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Table of contents

1. Dentistry as a science. Anatomy of the maxillofacial region (Anatomical structure of the maxillofacial region)
2. Diseases of the teeth
3. Equipment and equipment of the dental office
4. Anomalies of the dentoalveolar system (Anomalies of individual teeth. Anomalies of the dentition. Anomalies of the bite)
5. Increased tooth wear
6. Periodontitis)
7. Chronic focal infection of the oral cavity. Diseases of the oral mucosa (Diseases of the oral mucosa. Changes that occur on the oral mucosa in various diseases)
8. Mechanical trauma of the oral mucosa. Peculiarities of regeneration (Acute mechanical injury. Chronic mechanical injury (CMT). Chemical damage to the oral mucosa, types of anesthesia. Chronic chemical injury (CCT). Diagnosis of the state of the human body by language)
9. Periomandibular abscesses and phlegmon
10. Osteomyelitis of the jaws (Etiology, pathogenesis and pathological anatomy of osteomyelitis. Clinical picture and diagnosis of acute odontogenic osteomyelitis. Treatment)
11. Modern filling materials: classifications, requirements for permanent filling materials chemical curing (on the example of the microfilament composite "Degufil"). The method of using a light-curing composite material. The principles of biomimetic construction of teeth with restorative materials. The mechanism of adhesion of composites to enamel. Errors and complications in the use of composite materials, compomers, GRC)

LECTURE No. 1. Dentistry as a science. Anatomy of the maxillofacial region

Dentistry is a relatively young discipline in medicine: as a separate branch, it was formed only in the 20s of the XX century. Its name comes from two Greek roots "stoma" - mouth, hole and "logos" - teaching and literally means "science of the organs of the oral cavity." In the modern sense, dentistry is defined as a field of clinical medicine that deals with the study of diseases of the teeth, oral mucosa, jaws, face and part of the neck, and which develops methods for their diagnosis, treatment and prevention.

The prototype of modern dentistry in antiquity was dentistry, which at that time did not belong to traditional official medicine, and maxillofacial surgery, which was considered a branch of general surgery. The representatives of dentistry were mainly hairdressers and artisans, and sometimes simply self-taught. The first book on dentistry in Russia "Dentistry, or dental art about the treatment of diseases, with the application of children's hygiene" was written and published in 1829 by the head physician of the St. Petersburg Medical and Surgical Academy (today the St. Petersburg Military Medical Academy) Alexei Sobolev. But, despite this, the development of dentistry in Russia was very slow; the first dental school was founded only in 1881 by the works of N. V. Sklifosovsky, A. A. Limberg and N. N. Znamensky. The first society of dentists in Russia was organized in 1883.

In the late nineteenth - early twentieth centuries. dental care was mainly provided in private paid medical institutions, their services were available only to a small circle of the public, which also did not contribute to the rapid development of dentistry. Only after the First World War and then the October Revolution, with a change in the social way of life of the country, conditions appeared for the rapid development of the practical and scientific foundations of this area of ​​medicine. With the expansion and strengthening of the theoretical base and the accumulated experience, the prerequisites for the merging of dentistry and maxillofacial surgery into a single discipline appeared based on the similarity of pathological processes and approaches to treatment. A. A. Limberg, A. I. Evdokimov, G. A. Vasiliev, I. G. Lukomsky, A. E. Rauer, F. M. Khitrov, D. A. Entin, N. M. Mikhelson, M. V. Mukhin.

Later, with the development of a new discipline, independent sections were formed in it: therapeutic dentistry, surgical, pediatric and orthopedic.

1. Anatomical structure of the maxillofacial region

The oral cavity is represented by the following organs and anatomical formations: oral fissure, vestibule of the oral cavity, cheeks, lips, hard palate, soft palate, tongue, gums, teeth, upper and lower jaws.

The oral fissure is limited by the lips, which form the corners of the mouth on the sides. The thickness of the lips is represented by the circular muscle of the mouth and subcutaneous fat. The thickness of the cheeks is made up of adipose tissue (Bish's lump) and bundles of the buccal muscle. On the inner surface of the cheeks in the projection of the crown of the upper second large molar, there is a papillary eminence of the mucous membrane, on the top of which or under it in the vestibule of the oral cavity, the excretory duct of the parotid salivary gland opens. The vestibule of the oral cavity is formed in front - by the oral fissure (or closed lips) and the cheeks on the sides, behind - by the upper and lower gums and teeth. Gums - the alveolar processes of the upper jaws and the alveolar part of the lower jaw, covered with a mucous membrane, they cover the teeth in the cervical region. Paired parotid, sublingual and submandibular, as well as many small glands of the oral mucosa secrete saliva (up to 1,5 liters per day). Thanks to it, the mucous membrane and enamel of the teeth are constantly moistened. Saliva contains organic and inorganic substances, it contains about 18 amino acids, 50 enzymes, mucin, substances with antibacterial activity (leukins, opsonins, lysozyme). Saliva promotes the maturation of enamel, remineralization, has a cleansing effect, antibacterial activity and at the same time favors the formation of plaque and tartar, is a medium for the growth and reproduction of microorganisms. The hard palate is formed by the palatine processes of the upper jaws, which are perpendicular to the processes of the palatine bones. The soft palate is represented by muscle fibers covered with a mucous membrane with a large number of mucous glands; arches depart from it on the sides - palatoglossal and palatopharyngeal, between which there are accumulations of lymphoid tissue (palatine tonsil). The tongue is a muscular organ covered with a mucous membrane. In its structure, a root, a wider back, a body, a middle part and an apex are distinguished. In the rough mucous membrane of the tongue, four types of papillae containing taste buds are distinguished: filiform, leaf-shaped, mushroom-shaped, rough.

The upper jaw is a paired immovable bone. In its structure, the body, the palatine process, which takes part in the formation of the hard palate, the frontal process, which participates in the formation of the orbit, the zygomatic process (connects to the zygomatic bone), the alveolar process, which carries the holes of the teeth - alveoli, are distinguished. In the body of the upper jaw there is a cavity called the maxillary sinus, which contains air and is lined from the inside with a mucous membrane. In the immediate vicinity of it are the tops of the roots of large molars (especially the sixth), which creates conditions for the transition of the inflammatory process from the tooth and nearby tissues to the sinus and the development of sinusitis. The lower jaw is an unpaired movable bone that has the shape of a horseshoe. In its structure, a body is isolated, containing dental alveoli on the upper edge, two branches ending in the condylar and coronoid processes; the condylar process, connecting with the articular fossa of the temporal bone, participates in the formation of the temporomandibular joint, due to which movement in the lower jaw is carried out.

The laying of the dentition occurs in humans at the 6-7th week of intrauterine development from the ectodermal and mesodermal sheets. At the age of 6-7 months, the eruption of temporary, or milk, teeth begins, which ends by 2,5-3 years. The anatomical formula of the teeth of the temporary occlusion looks like: 212, i.e., on each side of the upper and lower jaws there are two incisors, one canine and two molars; the total number of temporary teeth is 20. At the same time, there is an active growth and development of the alveolar processes of the jaws. Teething is a complex and not yet fully understood process, regulated by neurohumoral factors of the body and largely influenced by environmental factors. At the age of 5-6 years, the teething of the permanent bite, or molars, begins, which completely replace the dairy ones by the age of 12-13; however, this process is completed only by the age of 22-24 with the appearance of the third large molars ("wisdom teeth"), and sometimes later. There are 32 teeth in the permanent bite, their anatomical formula is: 2123, i.e. two incisors, a canine, two premolars and three molars on each side of the upper and lower jaws.

In the structure of temporary and permanent teeth, the following formations are distinguished:

1) crown - part of the tooth protruding above the gingival margin into the oral cavity. In turn, a tooth cavity is isolated in the crown, which, when narrowed, passes into the root canal of the tooth, the pulp is a loose tissue that fills the tooth cavity and contains a large number of vessels and nerves;

2) neck - part of the tooth that separates its root from the crown and is located under the gingival margin;

3) root - part of the tooth, immersed in the alveolus of the jaw, in it passes the canal of the root of the tooth, ending with a hole; the main purpose of the root is to tightly fix the tooth in the alveolus with the help of a powerful ligamentous apparatus, represented by strong connective tissue fibers that connect the neck and root with a plate of compact bone substance of the alveolus. The bundles of these fibers, together with the gum and periosteum, form the circular ligament of the tooth.

The ligamentous apparatus of the tooth, together with the blood and lymph vessels supplying it, the nerves, is called the periodontium. It provides a tight fixation of the tooth, and due to loose fiber and interstitial fluid between the fibers, it also provides cushioning.

In the histological structure of the tooth, the following layers are distinguished:

1) enamel - the hardest tissue of the human body, close in strength to diamond, it covers the crown and neck of the tooth, its thickest layer is located above the tubercles of the tooth crown, towards the cervical region its thickness decreases. The strength of enamel is due to the high degree of its mineralization: 97% of it is represented by inorganic substances, most of which are hydroxylapatite crystals, 1% of the mass is accounted for by crystallization water, which forms the internal hydration shell of crystals. In its structure, enamel is represented by enamel prisms and interprism substance ("enamel lymph");

2) dentin - the second strongest tissue, which makes up the bulk of tooth tissues, consisting of collagen fibers and a large amount of mineral salts (70% of the mass of dentin is lime phosphate); in the outer layer of the main substance of dentin, collagen fibers are arranged radially (this layer is also called mantle), and in the inner (near-pulp) - tangentially.

In the peripulpal dentin, in turn, predentin is isolated - the most deeply located layer of constant growth of the dentin layer. In its structure, dentin is similar to coarse fibrous tissue, the main substance of which is penetrated by a huge amount (50-120 thousand per 1 mm²) of the thinnest (1-5 microns in diameter) dentinal tubules or tubules;

3) cement covers the root of the tooth, is similar in structure to bone tissue, contains collagen fibers and a large number of inorganic compounds. It is divided into primary (cell-free), adjacent directly to the dentin and covering the lateral surfaces of the tooth root, and secondary (cellular), containing cementocytes and covering the primary layer. Secondary cement is found only on the inter-root surfaces of molars and premolars, as well as on the apex of the tooth root. Cement - the place of attachment of the ligamentous apparatus to the tooth;

4) the pulp is represented by loose fibrous connective tissue with a large number of nerves and blood vessels, which are branches of the corresponding arteries and nerves of the jaws, as well as lymphatic vessels. Nerves and arteries in the form of a neurovascular bundle penetrate into the tooth cavity through the opening of the root canal. The pulp performs various functions: trophic, regenerative (due to the supply of cambial elements), manifested in the formation of new replacement dentin during the carious process, protective (it is a biological barrier to the penetration of microorganisms into the periodontium from the carious cavity through the root canal), sensitive (pulp receptors able to perceive various types of stimuli, including pain).

The high regenerative abilities of the tissues of the maxillofacial region are due to a rather abundant blood supply, mainly due to the external carotid artery, which branches into the lingual, facial, maxillary and superficial temporal. The venous outflow system is essentially the same as the arterial blood supply; blood from the maxillofacial region is ultimately collected by the facial vein, which merges with the mandibular and flows into the internal jugular.

The maxillofacial region is innervated by the following nerves:

1) trigeminal (V pair of cranial nerves), performing, in addition to sensory innervation, also motor (for masticatory muscles) and extending from the trigeminal node as part of three branches: ophthalmic, maxillary and mandibular nerves;

2) facial (VII pair of cranial nerves), which performs motor and autonomic (for the sublingual and submandibular salivary glands) regulation, in its course it gives off branches of the temporal, zygomatic, buccal, mandibular marginal and cervical.

The lymphatic network of the maxillofacial region is quite well developed and provides good lymph drainage. All lymph nodes of this zone are divided into lymph nodes of the face, submandibular region and neck. From the region of the tubercle of the upper jaw and the maxillary sinus, the lymph is directed to the deep cervical lymph nodes, which are usually not possible to palpate. On the way of outflow of lymph from the teeth, the first barrier is represented by the submandibular and submental nodes. From the tissues of the maxillofacial region, lymph through the lymphatic vessels of the neck enters the jugular lymphatic trunks.

The oral cavity, together with the dentition, performs various functions in the human body, such as:

1) mechanical processing of food. Thorough grinding, grinding, mixing and wetting prevents gross damage to the mucous membrane of the esophagus, contributes to the smooth passage of the food bolus through it;

2) chemical processing of food (the first stage of digestion, carried out due to the presence of the enzyme ptyalin in saliva, which breaks down many polysaccharides to disaccharides);

3) the function of sound production;

4) respiratory function;

5) sensitive (analyzer) function (perception of tactile, temperature, taste, physical and chemical stimuli by multiple receptors of the oral mucosa).

LECTURE No. 2. Diseases of the teeth

Dental diseases are the most common among all diseases. They are found in more than 95% of the world's population. These diseases include caries and its complications: pulpitis and periodontitis. Let's take a closer look at these nosologies.

The term "caries" from the Latin language is translated as "rotting". Initially, this term denoted a disease of the bone marrow substance, which was most often based on an inflammatory process. Later, D. A. Entin proposed to consider this tooth lesion as a carious disease, which subsequently became widespread and supported.

Currently, there are a huge number of theories of the occurrence of caries. One of them boils down to the fact that if oral hygiene is not observed, plaque appears, which is localized on the lateral surfaces of the teeth, fissures, in other words, in those places where it is not removed during chewing and is firmly associated with the surface of the teeth. The composition of plaque consists mainly of polysaccharides, mineral salts, which contribute to its compaction. In practical dentistry, such a formation is called "dental plaque", which, along with the above components, includes microorganisms, mainly represented by streptococci. Bacteria, in turn, produce lactic acid, which demineralizes the enamel and becomes the beginning of a carious process. It should be noted that the action of cariogenic bacteria in dental plaque manifests itself differently in different people. In some, resistance to caries is high, in others it is weak. Unfortunately, there are few people with high resistance, which explains such a widespread distribution of this disease. There is no doubt that the resistance of teeth to caries is associated with the body's natural defenses. It is noticed that in persons with a weakened resistance, soft plaque is more actively formed. According to another theory, it is believed that the frequency of occurrence of carious lesions is determined not only by the state of the body, but also by the properties and qualitative composition of saliva. In persons who are prone to caries, saliva is more viscous, the content of mineral salts in it is changed. In accordance with the latest data, dental caries occurs under the influence of local and general influences. To date, it has been proven that in the occurrence of caries, in addition to dental plaques, the presence of carbohydrates in saliva and the permeability of tooth enamel play a certain role.

Depending on the manifestations of the carious process, four forms of caries are distinguished.

Carious spot (macula cariosa) - a whitish spot, which is represented by an area of ​​enamel turbidity and weaker light refraction. There are no signs of enamel destruction. When probing this area, the enamel defect is not detected. The surface of this patch is smooth. In some cases, under unclear circumstances, the stain may disappear, which, in turn, indicates a significant role of the endogenous factor in the pathogenesis of teeth. However, the likely outcome of this stage is the transition to the next stage of superficial caries (caries superficialis). This stage is characterized by the appearance of roughness and pigmentation at the site of the chalky spot. In addition, it is possible to identify areas of softening of the enamel. This stage ends when the process extends to the entire thickness of the enamel. Medium caries (caries media) is characterized by the presence of a carious cavity, which is located in the dentin layer at a shallow depth. The condition in which a carious cavity of considerable size is formed (its bottom is a thin layer of dentin that separates this cavity from the dental chamber) is called deep caries (caries profunda).

The clinical picture is very clear: the absence of spontaneous pain, episodic pain attacks, which is due to thermal and chemical factors. After elimination of these irritants, the pain disappears. The appearance of pain with mechanical pressure indicates deep caries.

The division of caries into several types is very conditional and has no significant clinical significance.

In the treatment of caries, it is first necessary to remove the affected areas of dentin and enamel by mechanical treatment with a bur and a drill. After that, the resulting cavity, which is larger than the original carious cavity, is filled with filling material. Treatment of superficial and medium caries is performed in one session, deep - in 2-3 sessions to avoid the possibility of developing pulpitis. A patient with deep caries at the first visit is given a temporary filling, which is replaced with a permanent one after the control period of 7-10 days.

For the prevention of caries, it is necessary to carry out a planned sanitation of the oral cavity. Every person needs to visit the dentist about once every six months. Planned rehabilitation is also indicated for patients with chronic diseases. Such diseases include rheumatic heart disease, nephritis, etc.

Planned sanitation of the oral cavity is of great prophylactic importance in the prevention of diseases of the gastrointestinal tract. Of particular importance is the planned rehabilitation of workers in the chemical industry, who constantly deal with acids that can destroy enamel and dentin as a result of the dissolution of phosphorus, calcium, and fluorine salts. The basis of preventive measures should be individual precautions, which consist of periodic rinsing of the mouth with 1-3% sodium bicarbonate solution, in addition, it is necessary to improve production conditions.

As the carious process spreads to deeper layers of dentin, there comes a time when a thin layer of infected dentin remains between the bottom of the carious cavity and the cavity of the tooth. The ability of microorganisms to penetrate through the dentinal tubules into the layers of dentin that have not yet been destroyed causes infection of the pulp long before the first signs of communication between the carious cavity and the tooth cavity appear. According to the clinical course, the following types of pulpitis are distinguished: acute and chronic.

There is a direct relationship between the severity of the development of inflammation of the dental pulp and the virulence of microorganisms. In acute pulpitis, exudate compresses the nerve endings, which, in turn, leads to pain. In this case, the inflammatory process becomes irreversible due to a sharp violation of the pulp trophism.

The clinic is characterized by the appearance of acute spontaneous and paroxysmal pain. Often, patients cannot accurately indicate the location of the tooth, since the pain is diffuse in nature due to its irradiation along the branches of the trigeminal nerve. The paroxysmal pain is determined by the blood filling of the vessels, which, in turn, explains the appearance of night pains (increased influence of the vagus nerve).

It is not easy to identify the affected tooth, as noted above. In such cases, the doctor resorts to a little trick. Alternate irrigation of carious cavities with a thin jet of water gives its results in the form of pain in the affected tooth. The reaction with this type of irritation can be twofold: on the one hand, the pain can intensify and continue for a certain time after the cessation of irritation, on the other hand, it can subside and reappear after some time. In the clinic, several types of pulpitis are distinguished: acute serous-purulent focal and acute purulent diffuse pulpitis. In the case of serous-purulent pulpitis, the pain is aggravated by cold water, and with purulent it temporarily subsides. Thanks to pyogenic bacteria, the serous inflammatory process quickly progresses to a purulent one, which ultimately leads to pulp gangrene. In turn, purulent pulpitis is accompanied by increased pain.

In the treatment of pulpitis, analgesics are used to relieve pain, but this measure is not always effective. In the event of such a situation, each medical worker should have the following skill in providing emergency care. First of all, it is necessary to identify the affected tooth with a small curettage spoon (excavator), then free the carious cavity as much as possible in this situation. On 1-2 drops of 3% carbolic acid, novocaine powder is kneaded to a mushy state. Then a small amount of this mass is placed in the freed cavity. To prevent washing out of the anesthetic, this cavity is closed with a cotton ball. Carbolic acid is a strong fat solvent, so it penetrates well into the pulp. The analgesic effect is achieved by the cauterizing action of carbolic acid. The analgesic effect lasts approximately 1-2 days.

This disease proceeds much more slowly than acute pulpitis. It may be accompanied by intermittent aching pains. In some situations, any pathological sensations may be absent, which is explained from the pathological and anatomical point of view. The dead tissue is replaced by granulations. Sometimes these granulations can protrude into the cavity of the tooth - a tooth polyp.

Treatment consists in eliminating the inflammatory process and preventing its spread, pain relief. The classic method of treatment is the use of arsenic paste, which is applied to the bottom of the carious cavity. Arsenic is a protoplasmic poison that causes necrosis and mummification of the pulp and its elements. At the same time, pain sensations disappear within 3-5 hours after applying the paste. Pulp devitation begins to produce after 24-48 hours, which consists in the mechanical removal of the pulp. It is necessary to avoid leaving the paste for more than 48 hours, as this can lead to complications in the form of a necrotic process in the dental alveolus, and can also cause acute gastritis if the paste has been swallowed. For those patients who could not come to the dentist on the appointed day and hour, the paste should be removed by any medical worker.

After mechanical amputation of the pulp, the next stage is started, which consists in drug treatment, followed by filling the root canal with liquid cement, and the tooth cavity is filled with filling material. It should be added that the treatment of pulpitis can be carried out with the help of a local anesthetic, which greatly simplifies the procedure, since arsenic paste is not used in this case.

The death of the pulp significantly reduces the activity of the enamel and tissue resistance, which, in turn, can cause the spread of infection, the emergence of a new focus of carious lesions, or cause early tooth loss due to the fragility of the enamel.

Microorganisms can cause inflammation in the periodontium - the ligamentous apparatus of the tooth, and are also able to penetrate there in different ways, including hematogenous.

Allocate acute serous periodontitis and acute purulent periodontitis. In the first case, the clinic will be characterized by aching pains with a clear localization, a feeling of elongation of the affected tooth. In acute purulent periodontitis, local and general changes will be observed. The pain intensifies, takes on a pulsating character with rare light intervals.

Often there is irradiation of pain along the branches of the trigeminal nerve. Even a light touch can cause severe pain. The tooth becomes mobile as a result of melting of the ligamentous apparatus. Soft tissue edema and gingival hyperemia in the area of ​​the affected tooth are visualized.

During treatment, it is first necessary to ensure the outflow of exudate by creating drainage through the carious cavity. To do this, the gangrenous pulp is removed with an extractor.

As a rule, it proceeds in an asymptomatic form. There are the following types: fibrous, granulating, granulomatous chronic periodontitis. With fibrous periodontitis, there is practically no pain, the pulp is replaced by coarse fibrous connective tissue. Downstream, this type of periodontitis is sluggish. On the radiograph, it looks like a narrow uniform strip, limited by the contours of the tooth root and the line of the plate of the compact substance of the alveolus. In this case, deformation in the form of periodontal thickening is observed at the top of the tooth root. With granulating periodontitis, granulation tissue is formed in the periodontium. There is a destruction of the cortical plate in the alveolus. In contrast to fibrous periodontitis, in this case, the plate of the compact bone substance of the alveolus is destroyed. This form of periodontitis is the most active, since, in addition, it is accompanied by destruction of the periodontal gap and infiltrative growth of granulations. In some cases, fistulas can form, which can break through to the skin of the face in the perimaxillary region. When examined by a dentist, hyperemia and swelling are found at the root of the diseased tooth, and the presence of a fistulous passage facilitates the correct diagnosis. The radiological picture is usually characterized by the presence of a significant deformation of the peridontal gap. With granulomatous periodontitis, a connective tissue membrane is formed in the form of a sac attached to the top of the tooth root. This formation is called a granuloma. Due to the constant increase in the size of the granuloma, there is an increase in pressure on the surrounding tissue, which, in turn, leads to the melting and displacement of the bone elements of the alveoli. It should be noted that, despite the slow growth and the almost complete absence of symptoms, this type of periodontitis is no less dangerous than the others, as it can lead to the destruction of bone tissue (spontaneous fracture of the lower jaw).

The only possible treatment option for this pathology is a surgical intervention, which is aimed at removing pathological tissue from the peridental focus of inflammation and preventing the penetration of microorganisms through the root canal. The operation of choice is resection of the apex of the tooth root.

The following complications are distinguished: local and general. Common complications include the phenomena of intoxication as a result of the absorption of waste products of microorganisms from the focus of inflammation. Dissemination of bacteria to various organs, which, in turn, can lead to secondary diseases. Local complications include such as fistulous tracts and cysts. Let us consider in more detail several nosological units.

Odontogenic fistulas. They are formed as a result of the penetration of granulation tissue into the thickness of the alveolar process, under the periosteum, and then under the mucosa. As a result, a fistulous passage is formed at the level of the projection of the apex of the tooth root. In some cases, the granulation cord, bypassing the mucous membrane of the alveolar process above the arch of the vestibule of the mouth, can penetrate into the thickness of the soft tissues, thereby forming an accumulation of granulation tissue directly under the skin. In some cases, purulent fusion of the skin occurs with the formation of a fistulous tract, which, in addition to constant purulent discharge, creates a cosmetic defect and causes psychological discomfort to the patient.

To confirm the diagnosis of chronic periodontitis, it is necessary to conduct a thorough diagnosis with the maximum detail of diagnostic techniques. One of the main methods is radiography of the diseased tooth, as well as palpation determination of the granulation cord extending from the alveolar process into the soft tissues.

Treatment is aimed at sanitation of the source of infection (diseased tooth). At the same time, in some cases, the fistulous course is tightened on its own, otherwise curettage of granulations is performed.

If the diseased tooth is not amenable to conservative treatment, resection of the apex of the tooth root or replantation is performed. In order to avoid recurrence of the fistula, the granulation cord is transected, for which a 2-3 cm long incision is made, then the compact plate of the alveolar process and the exit site of the granulation cord from the bone are exposed. This cord is crossed, then the wound is plugged with gauze with iodoform for 3-4 days.

These are formations of a tumor-like form that occur as a result of an inflammatory process in the periodontium of the tooth. This disease is a consequence of a chronic inflammatory process, which involves the remains of the embryonic epithelium, which, in turn, forms the inner layer of the cyst membrane.

The clinic of this disease has an erased character, so the absence of pain can often lead to the destruction of the jaw, as in the previous case. Diagnosis of this disease, as in the previous case, is based mainly on X-ray data. This type of cyst is visualized as a clearly defined rarefaction of the bone tissue of a round or oval shape. In addition, there are such generally accepted research methods as palpation, with which you can determine the protrusion of the lower jaw. In some cases, resort to the puncture of the cyst to exclude the tumor process.

Treatment is only surgical, in which partial excision of the cyst membrane or complete removal of the membrane is performed. Before proceeding with this operation, the issue of preserving the tooth that caused this pathological process, as well as the neighboring teeth, the roots of which may be involved in the pathological process, is resolved. In cases where the tooth is stable, it is treated with canal treatment, cement filling and resection of the root apex.

LECTURE No. 3. Equipment and equipment of the dental office

In polyclinics and dental departments, it is desirable to allocate an initial examination room, a functional diagnostics room, an amalgam preparation room, a room for washing and sterilizing instruments, and a physiotherapy service room.

To organize one workplace in the dental office, if possible, a spacious room with good natural light should be allocated: its area should be about 15 m² (approximately 4,4 x 3,5 m). The height of the ceilings in the office should be at least 3,3 m. If it is planned to organize several workplaces in one room, then at least 7 m² of space must be added for each additional chair. If possible, the chairs should be placed in one row, opposite the windows, in order to ensure the highest level of natural illumination of the patient's oral cavity and free flow of fresh air to the workplace. In addition, the office should be equipped with supply and exhaust ventilation and sources of artificial lighting. It is preferable to paint the walls of the room with oil paints or nitro paints in soothing tones (for example, light blue or salad). It is important that the floor is flat, without gaps and recesses, covered with linoleum with a transition to the walls by 8-10 cm - this will ensure the overlap of the corner gaps between the floor and walls at the baseboards and thereby create the necessary hygiene requirements and the ability to work with amalgam.

You should also provide for a fume hood and a sealed vessel where mercury is stored, silver amalgam fillings are prepared, and instruments are sterilized: these precautions will help maintain an optimal microclimate in the office room.

It is very important to strive to use the premises of the dental office as rationally as possible: the room should not be cluttered with unnecessary items, the placement of furniture and equipment contributes to the fast, clear and fruitful work of the staff.

In daily activities, when providing qualified assistance, the dentist uses special equipment. It includes:

1) dental chair for the patient;

2) electric or turbine drill;

3) dental unit;

4) a chair for a doctor.

The dental chair is designed for comfortable positioning of the patient, fixing him in a sitting or lying position, facilitating the doctor's access to the surgical field, eliminating discomfort and tension of the patient, which, in turn, creates favorable conditions for manipulations in the oral cavity. The design and engineering solutions of dental chairs are being improved every year, old models are being replaced by new, more comfortable ones. However, they all have a number of similarities. The dental chair KZ-2 (one of the first models) is equipped with a massive metal base, it has a lift (oil tank and pump), thanks to which it is possible to move the seat to a height of 520 to 720 mm from the floor level. With the help of special screws, its back can be fixed at different heights and depths or tilted back up to a horizontal position, there are also a number of levers that provide it with an inclined position and the ability to move around a vertical axis. The remaining models of dental chairs are distinguished by a more advanced system of lifting and moving in different planes, better finish.

With the help of a drill, a dentist performs the main event in the clinic of therapeutic dentistry, namely, the preparation of hard dental tissues using rotating burs. The forerunners of modern electric and pneumatic drills were foot-operated machines, which were extremely inconvenient to use. Improving the design of drills is aimed at increasing the number of revolutions during the rotation of the drill and reducing the size of the installation itself. Electric drill with illuminator BEO-30-2 is a complex installation, it includes:

1) an electric drill with a rotation speed of 1000 to 30 thousand revolutions per minute;

2) a lamp that provides illumination of the surgical field, about 4000 lux at a distance of 1 m;

3) fan;

4) a saliva ejector system with a spittoon;

5) water supply system for boron cooling.

In the office, the drill is fixed permanently, it is supplied with electricity and water, it is connected to the general sewerage system.

The dental unit is designed to provide assistance in stationary conditions. Equipped with an electric motor, a lamp, a saliva ejector, a diathermocoagulator, an apparatus for electrodiagnostics, a water system unit, guns for water and air.

The chair for the dentist has a rotating seat, thanks to which you can change its height and turn freely, the back covers the doctor's lower back, preventing fatigue and the development of some occupational diseases.

Apparatus for electro-odontodiagnostics has become widespread in the practice of dentists; with their help, according to the study of the electrical excitability of tooth pain receptors, it seems possible to assess the state of the pulp and periapical tissues under normal conditions and under various pathological conditions.

In the clinical practice of examination, treatment of teeth and oral mucosa, the dentist uses a special set of tools. The main ones are:

1) dental mirror. With its help, areas of the oral cavity that are inaccessible to direct vision are examined, cheeks, tongue, lips are fixed, and they are also protected from injury while working with sharp instruments. Dental mirrors are of two types - flat, giving a true reflection of the object in question, and concave, increasing it. So that the mirror does not fog up during operation, it is suggested to wipe it with a mixture of alcohol and glycerin or lightly rub it along the inner surface of the patient's cheek;

2) dental probe. Depending on the shape, it can be angular or straight, sharp or blunt. A pointed probe is used to detect carious cavities, determine soreness and softening of dental tissues, communicate the tooth cavity with a carious cavity; using a blunt probe, the depths of periodontal pockets, the degree of exposure of the tooth root are detected and measured;

3) dental tweezers, used to hold and transfer cotton swabs into the oral cavity to isolate the tooth from saliva, drug treatment of carious cavities, study the degree of tooth mobility, hold and transfer small instruments;

4) trowels. With the help of a trowel (straight or curved spatulas), medicinal substances, filling material are introduced into the carious cavity of the tooth, and a filling is formed;

5) dental hooks, having the form of a straight or curved spatula with pointed ribs, they serve to remove dental deposits;

6) an excavator, which is a handle with sharp spoons on both sides, it is used to remove food debris, temporary fillings and softened dentine residues from carious cavities, supragingival and subgingival dental deposits.

Sterilization of dental instruments is carried out by the dry-air method (in a drying cabinet) or in special chambers at a temperature of 120 ° C and an exposure time of 30-40 minutes; at a temperature of 180 ° C, the exposure time is reduced to 20 minutes. However, dental mirrors, plastic products, as well as sharp and cutting instruments become unusable under the action of dry heat and boiling, so it is advisable to subject them to chemical (cold) sterilization. To do this, they are placed in an enameled or plastic container with an antiseptic liquid for 40-45 minutes, tightly closed with a lid. Before sterilization, objects are cleaned with a 0,5% hydrogen peroxide solution. It is possible to use a triple solution consisting of sodium bicarbonate - 15 g, formalin - 20 g, phenol - 3 g per 1000 ml of distilled water. For chemical sterilization, it is permissible to use a 1% solution of chloramine, a 1% solution of chlorhexidine, a 3% solution of formalin, a 6% solution of hydrogen peroxide, a 10% solution of dimexide and other compositions.

LECTURE No. 4. Anomalies of the dentoalveolar system

Anomalies of the dentoalveolar system are mainly a congenital pathology, therefore, it manifests itself at an early age. All violations can be divided into several groups:

1) anomalies of individual teeth (violations may relate to the shape of the teeth, their size, position in the oral cavity, number);

2) incorrect construction of dentition;

3) malocclusion.

1. Anomalies of individual teeth

Giant teeth are teeth with very large, incongruous crowns. This pathology occurs most often with permanent occlusion and somewhat less frequently with milk. Usually, the incisors of the upper or lower jaw are affected, but other teeth can also be affected. This anomaly of the shape of the teeth occurs more often when the developmental processes are disturbed, leading to the fusion of the rudiments of the teeth, as a result of a violation of the endocrine system and changes in the hormonal background. Giant teeth, in turn, can affect neighboring teeth - cause their anomalies, prevent the eruption of other teeth, and lead to crowding of teeth. They can also be located outside the dentition. The main disadvantage of giant teeth is a cosmetic defect on the face: their unusual appearance, which attracts the attention of others. The treatment for this defect consists in the removal of giant or adjacent teeth. In the event that after the removal of these teeth and correcting the position of the rest, gaps remain between the teeth, they resort to prosthetics and close the corresponding defects.

Often there is a directly opposite anomaly of size - small teeth. These are teeth that have the correct shape, but disproportionately small crowns. Such a defect is mainly found in permanent occlusion, most often the incisors are affected, especially the upper and lateral ones. The reasons for the development of this anomaly are unknown: it is assumed that such a discrepancy between the size of the teeth and jaws may be based on a hereditary predisposition, i.e. when a child "inherits" small teeth from one of the parents and a large jaw from the other. Small teeth, as a rule, are separated by large gaps and distort the harmony of the face with their appearance. To correct this defect, such teeth are covered with plastic crowns or removed with subsequent prosthetics.

Vestibular deviation is the displacement of the teeth outward from the dentition, such a deviation may affect one or even several teeth of the upper or lower jaw. Most often, this anomaly affects the incisors. The reasons for such violations can be a slowdown in the change of milk teeth by molars, a lack of free space in the dentition, bad habits, an incorrect position of the tooth germ, a violation of nasal breathing, and the presence of supernumerary teeth. In the treatment of this pathology, the teeth that are located vestibularly are moved in the palatal direction, they are given the correct position and fixed for a while to preserve it.

With a high or low arrangement of teeth, they are shifted in the vertical direction. In the upper jaw, supraocclusion is a high position of the tooth, while its tip does not reach the plane in which the dentitions close; infraocclusion - low position of the tooth. Sometimes there is a combination of supra- and infraocclusion of a group of teeth. The cause of such a defect may be the underdevelopment of the alveolar process or the presence of any mechanical obstacle that interferes with the normal growth of the teeth. Treatment: the tooth and the area of ​​the alveolar process adjacent to it are subjected to traction, for this purpose traction devices are used.

Mesiodistal displacement of teeth is understood as their incorrect location in front of the normal position in the dental arch or behind. The anterior and posterior teeth can be displaced equally. The most likely causes are the incorrect position of the tooth germ, adentia, early loss of milk and permanent teeth adjacent to the displaced tooth, and bad habits. The main principle of treatment is the movement, restoration and fixation of teeth in the correct position, which is achieved by using removable and non-removable orthodontic appliances.

Oral tilt - an incorrect position of the teeth, in which there is a displacement of the teeth inward from the dental arch, in the palatal direction or towards the tongue. Usually, when tilted, the root of the tooth is located in the alveolar process, and only its crown is deviated to the side, with corpus dystopia, the tooth is completely displaced outside the dentition. One or more teeth may be affected by this displacement. The reasons are: slowing down the change of milk teeth, incorrect position of the rudiments of permanent teeth, early removal of milk teeth, the presence of supernumerary teeth, shortening of the frenulum of the tongue, narrowing of the dentition, bad habits. An acceptable method of treatment is the separation of the bite and the movement of the teeth in the vestibular direction.

Diastema - a wide gap separating the central incisors, is observed mainly in the upper jaw. Various factors can contribute to the development of a diastema: adentia, low attachment of a powerful frenulum of the upper lip, the presence of supernumerary teeth, the presence of a wide dense bone septa between the central incisors, early loss of one of them, anomalies in the shape and size of the teeth, and incorrect location of the frontal teeth. Treatment can be only orthodontic or complex, including surgical intervention followed by hardware convergence of the incisors.

Rotation of the tooth - an incorrect position in which the tooth is in its normal place, but is rotated while causing cosmetic and functional defects. Most often, the incisors of the upper and lower jaws are subjected to deformation. This type of anomaly causes cosmetic and functional defects. Rotated teeth are often a traumatic factor for the teeth of the opposite jaw and can loosen them. They predispose to turning a lack of space in the dentition due to its narrowing or underdevelopment of the alveolar process, a slowdown in the change of temporary teeth by permanent ones, a lack of space in the dentition due to supernumerary teeth, or the presence of so-called impacted teeth. Treatment for this disorder consists in turning the tooth in the right direction, giving it the correct position and further fixing.

Transposition of teeth - a rearrangement of teeth in the dentition. The reason is the incorrect laying of the rudiments of the teeth.

Crowded position of teeth. With this anomaly, the teeth are located very closely, while they stand in a position rotated along the axis and overlap each other due to lack of space in the dentition. Such a defect often occurs with underdevelopment of the alveolar process or the basal part of the jaw, and the relatively large size of the dental crowns can also be the cause, which prevents them from being placed and growing in the correct position. The treatment is proper placement of the teeth.

Trema - the gaps between the teeth. There are physiological and pathological tremas. Physiological arise as a result of the growth of the jaws and relate to the features of the milk bite. Pathological tremas are observed after the replacement of milk teeth with molars with concomitant bite pathology, with anomalies in the location of the teeth, adentia, anomalies in the shape and size of the teeth, displacement of the teeth.

Ugly teeth - teeth that have a diverse, irregular shape, more often this defect is observed on the upper jaw in its frontal area. The etiology of the disease is not clear, a possible factor is a violation of the development of the jaws and tooth germs. The treatment is to correct the shape of the malformed tooth through prosthetics or to remove it.

Spike teeth are teeth that have crowns that are pointed in the shape of a spike. These can be the lateral teeth of both jaws, the central and lateral incisors also often suffer. The reasons for this deformation are not completely clear; consider that a possible cause may be a violation of the development of tooth germs. Treatment of such defects consists in prosthetics; often spiked teeth are removed and subsequently replaced with various prostheses, which can be both removable and fixed.

One of the most common examples of these anomalies is adentia - the congenital absence of teeth and their rudiments. There are two forms of adentia: partial and complete. The most likely causes are defects in the development of the outer (ectodermal) germ layer (subsequently, a tooth germ is formed from it), changes in the hormonal background, heredity plays a certain role. Treatment - prosthetics, which may be preceded by a course of orthodontic treatment.

Supernumerary teeth are excess teeth in number. They are located most often in the region of the anterior teeth and are often spike-shaped, but may resemble adjacent teeth. The etiology of the appearance of extra teeth is not completely clear, but it is assumed that the cause is the improper development of the epithelial dental plate, which gives rise to too many tooth germs. In determining the treatment tactics, the location of the extra tooth and its effect on the position of complete teeth are taken into account. In case of displacement of adjacent teeth, supernumerary teeth are removed and appropriate orthodontic treatment is carried out. However, it is also possible to save a supernumerary tooth if it is located in the arch and does not adversely affect the adjacent teeth, while the shape of the crown can be corrected by prosthetics.

2. Anomalies of the dentition

This violation is caused by narrowing of the alveolar processes of the jaws or expansion in various places and is expressed by crowding of teeth, vestibular or oral teething, partial adentia, their rotation along the axis, the presence of supernumerary teeth, diastemas. There are many forms of narrowed dentition, here are the most common:

1) acute-angled shape. With it, the dentition evenly narrows in the area of ​​the canines;

2) common form. All teeth (front and side) are closely spaced;

3) saddle shape. The dentition narrows in the region of the premolars;

4) V-shape. There is a narrowing in the lateral sections, and the anterior section acts as an acute angle;

5) trapezoidal shape. The row is narrowed and the frontal section is flattened;

6) asymmetrical shape. The narrowing is more pronounced on one side of the dentition of any of the jaws, as a result of which the bite becomes cross.

The main causes of deformation of the dental arches are the underdevelopment of the jaws caused by diseases of early childhood. The basis of treatment is the expansion and contraction of the dental arches and the correct placement of the teeth.

3. Bite anomalies

Bite anomalies are deviations in the relationship between the dentition of the upper and lower jaws. The following deviations are distinguished.

Prognathia (distal bite) is a discrepancy between the dentition, characterized by protrusion of the upper teeth or distal displacement of the lower jaw. Prognathia can be partial or total. Etiology: congenital feature of the facial skeleton, childhood diseases that affect the development of the skeletal system.

Progenia (medial bite) is a discrepancy between the dentition due to the protrusion of the lower teeth or the medial displacement of the lower jaw. It can be partial or complete. The reasons may be a congenital feature of the structure of the facial skeleton, improper artificial feeding, etc. Treatment is achieved by correcting the oral inclination of the upper incisors.

These include the narrowing of the dentition, the discrepancy between the width of the upper and lower dentition. vertical deviations.

Deep bite - closing of the dentition, while the front teeth overlap with antagonists. There are two types of bite - vertical and horizontal. The reasons may be a congenital feature of the structure of the facial skeleton, early loss of painters. Treatment consists in uncoupling the bite, expanding the dentition on the lagging jaw.

Open bite - the presence of a gap between the teeth. This gap is more common in the region of the anterior teeth.

A crossbite is a reverse closure of the teeth of the right or left half of the bite. The main reasons are the delay in the change of milk teeth, improper eruption

these teeth. Treatment consists in the elimination of etiological factors.

The main malformation of the palate is its through cleft, unilateral or bilateral. In the first case, the nasal septum, the premaxillary bone are connected to the palatine plates only on one side. Surgical treatment - elongation of the soft palate.

LECTURE No. 5. Increased abrasion of teeth

This is a natural process of erasing the upper layer of the tooth throughout life, which is observed in the horizontal and vertical planes. Erasure in the horizontal plane is observed on the tubercles of the canines, along the cutting edge of the incisors, on the chewing surface of premolars and molars. The associated decrease in the height of the crowns of the teeth should be considered as an adaptive reaction of the organism. The fact is that with age, the vascular system and other periodontal and temporomandibular joint tissues change. By vertical abrasion is meant, in particular, the abrasion of the contact surfaces of the tooth, whereby the interproximal contact parts are converted into contact areas over time. Disappearance of contacts between the teeth usually does not occur due to the medial displacement of the teeth. It is known that with age there is a settling (retraction) of the gums and interdental papilla. This should have resulted in the formation of triangular spaces between the teeth. However, their occurrence is prevented by the appearance of the contact area. In some people, natural functional wear is slow or absent. This could be explained by the use of soft food, a deep bite that makes lateral movements of the lower jaw difficult, and weakness of the masticatory muscles.

However, there are patients who have a normal bite, and they eat a wide variety of foods, and the abrasion is so weakly expressed that with age, the tubercles of the molars and premolars remain almost unchanged. The reasons for this are unknown. Often such patients suffer from periodontitis.

In addition to natural, there is also increased abrasion. It is characterized by a rapid course and significant loss of enamel and dentin. Increased tooth wear occurs in 4% of people aged 25 to 30 years and in 35% - up to 40-50 years (V. A. Alekseev). Increased abrasion violates the anatomical shape of the teeth: the tubercles and cutting edges of the incisors disappear, while the height of the crowns decreases. With a direct bite, the cutting edges and the chewing surface of all teeth are abraded, and with a deep bite, the surfaces of the lower teeth are abraded. Increased abrasion, having arisen once, is steadily increasing. It deepens in places where the dentin is exposed, and lingers somewhat where the enamel is preserved. The formation of crater-shaped facets is explained by the unequal hardness of enamel and dentin. The latter is softer and therefore wears off faster. This leads to the conclusion that with the loss of enamel, abrasion increases.

There are three degrees of abrasion. At the first degree, the tubercles and cutting edges of the teeth are erased, the second degree is characterized by the erasure of the crown of the contact pads, at the third - to the gums. In this case, not only enamel and dentin, but also secondary (replacement) dentin are subjected to abrasion. In response to abrasion, a protective reaction develops from the side of the tooth pulp. It is expressed in the deposition of secondary dentin, which deforms the tooth cavity, and sometimes causes its complete infection. With degeneration of the pulp, the deposition of replacement dentin may not keep pace with the loss of tooth tissue. As a result, the death of pulp tissue may occur without perforation of its cavity.

Enamel abrasion may be accompanied by increased sensitivity to thermal and chemical irritants. With the preservation of the plastic properties of the pulp, hyperesthesia can quickly disappear, since a layer of dentin is formed. With increased abrasion, periapical foci of inflammation (granulating or granulomatous periodontitis, cysts) are sometimes found, while carious changes are not always observed. This may be due to the death of the pulp.

Increased abrasion of teeth is polyetiological. The causes of the pathological process may be the following.

1. Functional insufficiency of hard tissues of teeth, due to their morphological inferiority:

1) hereditary (Stenson-Capdepon syndrome);

2) congenital (a consequence of a violation of amelo- and dentinogenesis in diseases of the mother and child);

3) acquired (a consequence of neurodystrophic processes, dysfunctions of the circulatory system and endocrine apparatus, metabolic disorders of various etiologies.

2. Functional overload of teeth with:

1) partial loss of teeth (with a decrease in the number of antagonistic pairs of teeth, mixed function, etc.);

2) parafunctions (bruxism, foodless chewing, etc.);

3) hypertonicity of the masticatory muscles of central origin and hypertonicity associated with the profession (vibration, physical stress);

4) chronic trauma of the teeth (including bad habits).

Occupational hazards: acid and alkaline necrosis, dustiness, hydrochloric acid intake with achilles. Some of the reasons listed can cause generalized abrasion, and some can only cause local damage. For example, with congenital insufficiency of enamel and dentin, a generalized form of increased abrasion can be predicted, while with functional overload, only teeth that hold the interalveolar height are involved in the process.

Obviously, the term "increased abrasion" combines various conditions of the dental system, the causes of which often remain unclear, but the pathological and anatomical characteristic is common to all: the rapid loss of enamel and dentin substance of all, perhaps only part of the teeth.

Over time, when the causes and pathogenesis are explained, it will be possible to identify the types of increased abrasion by etiological grounds. Then the therapy of this disorder will be not only symptomatic, but also etiopathogenetically directed.

Increased abrasion captures various surfaces of the teeth: chewing, palatine, labial and cutting edges. According to the localization of the defect, three forms of increased abrasion are distinguished: vertical, horizontal and mixed. With a vertical form, increased abrasion in patients with normal overlap of the anterior teeth is observed on the palatal surface of the upper anterior and labial surfaces of the lower teeth of the same name. In the case of reverse overlap - the areas of abrasion are located the other way around - the front upper teeth are erased from the labial side, and the lower ones of the same name - from the lingual. The horizontal form is characterized by a decrease in hard tissues in the horizontal plane, as a result of which horizontal abrasion facets appear on the chewing or cutting surface. Horizontal increased abrasion most often captures both the upper and lower dentition. There are patients with intensely pronounced abrasion of tooth tissues, observed only in the upper jaw, with normal abrasion of teeth in the lower jaw. With a mixed form, abrasion can develop both in the vertical plane and in the horizontal.

The tendency to increased abrasion is limited and spilled. Limited or localized increased abrasion captures only individual teeth or groups of teeth, without spreading along the entire arch. Usually, the anterior teeth are affected, but premolars and molars can also be involved in the destructive process. With a generalized (diffuse) form, increased abrasion is noted throughout the entire dental arch.

Depending on the compensatory-adaptive reaction of the dentition, the increased abrasion of dental tissues is divided into the following clinical variants: uncompensated, compensated and subcompensated. These options are both with generalized erasure and with localized. Localized uncompensated increased abrasion is characterized by a decrease in the size of the crowns of individual teeth and the subsequent appearance of a gap between them (open bite). The interalveolar height and shape of the face are preserved due to the presence of intact teeth. Localized compensated abrasion causes shortening of the crowns of individual teeth, worn teeth, while in contact with antagonists due to hypertrophy of the alveolar part (vacant hypertrophy) in this zone, which leads to dentoalveolar elongation. The interalveolar height and face height remain unchanged. Generalized uncompensated increased abrasion of hard dental tissues inevitably leads to a decrease in the height of the crowns of the teeth, which is accompanied by a decrease in the interalveolar height and face height. The lower jaw approaches the upper, its distal displacement is possible. The facial skeleton in patients with this form of abrasion, according to X-ray cephalometric analysis (V. M. Shulkov), is characterized by:

1) a decrease in the vertical dimensions of all teeth, mainly due to the shortening of their crowns;

2) deformation of the occlusal surface;

3) a decrease in the depth of incisal overlap and sagittal inter-incisal distance;

4) decrease in interalveolar height;

5) dentoalveolar reduction in the region of the upper canines and first premolars;

6) reduction of the roots of the anterior teeth and premolars;

7) a decrease in the alveolar parts in the region of the upper anterior teeth, upper premolars;

8) changing the shape of the lower jaw by reducing its angle;

9) convergence of the jaws;

10) decrease in vertical facial dimensions and area of ​​the face;

11) reduction in the length of the dental arches;

12) an increase in the interocclusal space in the resting position of the lower jaw.

Generalized compensated increased abrasion of dental tissues is expressed in a reduction in the vertical dimensions of the crowns of all teeth, a decrease in the interalveolar height, and the height of the lower third of the face does not change. The decrease in crowns is compensated by the growth of the alveolar process. The facial skeleton in patients with this form of abrasion is characterized by:

1) a decrease in the vertical dimensions of all teeth;

2) the absence of changes in the position of the lower jaw and the preservation of the vertical dimensions of the face;

3) deformation of the occlusal surface and a decrease in the depth of the incisal overlap;

4) dentoalveolar elongation in the area of ​​all teeth;

5) decrease in interalveolar height;

6) shortening of the length of the dental arches;

7) an increase in the length of the base of the lower jaw;

8) a decrease in the length of the roots of the front teeth.

A generalized subcompensated form of increased tooth wear is a consequence of insufficiently pronounced dentoalveolar elongation, which does not fully compensate for the loss of hard tooth tissues, which contributes to a decrease in the vertical dimensions of the lower third of the face and the approach of the lower jaw. Increased abrasion can be combined with the loss of part of the teeth, pathology of the masticatory muscles and temporomandibular joints. The clinical picture becomes even more complex.

Orthopedic treatment for increased abrasion.

The following methods of examination of patients are distinguished:

1) a detailed study of the anamnesis of life and illness of the patient;

2) radiography of all teeth;

3) electroodontodiagnosis of all teeth;

4) study of diagnostic models of jaws;

5) radiography of the temporomandibular joints.

It is desirable to conduct an electromyographic examination of the masticatory muscles and an X-ray cephalometric analysis of the facial skeleton. Therapy for patients with increased tooth wear should include:

1) elimination of the cause (treatment of parafunctions, elimination of hypertonicity of masticatory muscles, exposure to solid food, etc.);

2) replacement of loss of hard tissues of teeth by orthopedic methods.

Prosthetics with increased abrasion of teeth provides for both therapeutic and prophylactic purposes. The former means improving the function of chewing and the appearance of the patient, the latter - preventing further erasure of hard tissues of the tooth and preventing diseases of the temporomandibular joints.

Goals and objectives, methods of orthopedic treatment of patients are determined by the form of increased abrasion (compensated, subcompensated, non-compensated), the degree of tooth wear, associated complications (distal displacement of the lower jaw, partial loss of teeth, dysfunction of the temporomandibular joint). The treatment of patients is:

1) restoration of the anatomical shape and size of the teeth;

2) restoration of the occlusal surface of the dentition;

3) restoration of interalveolar height and height of the lower third of the face;

4) normalization of the position of the lower jaw.

After defining the tasks, the means for their implementation are selected. These include various types of artificial crowns, inlays and removable dentures with occlusal linings.

When choosing therapeutic agents, one should take into account the degree of erasure, the condition of the periodontium and the requirements of aesthetics. Therapy of patients with generalized uncompensated abrasion in the early stages is prophylactic and consists of prosthetics with counter crowns or inlays. Crater-shaped cavities are filled with composite materials.

With increased abrasion of the II degree, prosthetics are carried out with artificial crowns (cermet, metal-plastic, porcelain) or removable dentures with cast occlusal platforms. Restoration of the shape of the tooth at the III degree of abrasion is carried out using stump crowns, since root canals with increased abrasion are often obliterated and the treatment of such teeth is difficult. In this case, the stump is fixed on parapulpal pins. The creation of channels in the tooth is carried out taking into account the safety zones and with the help of an intraoral parallelometer. Channels (in the amount of 3-4) should be parallel to the long axis of the tooth and located at an equal distance from the pulp and the root surface.

Restoring the occlusal surface of worn dentition is a difficult task, it is carried out by various methods. One of them is recording the movements of the lower jaw using a pantograph and further modeling of fixed prostheses or occlusal linings in an individual articulator.

The second method consists in the modeling of bridges and crowns on individual occlusal surfaces obtained using intraoral recording of the movement of the lower jaw on hard wax bite ridges. Wax occlusal rollers are applied to the upper and lower dentition along the width of the corresponding teeth 2 mm above the expected height of the crowns. Further, the required interalveolar height is determined and a prosthetic plane is built. The next step is the rubbing of the rollers with various movements made by the lower jaw. In the occluder, modeling and selection of artificial crowns are carried out first on the upper dentition along the lower plane, and then, according to the shape of the opposing teeth, the lower teeth are modeled in full compliance.

The third technique involves a two-stage orthopedic treatment. First, temporary plastic crowns and bridges are made according to the method described above; patients use them for a month. During this period, the formation of occlusal surfaces of temporary prostheses takes place. At the second stage, temporary prostheses are replaced by permanent ones. To do this, impressions are taken from temporary prostheses, models are cast, then they are crimped in a thermal vacuum apparatus using polystyrene. In the oral cavity, after the removal of temporary prostheses, impressions are obtained and collapsible models are created. Teeth prints in polystyrene are filled with melted wax and a template is applied to the model. After the wax has hardened, the polystyrene templates are removed and a wax impression of an individually shaped chewing surface remains on the model. The final modeling of frames of fixed prostheses and other stages are carried out according to the generally accepted method (I. I. Abdullov).

Restoration of the height of the lower third of the face and the position of the lower jaw in patients with uncompensated generalized increased abrasion is performed simultaneously or gradually. At the same time, the interalveolar height can be increased within 4-6 mm in the region of the lateral teeth in the absence of a disease of the temporomandibular joint and masticatory muscles. It is obligatory to maintain a free interocclusal distance of at least 2 mm. A decrease in the interalveolar height by more than 6 mm is dangerous for the masticatory muscles, periodontal teeth and the temporomandibular joint by the development of pathological changes and necessitates its gradual restoration on therapeutic bite prostheses. The change in the position of the lower jaw is carried out simultaneously by prosthetics or on a medical device with an inclined plane, followed by prosthetics. Simultaneous movement of the lower jaw is indicated for patients in whom erasure developed quickly, who developed the habit of holding it in an advanced position. Changing the position of the lower jaw should be carried out under the control of the x-ray machine. Treatment and restoration of the form from an anatomical point of view of the function of the teeth and the appearance of patients without changing the interalveolar height. The method of orthopedic treatment of patients is determined primarily by the degree of tooth wear. With grade I abrasion, the treatment is prophylactic and consists in creating a three-point contact on opposite crowns or inlays without changing the interalveolar height. With grade II wear, it becomes necessary to restore the anatomical shape of the teeth without a significant increase in the height of the lower third of the face, since the latter is not changed. Therefore, patients need special preparation, which consists in restructuring the alveolar part and changing the position of the relative functional rest of the lower jaw with the help of a therapeutic bite plate. To accelerate the processes of restructuring of the alveolar part, it is advisable to use corticotomy (compact osteotomy). After a place has been created for the prostheses, the restoration of the normal anatomical shape of the teeth is carried out with the help of fixed and removable structures. When erasing teeth of the XNUMXst degree, orthopedic treatment is carried out in several ways. In some patients, in order to carry out the restructuring of the alveolar parts, followed by prosthetics with stump crowns, special training is carried out. In other patients, a special preparation of the oral cavity is carried out: filling the roots of the teeth according to the Elbrecht method and prosthetics with removable dentures. In the third patients, special surgical preparation is carried out, which consists in the extraction of the roots of worn teeth and part of the alveolar ridge. Prosthetics in these patients is staged: immediate and remote. Treatment of patients with localized erasure is carried out according to the principles described above, and depends on the form of erasure. Partial loss of teeth can occur against the background of already developing increased abrasion. On the other hand, the loss of molars and premolars can lead to increased abrasion of the anterior teeth due to their mixed function. The clinical picture in this case is very complex, since the symptoms of partial loss of teeth are superimposed on increased abrasion. In this regard, the tasks of prosthetics are also expanding. To the tasks that are pursued in prosthetics for increased abrasion, the replacement of defects resulting from tooth loss is added. The designs of prostheses used in solving the latter problem are determined by a specific clinical picture. With included defects without changes in the configuration of the lower third of the face, it is possible to use fixed prostheses. With a decrease in the height of the lower part of the face, prosthetics provides, in addition to replacing defects, and increasing the interalveolar height on all remaining teeth. As a therapeutic agent, one-piece cast bridges can be used. With end defects, the use of various designs of removable dentures is shown.

LECTURE No. 6. Periodontitis

Periodontitis is the second most common disease encountered by dentists. Approximately 50% of people over 30 who seek dental care suffer from this disease to some extent. Periodontitis is a pathological process that involves the gums, periodontium, bone tissue, alveoli.

Many scientists have studied the causes of periodontitis, among them an important role belongs to domestic specialists. So, A. I. Evdokimov developed a theory according to which the cause of the development of pathology in the periodontium is a violation of its nutrition. Trophic changes, in turn, are the result of narrowing of the lumen of the supply vessels due to their sclerosis and neurovascular changes in the functional state of the central nervous system. According to the theory of A. I. Evdokimov, a violation of the blood supply and nutrition of the periodontium invariably leads to the development and progression of atrophy of the alveolar processes of the upper jaw, as well as the circular ligament and the entire ligamentous apparatus of the tooth. In contrast to his theory, other researchers consider the following reasons for the development of periodontitis:

1) the presence of any local irritant (for example, tartar), which constantly affects the gum, leading to the development of local inflammation, a decrease in tissue immunity, the addition of a bacterial component, the occurrence of chronic inflammation and a change in the state of blood vessels;

2) the presence in the oral cavity of specific microorganisms, such as amoeba, dental spirochete, which have a pathogenic effect on the soft tissues of the tooth and lead to the development of inflammation;

3) a change in the hormonal background and a lack of vitamins (primarily vitamin C), which entails a change in the sensitivity of blood vessels to neurohumoral impulses and, consequently, to a narrowing of their lumen and impaired blood supply and nutrition of periodontal tissues.

The clinical symptoms of periodontitis are varied. The main manifestations are symptomatic gingivitis (inflammation of the gums), the formation of pathological gum pockets, the release of pus from the alveoli, atrophy of the alveolar processes. The first sign signaling the occurrence of a pathological process in the periodontal tissues is discomfort, discomfort in the form of itching, burning and paresthesia in the region of the gum margin. Later, swelling and swelling of the gingival papillae joins these symptoms, cyanosis of the gums appears as a result of congestion. Often, patients complain of bad breath and bleeding gums. Metal crowns, prostheses, sharp edges of previously damaged teeth, tartar deposits often provoke an exacerbation of periodontitis and aggravate its course.

Atrophy of the alveolar process and changes in the shape of the gums lead to the formation of pathological gingival pockets, the depth of which is more than 2 mm. The presence of saliva, stuck food residues, epithelium exfoliating from the gums are a favorable condition for the development of microorganisms in these pockets and the formation of purulent fluid. If you press on the edge of the gum with a hard tool, you can see the discharge of pus from under it. The presence of a focus of chronic inflammation leads to the formation of granulation tissue and its replacement of the ligamentous apparatus of the tooth, the deposition of remnants of decayed tissues, inorganic substances, which exacerbates atrophic changes in bone tissue. Common signs of inflammation (a slight increase in temperature, headache, loss of appetite, lethargy) are also characteristic, due to the constant absorption into the bloodstream of the decay products and vital activity of microorganisms. In the clinical picture of periodontitis, destructive phenomena can prevail over inflammatory ones: in this case, cyanosis and pallor of the gums, a decrease in its volume and elasticity, slipping from the tooth, suppuration in this case is not typical, but the process invariably ends with atrophy of the alveolar process, destruction of the ligamentous apparatus tooth and its loss.

Due to the incompleteness of disputes about the etiology of periodontitis, it is difficult to clearly formulate a scheme of pathogenetic therapy. To establish the possible causes of a particular disease and prescribe a plan of therapeutic measures, it is advisable to invite other specialists (neuropathologist, endocrinologist) for consultation. We must not forget about the possible secondary development of periodontitis against the background of a pathological process already existing in the body. General treatment contributes to the normalization of metabolic processes in the body, replenishing the lack of vitamins (primarily vitamins C and P), increasing the reactive abilities of the body, protective and regenerative forces, stabilizing the neuropsychic state: aloe, vitreous, immunomodulators, antihistamines are used, autohemotherapy. Local treatment is designed to normalize the anatomical and physiological state of the periodontium. To do this, sanitation of the oral cavity is carried out, gum pockets are washed with hydrogen peroxide, various antiseptics, teeth with III degree of mobility are removed. Then curettage is performed to remove granulation tissue. In order to create favorable conditions for scarring of the wound surface, magnetic laser therapy and solcoseryl are used. Surgical treatment of periodontitis is carried out under local anesthesia, in order to expose the gingival pocket, the gingival mucosa is dissected and thrown back, granulations, deeply located remnants of tartar and vegetation of the epithelium are removed with a sharp spoon, bur or laser beam. To stimulate bone formation in damaged areas, gum pockets are filled with bone filings; transplantation of formalized homobone is possible. To stimulate local blood circulation in the area affected by periodontitis, V. I. Kulazhenko proposed the method of vacuum therapy: a special apparatus creates negative pressure in certain areas of the gums, leading to the destruction of capillaries, new, intact vessels are formed at the site of the formed hematoma, which greatly improves tissue trophism. In the complex therapy of periodontitis, it is advisable to prescribe physiotherapy: electrophoresis of vitamins, novocaine, gum massage (finger, hydromassage). To reduce the load on the affected teeth during the treatment period, it is possible to use special prostheses and orthopedic devices.

LECTURE № 7. Chronic focal infection of the oral cavity. Diseases of the oral mucosa

Chronic infection of the oral cavity has long been a subject of increased interest for physicians as a possible cause of many somatic diseases. For the first time, the idea that a tooth affected by an infectious process as a primary focus can cause secondary lesions of internal organs was expressed by the English scientist D. Genter at the end of the 1910th century. based on long-term clinical observations. A little later, in XNUMX, he was the first to propose the concepts of "focal infection of the oral cavity" and "oral sepsis". Following D. Genter, the American researcher I. Rosenow, in the course of numerous experiments, came to the conclusion that every depulped tooth inevitably becomes the cause of infection of the body. This conclusion led to an unjustified expansion of indications for the extraction of teeth with pulp damage. Domestic dentists have made a significant contribution to the development of ideas about chronic infection of the oral cavity. So, I. G. Lukomsky in his writings showed and then proved in practice that due to the prolonged course of chronic inflammation in the root zone, serious pathophysiological changes occur in its tissues, leading, in turn, to the accumulation of toxins and antigens that change the reactivity of the body and pervert immunological responses to many factors. To date, it is reliably known that all forms of chronic periodontitis and periodontitis with a diverse microflora, sometimes persisting for several years, are sources of chronic inflammation and sensitization of the body, invariably affecting many organs and systems.

Odontogenic sources of infection as chronic foci of intoxication are the cause of such diseases as nephritis, endocarditis, myocarditis, iridocyclitis, rheumatism. In this regard, a practicing physician of any specialty should never lose sight of the condition of the patient's oral cavity as a possible cause of the development of the disease or the aggravation of the condition and the occurrence of complications. The danger of these violations due to the need for thorough sanitation of the oral cavity. With the development of chronic periodontitis, various types of conservative treatment are recommended for practically healthy people, while for patients with existing somatic pathology, the affected tooth should be removed to prevent the spread of odontogenic infection throughout the body. Preventive measures to prevent the development of chronic foci of inflammation in the oral cavity are the planned sanitation of the oral cavity for the entire population, regular preventive examinations 2 times a year to identify new local foci of infection, the provision of qualified dental care to all patients who are under dispensary observation and undergoing treatment in general medical clinics.

1. Diseases of the oral mucosa

Lesions of the oral mucosa are, as a rule, local in nature and can be manifested by local and general signs (headaches, general weakness, fever, lack of appetite); in most cases, patients turn to the dentist with already pronounced general symptoms. Diseases of the oral mucosa can be primary or be symptoms and consequences of other pathological processes in the body (allergic manifestations, diseases of the blood and gastrointestinal tract, various vitamin deficiencies, hormonal disorders and metabolic disorders). All diseases of the oral mucosa of inflammatory etiology are called the term "stomatitis"; if only the mucous membrane of the lips is involved in the process, then they speak of cheilitis, of the tongue - of glossitis, of the gums - of gingivitis, of the palate - of palatinitis.

Despite a large number of publications and various studies of the etiology, pathogenesis and relationship of clinical manifestations of stomatitis, much in their development remains unexplored and unclear. One of the most determining factors in the occurrence of an inflammatory process in the oral mucosa is the presence of a systemic disease that reduces the overall resistance to the action of the bacterial flora; the risk of developing stomatitis increases with existing diseases of the stomach, intestines, liver, cardiovascular system, bone marrow and blood, endocrine glands. Thus, the state of the oral mucosa is often a reflection of the state of the whole organism, and its assessment is an important measure that allows one to suspect a particular disease in time and refer the patient to the appropriate specialist.

As in the case of the etiology of stomatitis, there is still no consensus on their classification. The most common classification proposed by A. I. Rybakov and supplemented by E. V. Borovsky, which is based on the etiological factor; according to this qualification are distinguished:

1) traumatic stomatitis (develops due to the action of a mechanical, chemical, physical stimulus on the mucous membrane);

2) symptomatic stomatitis (are manifestations of diseases of other organs and systems);

3) infectious stomatitis (these include pathological processes that develop with measles, diphtheria, scarlet fever, influenza, malaria, etc.);

4) specific stomatitis (lesions that occur with tuberculosis, syphilis, fungal infections, toxic, radiation, drug injuries).

Traumatic, symptomatic and infectious stomatitis can occur both acutely and chronically, depending on the causative agent, the state of the body and the therapeutic measures performed, while specific stomatitis occurs, as a rule, chronically in accordance with the characteristics of the course of diseases, secondary manifestations of which they are.

There is also a classification of stomatitis according to clinical manifestations: catarrhal, ulcerative and aphthous. This classification is more convenient for studying pathological changes and features of individual forms of stomatitis.

Catarrhal stomatitis is the most common lesion of the oral mucosa; develops mainly in case of non-compliance with hygiene measures, lack of oral care, which leads to the appearance of massive dental deposits and tooth decay. This type of stomatitis is often found in seriously ill patients, for whom it is difficult to perform the necessary hygiene measures. Causes can also be chronic gastritis, duodenitis, colitis, various helminthiases. Clinically, catarrhal stomatitis is manifested by severe hyperemia and swelling of the mucous membrane, its infiltration, the presence of white plaque on it, which then becomes brown; characterized by swelling and bleeding of the gingival papillae. Like most inflammatory diseases of the oral cavity, stomatitis is accompanied by the presence of bad breath, a large number of leukocytes is determined in a laboratory scraping from the mucous membrane. Treatment of catarrhal stomatitis should be etiotropic: it is necessary to remove deposits of tartar, smoothing the sharp edges of the teeth. To accelerate healing, the mucous membrane is treated with a 3% hydrogen peroxide solution, the oral cavity is rinsed several times a day with warm solutions of chamomile or calendula. Food must be mechanically, chemically and thermally gentle. Under these conditions of treatment, the phenomena of stomatitis quickly disappear.

The course of ulcerative stomatitis is more severe, the disease can develop independently or be the result of advanced catarrhal stomatitis (with untimely seeking medical help, improper treatment). Most often, ulcerative stomatitis occurs in patients with peptic ulcer of the stomach and duodenum or chronic enteritis during the period of exacerbation, it can also be observed in diseases of the blood system, some infectious diseases, poisoning with salts of heavy metals. With ulcerative stomatitis, unlike catarrhal, the pathological process affects not only the surface layer of the oral mucosa, but its entire thickness. In this case, necrotic ulcers are formed, penetrating deep into the underlying tissues; these areas of necrosis can merge with each other and form extensive necrotic surfaces. The transition of the necrotic process to the bone tissue of the jaws and the development of osteomyelitis are possible.

Clinical manifestations in ulcerative stomatitis are similar to those in catarrhal (bad breath, hyperemia and swelling of the mucosa), but are more pronounced, the appearance of general intoxication: headache, weakness, fever up to 37,5 ° C. Approximately 2- On the 3rd day of the disease, whitish or dirty-gray plaques form on separate parts of the oral mucosa, covering the ulcerated surface. Saliva acquires a viscous consistency, the smell from the mouth is putrid. Any irritation of the mucous membrane causes severe pain. The disease is accompanied by an increase and soreness of regional lymph nodes. In the general analysis of blood, leukocytosis and an increase in the level of ESR are observed.

Treatment should begin as soon as possible. Antiseptic and deodorizing agents are used locally for irrigation: 0,1% potassium permanganate solution, 3% hydrogen peroxide solution, furacillin solution (1: 5000), ethacridine lactate (rivanol), these drugs can be combined in various ways, but the presence hydrogen peroxide and potassium permanganate in any scheme is required. To eliminate pain, an aerosol of proposol, ointments and powders with anesthesin, intraoral baths with a 2-4% solution of novocaine are used. At the same time, measures are taken to eliminate the signs of general intoxication, vitamin therapy, food is prescribed sparing with a high energy value. If necessary, antibiotics, antihistamines, calcium chloride are also used. If the treatment is started on time and carried out correctly, then the ulcerative surfaces are epithelialized in 8-10 days, after which a thorough sanitation of the oral cavity is required.

This disease is characterized by the appearance of single or multiple aphthae on the oral mucosa. Most often, it affects people suffering from various allergies, rheumatism, diseases of the gastrointestinal tract, who have been attacked by a viral infection. The first symptoms of incipient aphthous stomatitis are general malaise, fever, apathy and depression, accompanied by pain in the mouth, a slight leukopenia and an increase in ESR to 45 mm / h are noted in the general blood test. Then, aphthae appear on the mucous membrane of the oral cavity - small (with lentil grain) foci of a round or oval shape, clearly delimited from healthy areas by a narrow red border, in the center they are covered with a grayish-yellow coating due to the deposition of fibrin. In their development, they go through four stages: prodromal, aphthous, ulcerative and healing stage. Aphthae can heal on their own, without a scar. In the treatment of aphthous stomatitis, rinsing the oral cavity with disinfectant solutions is locally prescribed, aphthae are treated with a 3% solution of methylene blue, sprinkled with a powder mixture consisting of nystatin, tetracycline and white clay. For anesthesia, a suspension of 10% anestezin in oil or an aerosol of proposol is used. General treatment involves the appointment of antibiotics (biomycin, tetracycline), antihistamines, anti-inflammatory drugs (acetylsalicylic acid, amidopyrine 500 mg 2-5 times a day). In some cases, it is possible to use glucocorticosteroids. The patient's diet is sparing. Sometimes (more often in patients suffering from chronic diseases of the large intestine) aphthous stomatitis can take a chronic course. In this case, acute manifestations of the pathological process may be absent, aphthae appear in small quantities, periods of exacerbation occur more often in spring and autumn and last about 7-10 days.

Chronic recurrent aphthous stomatitis is one of the most common diseases of the oral mucosa.

Chronic recurrent aphthous stomatitis (CRAS) is a chronic disease of the oral mucosa (OM), characterized by periodic remissions and exacerbations with a rash of aphthae. According to the literature, the disease is relatively common in people of both sexes older than 20 years and accounts for 5-30% of patients among other diseases of the oral mucosa.

The etiology and pathogenesis of CRAS have not yet been clearly elucidated. The earliest view on the cause of stomatitis should be considered the theory of mechanical stimulation of the oral mucosa. In fact, trauma is only a provocative factor. Many authors speak in favor of the viral etiology of CRAS. However, experimental work did not confirm the viral nature of the disease. Recently, CRAS is considered not as a local pathological process, but as a manifestation of a disease of the whole organism. The factors provoking relapses include trauma to the oral mucosa, hypothermia, exacerbation of diseases of the digestive system, stressful situations, and climatic and geographical factors.

At the same time, attention is drawn to the fact that stomatitis occurred mainly in men who had never smoked before. The effect of smoking is associated with increased keratinization of the oral mucosa, which occurs in response to the constant exposure to the temperature factor. Of course, this does not mean that smoking should be promoted as a means to prevent stomatitis. Smoking, as proven by numerous studies, is the cause of many serious human diseases.

The important role of the sialogens factor in the pathogenesis of CRAS is evidenced by the results of clinical and experimental observations by E. E. Sklyar (1983). A large number of works also suggests that the role of the nervous system in the development of CRAS should be considered from the standpoint of disorders of the nervous trophism. Clinical and experimental studies made it possible to confirm the reflex principle of the pathogenetic connection of CRAS with diseases of the digestive system. Often, the defeat of the oral mucosa is the first symptom of diseases of the stomach, liver, intestines, etc.

Recently, a fairly large number of works have appeared in the literature confirming the stress mechanism of CRAS development. The stress factor leads to the release of noradrenaline and dopamine, which lead to ischemia of the oral mucosa, and subsequently to destruction with the formation of deep aphthae and ulcers. Many researchers compare CRAS with myocardial infarction, since under the influence of psycho-emotional factors, the blood coagulation system is disturbed. In 40% of cases, rheological disorders in CRAS are characterized by plasma sweating through the walls of postcapillary venules, an increase in blood viscosity and concentration, a slowdown in blood flow, and the formation of erythrocyte aggregates.

Developing deep hypovitaminosis C in CRAS should be considered one of the triggers of numerous metabolic disorders, which requires the use of this vitamin in treatment. Against the background of hypovitaminosis C, first of all, the process of collagen formation is inhibited, and, consequently, the development of granulation tissue. Inhibition of the phagocytic and digestive functions of neutrophils, a decrease in the complementary and bactericidal activity of blood serum and saliva, and a sharp decrease in the level of lysozyme were found.

Noteworthy is the hypothesis that oral microorganisms having common antigenic determinants of an autoallergic nature, together with the mucosal epithelium, can stimulate cellular and humoral immune responses and cause damage to epithelial tissues. In cases of CRAS, the culprit is certain types of oral streptococcus and its L-form. CRAS develops as a type of delayed hypersensitivity, as well as a mixed type of allergy, in which reactions of types II and III are observed. These processes involve the use of desensitizing and antiallergic therapy in treatment, as discussed below.

The cytotoxic type (II) is mediated by IgE and IgM. The antigen is always bound to the cell membrane. The reaction proceeds with the participation of complement, which damages the cell membrane. With an immunocomplex type (III) of an allergic reaction, immune complexes are formed in the vascular bed with a rather large intake of antigen into the body. Immune complexes are deposited on the cell membranes of blood vessels, thereby causing necrosis of the epithelium. IgZ and IgM are involved in the reaction. Unlike the second type of allergic reaction, the antigen in the immunocomplex type is not associated with the cell.

In autoimmune processes, autoantibodies or sensitized lymphocytes are produced to the antigens of one's own tissue. The reason for the violation of the "prohibition" of the immune response to "one's own" may be the modification of one's own antigens as a result of any damaging effects or the presence of so-called cross-reacting antigens. The latter have structurally similar determinants inherent in both body cells and bacteria.

Autoimmune diseases are often combined with lymphoproliferative processes and with T-cell immunodeficiency. In particular, with CRAS, a defect in T-suppressors is noted. It is noteworthy that among the populations of lymphocytes in patients with CRAS, the number of cells is 40% at a rate of 25%.

The development of an allergic reaction in CRAS is accelerated in the presence of predisposing factors, among which heredity is generally recognized.

It is interesting to note that CRAS most often occurs in persons with blood type II. Obviously, this is due to a large number of class Z immunoglobulins.

Characteristic morphological elements in CRAS are aphthae, which are usually localized in any area of ​​the OM and have a development cycle of 8-10 days. Aftas are more often solitary, round or oval in shape, have regular outlines, bordered by a thin bright red rim. Elements of the lesion are localized more often on the hyperemic (with sympathetic tone) or pale base of the oral mucosa (with parasympathetic tone). The size of the aft varies from finely punctate to 5 mm in diameter or more. They are covered with a yellowish-white fibrous film, which is on the same level with the mucous membrane or slightly protrudes above its level.

It was noted that during the initial rash, aphthae are localized mainly in the vestibular region of the oral cavity, and during subsequent relapses, they usually occur in the places of their initial appearance. Often, aphthous elements migrate, involving in the pathological process any area or area with a tendency to cover the posterior sections of the oral cavity. With localization of aphthae in the area of ​​the floor of the mouth, on the frenulum of the tongue, gums, retromolar region and palatine arches, aphthae have an elongated horseshoe shape, in the form of cracks or even geometric shapes with not quite even edges. Most patients at the time of treatment complain of moderate pain, which increases dramatically when eating, talking. Moreover, the shorter the interval between relapses, the more painful the process. Quite often, the general condition of the patient worsens, headaches, dizziness, insomnia, nausea appear, subfebrile temperature and dyspepsia may be added.

CRAS can be divided into several forms: fibrinous, necrotic, glandular, scarring, deforming, lichenoid. (G. V. Banchenko, I. M. Rabinovich, 1987).

The fibrinous form appears on the mucous membrane in the form of a yellowish spot with signs of hyperemia, on the surface of which fibrin precipitates, tightly soldered to the surrounding tissues. With the progression of the process, fibrin is rejected and an aphtha is formed, which epithelizes for 6-8 days. When staining fibrin with methylene blue (1% solution), the latter is not washed off with saline or saliva. This form of HRAS develops in those areas of the oral mucosa where there are no minor salivary glands.

In the necrotic form, a short-term vasospasm leads to necrosis of the epithelium, followed by ulceration. Necrotic plaque is not tightly soldered to the underlying tissue and is easily removed by scraping. A solution of methylene blue is easily fixed on fibrinous plaque, but is easily washed off with saline. Epithelialization of this form of CRAS is observed on the 12-20th day. The necrotic form of CRAS is localized in the abundantly vascularized areas of the oral mucosa.

In cases of the glandular form, in addition to the oral mucosa, the small salivary glands in the area of ​​the lips, tongue, and lymphopharyngeal ring are also involved in the inflammatory process. Areas of hyperemia appear, against which the salivary glands seem to be raised due to edema. A solution of methylene blue is fixed only in the area of ​​non-functioning minor salivary glands. Then erosion appears, which quickly turns into an ulcer, at the bottom of which the terminal sections of the small salivary glands are visible. The base of erosions and ulcers is infiltrated. The stage of epithelialization lasts up to 30 days.

The scarring form is accompanied by damage to the acinar structures and connective tissue. The function of the salivary glands is markedly reduced. Healing goes with the formation of a rough scar.

The deforming form is characterized by a deeper destruction of the connective tissue up to the muscle layer. An ulcer in this form is sharply painful, has a migratory character, small erosions and aphthae often appear along its periphery.

In the case of the lichenoid form, limited areas of hyperemia appear on the oral mucosa, bordered by a whitish ridge of hyperplastic epithelium. Most often, this form of HRAS is found in the tongue.

In the process of clinical observation, it is sometimes possible to note aphthous elements with a short development cycle - 3-4 days. B. M. Pashkov (1963), A. I. Rybakov (1965), V. A. Epishev (1968) call them the "abortive form".

The cytomorphological picture of cellular elements in chronic recurrent aphthous stomatitis is characterized by certain features: the cytological composition of smears in patients from the surface of aphthae is represented by cells of a slightly altered epithelium and a small number of leukocytes, with the formation of ulcers, epitheliocytes are less common, the number of leukocytes with noticeable dystrophic changes increases dramatically.

G. M. Mogilevsky (1975) pathologically distinguishes three stages of the process during CRAS:

1) the stage of depigmented and erythematous spots. At this stage, there is intercellular edema, destruction of intercellular contacts, cytolysis; in epitheliocytes, membrane structures are damaged. In the subepithelial basis - edema, destruction of fibrous structures;

2) erosive-ulcerative stage. Necrobiotic and necrotic processes are noted, leukocyte infiltrate is expressed;

3) stage of healing. The epithelium regenerates, the functional activity of epitheliocytes is noted.

The primary element of the defeat of this disease should be considered a vesicle, which is formed as a result of vacuolar degeneration of the cells of the epithelial cover. Vesicles are usually not visible on clinical examination. Aphtha, therefore, is a secondary element of the lesion and is an ulcer with all its common features. The distinguishing features of aphthae-ulcer in CRAS include the presence in the zone of complete destruction of the epithelial cover of individual clusters of cells of its basal and parabasal layers, retaining their inherent reproductive properties. This fact explains the absence of cicatricial changes in most cases during the healing of large and deep aphthae.

The effectiveness of the treatment of patients with CRAS is largely determined by timely diagnosis, since diagnostic errors are quite common. Particular attention should be paid to the differential diagnosis of CRAS and chronic herpetic stomatitis (CHC). Clinical differences between these two nosological forms are indistinct, hardly perceptible. However, a closer observation of the dynamics of these two diseases, taking into account amnestic data and a deep clinical analysis of the condition of patients, makes it possible to identify certain features inherent in these etiologically different diseases.

The onset of inflammation in CHC was characterized by the appearance of small vesicles filled with a transparent or yellowish content.

Patients with CRAS have lesions in the form of opal or cloudy milky spots, barely protruding above the level of the oral mucosa. Scraps of the epithelium in such places, due to maceration with saliva, covered the lesion in the form of a pseudo-membranous plaque. Subsequently, the lesions in patients acquired the form of yellowish-gray erosion, rounded or oval. For herpetic stomatitis, small (from 1 to 3 mm in diameter) lesions are more characteristic, which are located mainly grouped, in large numbers. With CRAS, large aphthae (from 3 to 6 mm in diameter) with a soft base, cone-shaped, towering above the mucosa, scattered and single, are observed. With a herpes infection, lesions are more often localized on the lips. With aphthous stomatitis, the most frequent localization of aphthae was noted on the buccal mucosa and tongue. Exacerbations of CHC are most often combined with acute respiratory diseases, CRAS most often occurs during exacerbation of diseases of the gastrointestinal tract. Differential diagnosis of CRAS and CHC is presented in Table 1.

CRAS must also be differentiated from the so-called neutropenic aphthae, which develop in patients with neutropenia during a sharp decrease in neutrophils in the peripheral blood.

From syphilitic papules, aphthae differ in sharp soreness, bright hyperemia around erosion, short duration of existence, absence of pale treponemas, and negative serological reactions to syphilis.

Aphthae that occur on the oral mucosa are one of the symptoms of Behcet's disease, in which they are preceded or appear simultaneously with other symptoms associated with damage to the eyes and skin of the genital organs, where aphthous-ulcerative rashes occur. Behcet's disease has a septic-allergic genesis. Often, in addition to lesions of the eyes, oral mucosa, genital organs, it is accompanied by severe general phenomena, fever, rheumatoid arthritis, etc.

A similar process without eye damage, but with intestinal pathology with aphthous-ulcerative rashes around the anus, can be diagnosed as Touraine's large aphthosis. The scarring and deforming forms must be differentiated from tuberculosis, syphilis, neoplasms, blood diseases. Differential diagnostic signs of CRAS with manifestations of tuberculosis, syphilis and neoplasms of the oral mucosa are presented in Table No. 2.

Treatment of chronic recurrent aphthous stomatitis should be comprehensive and individually selected. It can be divided into general and local.

The etiology of the pathogenesis of CRAS still cannot be considered definitively elucidated. This circumstance to a high degree limits the appointment of rational therapy for patients. It is not always possible to achieve a stable therapeutic effect. The choice of treatment method should be based primarily on the data of a detailed examination of the patient, which makes it possible to develop an individual treatment plan.

Based on the close anatomical and functional dependence of the oral cavity and the gastrointestinal tract, the treatment of CRAS should begin with the treatment of diseases of the digestive system. G. O. Airapetyan, A. G. Veretinskaya (1985) suggest using anaprilin in the general treatment of CRAS. This drug, selectively blocking the transmission of nerve impulses in the sympathetic division of the autonomic nervous system, interrupts the reflex effect from damaged abdominal organs and protects the tissues of the oral mucosa from the damaging effects of high concentrations of norepinephrine.

In practice, adrenoblockers are most often used: anaprilin, obzidin, trazikor. Assign these medications in small doses of 1/2-1/3 tablets 1-2 times a day. To block acetylcholine, M-anticholinergics are used: atropine, platifillin, aeron, bellataminal.

If an allergen that provokes CRAS is not detected or a polyallergy is detected, then nonspecific hyposensitizing therapy is prescribed. For this, antihistamines are used: diphenhydramine (0,05 g), tavegil (0,001 g), suprastin (0,025 g). Recently, peritol (0,04 g), which also has an antiserotonin effect, has proven itself to be good. The drug is prescribed 1 tablet 2-3 times a day. It is good to combine antihistamines with E-aminocaproic acid (0,5-1,0 g 4 times a day). Antihistamines are prescribed in short courses, alternating them for 7-10 days for one drug for a month. Drugs such as intal, zoditen, prevent the release of the contents of the granules from mast cells, and they can be combined with antihistamines.

Hyposensitizing agents are also used (a decoction of string, wild strawberries, vitamin teas containing rose hips, black currants, rowan fruits, 10% gelatin solution) inside 30 ml 4 times a day before meals with simultaneous intake of ascorbic acid up to 1-1,5 .2 g per day in a course of 1 weeks, sodium thiosulfate and hyperbaric oxygenation: (pressure 45 atm, session duration XNUMX minutes).

Given the great importance in the pathogenesis of CRAS activation of the kallikrein-kinin system, patients should be prescribed prostaglandin inhibitors, which have analgesic, desensitizing effects. The following drugs have a good effect: mefenamic acid (0,5 g 3 times a day), pyrroxane (0,015 g 2 times a day), etc.

Sedatives are used to normalize the functions of the nervous system. A good effect was obtained from the imported drug novopassita. Herbal preparations do not cause hyposalivation and give a persistent sedative effect. Recently, tinctures of valerian, peony, passion flower extract have been widely used.

Against the background of severe neurotic conditions with sleep disturbance, tranquilizers and neuroleptic drugs are prescribed: chlozepid (0,01 g 2-3 times a day), nozepam (0,01 g 3 times a day), etc.

In recent years, various bacterial antigens as stimulators of the immune system have been successfully used in foreign practice to treat patients with CRAS. For CRAS immunotherapy, bacterial allergens of Staphylococcus aureus, pyogenic streptococcus, Escherichia coli are used.

Very quickly, autohemotherapy leads to remission, which has a desensitizing and pronounced stimulating effect on the body. Intramuscular injections of the patient's blood taken with a syringe from a vein are made after 1-2 days, starting with 3-5 ml of blood and gradually increasing the dose to 9 ml. UV-irradiated and reinfused blood increases the body's resistance to infection, favorably affects the hemostasis system, accelerates the change in inflammation phases, favorably affects the patient's immunological status, does not cause complications and has no contraindications for use.

The leading place in the general treatment of CRAS is occupied by vitamin therapy. When prescribing vitamins, it is advisable to take into account the synergism and antagonism of vitamins, the interaction with hormones, microelements and other physiologically active substances, with some groups of drugs.

However, in case of exacerbation of CRAS, it is advisable not to prescribe B vitamins, as they can aggravate the severity of the disease due to allergic reactions. The appointment of vitamin Y to patients is very effective. When using this drug, a positive result is observed in 60% of patients in whom relapses were not observed within 9-12 months.

Patients in the period of exacerbation of CRAS are prohibited from using spicy, spicy, rough foods, alcoholic beverages.

Drugs used at the first stage of the process should have an antimicrobial, necrolytic, analgesic effect, contribute to the suppression of microflora and the speedy cleansing of aphthae or ulcers. At the stage of hydration, HRAS is prescribed all kinds of antiseptics in the form of rinses and applications. It must be remembered that the more pronounced the inflammatory process, the lower the concentration of the antiseptic. Among the old antiseptics, only hydrogen peroxide, preparations of iodine and potassium permanganate have retained a certain value. Over the past decades, new chemotherapy drugs have been created that have pronounced antimicrobial properties, low toxicity and a wide spectrum of action. An antiseptic such as dioxidine has proven itself well. The drug gives a direct bactericidal effect against gram-positive and gram-negative microflora, including Escherichia coli, Proteus.

Chlorhexidine is characterized by a wide spectrum of action, most active against staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa. The drug has low toxicity, has significant surface activity and disinfectant properties. For CRAS, rinsing the mouth with a solution of chlorhexidine bigluconate is effective.

Despite the high bactericidal activity of iodine preparations, their use for the treatment of CRAS is limited due to the irritating and cauterizing effect. The drug iodopyrone does not have such a negative effect due to the presence of a polymer - polyvinylpyrrolidone. Most often, a 0,5-1% solution of iodopyrone is used in the form of applications for 10-15 minutes. In recent years, there have been numerous reports of favorable results in the treatment of ulcerative lesions of the oral mucosa with lysozyme, dioxidin, citachlor, biosed, peloidin, ionized silver solution, 0,1% chinosol solution, 1% alcohol solution of chlorophyllipt (2 ml is diluted in 100 ml water).

There is a positive experience with the use of a mixture of 0,1% Novoimanin, 0,1% chinosol, 1% citral-I in equal amounts. Applications are carried out on the affected areas for 12-15 minutes. For better penetration of drugs into the submucosal layer, dimexide is used, which is able to penetrate cell membranes without damaging them during active transport of drugs.

As anti-inflammatory drugs, decoctions of St. John's wort, calamus, birch leaves, large burdock, calendula are used. Tissue edema and vascular permeability are significantly reduced under the influence of herbal preparations with astringent and tanning properties. These include chamomile, quince, oak bark, alder seedlings. For anesthesia use infusion of sage leaves, Kalanchoe juice. For local anesthesia, local anesthetics are used - anestezin emulsion in sunflower, peach oils, anestezin concentration 5-10%, novocaine solution (3-5%), 1-2% pyromecaine solution, 2-5% trimecaine solution ; 1-2% lidocaine solution.

Non-narcotic analgesics have analgesic and anti-inflammatory effects. Salicylic acid derivatives, 3-5% sodium salicylate solution, pyrozolone derivatives (10% antipyrine solution), 5% Butadion ointment are used, a good effect is noted when using a solution of reopirin.

Anthranilic acid derivative - mefenamic acid. The mechanism of its action is associated with the inhibition of proteases, which activate the enzymes of the kallikrein-kinin system, which cause a pain reaction during inflammation. Apply a 1% solution in the form of applications for 10-15 minutes. The analgesic effect persists for 2 hours.

In the initial stage of CRAS, agents are shown that have the ability to stabilize lysosome membranes, thereby preventing the formation of inflammatory mediators (mefenamic acid derivatives; salicylates; drugs that inhibit the action of hydrolytic enzymes (trasilol, contrycal, pantrypin, amben, aminocaproic acid); agents that suppress the action of mediators inflammation due to the presence of functional antagonism (antihistamines (diphenhydramine, suprastin, diazolin), serotonin antagonists (butadion, peritol), bradykinin (mefenamic acid), acetylcholine (diphenhydramine, calcium, magnesium electrolytes). An important link in the local treatment of CRAS is the use drugs that eliminate intravascular microcirculation disorders.For this purpose, the use of drugs that reduce and prevent the aggregation of blood cells, reduce viscosity, and accelerate blood flow.These include low molecular weight dextrans, anticoagulants and fibrinolytic agents (heparin, fibrionolysin, acetylsalicylic acid).

At present, hydrophilic-based ointments have been developed and can be used in the treatment of CRAS: ointment "Levosina", "Levomekol", "Dioksikol", "Sulfamekol". These drugs have pronounced antimicrobial properties, have an analgesic effect and a non-political effect.

Medicinal films for the treatment of CRAS have been developed. Biosoluble films contain 1,5 to 1,6 g of atropine sulfate. The biofilm is applied to the pathological focus 1 time per day, regardless of the meal. Due to the slow solubility of the special polymer composition, a long-term contact of atropine with the mucous membrane is ensured.

Considering the presence of an allergic component in the pathogenesis of CRAS, patients need to undergo a complex method of treatment, including the use of proteolysis inhibitors. It is possible to carry out applications with the following mixture: contrical (5000 units), heparin (500 units), 1 ml of 1% novocaine, hydrocortisone (2,5 mg). This should be preceded by antiseptic treatment of oral mucosa and removal of necrotic layers with the help of enzyme preparations: trypsin, chymotrypsin, terrilitin.

In the second stage of the course of CRAS, the use of drugs capable of stimulating regeneration is pathogenetically justified. These include vinylin, acemin ointment, vitamin A, methyluracil. Solcoseryl, an extract of the blood of cattle, freed from proteins and not possessing antigenic properties, has a good effect. The drug accelerates the growth of granulations and epithelialization of erosion or ulcers. To stimulate the epithelialization of aft-elements, it is advisable to prescribe a 1% solution of sodium mefenaminate, acemin ointment, and a 1% solution of citral. Applications are made 3-5 times a day after meals. Natural oils have a good keratoplastic effect: rosehip, sea buckthorn, plum, corn, etc.

Recently, quite often in the literature there are reports of the use of propolis. Propolis is represented by a mixture of pollen, cinnamic acid, esters, provitamin A, vitamins B₁, AT₂, E, C, PP, N. Propolis has a pronounced antimicrobial, anti-inflammatory, analgesic, deodorizing, tonic effect.

You can not neglect the experience of traditional medicine. Many recipes of Russian healers help people cope with ailments. So, with stomatitis, a decoction of aspen buds or bark is effective, and they can rinse the mouth with CRAS, as well as take it orally. The leaves and fruits of sorrel have an astringent and analgesic effect. Rinsing the mouth with an infusion of fresh lettuce leaves, as well as drinking it, quickly leads to the disappearance of aphthae.

For long-term non-healing stomatitis, an ointment is used, consisting of 75 g of crushed fresh burdock root, which is infused for a day in 200 g of sunflower oil, then boiled for 15 minutes on low heat and filtered. Shilajit is considered one of the strongest remedies for CRAS in folk medicine. Shilajit is diluted at a concentration of 1 g per 1 liter of water (a good mummy dissolves in warm water without signs of turbidity). Take in the morning 1 time per day for 50-100 g of solution. To improve regeneration, you can rinse your mouth with a mummy solution 2-4 times a day.

Given the etiology and pathogenesis of CRAS, it is necessary for people suffering from frequent relapses to conduct 2-3 therapeutic physiotherapy courses per year. During the period of remission, UV irradiation is performed to normalize the immunobiological reactivity of the organism. UV rays enhance oxidative reactions in the body, favorably affect tissue respiration, and mobilize the protective activity of the elements of the reticulohistiocytic system. UV rays contribute to the formation of a special photoreactivation enzyme, with the participation of which reparative synthesis occurs in nucleic acids. The course of treatment is prescribed from 3 to 10 exposures daily.

During the epithelialization of aft, darsonvalization can be used. Sessions lasting 1-2 minutes are carried out daily or after 1 day, for a course of 10-20 procedures. With multiple aphthae, in order to improve the body, aero-ionotherapy is proposed. The physiological effect of aeroionotherapy depends on the electric charges of air ions, which, after the loss of charges, acquire the ability to enter into biochemical reactions.

Under the influence of this procedure, the body temperature normalizes, the electrical potential of the blood changes, the epithelialization of aphthae and ulcers accelerates, pain sensations decrease.

Despite the fact that there are numerous publications devoted to the problem of the etiology and pathogenesis of CRAS, the essence of this pathological process remains insufficiently elucidated. In this regard, there are still no reliable methods of treating CRAS.

In the treatment of CRAS, it is necessary to prescribe means of correction aimed at restoring the function of the digestive system. In the general treatment of CRAS, the appointment of tranquilizers, sedative therapy takes place. In the interrecurrent period, patients are prescribed drugs that regulate interstitial metabolism: biostimulants, adaptogens, vitamins. The clinical practice of recent years convinces of the need for HRAS immunotherapy. With the help of immunostimulants, it is possible to achieve a faster recovery, achieve a stable remission. In the local treatment of CRAS, it is important to take into account the phase of the process, the degree of severity, and the localization of eruptive elements. Recently, clinicians have noted a good effect when using herbal remedies.

There are still many unresolved issues in the treatment of such a common oral disease as chronic recurrent aphthous stomatitis. The best results can be achieved by combined treatment aimed simultaneously at various pathogenic elements, including herbal medicine and physiotherapy.

Leukoplakia is a chronic disease of the oral mucosa, manifested by thickening of the mucosal epithelium, keratinization and desquamation; the most common localization is the buccal mucosa along the line of teeth closure, on the back and lateral surfaces of the tongue, at the corner of the mouth. This disease occurs more often in men over 40 years of age. The reasons for the development of leukoplakia have not yet been fully elucidated, but it is known that the predisposing factors are constant mechanical irritation (parts of the prosthesis, damaged edge of the tooth), smoking, alcohol abuse, frequent use of hot spices, frequent thermal lesions. The disease begins, as a rule, asymptomatically, a slight itching or burning sensation is possible. Morphologically, leukoplakia is a focus of thickening of the mucous membrane of a whitish color, its size can vary from the size of a millet grain to the entire inner surface of the cheek. There are three forms of leukoplakia:

1) a flat form (the lesion does not rise above the intact mucosa, there are no signs of inflammation);

2) verrucous form, characterized by compaction and vegetation of the epithelium in the affected areas;

3) an erosive-ulcerative form, characterized by the presence of cracks, ulcers, furrows, which is dangerous due to the possibility of malignancy.

Treatment involves the elimination of all possible provoking factors: oral hygiene, abstinence from smoking, eating too hot or too spicy food, and avoiding alcoholic beverages. The use of cauterizing agents is strictly prohibited. The patient must be registered with a dentist or oncologist. If the verrucous form is accompanied by the appearance of deep cracks, it is necessary to excise the lesion and its mandatory histological examination, which will determine further treatment tactics.

2. Changes that occur on the oral mucosa in various diseases

Since the oral mucosa is often involved in certain pathological processes occurring in the body, the study of its condition is very informative. Changes on the walls of the oral cavity can appear both during the course of the disease and long before its first symptoms, indicating disorders in organs and systems.

Even in the absence of patient complaints about any disorders of the gastrointestinal tract, certain symptoms may appear on the mucous membrane, usually indicating an exacerbation of an existing chronic disease. The presence and color of plaque on the tongue is especially indicative. Normally, early in the morning before breakfast, the tongue is covered with a small amount of light coating, which disappears after eating. Coating of the tongue during exacerbations of chronic diseases of the gastrointestinal tract and some infectious diseases does not require specific treatment. If, in the presence of a large amount of dense plaque, the patient feels awkward, then the surface of the tongue should be treated with a swab previously moistened with a solution of hydrogen peroxide, after each such procedure it is necessary to rinse the mouth with clean water.

Cyanosis of the mucous membrane of the lips, cheeks, tongue, floor of the mouth quite often accompanies hypertension and some heart defects. In this case, often on the surface of the mucosa there is a burning sensation, tingling, itching. Small-focal myocardial infarction is characterized by cyanotic color of the mucous membrane, its edema, and dry mouth. In acute myocardial infarction, the mucous membrane becomes cyanotic, cracks appear on it, erosions, sometimes ulcers, and even hemorrhages. Ulcerative-necrotic lesions of the mucous membrane, sometimes reaching the submucosal tissue, often develop with circulatory failure in stages III-IV, sometimes these defects bleed, especially when pressed. In this case, careful, careful and regular care of the oral cavity and the exclusion of any possibility of traumatizing the oral mucosa is necessary.

Granulocytosis, which in itself is characterized by a very vivid clinical picture, is also accompanied by ulcerative necrotic changes on the lips, tongue, gums, buccal surface of the mucous membrane, on the tonsils and even in the oropharynx. Local treatment consists in carrying out antiseptic treatment, a thorough toilet of the oral cavity, the use of painkillers, the appointment of baths; it is also important to avoid injury to the mucous membrane.

With the development of leukemia, pathological changes in the oral mucosa in the form of hemorrhages, bleeding gums, and the appearance of ulcers in 20% of patients precede other clinical manifestations. Treatment is reduced to regular, gentle oral care and treatment of the underlying disease.

Hypochromic iron deficiency and pernicious anemia. The main manifestations of these diseases in the oral cavity are burning, itching and tingling in the tongue, atrophy and deformation of the papillae of its mucosa, dry mouth. General treatment is necessary, antiseptic solutions can be applied locally.

Thrombocytopenia (Werlhof's disease) is characterized by recurrent bleeding (usually from the gums, but other localization is possible), which often occur unexpectedly against the background of complete well-being, without previous violation of the integrity of the mucous membrane. Often there are hemorrhages in the submucosa and under the skin, nosebleeds may develop. Constant blood loss causes pallor of the skin, cyanosis of visible mucous membranes, low hemoglobin levels in blood tests.

Syndrome of disseminated intravascular coagulation. DIC can complicate the course of a number of diseases, such as sepsis, severe injuries, burn disease, complicated childbirth, and various poisonings. At the same time, changes also affect the outer integument of the body along with mucous membranes: elements of a rash appear, multiple hemorrhages under the skin and in the submucosal layer, bleeding of the skin and gums.

In this disease, the back of the tongue is covered with red, pink and white areas, alternating with each other, the tongue becomes similar to a geographical map ("geographic tongue"), while the defects do not cause any discomfort to the patient. The picture of the "geographic language" persists in patients throughout life, but due to the benign course of any treatment, this condition does not require.

Since the number of HIV-infected people reaches a large number, mucosal lesions characteristic of AIDS can be found extremely often. The appearance of defects in the oral mucosa is one of the first manifestations of the pathological process; they are caused by the fact that, due to a violation of the immune processes in the body and a decrease in its protective forces, the opportunistic microflora of the oral cavity is activated. Most often, AIDS is manifested by gingivitis, periodontitis, fungal infection, cheilitis, dry mouth, enlarged salivary glands. Patients complain of dryness of the oral mucosa, white plaque on the tongue, burning sensation in various parts of the oral cavity, periodic itching, bleeding gums and their pale anemic color, painful erythematous spots, exposure of the necks of the teeth and interdental septa. These changes occur in many diseases of the body and the oral cavity in particular, so the dentist needs to pay attention to other characteristic features of the patient's condition: a change in the general appearance of the patient, weight loss, tired, haggard appearance, insomnia, decreased appetite, the duration of the disease, an increase in neck lymph nodes can indirectly indicate AIDS. In addition, signs and lesions of the dentoalveolar system, such as the appearance of warts, long-term non-healing wounds and seizures (especially in the corners of the mouth), periodontitis of non-carious origin, and others, allow suspecting the presence of immunodeficiency.

When the diagnosis of AIDS is confirmed, the patient is prescribed a thorough and careful toilet of the oral cavity, its sanitation is carried out; antifungal drugs (nystatin, decamin, levorin, nizoral) and antiviral agents (azidothymidine, etc.) are used to irradiate the lesion of microflora and prevent the introduction of viruses.

When working with HIV-infected people, it is necessary to remember the extremely high degree of their contagiousness. Even if invasive methods of diagnostics and treatment are not used, the probability of getting HIV into a susceptible organism from a patient while providing assistance to him is from 0,9 to 5%, therefore, when examining AIDS patients, you need to work very carefully, if possible, avoid contamination of hands and clothes with their secretions from the nose, eyes, skin and oral mucosa.

LECTURE No. 8. Mechanical trauma of the oral mucosa. Features of regeneration

1. Acute mechanical injury

Mechanical damage can be caused by acute trauma as a result of biting the mucosa while eating, an attack of epilepsy, a blow, preparing teeth for crowns (bur, probe, disk), filling teeth, as well as injuring it with a knife, fork, bone, etc.

Acute trauma to the oral mucosa can be:

1) open, i.e., with violations of the integrity of the mucous membrane, epithelial cover;

2) closed, i.e., without violating the integrity of the oral mucosa and the epithelial cover.

They often occur in practically healthy people from the simultaneous impact of a traumatic agent and quickly disappear after its elimination.

Depending on the strength, duration of the traumatic factor, the following may occur:

1) excoriations (abrasions) (the layer of the mucous membrane itself is not affected);

2) erosion (surface layers are involved in the process);

3) wounds.

Excoriation is a lesion in which the layer of the mucosa itself is not affected, a pain symptom is expressed, but there may not be bleeding, which indicates that the papillary layer has not been opened.

Erosion is a superficial injury when the epithelial and papillary layers are involved, which is explained by the appearance of blood droplets, like "dew".

Depending on the acting factor, the damaging agent, the wound can be:

1) chopped;

2) cut;

3) torn;

4) bitten.

The clinical manifestations of these wounds depend on the depth of the lesion, the type of injury, and vascular involvement. So, a bitten wound is the most severe, as there is a powerful infection. During a bite, up to 170 types of pathogens enter the wound. The very type of wound (lacerated) contributes to a significant disruption of microcirculation. Healing, as a rule, occurs by secondary intention, through granulation tissue, with the formation of scars, sometimes deforming the skin.

The course of an open wound, regardless of the type of damage, goes through the following stages:

1) stage of hydration (exudation), which lasts 1-2 days. Patients complain of burning, pain, aggravated by eating, talking. There are pronounced hyperemia and edema around the lesion. Immediately after the injury, ice or a cold compress can be applied to the wound. The pain is relieved by the use of painkillers. The wound is washed with antiseptic solutions. You can use decongestants in cases of extensive lesions (up to diuretics). In order to prevent infection of the wound, anti-inflammatory drugs are prescribed;

2) stage of dehydration (after 1-3 days). The pain subsides. This stage is characterized by the formation of crusts on the skin and plaque on the mucosa. During this period, in addition to anti-inflammatory drugs, enzymes can be prescribed that clean the wound surface from crusts, scales, and plaque; NB!!! if the wound heals by secondary intention, then enzymes are contraindicated, as they are able to melt the young, newly formed granulation tissue. Microcirculation is improved by ASA, heparin. Acemin, dibunol improve proliferative regenerative processes;

3) stage of epithelialization. Epithelialization of acute traumatic lesions occurs quickly, within 1-3 days. When a secondary infection is attached, they do not heal for a long time. Healing is possible through scarring. Reparants have proven themselves well: vitamins A, E, groups B, C, K, their oil solutions containing O₂, keratoplasty. Promotes the regeneration of solcoseryl, honsuride, methyl-uracil, sodium nucleinate, pentoxyl, actovigen, aloe juice or colanchoe, vinylin, Shestakovsky's balm.

Closed wound - hematoma - hemorrhage into the tissue surrounding the vessels. The hematoma undergoes changes over several stages, which are called the stages of the course of the hematoma:

1) red hematoma - 1st day. The color of the hematoma is due to hemorrhage into the surrounding tissues of red blood cells. In case of injury, there is a rupture of blood vessels, thrombosis, and the release of blood cells. Immediately after the injury, it is good to apply cold, to carry out cryoapplication. Adrenaline, mezaton, galazalin, ephedrine, sanarin, naphthyzine - locally, especially if the oral mucosa is damaged. Ultrasound, laser, UHF, Darsanval currents;

2) blue hematoma - 2-3rd day - due to venous congestion, changes in uniform elements. It is good to use FTL, anti-inflammatory therapy, absorbable agents (bodyagu, heparin) during this period;

3) green hematoma - 4-5th day. The color is due to the formation and release of hemasiderin;

4) yellow hematoma - 6-7th day. Resolving therapy is recommended: ranidase, lidase, hyaluronidase, bee venom, snake venom.

2. Chronic mechanical injury (CMT)

They are more common than acute. They are mainly caused by the following active causes: carious teeth, poor-quality fillings, prostheses and their clasps, lack of a contact point, tartar, bad habits, anomaly in the location of the teeth, malocclusion, etc. 65-70% of CMT develops as a result of orthopedic treatment; 13-15% - due to fillings, sharp edges of teeth; 10-15% - due to malocclusion; 5-6% - because of a bad habit, panto-facial expressions.

in literature until the 1970s. CMT was considered in the form of the following nosological units: decubital ulcer, prosthetic stomatitis, prosthetic granuloma. Currently, it is believed that the above diseases are different stages of the course of one pathology - chronic mechanical injury.

The process develops over months, years. Initially, the phenomena of catarrhal inflammation (hyperemia, swelling, soreness) appear in the tissue. But with a long course of the process, hyperemia from bright red becomes cyanotic, the edges and bases of the lesion become denser not only due to edema, but also as a result of the development of dense connective tissue. Prolonged exposure to a pathogenic factor leads to the development of ulcers, erosion, surrounded by cloudy epithelium and covered with plaque.

Such lesions are more often observed in older people who have prerequisites for their development. They have reduced mucosal turgor, increased density, change in compliance and mobility of the oral mucosa.

During chronic mechanical injury, the following stages can be distinguished:

1) catarrhal stage. It is characterized by burning, tingling, feeling of soreness. Possible glossalgia, paresthesia.

Objectively: hyperemia and edema develop on the mucosa in places according to the action of the traumatic factor. Morphological examination: acanthosis, vacuolar degeneration of the epithelial layer, stagnant capillaries.

2) violations of the integrity of the epithelium (erosion, aphtha, ulcer). More often they are localized on the lateral surfaces of the tongue, cheeks, hard palate. They can be small or large, covering a large area of ​​tissue. A long-lasting ulcer can spread to muscle tissue, and move from the palate to the bone, causing its perforation. Usually the edges and bottom of the ulcer are hyperemic, edematous, dense on palpation, slightly painful. Regional lymph nodes are enlarged, mobile, painful. Decubital ulcers can degenerate into cancer.

The epithelium normally regenerates within 3 days. If erosion, aphtha, ulcer do not pass to the next stage, but persist for 14 days, then rebirth occurs.

3) the stage of proliferative processes. This is vegetation, papillomatosis. The latter may be accompanied by hyperkeratosis.

A type of chronic traumatic injury to the mucosa is decubitus or prosthetic stomatitis. Under the prosthesis, catarrh occurs first, then erosion and even an ulcer, which can disappear immediately after the timely correction of the prosthesis. Prolonged wearing of such a prosthesis leads to the development of a chronic inflammatory process, which is accompanied by the growth of connective tissue in the area of ​​injury - lobular fibroma or papillomatosis occurs. A secondary infection joins the injury, which complicates the course of the process. Papillomatosis can occur on the hard palate when wearing a complete removable denture.

Differential diagnosis is carried out with the following diseases:

1) lichen planus;

2) lupus erythematosus;

3) candidiasis;

4) syphilis;

5) tuberculosis;

6) ulcerative necrotic gingivostomatitis of Vincent;

7) trophic ulcer;

8) blood diseases;

9) allergic diseases.

Eliminating the cause is the key to success in treating the disease. The oral cavity is being rehabilitated. Antiseptic rinses with potassium permanganate 1: 5000, furatsilin 1: 5000, 1-2% sodium bicarbonate solution (soda), heparin applications on the mucosa are shown. In the stage of violation of the integrity of the epithelial cover, apply:

1) enzymes that help clean the surface of the necrotic film;

2) anti-inflammatory and antiseptic applications, painkillers;

3) from the 3rd day - applications of keratoplastic agents: galascarbine, rosehip oil, keratolin, oil solutions of vitamins A and E, solcoseryl ointment.

In traumatic lesions, if the ulcer does not heal within 10-14 days during treatment, a biopsy should be done.

3. Chemical damage to the oral mucosa, types of anesthesia

Chemical damage to the oral mucosa can result from acute or chronic exposure to various substances.

An acute lesion occurs when a potent substance accidentally enters the mucous membrane. These lesions are rare. It is possible to take substances for the purpose of suicide (acetic acid and alkali - electrolytes). In the hospital. Kalinin on holidays, you can often find an acute chemical injury to the oral mucosa.

Medication-induced lesions of the oral mucosa are more common (50% of all lesions). These mucosal burns are the result of mistakes made by dentists when treating with the following drugs: silver nitrate, resorcinol-formalin mixture, EDTA, acid for expanding root canals (nitric, sulfuric, aqua regia). When they get on the mucous membrane, they cause severe burns, the patient feels a sharp pain, a strong burning sensation.

Burn stages:

1) the stage of intoxication (hydration, catarrhal changes);

2) stage of necrosis. In the affected area, coagulation of the mucosa occurs, and, depending on the duration and strength of the impact of the pathogenic object, necrosis occurs, followed by the formation of erosion or ulcers. With acid necrosis, the affected area is covered with a dense film (brown from sulfuric acid, yellow from nitric acid, white-gray from other acids). The mucosa around and the subject are inflamed, tightly soldered to the tissues of necrosis. Alkali burns have a loose surface, their consistency is similar to jelly. After rejection of necrotic masses, extensive erosive surfaces and ulcers are formed - sharply painful when eating, talking. Burn ulcers heal very slowly;

3) stage of scarring. Erosion or ulcer, covered with necrotic plaque, passes into the next stage - the stage of scarring, epithelialization. Possible vegetation, papillomatosis with symptoms of hyperkeratosis.

When providing first aid, one must act on the principle of neutralizing acids with alkalis, and vice versa. Abundant rinsing, irrigation, washing. The simplest thing that can be done with acid burns is to wash the affected area with soapy water, 1-2% sodium bicarbonate solution, magnesium oxide with water, 0,1% ammonia solution. Alkalis are neutralized with weak solutions of acids - 0,5-1% solutions of citric, acetic acids, 0,1% hydrochloric acid.

Patients are prescribed a diet, cold on the affected areas.

The emerging necrosis is treated with painkillers, antiseptics in the form of applications, nitrofuran preparations (such as furacilin, furazolidone, furagin). The necrotic film is removed by enzymes. In order to regenerate the epithelial layer, applications of keratoplastic agents are used: vinylin, oil solutions of 1% citral, vitamin A and E concentrate, cigerol, keratolin, rosehip oil, Shostakovsky balm, tezan liniment).

In the formation of contractures, surgical excision of scars is used.

Drug-induced lesions have a specific management, which consists in the use of special antidotes.

There are the following antidotes.

Phenol, carbolic acid, resorcinol:

1) 40% alcohol;

2) castor oil;

3) sodium usninate on fir balsam;

4) sodium usninate with anesthesin in castor oil.

Silver nitrate (lapis):

1) table salt;

2) Lugol's solution;

3) tannin;

4) strong tea.

Arsenic anhydride:

1) 2% tincture of iodine;

2) Lugol's solution;

3) iodinol;

4) iodopyrone;

5) unithiol;

6) eugenol;

7) burnt magnesia;

8) 10% Ca, Cl₂.

Alcohol tincture of iodine, formalin, sodium fluoride:

1) drinking soda;

2) sodium thiosulfate;

3) hyposulfite;

4) soapy water;

5) lime water;

6) burnt magnesia;

7) 10 drops of ammonia in 1 glass of water.

Potassium permanganate:

1) hydrogen peroxide;

2) ascorbic acid;

3) citric acid.

Ammonia, ammonia, antidurgelen (alkali):

1) citric acid;

2) 0,5% acetic acid;

3) ascorbic acid;

4) nicotinic acid.

Lactic acid:

1) chloramine 0,25%;

2) drinking soda.

4. Chronic chemical injury (CCT)

The cause of XHT is more often occupational injuries. Chemical laboratory assistants, pharmacy workers, smokers, etc. are susceptible to damage.

Chronic chemical injuries of the mucous membrane have a special character of manifestation. In some cases, they can be in the form of a delayed-type allergic reaction, in others - in the form of intoxication of the body.

In industrial enterprises where work is underway to eliminate harmful factors, occupational pathology is very rare. Mercury, lead stomatitis in severe forms are absent.

However, in the chemical industry (in the production of radioactive substances, polymers, etc.), where potent substances are used, workers who neglect safety precautions experience mucosal lesions.

The following information is used to make a diagnosis.

1. Anamnestic data.

2. Objective data:

1) general manifestations (correspond to the specific symptoms of intoxication);

2) local manifestations (non-specific - catarrhal phenomena, specific manifestations are characteristic for each agent of their own).

So, professional leukoplakia is observed in workers in contact with benzenes. The same phenomena were found in drivers, workers of coke plants, workshops where phenol is produced.

Prolonged contact with pesticides causes chronic inflammation of the oral mucosa, exfoliative cheilitis, leukoplakia of the palate, hyperkeratosis.

Mucosal changes in the form of hyperkeratosis are caused by the action of phenol, mercury, anthracite, liquid resins, arsenic, etc. Differential diagnosis of chemical lesions is presented in Table No. 3.

On April 26, 1986, the Chernobyl tragedy occurred, the consequences of which will be unpredictable for a long time. The Chernobyl nuclear power plant ran on cesium, which has a half-life of 33 years. This explains this terrible tragedy.

Radiation units

Roentgen is an off-system unit of the exposure dose of gamma radiation, which is determined by its ionizing effect on the air.

Curie is an off-system unit of activity of a radioactive isotope.

Rad is a unit of ionizing radiation dose absorption.

1 rad \u0,01d 100 J / kg. 1 ergs are absorbed by a mass of XNUMX kg.

Absorption dose (SI system) - 100 rad - 1 Gy - 1 J / kg.

Radiation sickness. Manifestation in the mouth

There are acute and chronic forms of radiation sickness (ARS). Acute develops after a single exposure to doses of 100-1000 rad. It appears in four periods.

The dose of a single irradiation is the total exposure for 4 days. The leukocyte lives for 4 days, is loaded during this time and dies. The dose of a single irradiation should not exceed 100 rad.

ARS occurs with total X-ray exposure, gamma exposure, and therapeutic exposure.

The most dangerous bomb is the proton bomb, as it causes chromosomal aberration (mutation). The most sensitive tissues to the action of radiation are tissues where the cells have a high methotic activity, a high methotic number. These fabrics include:

1) lymphoid tissue (where lymphocytes are trained - "university" or "school" for lymphocytes. The tissue dies, the cells do not have time to learn, the defense is sharply reduced;

2) bone tissue - maturation of cells of the hematopoietic system;

3) intestinal epithelium (gastrointestinal lesions);

4) the epithelium of the testicles in boys and the ovaries in girls (infertility and heredity disorders).

The severity of ARS depends on the radiation dose.

*cm. Table number 4.

Clinical forms of ARS:

1) typical;

2) intestinal;

3) toxic;

4) nervous.

The diagnosis is made on the basis of a combination of the following data:

1) anamnestic data;

2) clinical manifestations, such as:

a) symptoms of the primary general reaction (nausea, vomiting, weakness);

b) blood changes (neutrophilic leukocytosis, relative (absolute) leukopenia, damage to young generation cells (hemocytoblasts, erythroblasts, myeloblasts, mature basophilic normoblasts, promyelocytes);

c) change in the latent period (leukopenia, thrombocytopenia).

The prognosis depends on the radiation dose, clinical manifestations, blood test data:

1) disorders of the nervous system - the earlier they appear, the worse the prognosis;

2) manifestations of dyspeptic syndromes 1-2 hours after irradiation - the prognosis is unfavorable;

3) blood changes in the first day - poor prognosis;

4) early erythema, hair removal - poor prognosis.

The period of the primary reaction develops 1-2 hours after irradiation and lasts up to 2 days.

Nausea, vomiting, dyspepsia appear, salivation is disturbed, neurological symptoms are expressed, leukocytes decrease in the peripheral blood.

Clinic: dryness or hypersalivation in the oral cavity, decrease in taste and sensitivity of the mucous membrane, swelling of the lips and mucous membranes of other departments, hyperemia, petechial hemorrhages appear.

It is recommended to reduce the intake of radioisotopes into the body:

1) take a shower;

2) wash the mucous membranes with soda solution;

3) wash the stomach, intestines;

4) prescribe radioprotectors - substances that reduce the intake of isotopes (cuprinil, selenium, peracil, tincture of iodine).

Hypotension is recommended:

1) caffeine;

2) adrenaline;

3) strychnine;

4) glucose;

5) polyglucin;

6) 0,004 g of etaperazine.

Latent period - imaginary well-being (from several hours to 2-5 weeks). During this period, clinical symptoms are not expressed: there may be epilation, impaired salivation, herpetic lesions of the oral mucosa are possible, and in non-keratinized areas there may be candidiasis, spirochitosis, a decrease in hemoglobin is noted in the blood. Agranulocytosis is the main manifestation that leads to a violation of the body's defenses.

In this regard, the use of antiseptics, antibiotics is not desirable, as it enhances agranulocytosis.

On ORM - xerostomia, which can be removed with pilocarpine. It is possible to take bitterness, which have salivary properties (coltsfoot, yarrow). This is a period of active rehabilitation of the oral cavity, taking drugs that restore or protect the activity of hematopoietic organs (blood substitutes - leukocyte and platelet masses). M-anticholinergics (atropine, metacin).

The third period (the height of the disease). Against the background of a sharp deterioration in the general condition in the oral cavity, a clinical picture of a severe form of ulcerative necrotic gingivostomatitis occurs. The mucosa swells, the gingival papillae loosen, necrotic, the bone tissue of the alveolar process is resorbed, necrotized (radiation necrosis), sequestered, and jaw fractures are possible. The mucosa of other parts of the oral cavity is subjected to an ulcerative necrotic process with severe bleeding of the tissues. Accession of a secondary infection complicates the clinical picture of the ulcerative necrotic process. It is characterized by the vastness of distribution, the absence of sharp boundaries and the inflammatory reaction of surrounding tissues. The ulcers are covered with a dirty gray necrotic coating that emits a putrid odor. On the mucous membrane of the tongue there may be cracks, loss of taste.

The skin becomes marble due to hemorrhages. The septic state of the body is accompanied by clinical manifestations of infection.

Assign to combat septic conditions:

1) antibiotics (biseptol);

2) means that change hematopoiesis;

3) agents that normalize leukoposis (folic acid);

4) zymosan (in / m (suspension) at 0,002 g 1 time per day);

5) radioprotectors (cytostatics); Non-specific stimulation of hematopoiesis:

1) methyluracil (tablets, in suppositories). Improves cell reproduction, stimulates leukoposis;

2) mixatin 0,05. Radioprotective effect, sedative, hypnotic effect, vasoconstrictor effect, as it acts on smooth muscles;

3) antihemorrhagic agents (vikasol, ascorbic acid, vitamins B₁, AT₆, steroid hormone (10-15 mg per day)).

5. Diagnosis of the state of the human body by language

Of all the parts of the mucous membrane of the oral cavity, the surface of the tongue reacts most sensitively and early to various changes in the human body. Ancient Indian doctors, using Ayurvedic knowledge, determined the affected organ and diagnosis by the state of the tongue. Informational value is the color of the tongue, humidity, the presence and location of furrows, the state of individual zones, which are a reflection of certain organs, the presence and color of plaque. So, the anterior third corresponds to the heart and lungs in the tongue, the middle third corresponds to the stomach, spleen and pancreas, the intestines are projected onto the root of the tongue, the liver and kidneys are projected onto its lateral surfaces, the fold running along the middle of the tongue reflects the state of the spine. Increased sensitivity and discoloration of various areas indicate a violation of the functioning of those organs with which these areas are associated, the curvature of the median fold indicates damage to the spine, and the places of the bends indirectly indicate the suffering department. Uneven desquamation and regeneration of the epithelium are characteristic of lesions of the gastrointestinal tract, diathesis, helminthic invasions, and toxicosis during pregnancy. Tremor of the tongue indicates dysfunction of the autonomic nervous system, beginning neurosis, thyrotoxicosis. The presence of cracks, deep folds in the tongue indicates a violation of the bioenergetics of the body; the appearance of persistent imprints of teeth on it indicates a violation of the digestive processes.

Diagnosis by the color of plaque and the color of the mucous membrane of the tongue:

1) the tongue without plaque, cracks and lines is pale pink - the body is healthy;

2) yellow plaque - a violation of the functions of the digestive organs;

3) dense white coating - intoxication, constipation;

4) dense white plaque, thinning over time - a sign of improvement in the patient's condition;

5) black plaque - severe chronic dysfunction of the digestive organs, accompanied by dehydration and acidosis;

6) brown plaque - diseases of the lungs and gastrointestinal tract;

7) pale tongue - anemia and exhaustion of the body;

8) shiny, smooth tongue - anemia;

9) purple tongue - diseases of the blood and lungs in an advanced stage;

10) red tongue - disorders of the cardiovascular system, lungs and bronchi, hematopoietic system, also indicates an infectious process;

11) dark red tongue - speaks of the same disorders, but the prognosis is worse, the development of a life-threatening condition is possible;

12) blue tongue - diseases of the cardiovascular system, kidneys, lungs in an advanced stage;

13) bright blue tongue - preagonal state; Collagen diseases are a widespread group of diseases; most often they affect women of young and middle age. Although the etiology and pathogenesis of collagenoses have not yet been precisely established, it is known for certain that they are of an allergic nature and are accompanied by the development of autoimmune reactions that damage the connective tissue of the body. The course of collagenosis is long, cyclic, progressive, accompanied by an increase in body temperature. At the same time, signs of allergy are detected, their development is provoked by various exogenous factors, such as cooling, injury, infection in the body, taking medications, and physiotherapy procedures.

The most common manifestations of rheumatism in the maxillofacial region are pallor of the skin of the face, anemic mucous membranes, catarrhal inflammation of the gums, their thickening in the form of a roller, the severity of the vascular pattern, the formation of precarious chalky spots, multiple caries.

With this form of collagenosis, the color of the teeth changes, the enamel becomes thinner, light yellow spots (translucent dentin) appear on it, the edges of the teeth are erased and can be completely destroyed, vasculitis, submucosal hemorrhages, and petechial rashes on the mucosa may develop. In the temporomandibular joint, articular syndrome is expressed, which is manifested by short-term stiffness of the masticatory muscles, limitation and pain in opening the mouth, and a feeling of discomfort in this joint.

In addition to the presence of characteristic erythematous spots on the face in the form of a butterfly, with systemic lupus erythematosus, hard tissues of the teeth are affected, due to which their color changes, they become dull, chalk spots appear in the cervical zone of the teeth, areas of enamel necrosis with yellow or black pigmentation. The mucous membrane of the oral cavity at this time becomes hyperemic, edematous; along the line of closure of the molars, foci of clouded epithelium, the so-called lupus spots, rising above the rest of the surface, can form. In the acute stage of systemic lupus erythematosus in the oral cavity, a sharp fiery red lesion of the entire mucous membrane can be observed, on which erythematous edematous areas with clear boundaries are distinguished, as well as foci of desquamated epithelium, erosion in the soft palate. Such a lesion is called an enanthema, it is a characteristic diagnostic feature.

This disease is manifested by severe microcirculation disorders and the development of sclerotic processes leading to tissue thickening. At the same time, the appearance of a person changes significantly: the mobility of the soft tissues of the face decreases, facial expressions are almost absent, wrinkles are smoothed out, a microstoma develops - a decrease in the mouth opening, the lips are thinned, due to the shortening of the frenulum of the tongue, its mobility is limited.

Trigeminal neuralgia. The disease is manifested by bouts of pain along one or more branches of the trigeminal nerve, it is not uncommon. Trigeminal neuralgia is a polyetiological disease, its causes can be various infections (syphilis, tuberculosis, malaria, influenza, tonsillitis), gastrointestinal diseases, acute and chronic intoxications, oncological lesions, vascular changes in the brain, such as sclerosis, abnormal development , dental diseases (sinusitis, chronic periodontitis, the presence of an impacted tooth, cysts, bite pathology), arachnoiditis. More often trigeminal neuralgia affects people over 40 years old, and women get sick more often than men.

Allocate true and secondary neuralgia. True (or idiopathic) neuralgia is an independent disease, the cause of which cannot be established. Secondary (or symptomatic) neuralgia is a companion of any underlying disease (tumors, infections, intoxication, stomatogenic processes, brain diseases). Clinically, trigeminal neuralgia is manifested by attacks of sharp, jerking or cutting short-term pain, a burning sensation in a certain area of ​​the face, the area of ​​the oral mucosa, or in the jaw itself. The pain is unbearable, it can radiate to the neck, neck, temples, patients cannot speak, eat, turn their heads, as they are afraid to provoke a new pain attack. The pain ends as quickly as it begins. A painful attack may be accompanied by dilated pupils, hyperemia of the area of ​​innervation of the trigeminal nerve, increased salivation, lacrimation, an increase in the amount of nasal secretion, convulsive contractions of the mimic muscles. There is no pain during sleep.

One of the branches of the trigeminal nerve is usually affected: with neuralgia of the first branch (involved in the pathological process less often than the second and third), the pain is concentrated in the forehead, superciliary arches, anterior temporal region; neuralgia of the second branch is characterized by pain in the region of the upper lip, lower eyelid, wing of the nose, nasolabial groove, zygomatic zone, upper teeth, soft and hard palate; with neuralgia of the third branch, pain is determined in the region of the lower lip of the chin, teeth, cheeks, and tongue.

During palpation of the zones innervated by the trigeminal nerve, with its neuralgia, paresthesia of the skin is determined, the most painful points corresponding to the places where its branches exit: the eyebrow, infraorbital and mental foramina.

Treatment of trigeminal neuralgia should include the elimination of the primary disease, along with the aim of relieving painful symptoms for the patient, painkillers, B vitamins, prozerin, tegretol, chlorpromazine can be prescribed, in some patients a pronounced positive effect was observed after the use of bee venom, recommend the appointment of anticonvulsants and blockade of the affected branch with novocaine (the course of novocaine blockades consists of 20-25 injections of 3-5 ml of a 1% solution daily). Physiotherapeutic procedures are also prescribed: novocaine electrophoresis, paraffin therapy, Berganier half mask. In advanced cases that are not amenable to conservative treatment, they resort to surgical treatment, the main type of which is neurotomy.

LECTURE No. 9. Periomandibular abscesses and phlegmon

An abscess is a limited purulent inflammation of the cellular tissue with the formation of a cavity (and a granulation shaft), a purulent-inflammatory process is limited to the limits of any one isolated cellular space.

Phlegmon - acute diffuse purulent inflammation of the tissue (subcutaneous, intermuscular, interfascial), characterized by a tendency to further spread; diffuse purulent-inflammatory process, extending to 2-3 or more adjacent cellular spaces.

Cellulite is a serous inflammatory process in certain cellular spaces (MCF) (serous inflammation of the cellular tissue - according to the international nomenclature of diseases). If the inflammatory process becomes diffuse, then it is already interpreted as a phlegmon.

Etiology: These two pathological processes are considered together in view of the great difficulty in differential diagnosis.

The main features of the topical diagnosis of purulent maxillary phlegmon of odontogenic origin:

1) the sign of the "causal tooth". This refers to a tooth in the periapical or marginal tissues of which inflammation develops or has developed, which was the result of gangrene of the pulp or a consequence of the formation of marginal periodontitis. Such a tooth is a "generator of infection" that spreads and affects the tissues adjacent to it, therefore it is conditionally called causal;

2) a sign of "severity of inflammatory infiltrate" of the soft tissues of the maxillary region. This symptom is pronounced in superficial phlegmons and weakly expressed or absent in deep phlegmons. Any phlegmon is accompanied by intense inflammatory tissue infiltration. Here we are talking only about visible manifestations of infiltration and, as a result, a violation of the configuration of the face or, conversely, about the absence, asymmetry;

3) sign "impaired motor function of the lower jaw". Any inflammatory process in the localization zone of at least one of the masticatory muscles to some extent impairs the motor function of the lower jaw. Knowing the nature of the functions performed by the masticatory muscles and finding out the degree of their violation during the examination of the patient, it is possible to assume with sufficient certainty the localization of the development of the focus of inflammation;

4) sign "difficulty swallowing". The manifestation of this symptom is associated with compression of the lateral wall of the pharynx by the resulting inflammatory infiltrate, and, consequently, the appearance of pain that increases when trying to swallow something.

Classifications of abscesses and phlegmons of the maxillofacial region:

1) according to topographic and anatomical features;

2) according to the location of the tissue in which phlegmons appear (dividing them into phlegmons of the subcutaneous tissue and phlegmons of the intermuscular tissue);

3) according to the initial localization of the infectious-inflammatory process, highlighting osteophlegmons and adenophlegmons;

4) by the nature of the exudate (serous, purulent, putrefactive-hemorrhagic, putrid-necrotic, etc.).

Clinical picture: inflammation, as a rule, begins acutely. There is a rapid increase in local changes: infiltration, hyperemia, pain. In most patients, there is an increase in body temperature up to 38-40 ° C, in some cases there is a chill, which is replaced by a feeling of heat. In addition, general weakness is noted, which is due to the phenomenon of intoxication.

The following stages of the inflammatory process are distinguished:

1) serous inflammation;

2) serous-purulent inflammation (with signs of alteration expressed to one degree or another);

3) the stage of delimitation of the infectious focus, cleansing the surgical wound with proliferation phenomena.

Depending on the ratio of the main components of the inflammatory reaction, phlegmon with a predominance of exudation phenomena (serous, purulent) and phlegmon with a predominance of alteration phenomena (putrefactive necrotic) are distinguished.

The ultimate goal of the treatment of patients with abscesses and phlegmon of the maxillofacial region is the elimination of the infectious process and the complete restoration of impaired body functions in the shortest possible time. This is achieved through complex therapy.

When choosing specific therapeutic measures, the following should be taken into account:

1) the stage of the disease;

2) the nature of the inflammatory process;

3) virulence of the infectious beginning;

4) type of body response;

5) localization of the focus of inflammation;

6) concomitant diseases;

7) age of the patient.

The main task of treating patients in the acute stage of the disease is to limit the spread of the infectious process, to restore the balance that existed between the focus of chronic odontogenic infection and the patient's body.

Abscesses and phlegmon are located near the upper jaw - in the infraorbital region, zygomatic region, orbital region, temporal region, in the region of the infratemporal and pterygopalatine fossae, hard and soft palate.

The opening of the abscess of the infraorbital region is performed along the transitional fold of the mucous membrane at the level of the 1st-2nd-3rd teeth, however, unlike the periostectomy, it is recommended to go up into the canine fossa in a blunt way (with a hemostatic clamp) and push the muscles apart. In addition, it must be borne in mind that conventional drainage with a rubber or cellophane strip is sometimes not enough, since the abscess cavity, despite drainage, constantly continues to fill with purulent exudate. This is due to the fact that the drainage strip is infringed by contracted mimic muscles. To achieve full drainage, a perforated narrow rubber tube can be used, and sometimes it is necessary to open the abscess through the skin.

If the surgical opening of the abscess of the zygomatic region is performed along the lower edge of the greatest protrusion of the abscess from the side of the skin, then the opening of the phlegmon most often has to be performed depending on the spread of the abscess to the adjacent cellular spaces. The most rational method is a wide incision along the projection of the lower edge of the abscess from the side of the skin with the simultaneous imposition of counter-opening in the area of ​​the emerging spread of the process.

Among the phlegmon located near the lower jaw, the most common phlegmon of the submandibular triangle. It occurs as a result of the spread of infection from inflammatory foci in the region of the lower large molars.

Its initial clinical manifestations are characterized by the appearance of edema, and then infiltration under the lower edge of the body of the lower jaw. The infiltrate relatively quickly (within 2-3 days from the onset of the disease) spreads to the entire submandibular region. Puffiness of soft tissues passes to the cheek area and the upper lateral part of the neck. The skin in the submandibular region is stretched, shiny, hyperemic, not taken into a fold. Mouth opening is usually not impaired. In the oral cavity on the side of the purulent-inflammatory focus - moderate swelling and hyperemia of the mucous membrane.

The clinical manifestations of this phlegmon are quite typical and do not cause difficulties in differential diagnosis.

With an isolated lesion of the submandibular region, external access is used. A skin incision 6-7 cm long is made in the submandibular region along a line connecting a point 2 cm down from the top of the jaw angle with the middle of the chin. This direction of the incision reduces the likelihood of damage to the marginal branch of the facial nerve, which in 25% of people descends in a loop below the base of the mandible. The subcutaneous adipose tissue and the subcutaneous muscle of the neck with the superficial fascia of the neck enveloping it are dissected over the entire length of the skin incision. Above the grooved probe, the superficial plate of the own fascia of the neck is also dissected. Then, stratifying and pushing the fiber with a hemostatic clamp, they penetrate between the edge of the jaw and the submandibular salivary gland into the depths of the submandibular triangle - to the center of the infectious and inflammatory focus. If the facial artery and the anterior facial vein meet on the way, it is better to cross them between the ligatures. In order to avoid damage to the facial artery and anterior facial vein, when dissecting tissues during surgery, do not approach the bone of the body of the lower jaw with a scalpel, over the edge. This improves access to the infectious focus and reduces the likelihood of secondary bleeding. After evacuation of pus and antiseptic treatment, drains are introduced into the wound.

An abscess and phlegmon of the submental region is opened parallel to the edge of the lower jaw or along the midline (in the direction from the lower jaw to the hyoid bone), the skin, subcutaneous fatty tissue and superficial fascia are dissected; to the abscess penetrate the blunt way.

The prognosis for isolated phlegmon of the submandibular and submental areas in the case of timely complex treatment is usually favorable.

Duration of inpatient treatment of patients with phlegmon of the submandibular region - 12 days, submental region - 6-8 days; the total duration of temporary disability for patients with phlegmon of the submandibular region is 15-16 days, the submental region is 12-14 days.

The configuration of the face is sharply changed due to infiltration, swelling of the cheeks and adjacent tissues: there is swelling of the eyelids, lips, and sometimes in the submandibular region. The skin of the cheek is glossy, does not fold; the mucous membrane is hyperemic, edematous.

The choice of operative access depends on the localization of the infiltrate. The incision is made either from the side of the oral cavity, drawing it along the line of closure of the teeth, taking into account the course of the parotid duct, or from the side of the skin, taking into account the course of the facial nerve. After evacuation of purulent exudate, drainage is introduced into the wound.

Surgical opening of the phlegmon is performed by a vertical incision parallel to the posterior edge of the lower jaw branch and, depending on the spread of the abscess, the angle of the jaw is included. Drain the cavity with a rubber tube. When the abscess spreads into the peripharyngeal space, the incision is continued down, bordering the angle of the jaw with the transition to the submandibular triangle, and after a thorough digital revision of the cavity, drainage is performed during the day.

Surgical opening of the phlegmon of the pterygo-maxillary space is performed from the side of the skin in the submandibular region with an incision bordering the angle of the lower jaw, departing from the edge of the bone by 2 cm. A part of the tendon of the medial pterygoid muscle is cut off with a scalpel, the edges of the entrance to the cellular space are bluntly pushed apart with a hemostatic clamp. Purulent exudate comes out from under the muscles under pressure, a rubber outlet tube is inserted into the cavity.

Surgical opening of the abscess of the peripharyngeal space in the initial phase is performed by an intraoral incision passing somewhat medially and posteriorly from the pterygo-mandibular fold, the tissues are dissected to a depth of 7-8 mm, and then stratified with a blunt hemostatic forceps, adhering to the inner surface of the medial pterygoid muscle, until pus is obtained . A rubber strip is used as drainage.

With a phlegmon of the peripharyngeal space that has spread downward (below the dentition of the lower jaw), the intraoral opening of the abscess becomes ineffective, so it is immediately necessary to resort to an incision from the side of the submandibular triangle closer to the angle of the lower jaw.

After dissection of the skin, subcutaneous tissue, superficial fascia, subcutaneous muscle and outer leaf of the own fascia of the neck, the inner surface of the medial pterygoid muscle is found and the tissue is bluntly stratified along it until pus is obtained. After a digital revision of the abscess and combining all its spurs into one common cavity for drainage, a tube and a loose-gauze swab moistened with an enzyme solution are inserted on the first day. The swab is removed the next day, leaving 1-2 tubes.

The duration of inpatient treatment of patients with phlegmon of the pterygo-mandibular space - 6-8 days, peripharyngeal space - 12-14 days; the total duration of temporary disability for patients with phlegmon of the pterygo-mandibular space - 10-12 days, peripharyngeal - 16-18 days.

Phlegmon of the floor of the mouth is a purulent disease, when the sublingual, submandibular regions, submental triangle are affected in different combinations.

With the diffuse nature of phlegmon, only wide incisions can be recommended parallel to the edge of the lower jaw, retreating from it by 2 cm. This incision can be made according to indications of any length up to the collar with partial clipping of the attachment of the maxillohyoid muscle on both sides (for 1,5- 2 cm).

With a spilled abscess that has descended far, it can be opened with another collar incision in the area of ​​\u7b\u10bits lower edge, passing along the upper cervical fold. Both methods of opening provide good drainage, comply with the laws of purulent surgery. In order to avoid diagnostic errors when opening a diffuse phlegmon of the bottom of the oral cavity, it is necessary to revise the peripharyngeal space. This event should be considered not only as a therapeutic and diagnostic, but also as a preventive one. In order to obtain a cosmetically full-fledged scar on the XNUMX-XNUMXth day after the operation, after the cessation of purulent exudation, secondary sutures can be applied, leaving rubber drainage strips.

Putrid-necrotic phlegmon of the floor of the mouth is opened with a collar-shaped incision. It can be recommended to make only wide incisions (which achieve drainage and aeration of the tissues) parallel to the edge of the lower jaw, retreating from it by 2 cm. 1,5-2 cm). With a spilled abscess that has descended far, it can be opened with another collar incision in the region of its lower edge, passing along the upper cervical fold. Both methods of opening provide good drainage, comply with the laws of purulent surgery. All cellular spaces (submandibular, submental, sublingual) involved in the inflammatory process are widely opened and drained. At the same time excised necrotic tissue. With the localization of putrefactive-necrotic phlegmon in other cellular spaces, they are widely opened and drained from the side of the skin according to generally accepted rules.

Thus, surgical treatment for putrefactive-necrotic phlegmon in a number of cases includes tracheotomy with tracheostomy, wide opening of phlegmon, necrotomy, necrectomy, removal of the causative tooth (with the odontogenic nature of the disease), etc.

Pathogenetic treatment: local oxygenation, achieved by periodic insufflation of oxygen through a catheter into the wound, (HBO) tissues.

Regional infusion of antibiotics is carried out. Proteolytic enzymes are widely used to accelerate wound cleansing from necrotic tissues. FTL - UV irradiation of the wound.

For common, extensive phlegmon, a hyperergic reaction of the body is characteristic, they are often complicated by mediastinitis, thrombophlebitis and thrombosis of the vessels of the face and brain, sinuses of the dura mater, sepsis.

The incidence of progressive course of purulent diseases is 3-28%. Mortality with widespread phlegmon ranges from 28 to 50%, and with intracranial complications, mediastinitis, sepsis - from 34 to 90%.

According to M. A. Gubin, the following phases of the disease are distinguished - reactive, toxic and terminal.

The phase of a progressive purulent disease determines the tactics, the choice of methods and means of treatment, the duration of the course.

Immediate complex of treatment (surgical, therapeutic type of intensive care, FTL). Focus on the regulation of the functions of respiration, circulation, metabolism, nervous and endocrine systems.

Hemo-, lymphosorption, lymphatic drainage, plasmapheresis should be widely used. In the local treatment of wounds, it is advisable to use local dialysis, vacuum suction of exudate, sorbents, immobilized enzymes, antibiotics that have an immunocorrective effect, ultraviolet irradiation, laser, ozone and other types of influence on the wound process, depending on its phase.

The prognosis for phlegmon of the floor of the mouth, especially putrefactive necrotic and with the development of complications, is serious for the life of patients. With putrefactive-necrotic phlegmon, inflammatory phenomena are prone to progression. Mediastinitis develops more often, but there may be an upward spread of infection. The inflammatory disease can be complicated by septic shock, acute respiratory failure, and sepsis.

The duration of inpatient treatment of patients with phlegmon of the floor of the mouth is 12-14 days, the total duration of temporary disability for patients with phlegmon of the floor of the mouth is 18-20 days. The development of complications leads to long-term disability, disability, and sometimes death.

LECTURE No. 10. Osteomyelitis of the jaws

Osteomyelitis is an infectious inflammatory process of the bone marrow that affects all parts of the bone and is often characterized by generalization. The meaning of the word osteomyelitis is inflammation of the bone marrow, although from the very beginning it meant inflammation of the entire bone. This term was introduced into the literature in 1831 by P. Reynaud to denote an inflammatory complication of a bone fracture. Attempts by some authors to replace the term "osteomyelitis", such as "panostitis", "osteitis", were unsuccessful, and most surgeons adhere to the original term.

Bone inflammation has been known for a long time. It is mentioned in the works of Hippocrates, Abu Ali Ibn Sina, A. Celsus, K. Galen and others. But the traditional image of the clinical picture of acute osteomyelitis in 1853 was given by the French surgeon Ch. M.E. Chassaignac. The modern classification of osteomyelitis has been compiled taking into account the need for a report based on the principles of quantitative assessment of various aspects of the disease. Thus, a detailed working classification of osteomyelitis was developed, taking into account its etiology, staging, phasing, localization of the pathological process and clinical course.

Classification of osteomyelitis

1. By etiology:

1) monoculture;

2) mixed, or associated, culture:

a) double association;

b) triple association.

2. By clinical forms:

1) acute hematogenous osteomyelitis;

2) generalized form:

a) septicotoxic;

b) septicopyemic;

3) local (focal) form:

a) developed after a bone fracture;

b) gunshot;

c) postoperative form (including needle);

d) postradiation form;

4) atypical forms:

a) Brodie's abscess (sluggish intraosseous process);

b) albuminous (Ollier osteomyelitis);

c) antibiotic;

d) sclerosing (osteomyelitis Garre).

3. Stages and phases of hematogenous osteomyelitis:

1) acute stage:

a) intramedullary phase;

b) extramedullary phase;

2) subacute stage:

a) recovery phase;

b) the phase of the ongoing process;

3) chronic stage:

a) an exacerbation phase;

b) remission phase;

c) recovery phase.

4. Localization of the process and clinical forms:

1) osteomyelitis of tubular bones;

2) osteomyelitis of flat bones.

Morphological forms:

a) diffuse;

b) focal;

c) diffuse-focal.

5. Complications:

1) local:

a) pathological fracture;

b) pathological dislocation;

c) false joint;

2) general.

1. Etiology, pathogenesis and pathological anatomy of osteomyelitis

In 1880, Louis Pasteur isolated a microbe from the pus of a patient with osteomyelitis and named it staphylococcus. Subsequently, it was found that any microorganism can cause osteomyelitis, but its main causative agent is Staphylococcus aureus. However, since the mid-70s 40th century the role of gram-negative bacteria has increased, in particular Proteus vulgaris, Pseudomonas aeruginosa, Escherichia coli and Klebsiella, which are more often sown in association with staphylococcus aureus. Viral infections can also be an important etiological factor, against which 50-XNUMX% of cases of osteomyelitis develop.

There are many theories of the pathogenesis of osteomyelitis. The most famous of them are vascular, allergic, neuroreflex.

One of the founders of the vascular theory in 1888 at the III Congress of Russian doctors pointed out the features of the vessels of children that contribute to the occurrence of osteomyelitis. He believed that the arteries that feed the bone in the metaphyses branch out, forming an extensive network in which the blood flow slows down sharply, which contributes to the settling of pyogenic microbes in it. However, subsequent morphological studies have established that the terminal vessels in the metaphyses of long bones disappear by the age of 2 years, and therefore Bobrov's idea turned out to be one-sided. But A. Vilensky in 1934, without denying the embolic theory of the occurrence of osteomyelitis, believed that the obstruction of the arterial system of the pineal gland was caused not by passive blockage by a microbial embolus, but by the development of inflammatory thrombobarteritis or thrombophlebitis. However, the latter should be correctly interpreted as arising secondarily.

A significant contribution to the development of the theory of the pathogenesis of osteomyelitis was the experiments of the Smolensk pathologist Professor S. M. Derizhanov (1837-1840). The author sensitized rabbits with horse serum. Then, introducing a resolving dose of serum into the bone marrow cavity, he received aseptic allergic osteomyelitis. Based on these experiments, S. M. Derizhanov believed that bacterial emboli do not play any role in the pathogenesis of osteomyelitis. The disease develops only on the basis of sensitization of the body and the occurrence of aseptic inflammation in the bone, which occurs from a variety of reasons. In the osteomyelitic focus, proliferative changes in the periosteum and Haversian canals compress the vessels from the outside, and swelling of the walls of the vessels themselves reduces their lumen from the inside. All this makes it difficult and disrupts blood circulation in the bones, contributing to the occurrence of osteomyelitis.

According to the neuroreflex theory, the occurrence of osteomyelitis is promoted by a prolonged reflex vasospasm with impaired blood circulation. Factors that provoke vasospasm can be any irritants from the external environment. At the same time, the role of sensitization of the body and the presence of latent infection is not denied.

In the pathogenesis of acute osteomyelitis, autogenous sources of microflora are of particular importance. Foci of latent or dormant infection in carious teeth, tonsils, constantly releasing toxins and decay products, contribute to the development of a delayed-type allergic reaction, create a predisposition of the body to the onset of the disease. In this situation, in a sensitized organism, nonspecific stimuli (trauma, hypothermia, overwork, illness) play the role of a resolving factor and can cause aseptic inflammation in the bones. Under these conditions, when microbes enter the bloodstream, it is converted into acute hematogenous osteomyelitis. In other cases, as a result of a past illness or the influence of another non-specific stimulus in a premorbid state, the body may be exhausted. In this situation, an exogenous infection, once in a weakened body, can play the role of a trigger. Odontogenic osteomyelitis of the jaws develops just as a result of infection from the periodontal focus into the jawbone.

Pathological changes in osteomyelitis are currently well studied. On the 1st day, reactive inflammation phenomena are noted in the bone marrow: hyperemia, dilation of blood vessels, blood stasis with the release of leukocytes and erythrocytes through the altered vascular wall, intercellular infiltration and serous impregnation. On the 3rd-5th day, the medullary cavity is filled with red and yellow bone marrow. In some of its areas, accumulations of eosinophils and segmented neutrophils, single plasma cells are found. The accumulation of segmented neutrophils is also noted in the dilated Haversian canals of the cortical bone. On the 10-15th day, purulent infiltration progresses with the development of severe bone marrow necrosis throughout; sharply dilated vessels with foci of hemorrhages between the bone crossbars, multiple accumulations of exudate with a huge number of decaying leukocytes are revealed. Growth of granulation tissue in the elements surrounding the bone marrow was noted. On the 20th-30th day, the symptoms of acute inflammation persist. Fields filled with necrotic masses, detritus and surrounded by large accumulations of segmented neutrophils and lymphocytes are visible in the bone marrow. Separate areas of endosteal bone formation are outlined in the form of primitive bone crossbars. In the cortex, the Haversian canals are dilated and corroded, and the bony bars are thinned. On the 35th-45th day of the disease, necrosis spreads to almost all elements of the bone tissue, the cortical substance becomes thinner. The bone continues to collapse, there is no endosteal formation, the cavities are filled with homogeneous masses, in which sequesters are found surrounded by purulent exudate. Sequesters are adjacent to necrotic tissue, which, without sharp boundaries, passes into fibrous connective tissue. Near the endosteum, granulation tissue appears, in which massive foci of necrosis are visible with areas of the bone marrow and sharply dilated vessels, densely infiltrated with myeloid elements of varying degrees of maturity.

The timing of the formation of sequesters is different. In some cases, they are determined on radiographs by the end of the 4th week, in others, especially with extensive destruction, it takes 3-4 months for the final rejection of dead areas. The presence of separated sequesters indicates the transition of the inflammatory process to the chronic stage. After the transition of an acute inflammatory process into a chronic one, the vessels of the newly formed bone tissue gradually become empty, calcium salts are deposited in the intercellular substance, giving a special density to the bone tissue. The more there is a focus of destruction, the more pronounced sclerotic changes in the bone. After several years of the eburnation process, the bone acquires exceptional density. Vessels are almost not defined in it; when it is processed with a chisel, it crumbles. However, at the site of the transferred osteomyelitis for a long time, even for years, microabscesses and foci of latent infection can be detected. These foci, under certain conditions, give an exacerbation or relapse of the disease even after many years.

With long-term osteomyelitis with fistulas and frequent exacerbations, significant changes occur in the surrounding soft tissues. Fistulas often have convoluted passages that communicate with cavities located in the surrounding muscles. The walls of the fistulas and their ramifications are covered with granulations that produce a wound secret, which, accumulating in the cavities and not having sufficient outflow, periodically causes an exacerbation of the inflammatory process in the soft tissues. During remission, granulations are scarred, fistulas are closed. The alternation of periods of exacerbation and remission leads to cicatricial degeneration and atrophy of muscles, subcutaneous fat. In dense scar tissues, calcium salts are sometimes deposited, and ossifying myositis develops.

2. Clinic and diagnosis of acute odontogenic osteomyelitis

With a relatively slow development of osteomyelitis, the initial symptom is pain in the region of the causative tooth. Percussion of the tooth is acutely painful, first weakened, and then its significant mobility is detected. The mucous membrane in the area of ​​the gingival margin on both sides is edematous and hyperemic. Palpation of this area is painful. Body temperature rises to 37,5-38 o C, more often patients experience general malaise. A similar formation of osteomyelitis may resemble a picture of periostitis. With the active dynamics of osteomyelitis that has arisen in a certain area of ​​the jaw, the pain is rapidly spreading and intensifying. In the next few hours, the body temperature reaches 40 ° C. Chills are noted. In especially severe cases, twilight states are noted in patients. The development of osteomyelitis in such cases is very similar to the course of acute infectious diseases.

When examining the oral cavity, a picture of multiple periodontitis is revealed: the teeth adjacent to the causative ones are mobile, painful on percussion. The mucous membrane of the gums is sharply hyperemic, loose and edematous. Subperiosteal abscess occurs early. Interest in the inflammatory process of masticatory muscles causes their contracture. At the height of the development of an acute process, a decrease in the sensitivity of the skin of the chin area (Vincent's symptom) is determined, which is the result of compression of the lower alveolar nerve by inflammatory exudate. Already in the acute period, lymphadenopathy of regional lymph nodes is noted.

Under favorable conditions, purulent exudate breaks under the periosteum and, melting the mucous membrane, pours into the oral cavity. Quite often, thus, osteomyelitis is complicated by phlegmon.

Also, purulent exudate can break through, depending on the localization of the process, into the maxillary sinus, causing acute sinusitis, into the pterygopalatine fossa, into the orbit, into the infratemporal region, to the base of the skull.

The acute stage of osteomyelitis of the jaws lasts from 7 to 14 days. The transition to the subacute stage occurs during the formation of a fistulous tract, which ensures the outflow of exudate from the focus of inflammation.

In subacute osteomyelitis of the jaw, pain decreases, inflammation of the oral mucosa subsides, body temperature drops to subfebrile, blood and urine tests are close to normal. Pus is abundantly secreted from the fistula. Pathologically, the subacute stage of osteomyelitis is characterized by a gradual limitation of the area of ​​the bone lesion and the beginning of the formation of sequesters. In the same period, along with the necrotic process, reparative phenomena are observed. On the radiograph, an area of ​​osteoporosis of the bone with a noticeable border between healthy and affected tissue is determined, but there are still no clear outlines of the sequester. Due to the resorption of mineral salts in the damaged area of ​​the bone on the x-ray, it is determined as a structureless bone tissue with a fairly clearly manifested change in areas of enlightenment and bone compaction.

Subacute osteomyelitis lasts an average of 4-8 days and without noticeable signs becomes chronic.

The chronic form of osteomyelitis of the jaws can last from 4-6 days to several months. The final outcome of chronic osteomyelitis is the final rejection of necrotic bone areas with the formation of sequesters. Self-healing occurs only after the elimination of all sequesters through the fistulous course, but treatment is still mandatory.

The diagnosis of chronic osteomyelitis does not cause great difficulties. The presence of a fistulous tract with a purulent discharge, a causative tooth and radiograph data (a sequestral cavity filled with sequesters of various sizes is found on the radiograph) in most cases exclude an error. In some cases, it is necessary to conduct a study of pus to exclude the bone form of actinomycosis.

3. Treatment

In acute osteomyelitis of the jaw, early wide periostotomy is indicated to reduce intraosseous pressure by ensuring the outflow of exudate and preventing the spread of the process to neighboring areas. It is also necessary to eliminate the main factor that caused the development of osteomyelitis (removal of the causative tooth). Tooth extraction must be combined with antibiotic therapy.

You can also use the method of intraosseous washing. To do this, two thick needles are inserted through the cortical plate into the thickness of the bone marrow. The first - at one pole of the border of the bone lesion, the second - at the other. An isotonic sodium chloride solution with an antiseptic or antibiotic is dripped through the first needle, and the liquid flows out through the second needle. The use of the method contributes to the rapid relief of the process, the removal of intoxication, and the prevention of complications.

In the subacute stage of osteomyelitis, the previously prescribed therapy is continued. In the chronic stage with the end of the formation of sequesters, it is necessary to choose the right time for surgical intervention. Removal of sequesters should be done with their final rejection, without injuring a healthy bone; on roentgenograms the sequesters freely lying in a sequestral cavity are visible.

Sequestrectomy is performed, depending on the area of ​​the jaw lesion, either under local anesthesia or under general anesthesia. The approach to the sequester cavity is usually determined by the exit site of the fistulous tract. A wide incision exposes the bone. With a preserved cortical plate, it is trepanned in the place where it is pierced by the fistulous tract. Curettage spoon remove sequesters, granulations. Destruction of the natural barrier along the periphery of the sequester cavity should be avoided. If a sequester that has not yet completely separated is found, it should not be forcibly separated. It is necessary to leave it with the expectation of self-rejection and removal through the wound. The sequester cavity is washed with a solution of hydrogen peroxide and filled with an iodoform swab, the end of which is brought into the wound. The edges of the wound are sutured.

In the event of a spontaneous fracture of the lower jaw with the formation of a defect, bone grafting is indicated. After sequestrectomy and the creation of receptive sites on the fragments, the graft is placed overlay and strengthened with wire sutures.

The teeth involved in the inflammatory process and become mobile can become stronger as the acute events subside. However, the preservation of such teeth sometimes requires treatment similar to that of periodontal disease.

LECTURE No. 11. Modern filling materials: classifications, requirements for permanent filling materials

Filling is the restoration of the anatomy and function of the destroyed part of the tooth. Accordingly, the materials used for this purpose are called filling materials. At present, due to the emergence of materials capable of recreating tooth tissues in their original form (for example, dentin - glass ionomer cements, (GIC) compomers, opaque shades of composites; enamel - fine hybrid composites), the term restoration is more often used - restoration of lost tissues tooth in its original form, i.e. imitation of tissues in terms of color, transparency, surface structure, physical and chemical properties. Reconstruction is understood as a change in the shape, color, transparency of the crowns of natural teeth.

Filling materials are divided into four groups.

1. Filling materials for permanent fillings:

1) cements:

a) zinc phosphate (Foscin, Adgesor original, Adgesor fine, Unifas, Viscin, etc.);

b) silicate (Silicin-2, Alumodent, Fritex);

c) silicophosphate (Silidont-2, Laktodont);

d) ionomer (polycarboxylate, glass ionomer);

2) polymeric materials:

a) unfilled polymer monomers (Acryloxide, Carbodent);

b) filled polymer-monomer (composites);

3) compomers (Dyrakt, Dyrakt AP, F-2000);

4) materials based on polymer glass (Solitaire);

5) amalgams (silver, copper).

2. Temporary filling materials (water dentin, dentin paste, tempo, zinc-eugenol cements).

3. Materials for medical pads:

1) zinc-eugenol;

2) containing calcium hydroxide.

4. Materials for filling root canals.

The properties of filling materials are considered in accordance with the requirements for filling materials.

Requirements for permanent filling materials

1. Technological (or manipulation) requirements for the initial uncured material:

1) the final form of the material should contain no more than two components that are easily mixed before filling;

2) after mixing, the material should acquire plasticity or a consistency that is convenient for filling the cavity and forming an anatomical shape;

3) the filling composition after mixing must have a certain working time, during which it retains plasticity and the ability to form (usually 1,5-2 minutes);

4) the curing time (the period of transition from a plastic state to a solid state) should not be too long, usually 5-7 minutes;

5) curing must take place in the presence of moisture and at a temperature not exceeding 37 °C.

2. Functional requirements, i.e. requirements for the cured material. The filling material in all respects should approach the indicators of the hard tissues of the tooth:

1) show adhesion to the hard tissues of the tooth that is stable in time and in a humid environment;

2) during curing, give minimal shrinkage;

3) have a certain compressive strength, shear strength, high hardness and wear resistance;

4) have low water absorption and solubility;

5) have a coefficient of thermal expansion close to the coefficient of thermal expansion of the hard tissues of the tooth;

6) have low thermal conductivity.

3. Biological requirements: the components of the filling material should not have a toxic, sensitizing effect on the tissues of the tooth and organs of the oral cavity; the material in the cured state should not contain low molecular weight substances capable of diffusion and leaching from the filling; The pH of aqueous extracts from the uncured material should be close to neutral.

4. Aesthetic requirements:

1) the filling material must match the color, shades, structure, transparency of the hard tissues of the tooth;

2) the seal must have color stability and not change the quality of the surface during operation.

1. Composite materials. Definition, development history

In the 40s. 30th century Acrylic quick-hardening plastics were created, in which the monomer was methyl methacrylate, and the polymer was polymethyl methacrylate. Their polymerization was carried out thanks to the initiator system BPO-Amin (benzoyl and amine peroxide) under the influence of oral temperature (40-XNUMX ° C), for example Acryloxide, Carbodent. The specified group of materials is characterized by the following properties:

1) low adhesion to tooth tissues;

2) high marginal permeability, which leads to a violation of the marginal fit of the filling, the development of secondary caries and inflammation of the pulp;

3) insufficient strength;

4) high water absorption;

5) significant shrinkage during polymerization, about 21%;

6) discrepancy between the coefficient of thermal expansion and that of the hard tissues of the tooth;

7) high toxicity;

8) low aesthetics, mainly due to a change in the color of the filling (yellowing) during the oxidation of the amine compound.

In 1962, RL BOWEN proposed a material in which BIS-GMA, with a higher molecular weight, was used as a monomer instead of methyl methacrylate, and quartz treated with silanes as a filler. Thus, RL BOWEN laid the foundation for the development of composite materials. In addition, in 1965, M. Buonocore made the observation that the adhesion of the filling material to the tissues of the tooth improves significantly after pre-treatment of the enamel with phosphoric acid. These two scientific achievements served as prerequisites for the development of adhesive methods for the restoration of tooth tissues. The first composites were macrofilled, with the particle size of the inorganic filler from 10 to 100 microns. In 1977, microfilled composites were developed (particle size of inorganic filler from 0,0007 to 0,04 µm). In 1980, hybrid composite materials appeared, in which the inorganic filler contains a mixture of micro- and macroparticles. In 1970, M. Buonocore published a report on filling fissures with a material that polymerizes under the influence of ultraviolet rays, and since 1977, the production of light-cured composites polymerized under the action of blue color (wavelength - 450 nm) began.

Composite materials are polymeric filling materials containing more than 50% by weight of finished inorganic filler treated with silanes, therefore composite materials are called filled polymers, in contrast to unfilled ones, which contain less than 50% inorganic filler (for example: Acryloxide - 12%, Carbodent - 43%.

2. Chemical composition of composites

The main components of composites are an organic matrix and an inorganic filler.

There is the following classification of composite materials.

1. Depending on the particle size of the inorganic filler and the degree of filling, the following are distinguished:

1) macro-filled (ordinary, macro-filled) composites. The particle size of the inorganic filler is from 5 to 100 microns, the content of the inorganic filler is 75-80% by weight, 50-60% by volume;

2) composites with small particles (microfilled). The particle size of the inorganic filler is 1-10 microns;

3) microfilled (microfilated) composites. The particle size of the inorganic filler is from 0,0007 to 0,04 microns, the content of the inorganic filler is 30-60% by weight, 20-30% by volume.

Depending on the shape of the inorganic filler, microfilled composites are divided into:

a) inhomogeneous (contain microparticles and conglomerates of prepolymerized microparticles);

b) homogeneous (contain microparticles);

4) hybrid composites are a mixture of conventional large particles and microparticles. Most often, composites of this group contain particles ranging in size from 0,004 to 50 µm. Hybrid composites, which include particles no larger than 1-3,5 microns, are finely dispersed. The amount of inorganic filler by weight is 75-85%, by volume 64% or more.

2. According to the purpose, composites are distinguished:

1) class A for filling carious cavities of class I-II (according to Black);

2) class B for filling carious cavities III, IV, V classes;

3) universal composites (inhomogeneous microfilled, finely dispersed, hybrid).

3. Depending on the type of the original form and the method of curing, the materials are divided into:

1) light-cured (one paste);

2) chemical curing materials (self-curing):

a) type "paste-paste";

b) "powder - liquid" type.

The first composite, proposed by Bowen in 1962, had quartz flour as a filler with particle sizes up to 30 microns. When comparing macrofilled composites with traditional filling materials (unfilled polymer-monomer), their lower polymerization shrinkage and water absorption, higher tensile and compressive strength (by 2,5 times), and lower coefficient of thermal expansion were noted. Nevertheless, long-term clinical trials have shown that fillings made of macrofilled composites are poorly polished, change in color, and there is a pronounced abrasion of the filling and the antagonist tooth.

The main disadvantage of macrophiles was the presence of micropores on the surface of the filling, or roughness. The roughness arises due to the significant size and hardness of the inorganic filler particles compared to the organic matrix, as well as the polygonal shape of the inorganic particles, so they quickly crumble when polished and chewed. As a result, there is a significant abrasion of the filling and the antagonist tooth (100-150 microns per year), the fillings are poorly polished, surface and subsurface pores, they need to be eliminated (cleaning etching, washing, applying adhesive, polymerizing the adhesive, applying and polymerizing the composite); otherwise, they will be stained. Next, the final finishing (polishing) of the filling is performed. First, rubber, plastic heads, flexible disks, strips are used, and then polishing pastes. Most finishing companies produce two types of pastes: for preliminary and final polishing, which differ from each other in the degree of dispersion of the abrasive. It is necessary to carefully study the instructions, since the time of polishing with pastes of different companies is different. For example: Dentsply polishing pastes: polishing should be started with Prisma Gloss paste for 63 seconds on each surface separately. Polishing with this paste gives the surface a wet sheen (the filling shines when wet with saliva). Next, the "Frisra Gloss Exstra Fine" paste is used (also for 60 from each surface), which will give a dry shine (when drying the tooth with an air jet, the shine of the composite is comparable to the shine of enamel). If these rules are not observed, it is impossible to achieve an aesthetic optimum. The patient should be warned that dry sheen needs to be restored every 6 months. When filling cavities of II, III, IV classes, flosses are used to control the marginal fit of the seal in the gum area, as well as to control the contact point. Floss is introduced into the interdental space, without delay, but with great effort slides over the contact surface. It shouldn't tear or get stuck.

Ignoring the final illumination (illumination of each surface of the restoration for 1 minute) can compromise the strength of the filling, resulting in chipping of the restoration.

Composites with small particles (micro-filled) are similar in properties to macro-filled ones, but due to a decrease in particle size, they have a higher degree of filling, are less susceptible to abrasion (about 50 microns per year) and are better polished. For filling in the area of ​​the frontal group, Visio-Fill, Visar-Fill, Prisma-Fill (light-curing) are recommended, in the area of ​​chewing teeth are used: P-10, Bis-Fil II (chemical curing), Estelux Post XR, Marathon, Ful-Fil , Bis-Fil I, Occlusin, Profil TLG, P-30, Sinter Fil (light cured).

In 1977, microfilled composites were created, which include particles of an inorganic filler 1000 times smaller than those of macrophiles, due to this, their specific surface area increases by 1000 times. Microphilic composites are easily polished compared to macrophiles, they are distinguished by high color fastness (light-curing), less abrasion, since they are not characterized by roughness. Nevertheless, they are inferior to conventional composites in terms of strength and hardness, have a higher coefficient of thermal expansion, significant shrinkage and water absorption. An indication for their use is the filling of carious cavities of the frontal group of teeth (III, V classes).

A variety of microfilled composites are inhomogeneously microfilled composites, which include fine particles of silicon dioxide and microfilled prepolymers. In the manufacture of these composites, pre-polymerized particles (about 18–20 µm in size) are added to the main mass containing microfilled particles, thanks to this technique, the saturation with the filler is more than 80% by weight (for homogeneous microfilled particles, the filling by weight is 30–40%), in Therefore, this group of materials is more durable, and it is used for filling frontal and lateral teeth.

Representatives of microfilled (homogeneous) composites are the following composites.

- see Table No. 5.

The inorganic filler is a mixture of conventional large particles and microparticles. Contact with an etching agent on an adjacent tooth, if it is not isolated by a matrix, can lead to the development of caries.

Acid damage to the oral mucosa leads to burns. The etching solution must be removed, the mouth rinsed with an alkali solution (5% sodium bicarbonate solution) or water. With significant tissue damage, treatment is carried out with antiseptics, enzymes, keratoplastic preparations.

After etching, it is necessary to exclude contact of the etched enamel with the oral fluid (the patient should not spit, the use of a saliva ejector is mandatory), otherwise the microspaces are closed by saliva mucin, and the adhesion of the composites deteriorates sharply. If the enamel is contaminated with saliva or blood, the etching process must be repeated (cleaning etching - 10 s).

After washing, the cavity should be dried with an air jet, the enamel becomes matte. If dentine etching has been used, the principles of wet bonding must be kept in mind. Dentin must not be overdried, it must be moist, sparkling, otherwise air enters the dentinal tubules, demineralized dentin; collagen fibers stick together ("spaghetti effect"), as a result, the formation of the hybrid zone and strands in the dentinal tubules is disturbed. The result of the above phenomena may be the occurrence of hyperesthesia, as well as the strength of attachment of the filling to the dentin decreases.

At the stage of filling, the following errors and complications are possible. Wrong choice of composite, ignoring indications for its use. It is unacceptable, for example, to use micro-filled material on the chewing group of teeth due to low strength (or macro-filled - in the area of ​​the anterior teeth, due to unaesthetics.

*cm. Table No. 6. Representatives of finely dispersed hybrid composites.

1. Technological properties:

1) the final form of chemically curing composites contains two composites (mixed before filling): "powder - liquid", "paste - paste". Light-cured ones have one paste, so they are more homogeneous, there is no air porosity, they are accurately dosed, unlike chemically cured ones;

2) after mixing, chemically cured composites acquire plasticity, which they retain for 1,5-2 minutes - working time. During this time, the plasticity of the material changes - it becomes more viscous. The introduction of the material and its formation outside the working hours lead to a violation of adhesion and loss of the seal. Therefore, chemically curable materials have limited working time, while photopolymers do not;

3) the curing time for chemically cured ones is on average 5 minutes, for photopolymers - 20-40 s, but for each layer, therefore, the time for placing a filling from a photopolymer is longer.

2. Functional properties:

1) all composites have sufficient adhesion, which depends on etching, the type of bonds or adhesives used (etching increases the adhesion force of composites to enamel by 75%; enamel bonds provide an adhesion force of 20 MPa to enamel, and dentin adhesives create different adhesive forces with dentin in depending on the generation of the adhesive, which is in I generation - 1-3 MPa; II generation - 3-5 MPa; III generation - 12-18 MPa; IV and V generations - 20-30 MPa);

2) composites of chemical curing have the highest shrinkage, mostly of the "powder-liquid" type (from 1,67 to 5,68%). Photocurable - about 0,5-0,7%, which depends on the filler load: the more it is, the less shrinkage (macrophiles, hybrid ones have less shrinkage than microfilled ones); in addition, shrinkage in photopolymers is compensated by layer-by-layer curing, directed polymerization;

3) compressive and shear strength is the highest in hybrid and macrofilled composites, less in microfilled ones, so they are used in the area of ​​anterior teeth. The abrasion is greatest in macro-filled due to roughness - 100-150 microns per year, less in micro-filled ones, minimal in finely dispersed hybrids - 7-8 microns per year and inhomogeneous micro-filled ones. The wear rate of chemically cured composites is higher than that of light cured ones, which is associated with internal porosity and a lower degree of polymerization;

4) water absorption is greatest in microfilled ones, which significantly reduces their strength, less in hybrids and macrophiles, since they contain less organic component and more filler;

5) the coefficient of thermal expansion is closest to solid tissues in macrofilled and hybrids due to the high content of the filler;

6) all composites have low thermal conductivity.

3. Biological requirements (properties). Toxicity is determined by the degree of polymerization, which is greater for photopolymers, and therefore they contain fewer low molecular weight substances and are less toxic. The use of IV and V generation dentin adhesives makes it possible to dispense with insulating pads in case of medium caries, in case of deep caries, the bottom is covered with glass ionomer cement. Chemically cured composites, as a rule, are completed with enamel bonds, so the use of an insulating gasket (for medium caries) or an insulating and healing gasket (for deep caries) is suggested.

4. Aesthetic properties. All chemically cured composites: change color due to the oxidation of benzoyl peroxide, macrofilled - due to roughness. When opening and necrectomy, the classical principles of surgical treatment of the carious cavity are used. If it is intended to use only enamel bonds (adhesives), then traditional principles must be observed when forming a carious cavity: the walls and bottom of the treated cavity must be at a right angle, the formation of additional sites is carried out with cavities of II, III, IV classes. It is possible to completely abandon the classical principles of the formation of a carious cavity in the case of using enamel-dentin adhesive systems. In this case, the entire dentin or part of it (in the case of laying gaskets on the bottom of the carious cavity) is used for adhesion to the composite.

At the stage of processing the edges of the enamel, it is necessary to create a bevel at an angle of 45 ° or more with cavities of III, IV, V classes, and then finish it with a fine-grained diamond bur. By creating a bevel, the active surface of the tooth enamel is increased for adhesion to the composite. In addition, a smooth transition "composite - enamel" is ensured, which facilitates the achievement of an aesthetic optimum. If these rules are not observed, the filling may fall out and its cosmetic appearance may be violated. In class I and II cavities, enamel beveling is often not created, since the composite, which wears faster than enamel, wears out earlier, which worsens the marginal fit. In addition, chipping of the composite on the chewing surface along the fold line may occur. Finishing of the enamel edges is carried out in all cases when filling class IV cavities. As a result, the surface of the enamel becomes smooth, uniform, as the chips of enamel prisms that occur during the opening of the carious cavity are removed. There is a removal of the surface unstructured layer of enamel, which covers the beams of prisms, which facilitates the subsequent acid etching of the enamel. If finishing is not carried out, then chips of enamel prisms during the functioning of the filling lead to the formation of retention areas, which contributes to the accumulation of microorganisms, plaque and the development of secondary caries.

*cm. Table No. 7. Physical indicators of some composite filling materials used to restore chewing teeth.

The task of the dentist is not only to achieve an individual appearance, but also to provide for the variability of the color of natural teeth under any lighting conditions. The solution to this problem is possible if the doctor restores the crown of the tooth with materials that optically exactly imitate dental tissues:

1) enamel + surface enamel, enamel-dentine junction;

2) dentin + peripulpal dentin (does not imitate the pulp).

Finally, artificial dental tissues must be included in the restoration design within the topographical boundaries of natural dental tissues, such as:

1) the center (cavity) of the tooth;

2) dentin;

3) enamel.

To repeat the natural structure of the tooth is the essence of the biomimetic method of tooth restoration.

The most complete imitation of the appearance of the crown is possible if the restoration model matches 4 parameters:

1) form;

2) color;

3) transparency.

4) surface structure.

3. Mechanism of adhesion of composites to dentin

Pathophysiological features of dentin:

1) dentin consists of 50% inorganic matter (mainly hydroxyapatite), 30% organic (mainly collagen fibers) and 20% water;

2) the surface of the dentin is heterogeneous, it is penetrated by dentin tubules containing processes of odontoblasts and water. Water is supplied under pressure of 25-30 mm Hg. Art., when dried, the amount of water increases, so the dentin of a living tooth is always wet and cannot be dried. The degree of mineralization of dentin is heterogeneous. Allocate hypermineralized (peritubular) dentin and type-mineralized (intertubular);

3) after preparation, the surface of the dentin is covered with a smeared layer containing hydroxyapatites, collagen fragments, processes of odontoblasts, microorganisms, water. The smear layer prevents the penetration of the adhesive into the dentin.

Taking into account the above features, in order to obtain a strong bond between dentin and composite, it is necessary:

1) use hydrophilic low-viscosity adhesives (the use of hydrophobic viscous adhesives is unacceptable, since the dentin of a living tooth cannot be dried; in this case, an analogy can be drawn with applying oil paint on a wet surface);

2) remove the smear layer or impregnate it and stabilize it. In this regard, dentin adhesive systems can be divided into two types:

a) Type I - dissolving the smeared layer and decalcifying dentin;

b) Type II - preserving and including a lubricated layer (self-conditioning).

Technique for bonding composites to dentin

1. Conditioning - treatment of dentin with acid to dissolve the smear layer, demineralize the surface dentin, open the dentin tubules.

2. Priming - treatment of dentin with a primer, i.e. a solution of a low-viscosity hydrophilic monomer that penetrates into demineralized dentin, dentinal tubules, forming strands. As a result, a hybrid zone is formed (micromechanical bonding of the adhesive to the dentin).

3. Application of a hydrophobic adhesive (bond) that provides a bond (chemical) with the composite.

When using Type I dentin adhesive systems, an acid solution (conditioner) is used to remove the smear layer. If it is a weak organic acid of low concentration (10% citric, maleic, EDTA, etc.), then the enamel is treated traditionally, i.e., 30-40% phosphoric acid. At present, the method of total etching of enamel and dentin with a solution of 30-40% orthophosphoric acid is widely used. Acid etching of dentin does not irritate the pulp, since a zone of sclerosed dentin is formed during caries; pulpitis observed after filling is most often associated with insufficient tightness of the filling.

4. Insulation.

5. Conventional preparation of the cavity with an enamel bevel at an angle of 45°.

6. Medical treatment (70% alcohol, ether, 3% hydrogen peroxide are not used).

7. The imposition of therapeutic and insulating pads (with deep caries) and insulating - with an average. Glass ionomer cement should be preferred. Pads containing eugenol or phenol inhibit the polymerization process.

8. Etching of enamel. The etching gel is applied to the beveled enamel tap for 30-60 seconds (milk and pulpless teeth are etched for 120 seconds), then the cavity is washed and dried for the same time.

9. Mixing two-component bond 1:1, applying it to the etched enamel and gasket, spraying.

10. Mixing basic and catalytic paste 1:1 for 25s.

11. Filling the cavity. The time of use of the prepared material is from 1 to 1,5 minutes. Polymerization time 2-2,5 minutes after mixing.

12. Final processing of the seal.

Contraindications to the use of the material are allergic reactions, poor oral hygiene.

After applying the primer, a hydrophobic adhesive or bond is applied (on enamel and on dentin), it provides a chemical bond with the composite.

Type II adhesives are called self-etching or self-conditioning; the primer, in addition to the low-viscosity monomer of acetone or alcohol, includes acid (maleic, organic esters of phosphoric acid). Under the influence of a self-conditioning primer, a partial dissolution of the smear layer, opening of the dentinal tubules and demineralization of the superficial dentin occur. Simultaneously, impregnation with hydrophilic monomers occurs. The smeared layer is not removed, but sprayed, and its sediment falls on the surface of the dentin.

After applying the self-conditioning primer, a hydrophobic bond is used. The disadvantage of this type of dentin adhesives is their weak ability to etch enamel, therefore, at present, even when using these systems, a total etching technique is carried out.

Currently, IV and V generation adhesive systems are used in dental practice. Generation IV is characterized by a three-stage treatment: total etching, primer application, and then enamel bonding. In adhesives of the fifth generation, the primer and adhesive (bond) are combined; the adhesion force of IV and V generation adhesives is 20-30 MPa.

Adhesive systems IV generation:

1) Pro-bond (Caulk);

2) Opti-bond (Kerr);

3) Scotchbond Multipurpose plus (3M);

4) Аll bond, All bond 2 (Bisco);

5) ART-bond (Coltene), Solid bond (Heraeus Kulzer).

Adhesive systems of the fifth generation:

1) One step (Bisco);

2) Prime and bond 2.0 (Caulk);

3) Prime and bond 2,1 (Caulk);

4) Liner Bond - II tm (Kuraray);

5) Single Bond (3M);

6) Suntaс Single bond (Vivadent);

7) Solo bond (Kerr).

The disadvantage of all composites is polymerization shrinkage, which is approximately 0,5 to 5% The reason for shrinkage is the decrease in the distance between the monomer molecules as the polymer chain is formed. The intermolecular distance before polymerization is about 3-4 angstroms, and after it 1,54.

The impetus for the polymerization reaction is given by heat, a chemical or photochemical reaction, as a result of which free radicals are formed. Polymerization occurs in three stages: start, propagation and end. The propagation phase continues until all free radicals have combined. During polymerization, shrinkage occurs and heat is released, as in any exothermic reaction.

Composite materials have shrinkage in the range of 0,5-5,68%, while shrinkage in fast-hardening plastics reaches 21%. Polymerization shrinkage is most pronounced in chemically cured composites.

Dyract PSA One-Part Adhesive

The curing reaction initially occurs due to the light-initiated polymerization of the composite part of the monomer, and then the acid part of the monomer enters the reaction, leading to the release of fluorine and further cross-linking of the polymer.

Features:

1) reliable adhesion to enamel and dentine;

2) marginal fit, as in composites, but easier to achieve;

3) strength is greater than that of GIC, but less than that of composites;

4) shrinkage, as in composites;

5) aesthetics and surface properties close to composites;

6) prolonged release of fluorine.

Indications:

1) III and V classes of permanent teeth;

2) non-carious lesions;

3) all classes, according to Black, in milk teeth.

DyractAP Features:

1) reduced particle size (up to 0,8 microns). This increased resistance to abrasion, increased strength, fluorine release, improved surface quality;

2) a new monomer has been introduced. Increased strength;

3) improved initiator system. Increased strength;

4) new adhesive systems Prime and Bond 2,0 or Prime and Bond 2,1 are applied.

Indications:

1) all classes, according to Black, in permanent teeth, cavities of classes I and II, not exceeding 2/3 of the intertubercular surface;

2) to imitate dentine ("sandwich technique");

3) non-carious lesions;

4) for filling milk teeth.

Thus, Dyract AP is similar in properties to microhybrid composites.

4. Requirements when working with composite material

The requirements are as follows.

1. Subject the light source to periodic inspection, as deterioration in the physical characteristics of the lamp will affect the properties of the composite. As a rule, the lamp has a light output power indicator, if it is not there, you can apply a layer of filling material on a mixing pad with a layer of 3-4 mm and cure with light for 40 seconds. Then remove the layer of uncured material from below and determine the height of the fully cured mass. As a rule, the power density of curing lamps is 75-100 W/cm².

2. Taking into account the limited penetrating power of light, the filling of the carious cavity and the polymerization of the seal should be incremental, i.e. layered, with a thickness of each layer no more than 3 mm, which contributes to a more complete polymerization and reduced shrinkage.

3. In the process of working with the material, it should be protected from extraneous light sources, especially from the light of the lamp of the dental unit, otherwise, premature curing of the material will occur.

4. Low-power lamps less than 75 W suggest a longer exposure and a reduction in the thickness of the layers to 1-2 mm. In this regard, an increase in temperature below the filling surface at a depth of 3-2 mm can reach from 1,5 to 12,3 ° C and lead to damage to the pulp.

5. To compensate for shrinkage, a directional polymerization technique is used.

Thus, photopolymers have the following disadvantages: heterogeneity of polymerization, duration and complexity of filling, the possibility of thermal damage to the pulp, high cost, mainly due to the high cost of the lamp.

Most of the shortcomings of photopolymers are associated with the imperfection of the light source. The first photopolymers were cured with an ultraviolet emitter, later systems with longer wavelength light sources (blue light, wavelength 400-500 nm) were proposed, which are safe for the oral cavity, the curing time was reduced from 60-90 s to 20-40 s, the degree of polymerization with a material thickness of 2-2,5 mm. At present, the most promising light source is the argon laser, which can polymerize to a greater depth and width.

5. Mechanism of adhesion between composite layers

The construction of the restoration structure is based on gluing, which, according to its intended purpose, can be divided into gluing the restorative material with tooth tissues and gluing fragments of the restorative material (composite or compomer) together, i.e., a layered technique for building restorations. (Features of obtaining a reliable connection of the composite with enamel and dentin will be discussed in the section Adhesion of composites to enamel and dentin). The connection of fragments of the composite material with each other is due to the peculiarity of the polymerization of composites, namely, the formation of a surface layer (PS).

The surface layer is formed as a result of polymerization shrinkage of the composite or compomer and inhibition of the process by oxygen.

The polymerization of chemical curing composites is directed towards the highest temperature, i.e., towards the pulp or the center of the filling, therefore chemical curing composites are applied parallel to the bottom of the cavity, since shrinkage is directed towards the pulp. Shrinkage of photopolymers is directed towards the light source. If the direction of shrinkage is not taken into account when using photopolymers, then the composite detaches from the walls or bottom, as a result, the insulation is broken.

The method of directed polymerization allows you to compensate for shrinkage.

I class. To ensure a good connection of the composite with the bottom and walls, it is applied in oblique layers approximately from the middle of the bottom to the edge of the cavity on the chewing surface. First of all, the deposited layer is illuminated through the appropriate wall (to compensate for polymerization shrinkage), and then it is irradiated perpendicular to the composite layer (to achieve the maximum degree of polymerization). The next layer is superimposed in a different direction and is also reflected first through the corresponding wall, and then perpendicular to the composite layer. In this way, a good marginal fit is achieved and tearing off of the filling edges due to shrinkage is prevented. When filling large cavities, polymerization is carried out from four points - through the tubercles of the molars. For example: if the composite layer is first applied to the buccal wall, it is illuminated first through the buccal wall (20 s) and then perpendicular to the surface of the composite layer (20 s). The next layer is superimposed on the lingual wall and is reflected through the corresponding wall, and then perpendicularly.

II class. When filling, the most difficult is the creation of contact points and good marginal adaptation in the gingival part. For this purpose, wedges, matrices, matrix holder are used. To stop the shrinkage, the gingival part of the filling can be made from a chemically cured composite, CRC, since its shrinkage is directed towards the pulp. When using a photopolymer, light-conducting wedges are used or light is reflected using a dental mirror, placing it 1 cm below the level of the neck of the tooth at an angle of 45 ° to the longitudinal axis of the tooth.

III class. Layers are superimposed on the vestibular or oral walls, followed by reflection through the corresponding wall of the tooth, on which the composite layer was applied. Then polymerize perpendicular to the layer. For example, if the composite layer was first applied to the vestibular wall, then it is initially polymerized through the vestibular wall, and subsequently perpendicularly.

The gingival part of the filling in III and IV classes polymerizes similarly to II.

V class. Initially, a gingival part is formed, the fillings of which are polymerized by directing the light guide from the gum at an angle of 45°. The shrinkage is directed towards the gingival wall of the cavity, resulting in a good marginal fit. Subsequent layers are polymerized by directing the light guide perpendicularly.

After polymerization of the last layer, a finishing treatment is carried out to remove the surface layer, which is easily damaged and permeable to dyes.

Under conditions of wet (not overdried) dentin, the adhesion force of the SS with dentin is up to 14 MPa.

When using GIC - Vitremer for processing dentin, a primer containing HEMA and alcohol is used.

The strength of the GIC depends on the amount of powder (the more it is, the stronger the material), the degree of maturity, and the characteristics of the processing of the filler. For example, high-strength type II GRC (having inclusions of silver particles in crushed glass particles) and type III gasket cements have the highest strength.

GIC have low water absorption and solubility associated with the degree of maturity of the cement. The maturation of GIC, depending on the type of cement, occurs at different times (from several weeks to several months).

The coefficient of thermal expansion is close to the coefficient of thermal expansion of dentin.

When cement is made radiopaque, the aesthetic properties (transparency) deteriorate, so cosmetic cements are generally not radiopaque.

GIC have low toxicity to the pulp, as they contain a weak organic acid. With a dentin thickness of more than 0,5 mm, there is no irritating effect on the tooth pulp. In the case of significant thinning of the dentin, it is covered with a medical lining based on calcium hydroxide in a certain area.

GICs have an anti-caries effect due to the release of fluorine ions for several months, in addition, they are able to accumulate fluorine released from toothpastes when they are used, GICs containing silver additionally release silver ions.

Aesthetic properties are high in CRC for cosmetic work, in high-strength cements and lining cements they are low due to the significant content of powder and fluorine ions.

Powder: zinc oxide, magnesium oxide, aluminum oxide.

Liquid: 40% polyacrylic acid solution.

The cured material consists of zinc oxide particles bound in a gel-like zinc polyacrylate matrix. The calcium ions of the dentin combine with the carboxyl groups of the polyacrylic acid, and the zinc ions "crosslink" the molecules of the polyacrylic acid.

Properties: physical and chemical bond with hard tissues, slightly soluble in saliva (compared to CFC), does not irritate (liquid is a weak acid), but has low strength and poor aesthetics. Used for insulating gaskets, temporary fillings, fixation of crowns.

The ratio of liquid and powder is 1: 2, the mixing time is 20-30 s, the finished mass stretches behind the spatula, forming teeth up to 1 mm, and shines.

Insulating and medical pads

Composite materials are toxic to the dental pulp, therefore, with medium and deep caries, therapeutic and insulating pads are needed. It should be noted that the toxicity of composites is related to the amount of residual monomer that can diffuse into the dentinal tubules and damage the pulp. The amount of residual monomer is greater in chemically cured composites, since the degree of their polymerization is lower compared to photopolymers, i.e., light-cured composites are less toxic. The use of IV and V generation dentin adhesives (which reliably isolate the pulp and compensate for the shrinkage of composites) makes it possible to do without insulating pads in case of medium caries, and in case of deep caries, therapeutic and insulating pads are applied only to the bottom of the cavity. The use of eugenol-containing cements is unacceptable, since eugenol inhibits polymerization. When filling canals with materials based on resorcinol-formalin mixture and eugenol, an insulating gasket made of phosphate cement, glass ionomer or polycarboxylate cement is applied to the mouth of the canal.

Medical pads

With deep caries, the use of calcium-containing therapeutic pads is indicated. Calcium hydroxide, which is part of their composition, creates an alkaline pH level of 12-14, as a result of which it has an anti-inflammatory, bacteriostatic effect (pronounced dehydration) and an odontotropic effect - it stimulates the formation of replacement dentin.

Therapeutic pads are applied only to the bottom of the cavity in the projection of the pulp horns with a thin layer. An increase in volume and application of a gasket to the walls is undesirable due to low strength - 6 MPa (phosphate cement - 10) MPa) and poor adhesion, otherwise the fixation of a permanent filling deteriorates. Etching of enamel and dentine is carried out after the isolation of the medical lining with GIC (glass ionomer cement), since due to the high marginal permeability of the medical lining, an acid depot is created under it, in addition, it is dissolved by acid.

There are single-component medical pads of light (Basic-L) and chemical curing (Calcipulpa, Calcidont) and two-component chemical curing (Dycal, Recal, Calcimot, Live, Calcesil).

Insulating pads.

As insulating gaskets can be used:

1) zinc phosphate cements (CFC): Foscin, Phosphate cement, Visphate, Wiscin, Dioxyvisphate, Unifas, Adgesor, Adgcsor Fine. II. Ionomeric cements (IC);

2) polycarboxylate: Superior. Carbcfme, Carboxyfme, Belokor;

3) glass ionomer (GIC).

*cm. Table No. 7. Glass ionomer cements.

The priority of the invention of the JIC belongs to Wilson and Keith (1971).

Glass ionomer cements are materials based on polyacrylic (polyalkenic) acid and crushed aluminofluorosilicate glass. Depending on the type of the original form, there are:

1) type "powder - liquid" (powder - aluminosilicate glass, liquid - 30-50% solution of polyacrylic acid). For example, Master Dent;

2) type "powder - distilled water" (polyacrylic acid is dried and added to the powder, which increases the shelf life of the material, facilitates manual mixing, allows you to get a thinner film), the so-called hydrophilic cements. For example, Stion APX, Base Line. Nasta type. For example, lonoseal, Time Line.

According to the curing method, the following powders are distinguished (see table No. 8).

Glass ionomer cements are classified according to their purpose.

1 type. It is used for fixing orthopedic and orthodontic constructions (Aquameron, Aquacem, Gemcem, Fuji 1).

Type 2 - restorative cement for the restoration of defects in hard tissues of the tooth:

1) type for cosmetic work. Works requiring aesthetic restoration, with a slight occlusal load (Chemfill superivjr, Vitremer. Aqua Ionofill).

2) for work requiring increased strength of seals (Ketak-molar; Argion).

Type 3 - laying cements (Bond Aplican, Gemline, Vitrcbond, Vivoglas, Miner, Bond fotak, Ionobond, Ketak bond, Time Line, Stion APH, Base Line, lonoseal).

Type 4 - for root canal filling (Ketak endo applican, Stiodent).

Type 5 - sealants (Fugi III).

GIC properties

1. Technological properties (uncured material). The mixing time is 10-20 s, after which the material acquires plasticity, which is maintained for 1,5-2 minutes (for chemically cured materials).

2. Functional properties. Adhesion to enamel and dentin is of a chemical nature (A. Wilson, 1972) due to the combination of calcium ions of hard tooth tissues and carboxyl groups of polyacrylic acid. The necessary conditions for a strong bond are the absence of foreign substances: plaque, saliva, blood, smear layer on the surface of the dentin, therefore, it is necessary to pre-treat the enamel and dentin with a 10% solution of polyacrylic acid for 15 s, followed by washing and drying. The advantage of using polyacrylic acid is that it is used in cement and its residues do not affect the cement curing process, in addition, calcium ions are activated in enamel and dentin.

As a result of finishing - the surface is smooth, transparent, shiny. Under different lighting (direct, transmitted, side light), the restoration is monolithic, the border with dental tissues is not visible. If an optical boundary between the dental tissues and the filling (white stripe, "crack in the glass") is detected, it can be concluded that the bonding is broken, correction is necessary: ​​etching is carried out, an enamel adhesive is applied, followed by curing.

In conclusion, the final illumination of all surfaces of the filling is carried out, which achieves the maximum degree of polymerization of the composite.

Thus, the control tests for bonding the composite:

1) when applying the composite, the portion should stick to the surface and come off the capsule or trowel;

2) after plastic processing, a portion of the composite is not separated from the bonded surface, but is deformed;

3) after finishing, a monolithic connection of the composite and dental tissues, there are no white stripes of separation.

GIC for cosmetic work (Vitremer, Kemfil Superior, Aqua Ionophil).

The ratio of powder to liquid is from 2,2:1 to 3,0:1 (if the liquid is polyacrylic acid) and from 2,5:1 to 6,8:1 (for materials mixed with distilled water).

The CIC curing reaction can be represented as an ionic cross-link between polyacrylic acid chains. In the initial curing phase, cross-links are formed due to calcium ions located on the surface of the particles. These divalent bonds are unstable and easily dissolve in water, and dehydration is observed when dried. The duration of the initial phase is 4-5 minutes. In the second phase - the final curing - cross-links are formed between the chains of polyacrylic acid using less soluble trivalent aluminum ions. The result is a solid, stable matrix that is resistant to dissolution and drying. The duration of the final curing phase is, depending on the type of cement, from 2 weeks to 6 months. Especially significant absorption - loss of water - can occur within 24 hours, therefore, insulation with varnishes is necessary for this period. A day later, the seal is processed, followed by seal insulation with varnish (treatment of high-strength cements and sealing cements is possible after 5 minutes, since they acquire sufficient strength and resistance to dissolution). The length of curing time is determined by a number of factors:

1) Particle sizes matter (in general, cosmetic slow-curing cements have a particle size of up to 50 microns, while types I and III with a faster curing reaction are smaller particles);

2) An increase in the amount of fluorine reduces the ripening time, but worsens the transparency.

3) Reducing the calcium content on the surface of the particles reduces the maturation time, but reduces the aesthetics of the material.

4) The introduction of tartaric acid reduces the amount of fluorine, such materials are more transparent.

5) The introduction of a light-activated composite matrix into the composition of the GIC reduces the initial curing time to 20-40 s.

The final curing of light-activated glass ionomer cements (GIC) occurs within 24 hours or more.

GITs of increased strength (Argion, Ketak Molar)

An increase in strength is achieved by the introduction of an amalgam alloy powder, but the physical properties do not change much.

A significant increase in strength and resistance to abrasion is achieved by introducing into the composition about 40% by weight of silver microparticles, which are baked into glass particles - "silver cermet". Such materials have physical properties comparable to those of amalgam and composites, but not so significant as to form the edge of the tooth and fill extensive lesions.

Mixing powder and liquid in a ratio of 4: 1 by hand or capsule, introduction with a trowel or syringe. Curing time is 5-6 minutes, during which resistance to dissolution is acquired and processing of the seal becomes possible. After processing, the cement is insulated with varnish.

The cements of this group are radiopaque and not aesthetic.

Adhesion to dentin is slightly reduced due to the presence of silver ions.

Indications:

1) filling temporary teeth;

2) polymerization on the surface of the composite.

In its composition PS resembles an unfilled adhesive system. In air-permeable PS, the polymerization reaction is completely inhibited (if you place a chemical or light adhesive in the recess of the tray, you can see that the layer located on the bottom is cured, which demonstrates the formation of PS and the penetration of oxygen to a certain depth). The surface of a portion of the composite polymerized with access to air is shiny and moist. This layer is easily removed, damaged, and permeable to dyes; therefore, after the completion of the restoration, it is necessary to treat the entire accessible surface of the restoration with finishing instruments to expose a strong, well-polymerized composite.

PS also plays an important positive role, creating the possibility of joining a new portion of the composite with the previously polymerized one. Based on this idea, the formation of the restoration is carried out in a certain sequence.

1. Checking for the presence of a surface layer inhibited by oxygen - the surface looks shiny, "wet", the gloss is easily removed. When a portion of the composite is introduced, due to locally created pressure, the layer inhibited by oxygen is removed, and the portion of the introduced composite adheres to the surface. If the composite is pulled behind the instrument or capsule and does not adhere, then the surface is contaminated with oral or gingival fluid or there is no PS. The introduced portion is removed and the adhesive surface treatment is repeated (etching, adhesive application, polymerization).

2. Plastic processing of a portion of the composite. The glued portion is distributed over the surface with patting movements directed from the center to the periphery, while the oxygen-inhibited layer is displaced. When the ambient temperature rises above 24 °C, the material becomes excessively plastic and fluid, therefore it does not transfer the pressure of the trowel; in this case, the layer inhibited by oxygen is not displaced. Perhaps this is the reason for the frequent delamination of restorations made in the summer or in a hot room. As a result of plastic processing, when trying to separate a portion of the composite with a tool, it is deformed, but not separated. Otherwise, it is necessary to continue plastic processing.

3. Polymerization.

Gasket cements

They are not transparent and not aesthetic, therefore they are covered with restorative materials. They quickly cure, becoming resistant to dissolution within 5 minutes, have chemical adhesion to enamel and dentin, which prevents marginal permeability, emit fluorine, and are radiopaque.

The ratio of powder and liquid - from 1,5: 1 to 4,0 1,0; in a "sandwich" type structure, at least 3: 1, since a larger amount of powder increases strength and reduces curing time.

After 5 minutes, they acquire sufficient strength, resistance to dissolution, and can be etched with 37% phosphoric acid simultaneously with the enamel. Mixed manually or in capsules, injected with a spatula or syringe.

When filling several cavities, the CIC is inserted into one cavity and covered with another restorative material. If several cavities are filled at the same time, then to prevent overdrying, the GIC is insulated with varnish. The subsequent overlay of the composite should be layered, following the method of directed polymerization to prevent separation of the GIC from the dentin. The strength is sufficient to replace the dentine with subsequent coating with another restorative material.

Some cements have sufficient strength and can be used for insulating gaskets, the suitability criterion is the curing time (no more than 7 minutes).

Light-curing GICs contain 10% of a light-cured composite and harden under the action of a light activator in 20–40 s. The final curing time required for the formation of polyacrylic chains and the final strength of the cement is approximately 24 hours.

GIC modified with light-sensitive polymers are less sensitive to moisture and dissolution (in the experiment - after 10 min). The advantage of such cements is also a chemical bond with the composite.

Steps for applying glass ionomer cement:

1) tooth cleaning. Color matching using a shade scale (if the CIC is used for a permanent filling);

2) isolation of the tooth.

Mixing of the components is carried out manually and using a capsule system, followed by the introduction of a spatula or syringe. The capsule mixing system followed by injection with a syringe makes it possible to reduce the level of porosity and evenly fill the cavity. Curing time: mixing time 10-20 s, initial curing 5-7 minutes, final curing after a few months. These properties cannot be changed without losing transparency. After the initial curing, the cement is isolated with a protective varnish based on BIS-GMA (it is better to use a bond from light-activated composites), and the final treatment is carried out after 24 hours, followed by re-insulation with varnish.

Physical properties: GIC of the group under consideration is not sufficiently resistant to occlusal loads, therefore, their scope is limited to class III, V cavities, erosion, wedge-shaped defects, cement caries, fissure sealing, filling of milk teeth, temporary filling, some can be used as a lining material ( if the initial curing occurs within a period of not more than 7 minutes).

Radiopacity: Most cements in this group are not radiopaque.

Compomers

A new class of filling materials introduced into practice since 1993. The term "compomer" was derived from two words "composite" and "ionomer". The material combines the properties of composites and glass ionomers.

Adhesive bonding system, polymer matrix was taken from composites, chemical bond between glass particles (filler) and matrix, fluorine release from the mass, proximity of thermal expansion to tooth tissues were taken from CIC. In particular, in the Dyract AR material, both acidic groups and polymerizable resins are present in the monomer composition. Under the action of light, the polymerization of methacrylate groups occurs; further, in the presence of water, acidic groups react with filler particles. Strength, hardness, abrasion correspond to microhybrid composites, which allows us to recommend Dyract AR for the restoration of all groups of cavities, dentin imitation when filling with composites.

Many people associate the term "compomer" with "Dyract", which, indeed, was the first material of a new class. Currently, it has been improved and a new compomer is being produced - Dyract AR (anterior, posterior) with improved physical, chemical and aesthetic properties. Among other representatives of this class, F 2000 (ЗМ), Dyract flow are known.

Composition of composites (using Dyract as an example):

1) monomer (qualitatively new);

2) composite resin (BIS-GMA) and polyacrylic acid GIC;

3) special type powder;

4) liquid (from 1,67 to 5,68%) and least in light-cured composites (0,5-0,7%).

Chemically activated composites consist of two pastes or liquid and powder. The composition of these components includes an initiator system of benzoyl peroxide and amine. When kneading a base paste containing amine and catalytic components, free radicals are formed that trigger polymerization. The rate of polymerization depends on the amount of initiator, temperature and the presence of inhibitors.

The advantage of this type of polymerization is a uniform polymerization regardless of the depth of the cavity and the thickness of the filling, as well as a short-term heat release.

Disadvantages: possible errors during mixing (incorrect ratio of components), insignificant working time for filling modeling, impossibility of layer-by-layer application, darkening of the filling due to oxidation of the residue of the amine compound. In the process of working with such materials, the viscosity changes rapidly, therefore, if the material is not introduced into the cavity within the working time, its adaptation to the walls of the cavity is difficult.

As a polymerization initiator in light-polymerizable composites, a light-sensitive substance is used, for example, campferoquinone, which, under the influence of light with a wavelength in the range of 400-500 nm, is cleaved to form free radicals.

Light-activated materials do not require mixing, therefore they do not have air porosity inherent in two-component chemically cured composites, i.e. they are more homogeneous.

Polymerization occurs on command, so the working time of modeling fillings is not limited.

Possible layer-by-layer applications to a large extent allow you to more accurately select the color of the seal. The absence of a tertiary amine will give the material color stability. Thus, photohardening composites are more aesthetically pleasing.

However, it should be noted that the degree of polymerization is not uniform, polymerization shrinkage is directed towards the source of polymerization. The degree and depth of polymerization depend on the color and transparency of the composite, the power of the light source, and the exposure distance to the source. The concentration of underpolymerized groups is the lower, the closer the light source.

Curing time - 5-6 min. Final polymerization after 24 hours, therefore, after curing, it is necessary to protect with varnish (supplied), for example, Ketak Glaze, Finishing after 24 hours.

The presented description is indicative, it cannot take into account the peculiarities of the use of various representatives of a large group of glass-filled cements, therefore, in all cases, their use must comply with the manufacturer's instructions.

6. Method of working with composite materials of chemical curing (on the example of microfilament composite "Degufil")

Before working with these composite materials, it is necessary to determine the indications for its use (depending on the classification of cavities, according to Black), for the material in question - classes III, V, it is possible to fill cavities of other classes when preparing a tooth for fixed prosthetics.

1. Tooth cleaning (no fluoride-containing pastes are used).

2. Color selection is made by comparison with the scale in daylight; the tooth must be cleaned and moistened. In the material under consideration, pastes of color A are presented.₂ or A₃.

Total etch technique: acid gel is applied first to the enamel and then to the dentin. Etching time for enamel is 15-60 s, and for dentine - 10-15 s. Washing 20-30 s. Drying - 10 s.

Advantages:

1) saving time - the processing of tooth tissues is carried out in one stage;

2) the lubricated layer and its plugs are completely removed, tubules open, relative sterility is achieved;

3) the permeability of dentin is sufficient for the formation of a hybrid zone.

Disadvantages:

1) when the etched dentin is contaminated, the infection penetrates into the pulp;

2) with a high degree of shrinkage of the composite, hyperesthesia is possible.

The technique of working with etched dentine has some peculiarities. Prior to etching, dentine contains 50% hydroxyapatite, 30% collagen and 20% water. After etching - 30% collagen and 70% water. During the priming process, the water is replaced by the adhesive and a hybrid zone is formed. This phenomenon is possible only if the collagen fibers remain moist and do not collapse, therefore water and air jets should be directed to the enamel, only reflected ones to the dentin. After drying, the enamel is matte, and the dentin is slightly moistened, sparkling (the so-called wet bonding concept). When the dentin is overdried, collagen fibers fall off - the "spaghetti effect", which prevents the penetration of the primer and the formation of a hybrid zone (Edward Swift: connection with etched overdried dentin - 17 MPa, sparkling - 22 MPa).

The next step after conditioning is the application of a primer. The primer contains a low-viscosity hydrophilic monomer (eg, CHEMA - hydroxyethyl methacrylate), penetrating into wet dentin; glutaraldehyde (chemical bond with collagen, denatures, fixes, disinfects protein); alcohol or acetone (reduce the surface tension of water, contributing to the deep penetration of the monomer). Priming time - 30 s or more. As a result of priming, a hybrid zone is formed - a zone of monomer penetration into demineralized dentin and tubules, the penetration depth is limited by the odontoblast process. With significant shrinkage of the composite, negative pressure is created, causing tension in the process, which may be the cause of postoperative sensitivity.

7. Method of application of light-cured composite material

I stage. Cleaning the surface of the teeth from plaque, tartar.

II stage. Material color selection.

III stage. Insulation (cotton swabs, rubber dam, saliva ejector, matrices, wedges).

IV stage. Preparation of a carious cavity. When using a composite material with enamel adhesives, the preparation is carried out traditionally: a right angle between the bottom and the walls; in classes II and IV, an additional platform is required. Beveling is obligatory, the edges of the enamel are at an angle of 45 ° or more to increase the surface area of ​​contact between the enamel and the composite. With class V - flame-shaped bevel. If composites with IV, V generation enamel-dentin systems are used, traditional principles of preparation can be abandoned. Enamel bevel is carried out in cavities V and IV; III class - according to aesthetic indications.

V stage. Drug treatment (alcohol, ether, hydrogen peroxide are not used) and drying.

VI stage. The imposition of insulating and therapeutic pads (see section "Insulating therapeutic pads").

VII stage. Etching, washing, drying.

Solitare is a modification of the cladding material Artglass "Heraeus kulze" and therefore can be included in the group of materials based on polymer glass.

Composition:

1) organic matrix: high molecular weight esters of methacrylic acid, reaching an amorphous highly wettable structure, similar to organic glass. Organic glass is bonded to a silane-treated inorganic filler;

2) inorganic filler;

a) polyglobular particles of silicon dioxide in size from 2 to 20 microns;

b) fluorine glass, particle size - from 0,8 to 1 micron;

c) fluorine-containing glass based on barium aluminosilicate, the average particle size is less than 1 micron;

3) rheologically active silicic acid.

The total amount of inorganic filler is not less than 90%.

The material is recommended for filling I and II classes of carious cavities, according to Black.

It is applied with adhesive system of IV generation "Solid Bond". Shrinkage during polymerization is 1,5-1,8%, the material is resistant to chewing load, dissolution, well polished, color stable.

Used in a simplified way:

1) used with metal matrices and wooden wedges;

2) is applied in layers parallel to the bottom, polymerized with light for 40 s directed perpendicular to the filling, the thickness of the layers is 2 mm or more (except for the first layer).

The presentation of Solitare took place in 1997. Clinical trials are currently underway. The results obtained within 6 months allow us to hope that this material can serve as an alternative to amalgam and be used for filling the chewing group of teeth, along with fine hybrid composites.

8. Principles of biomimetic construction of teeth with restorative materials

A natural tooth is a translucent optical body, consisting of two optically different tissues: more transparent and light enamel and less transparent (opaque - opaque) and dark dentin.

The ratio of enamel and dentin creates differences in the appearance of different parts of the crown of the tooth, such as:

1) the cervical part of the crown, where a thin plate of enamel is combined with a large mass of dentin;

2) the middle part of the crown, where the thickness of the enamel increases and the amount of dentin decreases significantly;

3) the edges of the crown, where a thin plate of dentin is combined with two plates of enamel.

The combination of enamel and dentin also creates differences in the appearance of different teeth in one person: light incisors, in which enamel is combined with a small amount of dentin; more yellow fangs - enamel is combined with a large amount of dentin; darker molars - the amount of dentin is even more increased compared to enamel.

The crown of the tooth, due to translucency, has color variability under different lighting conditions (cold blue light prevails in the morning, warm red in the evening; the light intensity changes). The range of variability of the teeth depends on the individual transparency of the crown. Thus, more transparent teeth have greater variability, while less transparent teeth have the opposite.

According to the degree of transparency, teeth can be divided into three conditional groups:

1) absolutely opaque "deaf" teeth, when there is no transparent cutting edge, due to the peculiarities of the individual structure or abrasion - these are yellow teeth. The range of color changes of the vestibular surface is low and is detected when the tooth is translucent from the oral side;

2) transparent teeth, when only the cutting edge is transparent. As a rule, these are teeth of yellow-gray shades, the range of color changes of the vestibular surface is not significant;

3) very transparent teeth, when the transparent cutting edge occupies 1/3 or 1/4 and the contact surfaces are also transparent.

9. The mechanism of adhesion of composites with enamel

Adhesion comes from lat. Adhesio "sticking".

Bond comes from English. Bond "bond".

Adhesives and bonds are used to improve the micromechanical adhesion of composites to dental tissues, compensate for polymerization shrinkage, and reduce marginal permeability.

Enamel mainly consists of inorganic matter - 86%, a small amount of water - 12% and an organic component - 2% (by volume). Thanks to this composition, the enamel can be dried, so the hydrophobic organic component of the composite is the BIS-GMA monomer, which has good adhesion to the enamel. Thus, hydrophobic viscous adhesives (bonds) are used in the enamel area, the main component of which is the BIS-GMA monomer.

Method for obtaining a bond between composites and enamel

Stage I - the formation of a bevel at 45 ° or more. The bevel is necessary to increase the active surface of the bond between the enamel and the composite.

Stage II - etching the enamel with acid. 30-40% phosphoric acid is used in the form of a liquid or gel, and the gel is preferable, since it is clearly visible and does not spread. The etching period for enamel is from 15 s to 1 min. As a result of pickling:

1) organic plaque is removed from the enamel;

2) enamel microroughness is formed due to the dissolution of enamel prisms to a depth of approximately 40 μm, which significantly increases the surface area of ​​the adhesion of the composite and enamel. After applying the bond, its molecules penetrate into microspaces. The adhesive strength of the composite to the etched enamel is 75% higher than that of the unetched one;

3) etching allows to reduce the marginal permeability at the "enamel-composite" interface.

Stage III - the use of enamel (hydrophobic) bonds based on the organic matrix of the composite (BIS-GMA monomer), which penetrate into the microspaces of the etched enamel. And after polymerization, processes are formed that provide micromechanical adhesion of the enamel to the bond. The latter combines chemically with the organic matrix of the composite.

The identification of the patient's teeth is carried out immediately after cleaning with a nylon brush and professional toothpaste (not containing fluoride) in natural light, the surface of the teeth must be moist. The assessment of the result of the restoration is carried out no earlier than 2 hours after completion of the work, preferably after 1-7 days, then a decision is made on the need for correction. A properly executed restoration looks darker and more transparent immediately after completion of the work due to the drying of the enamel, which becomes lighter and less transparent. After water absorption, the color and transparency of artificial and natural dental tissues are the same.

Stage IV - application of the adhesive system.

Stage V - filling.

Stage VI - final processing.

Enamel treatment with fluorine preparations

Contraindications: allergic reactions to the components of the filling material, poor oral hygiene, the presence of an artificial heart rate stimulator.

10. Mistakes and complications when using composite materials, compomers, GIC

At the stage of tooth cleaning and color determination: before determining the color of the teeth and preparing the carious cavity, it is necessary to clean the tooth from plaque and remove the pellicle layer. For this, a nylon brush and a fluorine-free paste are used, otherwise the color determination will not be carried out correctly. It is also necessary to use the standard rules for determining the color of the teeth (shading scale, moistened tooth, natural light). In the case of aesthetic restorations, it is important to determine the individual transparency of the teeth.

Authors: Kapustin K.M., Orlov D.N.

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