Risk factors for the development of diseases of hard tissues of the tooth. Pathology of hard tissues of teeth

Send your good work in the knowledge base is simple. Use the form below

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Hosted at http://www.allbest.ru

Etiology, pathogenesis and clinic of diseases of hard tissues of the tooth

Brief information about the process of mineralization and ultrastructure of dental hard tissues

Enamel. Human teeth are an organ that performs the primary mechanical processing of food. The main function of the teeth determined the morphological features of their tissues. The crown part of the teeth is covered with enamel - the most durable tissue. Withstanding great pressure during chewing, enamel is also fragile and weakly resists sudden loads, such as impact, which causes cracks and spalling of the enamel.

The thickness of the enamel layer is not the same: at the neck of the tooth it barely reaches 0.01 mm, at the equator it is 1.0-1.5 mm, in the bottom of the fissures - 0.1-1.5 mm, at the cutting edge of unworn teeth - 1.7 mm, on the hillocks - 3.5 mm [Fedorov Yu. A., 1970]. The specific heat capacity of enamel is 0.23 J / (kg * K); its thermal conductivity is low (Ktp is equal to 10.5 * 10 -4 W / (m * K). Outside, the enamel is covered with a very dense, non-calcified, resistant to acids and alkalis film (Nasmite shell) 3-10 microns thick, which is near the neck The tooth is connected to the epithelium of the mucous membrane of the gums, being, as it were, its continuation.Shortly after teething, the film is erased, primarily on the contact surfaces of the teeth.The structural element of the enamel is the enamel prism.It is formed during the development of the tooth from adamantoblasts - the cells of the inner epithelium of the enamel organ.

The data obtained in recent years using electron microscopy make some adjustments to the understanding of the ultrastructure of enamel and its components. Enamel prisms consist of collagen protofibrils and isolated crystals oriented perpendicular to the dentin-enamel junction. The cross section of enamel prisms is 5-6 microns, their shape can be round, hexagonal, etc. The spaces between the prisms 1-3 microns wide are less mineralized and filled with fibrous tissue (an interprism substance that performs a nutritional function in enamel) with a smooth surface, facing the walls of the prism. The interprism substance appears to be amorphous, is located in the form of a thin, often barely noticeable strip, or forms clusters - enamel: bundles or plates. In cross section and at the base, prisms most often have an arcade, oval or polyhedral shape. With their opposite sharp ends, they wedged between the underlying prisms. The ends of the enamel prisms, wide at the base, are separated by tapered ones. The ends of the enamel prisms, wide at the base, are separated by the narrowed ends of the prisms of the overlying layer.

Enamel prisms are evenly mineralized, the degree of mineralization is high. With age, the crystals thicken the protein-rich interlayers between the prisms, and the "boundary lines" become thinner.

At the border of enamel with dentin, a continuous layer is formed from the adhesive substance - the so-called delimiting membrane. On its side, facing the dentin, a border is formed in the form of a brush, the fibers of which pass into the Korf fibrils of the dentin, which ensures a strong mechanical and physiological bond between the enamel and the dentin. The results of the study of the ultrastructure of the hard tissues of the tooth suggest that the enamel-dental connection as a morphological formation does not exist [Bushan M. G., 1979].

Dentine. Dentin makes up about 85% of the tissues of the tooth and contains collagen fibers, between which there is an amorphous adhesive substance. These formations make up the main substance of dentin. The number and nature of the location of these fibers are not the same in different layers of dentin, which determines the peculiar structure of the mantle, or peripheral, layer of dentin, in which radial fibers predominate, and the near-pulpal dentin, rich in tangential fibers.

Dentin belongs to highly mineralized tissues (about 73% of organic compounds) and is second only to enamel in terms of the degree of mineralization. The least mineralized is the zone of dentin facing the pulp and separated by a fibrous line. In the literature, this zone is described as the poedentine or dentinogenic zone, although it has nothing to do with dentinogenesis.

Except for the quality of very low mineralization, it is identical to peripulpal dentin.

Interglobular spaces are often found on the border of the mantle and peripulpal dentin, the origin of which is presumably associated with the uneven process of calcification. Similar but smaller formations, referred to as Tomes granular layers, are noted at the dentin-cement margin. Interglobular spaces and granular layers of Tomes, located in several rows, make up Owen's contour lines, which are identical to the Retzius lines in enamel by the mechanism of formation.

The ground substance of dentin is penetrated by a huge number of dentinal tubules, mainly of a radial direction. According to G. V. Yasvoin (1946), in the peripulpal dentin their number reaches 75 thousand per 1 mm 2 . Starting on the inner surface of the dentin and heading towards the periphery, the tubules narrow and diverge due to the radial direction. Near the enamel-dentine connection, their number reaches 15 thousand per 1 mm 2.

On electron microscopic replicas, non-decalcified dentin of intact teeth consists of the main substance (matrix) from which a network of dentinal tubules is determined. Dentinal tubules are tubules of different diameters. In areas located closer to the pulp chamber, their diameter is 0.5-0.8 µm on average. As it approaches the enamel-dentine junction, the tubules gradually become narrower - 0.2-0.4 microns.

The wall of the dentinal tubules is more mineralized and dense compared to the intertubular zone. 3 in the immediate vicinity of the dentinal tubules, collagen protofibrils are located more densely than on the periphery, which corresponds to the peritubular hypermineralized zone. This serves as evidence that the centers of apatite crystal formation are formed along the protofibrils of dentin collagen.

The width of the hypermineralized peritubular zone depends on the area of the dentin and the age of the person. At the age of 20-30 years, she is somewhat narrower than at 40-50 years old. As the dentinal tubule approaches the dentinal-enamel border, the hypermineralized peritubular zone becomes wider; it is also well preserved around the lateral branches.

The intertubular zone is a less mineralized area of dentin. In addition to crystals, the intertubular zone contains collagen fibers running in different directions. The density of grains of crystals and collagen fibers is lower compared to the peritubular zone.

In most cases, dentine crystals are needle-shaped with pointed ends. The bulk of the apatite crystals are of the same size: their average length is 30–60 nm, and their width is 2–13 nm.

The question of the existence of a Neumann membrane (peritubular dentin), which supposedly lines the dentinal tubules, has not been finally resolved. Some authors recognize its existence [Falin L.I., 1963]. In their opinion, the Neumann membrane consists of amorphous plasma substances and is located between the processes of Toms (the dentinal process of the ondoblast) and the inner surface of the wall of the dentinal tubules. The authors came to this conclusion on the basis of data obtained using an optical microscope. This information is still given in textbooks, although there are enough new data that completely refute the existence of the Neumann shell.

Dentinal tubules are limited only by the plasma membrane. Toms fibers are protoplasmic processes of odontoblast cells that go into the dentinal tubules.

These fibers act as a transfusion system that provides nutrition to hard tissues. Most of the fibers blindly end in the form of thickenings in the peripheral parts of the dentin. Some fibers penetrate the enamel in the form of flask-shaped swellings - enamel spindles or bushes.

The question of the presence of nerve cements in the dentin is also controversial, which is associated with significant difficulties that arise during neuro-otological processing of the object. Many authors deny the existence of these elements in the dentin, and the processes of odontoblasts are assigned the role of transmitters of irritation to the marginal zone of the pulp, which is supplied with nerve fibers. Nerve fibers penetrating the dentinal tubules perform a dual function - sensitive and trophic.

Cement. There are cellular and acellular cement covering the dentin of the tooth root. Cellular, or secondary, cement in certain areas of the root, mainly at the bifurcation of multi-rooted teeth and on the tops of the roots of all teeth, is superimposed on acellular, or primary. With age, the amount of cellular cement increases. Quite often, cavities with cells are found in the newly formed cementum. There is a known case when the newly formed cement acquired the character of lamellar bone.

No blood vessels were found in both cellular and acellular cement, and there is also no information about its innervation. The main substance of the primary cementum consists of collagen fibrils, which diverge mainly in the radial direction, sometimes in the longitudinal direction. Radial fibrils directly continue in the sharpei (perforating) fibers of the periodontium and then penetrate into the alveoli.

The tooth is not isolated from the surrounding tissues, but, on the contrary, forms an inseparable whole with them. It is believed that the tooth is genetically, anatomically and functionally associated with periodontal tissues. Connective tissue, vessels, nerves of the tooth and periodontium combine these anatomical formations into a single, interdependent complex that performs a single function.

Dentin hydroxyapatite crystals are similar in size and shape to bone tissue crystals. Due to the extremely small size of the crystals (length 20–50 nm, thickness about 10 nm, width 3–25 nm), favorable conditions are created for ion exchange. The crystals increase in size as the degree of mineralization of the tooth substance increases. Dentinal fluid (dental lymph) penetrates into the dentin and enamel through the processes of Toms, with which nutrients from the blood enter the hard tissues of the tooth.

Many issues of the physicochemical and biological nature of the process of formation of hydroxyalatite crystals and intracrystalline exchange have not yet been sufficiently studied. Their study was carried out mainly in vitro, so the data obtained cannot fully reveal the nature of these processes in the tissues of the tooth. At the same time, the presence of a close morphological and functional relationship between the organic and inorganic components of the tooth was established. It has also been proven that collagen protofibrils of hard dental tissues serve as a base, on the surface and inside of which crystallization centers are created. As a result of the deposition of inorganic salts of calcium and phosphorus, individual apatite crystals (hydroxyapatite, fluorapatite) gradually form in the centers of crystallization. As they grow, they approach neighboring ones, become cemented and form a group of crystals. The process of crystallization is characterized by certain intervals and periods.

Each crystal of hydroxyapatite is surrounded by the thinnest immovable liquid layer - the so-called hydrated layer. It is formed due to a pronounced electrical asymmetry, due to which a strong electric field is created on the surface of the crystals. As a result of this, layers of bound ions are formed, which constantly hold around the crystals a fixed solvent layer - the hydrate layer. The hydrated layer contains high concentrations of hydrated calcium ions and polarized phosphorus ions. The crystals themselves are composed of anions and cations, which form atomic crystal lattices repeating one after another. Anions and cations, being opposite in charge, are located in the crystal lattice at a strictly defined distance and are interconnected using the electric field formed around the ions.

Calcium and phosphorus in the bones and tissues of the teeth are presented in the form of two fractions - labile and stable. Labile calcium is 20-25%, phosphorus - 12-20%. The exchangeable and labile fractions are a kind of depot of ions, which provide an exchange reaction in the hydration layer of the liquid around the crystals and are in quantitative equilibrium with blood phosphorus and calcium. In the process of mineral metabolism, growth and formation of crystals, calcium and phosphorus pass from the labile to the stable fraction of crystals by precipitation (recrystallization).

In the process of isoionic exchange, calcium and phosphorus ions pass into hydroxyapatite crystals through three zones. The first of them is the transition from the diffusion layer to the hydrate layer, which is carried out due to the charge asymmetry on the crystal surface. The second zone is the transition from the hydrate layer to the crystal surface, which occurs under the action of ionic force. The third zone is the transition from the crystal surface to crystal lattices due to thermal motion and diffusion.

Calcium ions are polarizable, so a strong electric field is formed around them and the surface of the crystals has a mostly positive charge. Negative charges are located on their surface in the form of a mosaic. The rate of ion exchange also largely depends on the valency and the force of interionic attraction. The first two phases of ion exchange—between the diffuse and hydrate layers, as well as between the hydrate layer and the crystal surface—occur quite rapidly. Inside the crystals, the exchange rate depends on the number of free places and defects in the lattice, so the process proceeds rather slowly.

Functional morphology of teeth

In the dental system, the unity and interdependence of form and function is especially clearly traced. Various lesions of the hard tissues of individual or groups of teeth gradually lead to a change in their morphology, as a result of which there may be violations of the masticatory function of the dentition, the normalization of which is the main goal of dental prosthetics.

The ratio between the height of the clinical crown and the length of the root varies widely both in individual teeth or groups of teeth, and individually for each patient. In some cases, the clinical crown corresponds to the anatomical one, in others the length of the clinical crown is longer than the anatomical one. In childhood and adolescence, the clinical and anatomical contours of the tooth crown usually coincide: the transition of enamel into cement coincides with the line of the clinical neck. The root is usually not visible or palpable and can only be examined radiographically. Teeth with such a morphology are highly stable and can take additional load, which is important when choosing fixed and removable dentures.

With periodontitis, the dimensions of the clinical crown and root of the tooth undergo certain changes. Due to alveolar atrophy and gingival retraction, the root is exposed, and the clinical crown becomes longer than the anatomical one. As the clinical crown lengthens and the root shortens, the stability of the tooth and the reserve forces of the periodontium decrease. Changing the size of the arm of the resistance lever of the tooth complicates the choice of prosthesis design, excluding the functional overload of the periodontium.

It is known that the root surface is individually different, while the size of the surface of individual teeth is directly dependent on the size of the tooth crown and the function performed. With the exception of the second and third molars, the root surface increases as you move away from the midline to the distal side.

The anatomical equator divides the tooth surface into gingival and occlusal. The level at which the anatomical equator is located is different both on the oral and vestibular surfaces of one tooth, and on individual teeth.

In case of pathology of hard tissues of the teeth, the restoration of their anatomical shape should give not only an aesthetic, but also a preventive effect aimed at preserving periodontal tissues.

The pulp cavity in general follows the shape of the coronal part of the corresponding tooth and has different wall thicknesses. Knowing the thickness of hard tissues in different parts of the tooth crown eliminates the possibility of damage to the pulp during the preparation process. The thickness of various sections of the crown part of the teeth was first presented in the form of diagrams by Boisson, who proposed to distinguish between the so-called safety zones. He considered these zones to be areas of the crown part of the tooth, on which the thickness of hard tissues allows the necessary amount of grinding to be carried out without fear of opening the pulp chamber in the manufacture of fixed dental structures. Dangerous zones are called areas of the crown of the tooth, on which there is a small thickness of hard tissues and, therefore, the pulp cavity is close to the surface of the tooth. For example, incisor safety zones are located at the incisal edge, on the oral side, and on the proximal surfaces of the crown and neck of the tooth. Danger zones are the spaces between the safe zones of the incisal edge and the oral side, as well as the vestibular and oral sides of the neck of the tooth.

In fangs, the safety zones are located on the approximal surfaces, pass to the oral surface, and extend to the equatorial region. At the neck of the tooth, the safety zones are located on the proximal surfaces. The zone of the apex of the tubercle, the vestibular and oral sides of the neck of the tooth are easily vulnerable, since here the pulp is located close to the surface.

Safety zones of premolars are localized on the approximal surfaces, in the middle of the chewing surface, where the fissures end near the contact points, and also at the neck of the tooth. Dangerous places are the tops of the tubercles, the oral and vestibular sides of the neck of the tooth.

Molar safety zones are the contact points of the crown, the central part of the chewing surface, the spaces between the tubercles, the ends of the fissures on the vestibular, oral and contact points of the tooth, and the contact sides of the neck of the tooth. Dangerous places are the tops of the tubercles, the vestibular and oral sides of the neck of the tooth.

The structural features of each tooth are taken into account when determining the amount of grinding of hard tissues during the preparation of teeth, as well as when deciding whether it is advisable to create a ledge, its location, length and depth. In cases where the presence and topography of dangerous zones are not taken into account, complications arise during the grinding of hard dental tissues: opening of the pulp, pulpitis, thermal burns of the pulp. Approximately the dimensions of the safety zones can be determined by measuring on radiographs.

Immediately after teething, the pulp cavity is very voluminous, and as age increases, its volume decreases, this feature is taken into account when determining indications for the use of street crowns up to 16 years old and porcelain crowns - up to 18-19 years old.

The functional morphology of the anterior teeth corresponds to the necessary conditions for the initial act of chewing - cutting and tearing food, and the lateral teeth - for crushing and grinding food. The more often the anterior teeth are included in the function and the more often they cut hard food, the faster the crown height decreases due to wear, and the cutting surface increases. This functional wear is considered as physiological wear. However, under the influence of a number of factors, the wear of hard tissues of the teeth can progress and acquire the character of a pathological process, which leads to shortening of the crowns of the teeth up to the gum level, which is accompanied by a complex of other complications.

The front teeth, with the exception of the lower incisors, in most cases have a wide and easily passable root canal. This provides the possibility of their expansion and use for the manufacture of post teeth, post post inlays and post crowns. The roots of the lower incisors are flattened from the proximal sides, which excludes the possibility of expansion of their canals due to the risk of perforation.

Premolars, with the exception of the first upper ones, have one root canal. The second upper premolars sometimes have two canals in one root. Single-rooted premolars with a passable canal can be used for the manufacture of pin structures for prostheses.

The first and second molars of the upper jaw have three roots each: two buccal, shorter and less massive, diverge somewhat in the sagittal plane, and the palatine, longer and more voluminous, goes towards the sky. The characteristic direction of the palatine root, which is the result of functional adaptation, makes it possible to redistribute the masticatory load along the main axis of the tooth. The structural features of the palatine roots, in comparison with the buccal ones, provide more favorable conditions for the introduction and fixation of prosthesis pin structures.

During life, the morphology of the occlusal surface of the teeth may remain unchanged or change depending on the nature of the occlusal contacts during chewing. In persons in whom vertical articulated movements of the lower jaw predominate (with a deep bite), there are no pronounced changes in the occlusal surface of the teeth for a long time. With a direct bite, in which the horizontal sliding movements of the lower jaw are carried out freely, the relief of the occlusal surface of the teeth changes due to the erasure of the tubercles. This must be taken into account when studying the state of the dentoalveolar system, establishing a diagnosis and choosing a method of orthopedic treatment of patients.

J. Williams (1911) proved the presence of a certain dentofacial harmony. In particular, the shape of the central incisors corresponds to the shape of the face: in patients with a square face, the anterior teeth are most often square, in those with an oval face, an oval shape, and with a triangular face, the anterior teeth are most often also triangular. In the process of orthopedic treatment of the anterior teeth, the nature of modeling, the creation of the shape, direction and size of the teeth are directly related to the restoration of the aesthetic appearance of the patient.

The color of the teeth in each patient has individual characteristics, which is the result of the layering of the color of the enamel on the color of the dentin. Dentin has a yellow color of various shades. The color of the enamel is white with a yellow, blue, pink, gray tint or a combination of them. In this regard, the vestibular surface of the anterior teeth has three color nuances. The cutting edge of the front teeth, which does not have a dentin sublayer, is often transparent, the middle part, covered with a thicker layer of enamel, which does not allow the dentin to show through, is less transparent; in the cervical part, the enamel layer is thinner and the dentin shines through it more strongly, therefore this part of the tooth crown has a pronounced yellowish tint.

In young people, the color of the teeth is generally lighter, while in adults, especially the elderly, it has a more pronounced yellowish or grayish tint. In some cases, in particular in smokers, various pigmentations and atypical discolorations of the teeth appear. The color of the teeth largely depends on the observance of the rules of hygiene of the teeth and oral cavity.

Partial and complete destruction of the crown part of the tooth

To the pathology of hard tissues of the teeth include carious and non-carious lesions.

Tooth caries. The study of the problem of dental caries (etiology, pathogenesis, clinic, treatment and prevention) is devoted to a huge amount of scientific research. However, it remains very relevant throughout the world and the search for its resolution continues.

Teeth affected by caries are covered with dentures according to indications only after their thorough treatment. Along with other harmful effects on the dentition, the carious process disrupts the anatomical shape and structure of the tooth crown due to the formation of defects in hard tissues.

Tooth crown defects are divided into partial and complete. Partial defects can have different localization, size, shape and depth. The crown part of the tooth is not completely destroyed, and it is restored with the help of a filling material, and in some cases, according to indications, orthopedic treatment is carried out. Complete defects of the crown part of the tooth (complete absence of a crown) are eliminated using pin teeth.

Non-carious lesions of the teeth are divided into two main groups [Patrikeev V.K., 1968]: 1) lesions that occur during the period of follicular development of dental tissues, i.e. before eruption: enamel hypoplasia, enamel hyperplasia, dental fluorosis, anomalies of development and eruption teeth, changes in their color, hereditary disorders of tooth development; 2) lesions that occur after eruption: pigmentation of the teeth and plaque, erosion of the teeth, wedge-shaped defect, erasure of hard tissues, hyperesthesia of the teeth, necrosis of the hard tissues of the teeth, trauma to the teeth.

Enamel hypoplasia. Hypoplasia of tooth tissues occurs as a result of a violation of metabolic processes in the anamenoblasts of the rudiments of teeth. The occurrence of hypoplasia contributes to the violation of protein and mineral metabolism in the body of the fetus or child. According to etiological signs, focal odontodysplasia, systemic and local hypoplasia are distinguished.

Focal odontodysplasia (odontodysplasia, incomplete odontogenesis) occurs in several adjacent teeth of the same or different periods of development. The rudiments of both temporary and permanent teeth are affected, more often incisors, canines and permanent molars. The clinical picture of the disease is characterized by a rough surface, a yellowish color, a decrease in size and an uneven density of the tissues of the tooth crown.

Systemic hypoplasia occurs under the influence of various factors, primarily diseases that can disrupt metabolic processes in the child's body during the formation and mineralization of these teeth. Systemic hypoplasia is accompanied by a violation of the structure of the enamel of only that group of teeth, which is formed in the same period of time.

Enamel hypoplasia is characterized by the formation of cup-shaped depressions of a round or oval shape. At the bottom of the recesses, enamel may be absent (aplasia) or it may be thinned and yellowish dentin shines through it. The dimensions, depth and number of defects are different, the walls, edges of the recesses and the bottom are smooth. The cutting edges of teeth affected by hypoplasia form a semilunar notch.

With the striated form of hypoplasia, the defects are localized parallel and at some distance from the cutting edge or chewing surface and are more pronounced on the vestibular surface of the teeth. The number of grooves can be different, on their bottom there is a thinned layer of enamel, and in some cases there is no enamel.

Fournier, Getchinson and Pfluger teeth are considered a type of systemic hypoplasia. The crown of the tooth acquires a peculiar barrel-shaped shape with a semilunar notch on the cutting edge of the anterior incisors of the upper and lower jaws. Pfluger teeth are characterized by a cone-shaped permanent molars. Hypoplasia of the cutting edges and tubercles contributes to the development of increased abrasion of hard dental tissues and often leads to aesthetic dissatisfaction with the patient's appearance.

With local hypoplasia (Turier's teeth), one, less often two teeth are affected, and only permanent teeth. The disease develops under the influence of mechanical injury or inflammation.

Therapeutic treatments for hypoplasia are ineffective. Preference should be given to orthopedic methods: to cover the affected teeth with prostheses, the design of which depends on the clinical indications.

Enamel hyperplasia (enamel drops, pearls). This pathology is an excessive formation of tooth tissue during its development, most often in the area of the neck of the tooth on the line separating enamel and cementum, as well as on the contact surface of the teeth. Functional disturbances in enamel hyperplasia are usually absent. This damage to hard tissues must be taken into account when determining the indications for creating a ledge at the neck of the affected teeth in the manufacture of porcelain and metal-ceramic structures.

Dental fluorosis (spotted enamel, pockmarked enamel). This damage to hard tissues develops as a result of the use of drinking water with an excess content of fluoride compounds.

VK Patrikeev (1956) distinguishes five forms of dental fluorosis: dashed, spotted, chalky-mottled, erosive and destructive. The dashed form most often appears on the vestibular surface of the incisors of the upper jaw in the form of subtle chalky stripes. When spotted, the front teeth are most often affected, less often the lateral ones. The disease is manifested by the appearance of chalky spots located on different parts of the tooth crown. Chalky-speckled fluorosis is considered a more severe disease, affecting all teeth, the crowns of which acquire a matte shade, along with patches of pigmentation of light or dark brown. Small defects in the form of specks with a light yellow or dark bottom are formed in the enamel. The erosive form is characterized by degeneration and pigmentation of the enamel with the formation of deep extensive defects, accompanied by exposure of the dentin. The destructive form is the most advanced stage of fluorosis. This form is characterized by extensive destruction of the enamel, pathological abrasion, breaking off of individual sections of the tooth and a change in the shape of its crown part.

Thus, with fluorosis, depending on the form and degree of development of the process, various violations of both the shape and structure of hard tissues and the aesthetics of the face occur.

Local and general therapeutic treatment for severe forms of fluorosis (chalky-speckled, erosive, destructive) often does not give the desired effect. In such cases, orthopedic methods are indicated for restoring aesthetic norms and the anatomical shape of the tooth crown.

Capdepon's dysplasia(Stainton-Capdepon syndrome). With this disease, related to hereditary disorders of dental development, both temporary and permanent teeth are affected.

Erosion of hard tissues of the tooth. Erosion occurs mainly in middle and old age from the mechanical impact of a toothbrush and powder. The etiology of the disease is not well understood. Erosion mainly occurs on the anterior teeth of the upper jaw, the premolars of both jaws and the canines of the lower jaw. It appears on the vestibular surface of the tooth crown as a round or oval enamel defect with a smooth, hard and shiny bottom, gradually increases in the transverse direction and takes the form of a grooved chisel. With a large area of the lesion, when it is not possible to eliminate the defect with the help of a filling material, orthopedic treatment is performed.

wedge defect. This hard tissue lesion is more commonly seen on canines and premolars. less often - incisors and molars. The etiology of the disease has not been fully elucidated. Importance in the progression of wedge-shaped defects is attached to mechanical and chemical factors (toothbrushes and powder, demineralizing action. acids to as well as endocrine disorders, diseases of the central nervous system and gastrointestinal tract.

Wedge-shaped defects are most often located symmetrically (on the right and on the left) on the vestibular surface of the tooth in its cervical region. They develop slowly and are accompanied by deposition of replacement dentin. As the pathological process progresses, pain occurs under the action of mechanical (when brushing teeth), chemical (sour, sweet) and temperature (hot, cold) stimuli.

S. M. Makhmudkhanov (1968) distinguishes four groups of wedge-shaped defects:

1) initial manifestations without visible loss of tissue, which are revealed with a magnifying glass. Sensitivity to external stimuli is increased;

2) superficial wedge-shaped defects in the form of scallop-shaped damage to the enamel, localized near the enamel-cement border. The depth of the defect is up to 0.2 mm, the length is 3--3.5 mm. The loss of tissue is determined visually. Increased hyperesthesia of the necks of the teeth is characteristic;

3) medium wedge-shaped defects formed by two planes located at an angle of 40-45 °. The average depth of the defect is 0.2-0.3 mm, the length is 3.5-4 mm, the color of hard tissues is similar to the yellowish color of normal dentin;

4) deep wedge-shaped defects with a length of more than 5 mm, accompanied by damage to the deep layers of dentin up to the pulp cavity, as a result of which the crown may break off. The bottom and walls of the defects are smooth, shiny, the edges are even.

With wedge-shaped defects, a general treatment is carried out aimed at strengthening the structure of the tooth and eliminating dentin hyperesthesia, as well as local filling. In case of poor fixation of the filling and the risk of fractures of the tooth crown, orthopedic treatment is indicated.

Hyperesthesia of hard tissues of the tooth. Hyperesthesia - increased sensitivity of hard tissues of the tooth to mechanical, thermal and chemical stimuli, observed in carious and non-carious lesions of hard tissues of the teeth and periodontal diseases.

A. By prevalence.

1. Limited form, usually manifested in the area of individual or several teeth, more often in the presence of single carious cavities and wedge-shaped defects, as well as after the preparation of teeth for artificial crowns or inlays.

2. Generalized form, manifested in the area of most or all teeth, more often in the case of exposure of the necks and roots of teeth in periodontal diseases, pathological abrasion of teeth, multiple dental caries, multiple progressive form of tooth erosion.

B. By origin.

1. Hyperesthesia of dentin associated with the loss of hard tissues of the tooth:

a) in the area of carious cavities;

b) arising after the preparation of tooth tissues for artificial crowns, inlays, etc.;

c) concomitant pathological abrasion of hard tissues of the tooth and wedge-shaped defects;

d) with erosion of hard tissues of teeth.

2) Hyperesthesia of dentin, not associated with the loss of hard tissues of the tooth:

a) in the area of exposed necks and roots of teeth in case of periodontal diseases;

b) intact teeth (functional), concomitant with general disorders in the body.

B. According to the clinical course.

I degree - tooth tissues react to a temperature stimulus (cold, heat). The threshold of electrical excitability is 5-8 μA;

II degree - tooth tissues react both to temperature and chemical stimuli (cold, heat, salty, sweet, sour, bitter food). The threshold of electrical excitability is 3-5 μA;

III degree - tooth tissues react to all types of stimuli (including tactile ones). The threshold of electrical excitability is 1.5-3.5 μA).

Pathological abrasion of hard tissues of teeth. This form of hard tissue damage is quite common and causes a complex set of disorders in the dental system, and orthopedic treatment methods have their own specifics.

Crossbite

Crossbite refers to transversal anomalies. It is due to the discrepancy between the transversal sizes and the shape of the dentition. The frequency of crossbite, according to the literature, is not the same at different ages: in children and adolescents - from 0.39 to 1.9%, in adults - about 3%. Various terms are used that characterize crossbite: oblique, lateral, buccal, vestibulo-occlusion, buccoocclusion, lintaocclusion, lateral - forced bite, articular crossbite, laterognathia, laterogeny, lateroversion, latero-deviation, laterodgnathia, laterodyskinesia, lateroposition.

The development of a crossbite may be due to the following reasons: heredity, the incorrect position of the child during sleep (on one side, placing a hand, a fist under the cheek), bad habits (supporting the cheek with a hand, sucking fingers, cheeks, tongue, collar), atypical arrangement of the rudiments of teeth and their retention, delay in the change of milk teeth by permanent ones, violation of the sequence of teething, unworn tubercles of milk teeth, uneven contacts of the dentition, early destruction and loss of milk molars, nasal breathing disorder, improper swallowing, bruxism, uncoordinated activity of chewing muscles, violation of calcium metabolism in the body , facial hemiatrophy, trauma, inflammatory processes and associated jaw growth disorders, ankylosis of the temporomandibular joint, unilateral shortening or lengthening of the mandibular branch, unilateral overgrowth of the jaw body or growth retardation, residual defects in the palate after uranoplasty, neoplasms ania and others.

Considering the great variety of the clinic of cross-occlusion, it is advisable to single out the following forms [Uzhumetskene II, 1967].

The first form is the buccal crossbite.

1. Without displacement of the lower jaw to the side;

a) unilateral due to unilateral narrowing of the upper dentition or jaw, expansion of the lower dentition or jaw, a combination of these signs;

b) bilateral, due to bilateral symmetrical or asymmetric narrowing of the upper dentition or jaw, expansion of the lower dentition or jaw, a combination of these signs.

2. With the displacement of the lower jaw to the side:

a) parallel to the midsagittal plane;

b) diagonally.

3. Combined buccal crossbite - a combination of signs of the first and second varieties.

The second form is lingual crossbite:

1. One-sided, due to a unilaterally expanded upper dentition, a unilaterally narrowed lower dentition, or a combination of these disorders.

2. Bilateral, due to a wide dentition or a wide upper jaw, a narrowed lower jaw, or a combination of these features.

The third form is a combined (buccal-lingual) crossbite.

There are the following types of crossbite:

1) dentoalveolar - narrowing or expansion of the dentoalveolar arch of one jaw; a combination of disorders on both jaws;

2) gnathic - narrowing or expansion of the basis of the jaw (underdevelopment, excessive development);

3) articular - displacement of the lower jaw to the side (parallel to the midsagnt plane or diagonally). The listed types of crossbite can be unilateral, bilateral, symmetrical, asymmetric, and also combined (Fig. 1).

Rice. 1. Varieties of crossbite.

destruction crown tooth bite

With a crossbite, the shape of the face is disturbed, transversal movements of the lower jaw are difficult, which can lead to uneven distribution of masticatory pressure, traumatic occlusion, and periodontal tissue disease. Some patients complain of biting the mucous membrane of the cheeks, incorrect pronunciation of speech sounds due to a mismatch in the size of the dental arches. Often, the function of the temporomandibular joints is disturbed, especially with malocclusion with a displacement of the lower jaw to the side.

The clinical picture of each type of crossbite has its own characteristics.

With a buccal crossbite without displacement of the lower jaw to the side, asymmetry of the face is possible without displacement of the median point of the chin, which is determined in relation to the median plane. The median line between the upper and lower central incisors usually coincides. However, with a close position of the anterior teeth, their displacement, asymmetry in the development of the dental arches, it can be displaced. In such cases, determine the location of the bases of the frenulums of the upper and lower lips, tongue.

The degree of violation of the ratio of dental arches in the bite is different. The buccal tubercles of the upper lateral teeth may be in tuberous contacts with the lower teeth, may be located in the longitudinal grooves on their chewing surface, or not in contact with the lower teeth.

With a buccal crossbite with a displacement of the lower jaw to the side, asymmetry of the face is observed, due to the lateral displacement of the chin in relation to the midsagittal plane. The right and left profiles in such patients usually differ in shape, and only in preschool children is the asymmetry of the face hardly noticeable due to chubby cheeks. It progresses with age. The midline between the upper and lower central incisors usually does not coincide as a result of the displacement of the lower jaw, changes in the shape and size of the dental arches and often the jaws. In addition to shifting the lower jaw parallel to the midsagittal plane, it can move diagonally to the side. The articular heads of the lower jaw with its lateral displacement change their position in the joint, which is reflected in the meiodistal ratio of the lateral teeth in the occlusion. On the side of the displacement, a distal ratio of the dental arches occurs, on the opposite side, a neutral or mesial one. On palpation of the region of the temporomandibular joints during opening and closing of the mouth on the side of the displacement of the lower jaw, a normal or mild movement of the articular head is determined, on the opposite side - more pronounced. When opening the mouth, the lower jaw can move from the lateral position to the central position, and when closing, it can return to its original position. In some patients, there is an increase in the tone of the masticatory muscle proper on the side of the displacement of the lower jaw and an increase in its volume, which increases the asymmetry of the face.

To determine the displacement of the lower jaw to the side, the third and fourth clinical functional tests are used according to L. V. Ilina-Markosyan and L. P. Kibkalo (1970), namely, the patient is offered to open his mouth wide and study the facial signs of deviations; the existing asymmetry of the face increases, decreases or disappears depending on the cause that causes it (third test); after that, the lower jaw is set in the usual occlusion, and then, without the usual displacement of the lower jaw, the harmony of the face is assessed from an aesthetic point of view, the degree of displacement of the lower jaw, the size of the interocclusal space in the region of the lateral teeth, the degree of narrowing (or expansion) of the dentition, the asymmetry of the bones of the facial skeleton, etc. (fourth trial).

When studying a direct radiograph of the head, asymmetric development of the facial bones of the right and left sides, their unequal location in the vertical and transverse directions, and diagonal lateral displacement of the lower jaw are often established. Note the shortening of the body of the lower jaw or its branches on the side of displacement, the thickening of the body of this jaw and the chin on the opposite side.

With a lingual crossbite, on the basis of an examination of the face in front and profile, a displacement of the lower jaw and a flattening of the chin are often detected. Sometimes hypotension of the masticatory muscles, a disorder in the function of chewing, blocking of the lower jaw and a violation of its lateral movements are determined. Change the shape of the dental arches and bite. With an excessively wide upper dental arch or a sharply narrowed lower apex, the lateral teeth partially or completely slip past the lower ones on one or both sides.

Rice. 2. Orthodontic appliances for the treatment of crossbite.

With a combined buccal-lingual crossbite, facial signs of disorders, as well as dental, articular, muscular, etc., are characteristic of both literal and lingual crossbite.

The treatment of a crossbite depends on its type, causes of development, as well as the age of the patient. Basically, the width of the upper and lower dentition is normalized by unilateral or bilateral expansion, narrowing, setting the lower jaw in the correct position (Fig. 2).

During periods of milk and early mixed occlusion, treatment consists in eliminating the etiological factors that caused the violation: fighting bad habits and mouth breathing, removing delayed milk teeth, grinding off unworn milk tubercles - molars and canines, which impede transversal movements of the lower jaw. Children are advised to chew solid food on both sides of their jaws. In cases of habitual displacement of the lower jaw to the side, therapeutic exercises are prescribed. After an early loss of milk molars, removable dentures are made to replace defects in the dental arches. Removable dentures for the upper jaw with a neutral and distal ratio of the dental arches are made with a bead platform - in the anterior area. The bite is also increased on artificial teeth, which makes it possible to separate the teeth on the abnormally developed side. This makes it easier to correct their position with springs, inclined plane screws, and other devices.

In addition to preventive measures, orthodontic appliances are used. According to the indications, the bite is increased by means of crowns or mouthguards, fixed on the milk molars, which makes it possible to create conditions for the normalization of the growth and development of the dental arches and jaws and the elimination of mixing of the lower jaw. With a lateral displacement of the lower jaw, crowns or mouth guards are modeled taking into account its correct position. It is recommended to use a chin sling to normalize the position of the lower jaw, which is achieved with the help of a stronger rubber traction on the side opposite to its displacement. To establish the lower jaw in the correct position, plates or mouth guards are used for the upper or lower jaw with an inclined plane in the lateral area.

In the manufacture of devices for the treatment of crossbite, a constructive bite is determined: the dentitions are separated on the side of deformation in order to facilitate their expansion or narrowing and the lower jaw is set in the correct position with its lateral displacement.

For the treatment of crossbite, combined with a lateral displacement of the lower jaw, an inclined plane is modeled on the plate for the upper jaw - palatine, for the lower jaw - vestibular on the side opposite to the displacement. You can also make an inclined plane on the side of the displacement of the lower jaw: on the upper plate - from the vestibular side, on the lower - from the oral. In case of bilateral crossbite, an expanding plate with occlusal pads on the lateral teeth without imprints of the chewing surface of the opposing teeth is used, which facilitates the expansion of the dental arch. With a significant narrowing of the upper dental arch or jaw, both unilateral and bilateral, expansion plates are shown with a screw or springs, as well as with bite pads in the lateral areas. With the help of such devices, the lower jaw is set in the correct position, the lateral teeth are separated, which facilitates the expansion of the upper dentition, the bite is corrected, the tone of the chewing muscles is rebuilt, and the position of the articular heads of the lower jaw in the temporomandibular joints is normalized.

With a pronounced malocclusion, including those combined with sagittal and vertical anomalies at the age of 5-6 years, functionally guiding or functionally operating orthodontic appliances are used. Of the functional guide vanes, the activator is more often used. With a one-sided discrepancy between the position of the lateral teeth (narrowing of the upper dentition and expansion of the lower one), devices for moving the lateral teeth (springs, screws, levers, etc.) are added to the Andresen-Heupl activator. Occlusal adjustments are kept on the side of a correctly formed bite. The bite is normalized as a result of correcting the position of the teeth, the growth of the articular process and the branches of the lower jaw and the elimination of its displacement. You can use an activator with a one-sided sublingual pad (on the side of the correct closure of the dentition) or with a bilateral one. In the latter case, it should not fit (to the teeth subject to lingual inclination with the help of the vestibular arch.

Of the functionally operating devices, the Frenkel function controller is more often used. Treatment with this device is most effective in the final period of the milk and the initial period of mixed dentition. In buccal crossbite, the regulator is made so that the side shields are adjacent to the crowns and the alveolar process of the lower jaw and do not touch them in the region of the upper jaw on one side with a unilateral crossbite or on both sides with a bilateral one; with a lingual crossbite, the ratio of the lateral shields and dentoalveolar areas should be reversed. By compressing the median flexure of the palatine clasp of the regulator, it is possible to increase the pressure on the upper posterior teeth in the oral direction.

In the final period of mixed dentition and the initial period of permanent dentition, the same preventive and therapeutic measures are used as in the previous period.

During the change of milk molars and the eruption of goremolars, active orthodontic appliances are usually replaced with retention ones. After (eruption of the premolars at half the height of their crowns, they are pressured by an orthodontic apparatus in order to establish in the correct position. Uncoupling of the bite during this period of treatment is not required.

In the final period of permanent bite and in adults, it is possible to correct the position of individual teeth, change the shape of the dental arches and eliminate the displacement of the lower jaw. For treatment, mechanically acting devices are more often used, combining their relationship with intermaxillary traction, extraction of individual teeth, and compact osteotomy (Fig. 3). In case of lateral displacement of the lower jaw, the need for expansion or narrowing of individual sections of the dental arches, removal of individual teeth for orthodontic indications, compact osteotomy, or other types of surgical interventions is detected after the jaw is established in the correct position. Compactosteotomy is done near the teeth subject to vestibular or oral movement both from the vestibular and oral sides of the alveolar process, and with indications for dentoalveolar shortening or lengthening, also at the level of the apical basis of the dentition.

Rice. Fig. 3. Diagnostic models of the jaws of patient D. in front (a) and in profile (b). On the left - before treatment: mesial crossbite with displacement of the lower jaw to the right, on the right - after the removal of the lower first premolars, correcting the position of the teeth and lower jaw.

To move the upper and lower teeth in mutually opposite directions after bite disengagement with the help of a removable apparatus, rings are used on the upper and lower lateral teeth with intermaxillary traction. In the treatment of buccal crossbite, the rubber rings are hooked on the hooks soldered on the oral side of the rings on the movable upper lateral teeth, and on the hooks located on the vestibular side of the rings fixed on the lower lateral teeth. If occlusal contacts between the teeth remain on the side of tooth movement, the patient will bite through the rubber rings and the treatment will not be successful. Dental rows in these areas are subject to disassembly. It is necessary to ensure that the removable device that separates the teeth does not adhere to the teeth that are moved orally, to the alveolar process in this area.

Rice. Fig. 4. Patient P. Mesial crossbite with displacement of the lower jaw: on the left (a, c) - before treatment, on the right (b, d) - after treatment.

Angle appliances are used to correct the size of dental arches. The distance between the vestibular surface of the moved teeth and the springy arch is adjusted. For the treatment of crossbite with displacement of the lower jaw, to the side or combined with sagittal and vertical bite anomalies, Entl devices with intermaxillary traction, including one-sided (Fig. 4), are used.

...

General concept

Non-carious lesions of the teeth are an extensive group of diseases and pathologies. These include all damage to the enamel, diseases of a non-bacterial nature. In terms of prevalence, they rank second after caries. Such lesions can have a variety of symptoms and clinical picture, they have different causes and causes. But they are all congenital or acquired.

They can have a different distribution - affect one or all teeth in a row, individual sections in a certain order. Many of these diseases are difficult to diagnose, since the signs of different pathologies are similar and difficult to distinguish from each other. This may be due to insufficient knowledge of the disease, which complicates its detection and increases the risk of complications. In such a situation, only the best can help where they choose the right treatment option (for example, SM-Clinic, which has several branches in Moscow, Diamed or DentaLux-M).

Classification of non-carious lesions

Due to the variety of diseases that relate to the concept of "non-carious lesions of the teeth", their classification does not have one generally accepted standard. If you summarize all the data, you can get a generalized list of types of lesions.

1. Pathology of development during teething:

Anomaly of shape, size.
Fluorosis (mottled teeth).
Enamel hypoplasia (developmental disorder).
Pathologies of the structure of the teeth of a hereditary nature (odontogenesis, amelodentinogenesis).
Syphilis (congenital).
Other developmental pathologies associated with external factors (antibiotics, rhesus conflict).

2. Pathological changes in the hard tissues of the tooth:

Complete loss of a tooth.
Erosion.
Color change after cutting.
Increased tissue sensitivity.

3. Changes in the internal structure of the tooth:

Root fracture.
Root dislocation.
Fracture of the crown of the tooth.
Pulp opening.

In our country, another classification, proposed in 1968 by V.K. Patrikeev, is more often used. According to it, non-carious lesions of the teeth are divided into two groups.

1. Lesions occurring before eruption:

Anomaly of eruption and development.
Hypoplasia of the teeth.
Hyperplasia.
Fluorosis.
hereditary pathologies.

2. Lesions occurring after eruption:

Erosion.
wedge defect.
Necrosis of hard tissues.
Hyperesthesia of the teeth.
Erase.
Tooth trauma.
Pigmentation.

hypoplasia

This is the name of the pathology of the development of dental tissue during its formation, that is, in children before teething. Such a violation is caused by insufficient mineralization of tissues. The main symptom is the complete absence of an organ or its abnormally small development. Hypoplasia of the teeth can be either congenital or develop after the birth of a child. There are several reasons for this:

Rh factor conflict between mother and child
an infectious disease transmitted by the mother during pregnancy, infections in a child after birth,
severe toxicosis accompanying pregnancy,
premature birth, trauma during childbirth,
pathology of the development of the child after birth,
dystrophy, diseases of the gastrointestinal tract,
metabolic disease,
impaired development of brain activity,
mechanical damage to the jawbone.

There are two types of hypoplasia - systemic and local. The first is characterized by the defeat of all teeth, low thickness of enamel or its absence. Yellow spots appear. Local is characterized by damage to one or two organs. Here, there is a lack of enamel (partial or complete), structural defects of the teeth - they can be deformed. Such disturbances cause pain. Hypoplasia in severe form causes increased tooth wear, tissue destruction or complete loss of an organ, and the development of malocclusion. Treatment of hypoplasia includes teeth whitening (at an early stage) or filling and prosthetics (for severe disease). At the same time, the enamel is remineralized with medications (for example, calcium gluconate solution). In order to prevent the occurrence of hypoplasia in children, pregnant women are recommended a balanced diet containing vitamins for teeth (D, C, A, B), calcium and fluoride, as well as strict oral hygiene.

Hyperplasia

Hyperplasia - non-carious lesions of the teeth associated with excessive formation of tooth tissues. Their appearance is due to an anomaly in the development of epithelial cells, enamel and dentin. It appears in the form of "drops", which are also called "enamel pearls". They can be up to 5 mm in diameter. The main area of localization is the neck of the tooth. Such a drop consists of tooth enamel, inside there may be dentin or soft connective tissue resembling pulp. There are five types of such formations according to their structure:

true enamel - consist only of enamel,
enamel-dentine - the enamel shell contains dentin inside,
enamel-dentine drops with pulp - there is connective tissue inside,
drops Rodriguez - Ponti - enamel formations in the periodontium between the root and the alveolus,
intradentinal - located in the thickness of the dentin.

Hyperplasia of the tissues of the teeth does not manifest itself clinically, it does not cause pain, inflammation or any discomfort. You can only highlight the aesthetic factor if the anomaly affects the front teeth.

In this case, grinding and leveling of the surface is carried out. In other cases, if the patient is not bothered by anything, treatment is not carried out. Preventive measures are to protect milk teeth from caries, since their destruction can cause disturbances in the development of permanent ones.

Fluorosis

Fluorosis occurs during the formation of dental tissue due to the increased intake of fluoride in the body. It changes the correct structure of the enamel and causes its external defects - the appearance of spots, stripes, furrows, dark blotches. In the development of such a pathology, not only an excess of fluorine plays a role, but also a lack of calcium. In the children's body, fluorine accumulates more and faster than in adults, coming from food and water. There are such forms of fluorosis:

dashed - manifested by the appearance of white stripes without a clear outline;
spotted - characterized by the presence of yellowish spots with a smooth surface;
chalky-mottled - dull or shiny spots that are white, brown or yellow (can affect all teeth);
erosive - multiple erosions of the enamel surface;
destructive (a tooth broke off or completely collapsed) - the detrimental processes that accompany fluorosis.

Treatments for fluorosis vary depending on the form of the disease. So, with a spotted form, whitening and remineralization are carried out, if necessary, grinding of the upper layer of enamel. But the erosive form cannot be cured by such methods; here it is necessary to restore the teeth with veneers or crowns. General methods of treatment include remineralization, restoration of the shape and color of the organ, local effects on the body, control of fluorine intake.

Erosion

Non-carious lesions of the teeth include enamel damage such as erosion. Its formation leads to discoloration, aesthetic damage to the tooth, as well as increased sensitivity. Detected by visual inspection. Tooth erosion is characterized by progressive destruction of enamel and dentin, the course of the disease is chronic, and can take a long time. The cause of the pathology may be mechanical in nature, for example, when using hard brushes or pastes with abrasive particles. Also, erosion can be caused by a chemical effect on the enamel when eating foods and drinks with high acidity (picks, marinades, citrus juices, and others). Workers in industries associated with the constant inhalation of harmful substances most often suffer from such damage to the teeth. The use of certain drugs can contribute to the onset of the disease (for example, a large amount of ascorbic acid has a detrimental effect on enamel).

The cause may also be disturbances in the work of the stomach (increased acidity of its environment) or the thyroid gland. It is difficult to identify the disease at an early stage, since it is manifested only by a loss of luster in a separate small area of the tooth. The further course of the disease leads to a gradual decrease in enamel and dentin. It looks like worn teeth, most often at the base. Treatment is based on stopping the destruction of dental tissues. It includes the use of applications containing fluorine and calcium for about 20 days, then the affected area is covered with fluorine varnish. It is possible to use veneers or crowns to restore the aesthetic appearance. The complex therapy includes calcium and phosphorus preparations, as well as vitamins for teeth. If left untreated, erosion can cause tooth hyperesthesia.

Hyperesthesia

Hyperesthesia of the teeth is manifested by increased sensitivity of the enamel and in most cases is a concomitant symptom of other non-carious diseases. The prevalence of this pathology is high: about 70% of the population suffer from hyperesthesia, more often women are affected. Manifestation - a sharp, severe pain that lasts no more than thirty seconds and appears when exposed to external factors on the enamel. Hyperesthesia is divided into types according to several criteria:

1. Distribution:

limited form - affects one or more teeth;
generalized - characterized by sensitivity of all organs.

2. Origin:

a form of hyperesthesia associated with the loss of dental tissues;
not associated with loss, due to the general condition of the body.

3. Clinical picture:

pain occurs as a reaction to the temperature of external stimuli (cold water);
teeth react to chemical stimuli (sweet or sour foods);
reaction to all stimuli, including tactile ones.

Treatment of hyperesthesia is prescribed by a specialist, depending on the cause of its occurrence, the complexity of the problem and the form of the disease. In some cases, surgical intervention is necessary (for example, with pathological and denudation of the cervical region of the tooth), and sometimes therapeutic procedures can be dispensed with, such as the application of fluorine-containing applications to damaged areas. Orthodontic therapy may be required for hyperesthesia due to increased tooth wear. Preventive measures - eating all the necessary minerals and vitamins that strengthen dental tissues, regular and proper use of oral hygiene products, as well as an annual examination at the dentist.

wedge-shaped defect

A wedge-shaped defect is a tooth lesion in which its base is destroyed. Outwardly, it is manifested by damage to the neck of the tooth in the form of a wedge. Most often, fangs are defective. At the initial stage, it is invisible, it is difficult to diagnose. With a long course of the disease, a dark shade appears in the affected area. The main symptom of a wedge-shaped defect is that the teeth react painfully to the influence of high or low temperatures, sweet food, physical impact (cleaning). The reason for the development of the disease may be non-observance of oral hygiene, improper use of the brush - if after cleaning a bacterial plaque remains at the base of the bone formation, it destroys the enamel, leading to a wedge-shaped defect. It can also be caused by gum disease such as gingivitis and periodontitis, a malfunction of the thyroid gland, and increased acidity of the stomach, which causes heartburn. Treatment of a wedge-shaped defect depends on the severity of the damage.

With a slight destruction, it is enough to carry out restorative procedures that will replenish calcium and fluoride in the tooth enamel and reduce its susceptibility to external factors. In case of severe damage, a seal cannot be dispensed with. Due to the inconvenient location of the defect, such fillings often fall out. The best dental clinics are able to solve this problem by drilling a hole of a certain shape that holds the filling and using a material of special elasticity.

hard tissue necrosis

Necrosis of hard tissues of the teeth at an early stage is manifested by a loss of enamel luster, chalky spots appear. As the disease progresses, they turn dark brown. Softening of tissues occurs in the affected area, the enamel loses its strength, the patient may complain that his tooth has broken off. Dentin pigmentation occurs. Usually not one organ is affected, but several at once. Sensitivity to external stimuli increases. It is localized mainly at the neck of the tooth, as well as a wedge-shaped defect and erosion. But, despite the similar symptoms and the affected area, an experienced dentist can easily distinguish these diseases from each other and make the correct diagnosis. This pathology occurs against the background of hormonal disorders in the body. Treatment is aimed at strengthening dental tissues, eliminating hypersensitivity (hyperesthesia), and in case of severe damage, orthopedic therapy is prescribed.

Tooth trauma

The concept of “dental injury” combines damage to the mechanical nature of the external or internal parts of the tooth. The reasons for their occurrence can be called falls, blows to the jawbone during sports, fights, accidents. With prolonged exposure to a tooth with foreign objects or solid food, its tissues become thinner and become brittle. In this case, trouble can happen even when chewing food.

Injuries to the teeth can be the result of improper dental procedures, such as poor-quality pin installation. Some diseases can also lead to damage, such as hypoplasia, fluorosis, cervical caries, root cyst. Injuries include fractures of the crown or root, dislocation. The treatment of a bruise is based on the exclusion of physical impact on the diseased organ, the rejection of solid food. During treatment, it returns to the hole for further engraftment. If such an operation does not have prospects, according to the dentist, prosthetics or implantation is performed. A crown fracture needs immediate treatment to restore not only chewing functions, but also an aesthetic appearance, especially if the front teeth have been damaged. In this case, fixed crowns are installed. When a root is fractured, a complete tooth extraction is usually performed to install a post or implant.

Diseases of the dentoalveolar system and organs of the oral cavity are numerous and varied. They can be hereditary and congenital, but more often they are acquired.

Classification. Allocate diseases: 1) hard tissues of the tooth; 2) pulp and periapical tissues; 3) gums and periodontium; 4) jaws; 5) salivary glands; 6) lips, soft tissues of the oral cavity and tongue. The section presents the most common diseases.

Diseases of the hard tissues of the tooth

Among the diseases of hard tissues of the tooth, caries and some non-carious lesions of the teeth are of the greatest importance.

Caries

Tooth decay- a pathological process manifested by demineralization and progressive destruction of hard tissues of the tooth with the formation of a defect in the form of a cavity. This is one of the most common dental lesions, which, according to WHO, affects up to 90% of the world's population. It is observed at any age, but mainly in children and adolescents and equally often in both sexes. The teeth of the upper jaw are affected by caries somewhat more often than the lower, perhaps due to the fact that in the lower jaw they are in conditions of better blood circulation, they are better cleaned of food debris, which prevents the development of conditions for the occurrence of caries. Caries often affects the first large molars - molars (from lat. molares- millstones), since the greatest load falls on them when chewing. In second place are the second large molars, in the third - small molars (premolars) and upper incisors, in the fourth - fangs. The anterior teeth of the lower jaw are rarely affected. In molars and premolars, caries usually begins on chewing surfaces, in enamel folds - fissures and blind pits, where the enamel layer is much thinner, its mineralization is less pronounced. (fissure caries), or on adjacent surfaces. The buccal surfaces are less commonly affected, and very rarely the lingual ones. Relatively rare cervical caries and cement caries.

Etiology and pathogenesis. The cause of caries is still not clear enough. For a long time, localistic chemical and microbial theories of its origin and development dominated and have not lost their significance at the present time. According to these theories, organic acids, including lactic acid, formed in the oral cavity during bacterial fermentation of carbohydrates, damage the enamel and open access for bacteria to the dentinal tubules. Bacteria penetrating into the dentin extract calcium salts from it, soften it, which leads to the destruction of the hard tissues of the tooth.

Microorganisms of the oral cavity in greater or lesser quantities are found in plaque, which is formed in fissures, pits on the contact surfaces of the teeth, around the neck of the tooth under the gum. The formation of plaque has a certain sequence: from the attachment of bacteria to the pellicle (a derivative of saliva contains amino acids, sugars, etc.) and the formation of a matrix to the multiplication of bacteria and the accumulation of their metabolic products. Plaque with formation dental plaque currently given a leading role as a local factor in the appearance of the initial manifestations of caries.

Plaque also underlies the formation of supragingival and subgingival tartar(cm. gum and periodontal disease).

It has been established that microbial associations (streptococci, staphylococci, lactobacilli, etc.) have increased hyaluronidase activity. A direct relationship has been found between the activity of this enzyme, the pH of saliva and the degree of development of caries.

It has been shown that saliva hyposecretion and a lack of parotin (a hormone of the salivary glands) accelerate the development of caries, while an excess of parotin has an anti-caries effect and favors the normalization of protein and mineral metabolism in the teeth.

In the origin of caries, not only local chemical and microbial factors play a role, but also the general condition of the body, hereditary predisposition, age - periods of eruption and change of milk teeth, puberty. It is during these periods that the greatest damage to caries is observed. Of great importance are violations in the body of mineral, protein and carbohydrate metabolism, an incorrect ratio of the content of calcium and phosphorus salts in the teeth, a lack of vitamins, microelements, especially fluorine, and hormones. Due to the deficiency of these substances, apparently, the activity of the odontoblasts of the pulp with its neurovascular apparatus, which perform the function of intradental trophic centers in relation to the hard tissues of the tooth: enamel, dentin and cement, is disrupted. In the occurrence of caries, one should take into account geographical factors, living conditions, the nature of nutrition and other factors affecting the external environment on the body.

Pathological anatomy. The nature clinical and morphological manifestations There are 4 stages of caries development: spot stage, superficial, medium and deep caries. The nature currents distinguish between slow and fast current caries.

Spot stage- early stage of caries. The onset of caries is expressed by the appearance of white opaque against the background of the shiny surface of the enamel.

spots resembling chalk in color (chalk spot). The results of morphological and microradiographic studies of teeth sections showed that the pathological process begins with dis- and demineralization in surface area of the enamel. A decrease in the content of calcium, phosphorus, fluorine and other minerals was established. Initially, calcium salts disappear from the interprism substance, and then from the prisms. The interprism gaps expand, the contours of the prisms are erased, become fine-grained and turn into a structureless mass. As a result, the enamel loses its uniformity and luster, and later softens. The permeability of the enamel in this stage increases.

chalk stain may become pigmented (from yellowish to dark brown), which has not been properly explained. It is believed that pigmentation can be associated both with the penetration of organic substances and their splitting, and with the accumulation of tyrosine in the spot and its transformation into melanin.

The enamel layers and dentin-enamel junction are not broken at this stage. The carious process may subside, be accompanied by remineralization, and the enamel stain acquires clear boundaries. With the progression of caries in the stage of a pigmented spot, demineralization of the enamel increases.

Superficial caries- the process of ongoing demineralization and destruction of enamel within the dentin-enamel junction. Calcium salts disappear from the enamel prisms, the interprism substance is destroyed, the prisms look more prominent, they clearly show transverse striation, which is explained by the uneven dissolution of calcium salts. Prisms are arranged randomly and gradually undergo complete destruction. Microbes accumulate in the areas of the enamel defect, which begin to spread along the loosened interprism substance, along the cracks formed between the remaining prisms. With the rapid progression of caries, the process extends to the dentin, with its slow course, the softened area of enamel is again calcified (remineralization) and hardens.

Medium caries- the stage of progression of caries, in which the dentin-enamel junctions are destroyed and the process passes to the dentin. Dentinal tubules expand, fill with microbial masses, processes of odontoblasts under the action of microbial toxins undergo dystrophy and necrosis with disintegration into separate fragments. The shell lining the lumen of the tubules also perishes. This facilitates the penetration of microbial waste products into the deep-lying tubules of dentin and enhances its demineralization and softening.

(Fig. 348).

Formed carious cavity (hollow). The carious focus has the shape of a cone, with its apex facing deep into the tooth, and its base towards its surface. In the area of the bottom of the carious cavity, three zones can be distinguished. First- softened dentine zone: it is completely missing

Rice. 348. Medium caries. Destruction of enamel and strips of dentin, penetration of microbes into dentinal tubules

structure of dentin, it is soft, completely devoid of calcium salts, contains many different microbes. Second- zone of transparent dentin, this is calcified dentin, its tubules are narrowed, the tissue becomes homogeneous, as a result of which it becomes more transparent compared to the area of unaffected dentin. Third- zone of replacement (irregulatory, secondary) dentin, which is formed by odontoblasts, has no ordered tubules. The formation of replacement dentin should be considered as a compensatory reaction (reparative regeneration) that contributes to the stabilization of the process (Abrikosov A.P., 1914).

deep caries represents a further progression of the process with the formation of a cavity in the softened dentin (Fig. 349). Between the carious cavity and the pulp remains a narrow layer - the bottom of the carious cavity. In case of destruction (penetration) of this layer, the carious cavity reaches the pulp.

The data of microradiography of teeth affected by caries show that in all stages of its development, alternation of zones of demineralization, remineralization of enamel and dentin can be observed. Enamel mineralization processes are carried out mainly due to the intake of mineral salts from saliva. Mineralization increases as it approaches unaffected tissues. With deep caries, the most characteristic is the formation of an area of increased mineralization at the border of the dentin with the tooth cavity and the abrasion of the pattern on the rest of the dentin due to demineralization. It is also important

Rice. 349. deep caries. Softening of dentine, formation of a cavity

It should be noted that in the course of the development of caries, there is a decrease in calcium salts in the remaining hard tissues of the tooth, a decrease in the resistance of enamel and dentin, and a decrease in the activity of phosphatase in the teeth. On this soil, the mechanism of calcium phosphate deposition under the influence of phosphatase is weakened, which contributes to the progression of caries.

In addition to the typical morphological picture of caries described above, there are some variants of its development and course, observed mainly in children and relating to milk or malformed teeth in violation of calcium metabolism. These include: 1) circular caries, starting in the area of the neck of the tooth and covering it in an annular fashion; the course of the carious process is fast, without the formation of a zone of borderline transparent dentin and is accompanied by significant destruction of tooth tissues; 2) early, or subenamel, caries develops directly under the layer of enamel; 3) side caries, arising on the lateral sides of the tooth, resembling circular caries in terms of localization of the lesion, but differing from the latter in a slower course; 4) stationary caries is limited only to the dissolution of the enamel and stops there; occurs almost exclusively in first molars; 5) retrograde caries develops from the side of the pulp, affects the dentin and then comes to the surface of the tooth, destroying the enamel cover. The microscopic picture resembles a picture with ordinary caries, but, as it were, in reverse (Aprikosov A.I., 1914). It is observed with purulent pulpitis of hematogenous origin, with tooth injuries, with dental anomalies in both children and adults.

caries cement is rare, mainly when the root of the tooth is exposed and there are inflammatory processes in the periodontium. It is manifested by destructive changes in the cement and its resorption - cementolysis. Along with this, an increase in the cement layer is sometimes observed - hypercementosis.

Complications. A complication of medium and especially deep caries is pulpitis.

Non-carious lesions

To non-carious lesions dental hard tissues include wedge-shaped defects, fluorosis, dental erosion and acid necrosis.

Wedge-shaped defects- Defects of hard tissues of the tooth, located on the vestibular surface of the teeth, more often canines and premolars. Defects are formed in the neck of the tooth and occur on the soil trophic lesions of the organic matter of enamel and dentin usually in connection with past diseases of the gastrointestinal tract, endocrine system. Often these defects accompany periodontal disease. The pulp remains closed by secondary, compacted dentin, undergoes atrophy and sclerosis. The development of a wedge-shaped defect lasts for years.

Fluorosis(hyperfluorosis, enamel spotting) is a disease that develops with prolonged and excessive intake of fluorine (from lat. fluor- fluorine) and accompanied by damage not only to the teeth, but also to many organs. It occurs in separate endemic foci, where co-

the content of fluorine in water and foodstuffs exceeds 2 mg/l (the norm is 0.7-1.2 mg/l). In teeth with fluorosis, the processes of formation and calcification of enamel are disrupted.

There are 4 degrees of fluorous lesions of the teeth: I degree - a very weak lesion, in which single, small porcelain-like or chalky spots and stripes located on the labial, lingual half of the tooth surface and covering no more than 1/3 of its surface are hardly detected. II degree - weak lesion: porcelain-like and chalky spots and stripes are visible, occupying about half of the surface of the tooth crown. There are also pigmented spots, but the lesion is localized only in the enamel and does not touch the dentin. III degree - moderate damage: confluent spots are observed, occupying more than half of the surface of the tooth (Fig. 350). The spots are dark yellow and brown. Not only enamel is destroyed, but also dentin. IV degree - a severe lesion, in which single and multiple erosions of enamel of various shapes are formed - both colorless and pigmented (from yellow-brown to black). With lesions of III and IV degrees, pronounced disorders of mineralization are observed, as a result of which the teeth become brittle, brittle, easily erased and destroyed.

Erosion of the teeth- progressive bowl-shaped loss of enamel and dentin on the vestibular surface, first of the incisors, and then of the canines and premolars of the upper jaw. It occurs in middle-aged people. The reason has not been established. The course is chronic with gradual involvement of new unaffected teeth. Defects are very painful.

Acid necrosis of dental hard tissues- an occupational disease that occurs in people working in the field of production of inorganic acids. It is assumed that acid vapors reduce the pH of saliva, as well as the capabilities of the buffer systems of the oral fluid and the remineralizing properties of saliva. This contributes to the rapid wear (erasure) of the hard tissues of the tooth.

The defeat of the teeth is widespread, the process develops slowly. The crowns of the teeth are destroyed, but pulpitis does not occur due to the gradual formation of replacement dentin.

Rice. 350. Fluorosis. Multiple spots on the surface of the teeth (according to A.A. Zhavoronkov)

Diseases of the pulp and periapical tissues of the tooth

Pulp carries out tooth trophism and can undergo a wide variety of changes under the influence of general and local factors. It develops reactive changes, separate inflammation of the pulp (pulpitis).

Reactive pulp changes

Among the reactive changes in the pulp, there are disorders of blood and lymph circulation, atrophy, dystrophy, necrosis, hyalinosis, pulp calcification, as well as denticles and intrapulpal cysts.

Disorders of the blood and lymph circulation arise as a result of local and general processes. Anemia, plethora, hemorrhages, thrombosis and vascular embolism, edema are observed in the pulp. Intrapulpal hemorrhage can cause the development of pulpitis. pulp atrophy primarily for cells. First, the number and size of odontoblasts decrease, then pulpocytes. Against the background of depletion of cells, a somewhat sclerotic connective tissue base of the pulp is clearly visible, acquiring a mesh appearance. (net pulp atrophy). Dystrophy, more often hydropic, develops in odontoblasts; their fatty degeneration is also possible. Foci of mucoid swelling and fibrinoid swelling of the collagen fibers of the pulp may appear. Necrosis pulp can develop with purulent pulpitis with a closed cavity. When the pulp cavity communicates with the carious cavity and the anaerobic putrefactive flora penetrates, pulp gangrene is possible. Hyalinosis pulp can touch the walls of its vessels and collagen fibers. Sometimes in the pulp in atrophic conditions there are small amyloid bodies. Quite often, calcification is observed in the pulp (pulp petrification). The presence of significant deposits of calcium salts in the pulp disrupts metabolic processes in it, which affects the state of the hard tissues of the tooth, and in the presence of caries worsens its course. Denticli are round-oval formations, localized in the pulp in some cases freely, in others - parietal, connecting with the dentin of the tooth, or inside the mass of dentin (intrastitial denticles). Distinguish between highly and underdeveloped denticles. Highly developed denticles in their structure they are close to replacement dentin and are formed as a result of active activity of preserved odontoblasts. Underdeveloped denticles are areas of calcification of the connective tissue, and their appearance is observed most often in sclerotic coronal pulp. Denticles are especially common in chronic pulpitis and periodontal disease. Intrapulpal cysts(single and multiple) are formed as a result of various pathological processes.

Pulpitis

Pulpitis- inflammation of the dental pulp.

Etiology and pathogenesis. The causes of pulpitis are varied, but infection plays a leading role. Rarely, pulpitis can develop under aseptic conditions. Most often, pulpitis complicates medium and especially deep dental caries, when microbes and their toxins penetrate the pulp either through dilated dentinal tubules, or directly through a narrow strip of softened dentin of the bottom of the carious cavity and when it penetrates. Less often, the infection can penetrate into the pulp through the apical opening of the tooth with periodontitis, periodontitis in the presence of a periodontal pocket, very rarely - by lymphogenous and hematogenous routes in sepsis. Pulpitis can be caused by trauma to the tooth, exposure to physical factors, such as thermal (when processing a tooth for an artificial crown), radiation and decompression. Chemical factors, including medications used in the treatment of teeth and as filling agents, can also cause the development of pulpitis. The intensity and nature of inflammation in the pulp depend not only on microbes and their toxins (an association of streptococci and lactobacilli, less often staphylococci), but also on the state of local and general reactivity (sensitization) of the body.

The inflammatory process in the pulp as a closed cavity acquires, because of this, some features: it is accompanied by severe circulatory disorders (venous congestion, stasis occur, especially pronounced in the acute form of pulpitis). These vascular disorders are largely due to the difficulty of outflow from the inflamed pulp due to the narrowness of the root canals and the small size of the apical foramen. Violation of blood circulation adversely affects the vital activity of the structural elements of the pulp, intensifying dystrophic processes, and can lead to its necrosis.

Pathological anatomy. Depending on the localization allocate coronal, total and root pulpitis. By downstream pulpitis can be acute, chronic and chronic with exacerbation.

Acute pulpitis has several stages of development. It begins as focal near the carious cavity and manifests itself as serous inflammation. (serous pulpitis), in which there is a pronounced hyperemia of the vessels of the microvasculature in the pulp, especially the venular section, serous edema with a slight accumulation of poly- and mononuclear leukocytes (Fig. 351). Sometimes diapedesis of erythrocytes is noted with the formation of small foci of hemorrhages. Mild dystrophic changes in nerve fibers are revealed. This character of pulpitis lasts for several hours. Then a pronounced migration of neutrophils joins, a large number of which initially accumulates around the venules, dystrophic changes in the nerve fibers of the pulp with the breakdown of myelin intensify. There is focal or diffuse purulent pulpitis.

Focal purulent pulpitis has a limited character with the formation of a cavity filled with purulent exudate as a result of purulent fusion of the pulp, i.e. abscess (Fig. 352). At diffuse purulent

pulpitis exudate can fill not only the coronal, but also the root part of the pulp (phlegmon). The pulp has a grayish color. All its structural elements are sharply damaged.

When the pulp cavity communicates with the carious cavity and the anaerobic flora of the oral cavity penetrates, it may develop pulp gangrene. In this case, the pulp takes the form of a gray-black mass with a putrid odor; microscopically, it is structureless, sometimes granular, and may contain fatty acid crystals and microbes. With the transition of the inflammatory process to the root pulp, the development of apical periodontitis is possible. The total duration of acute pulpitis is 3-5 days.

Chronic pulpitis more often it develops gradually, as an independent form, but it can also be the outcome of acute pulpitis. By morphological features emit gangrenous, granulating (hypertrophic) and fibrous chronic pulpitis.

Gangrenous pulpitis can develop from acute after partial death of the pulp. In the preserved part of the pulp, where there are signs of serous inflammation, granulation tissue is formed, delimiting the dead masses.

Granulating (hypertrophic) pulpitis characterized by chronic productive inflammation. The tooth cavity is replaced by granulation tissue, which sometimes can also fill the carious cavity communicating with the tooth cavity. In these cases, it forms pulp polyp. It is soft, reddish in color, and bleeds easily. Its surface may be ulcerated or epithelialized due to the gingival epithelium. With this form of pulpitis, lacunar resorption can be observed.

areas of dentin by macrophages with its replacement by osteodentin (Migunov B.I., 1963). The maturation of granulation tissue leads to sclerosis. Petrificates and denticles may be found.

fibrous pulpitis- a process in which most of the cavity of the tooth is made of connective tissue with a significant amount of collagen fibers, with cellular infiltrates of lymphocytes, plasma cells. Over time, there are fewer cellular elements, collagen fibers are hyalinized, there are denticles and petrificates.

Complications and outcomes. They depend on the nature of the inflammation and its prevalence. Serous pulpitis, when the cause is eliminated, can resolve. Purulent pulpitis, especially its diffuse form, as a rule, ends with the death of the pulp and the transition to chronic forms. Chronic pulpitis ends with atrophic, sclerotic processes (see. reactive pulp changes). A frequent complication of pulpitis is periodontitis. Thus, purulent pulpitis can become the first link in the chain of development of odontogenic infection.

Periodontitis

Periodontitis called inflammation of the periodontium.

Etiology and pathogenesis. The cause of periodontitis is infection, trauma, chemicals, including medications. The value of infection in the development of periodontitis is very high, since it not only causes the development of inflammation itself, but also joins other pathogenic factors. Streptococci play the main role, other representatives of the microbial flora of the oral cavity are of lesser importance. The ways of penetration of the infection are different: intradental and extradental. Intradental (descending) path is the most frequent, the development of periodontitis is preceded by pulpitis. Extradental path can be contact - from surrounding tissues and, less often, ascending- lymphogenous or hematogenous.

Pathological anatomy. According to the localization of inflammation in the periodontium, apical(apical) and marginal(marginal, gingival) periodontitis(cm. gum and periodontal disease). Along the course, periodontitis can be acute, chronic and chronic with exacerbation.

Acute apical periodontitis may be serous and purulent. At serous inflammatory hyperemia of tissues in the region of the apex of the tooth, their edema with infiltration by individual neutrophilic leukocytes are noted. Very quickly serous exudate becomes purulent. In this case, as a result of purulent fusion of tissues, acute abscess or diffuse purulent infiltration periapical tissue with the transition of the process to the tooth socket, gum and transitional fold. At the same time, in the soft tissues of the cheek, transitional fold, palate, regional to the affected tooth, perifocal serous inflammation with severe tissue edema, called flux (parulis). Spicy

the process in the periodontium can last from 2-3 days to 2 weeks and end with recovery or transition to a chronic form.

Chronic apical periodontitis There are three types: granulating, granulomatous and fibrous. At granulating periodontitis in the region of the apex of the tooth, the formation of granulation tissue with greater or lesser infiltration of its neutrophils is noted. There may be osteoclastic resorption of the compact lamina of the alveolus, cementum, and sometimes the dentin of the root of the affected tooth. In the gums, fistulous passages can form, through which pus is periodically released.

At granulomatous periodontitis along the periphery of the periapical accumulation of granulation tissue, a fibrous capsule is formed, which is tightly soldered to the tissues surrounding the apex of the tooth. This variant of granulomatous periodontitis is called simple granuloma. Fibroblasts, macrophages predominate among the cell proliferate, lymphocytes, plasma cells, xanthoma cells, cholesterol crystals, sometimes giant cells such as foreign body cells are found. The bone tissue of the alveolar process, corresponding to the location of the granuloma, undergoes resorption. With exacerbation of inflammation, the granuloma can suppurate. The most common variant of granulomatous periodontitis is complex, or epithelial, granuloma(Fig. 353). Its difference from a simple granuloma lies in the fact that strands of stratified squamous epithelium are formed in it, penetrating the granulation tissue. The origin of the epithelium in the granuloma is associated with the proliferation of remnants of the odontogenic epithelium (Islets of Malasse). The third variant of granulomatous periodontitis is cystogranuloma. Morphogenetically, it is associated with an epithelial granuloma and is a cavity with an epithelial lining. The formation of cystogranuloma is associated with suppuration, dystrophic and necrobiotic processes in the granulation tissue. Cystogranuloma may

Rice. 353. Chronic periodontitis. Epithelial granuloma

have a diameter of 0.5-0.8 cm. Further evolution of cystogranuloma leads to the formation of a radicular cyst of the jaw (see Fig. diseases of the jaw).

Fibrous periodontitis represents the outcome of granulating periodontitis, due to the maturation of granulation tissue in the absence of an exacerbation of the process.

Any type of chronic apical periodontitis can aggravate and suppurate.

Complications and outcomes. In severe cases, purulent inflammation in the periodontium can spread to the periosteum, and then to the bone marrow of the alveolar process. Arises periostitis, possible development osteomyelitis wells. Regional lymph nodes may be involved in the process. Purulent periodontitis of the teeth of the upper jaw, projected into the maxillary (maxillary) sinus, may be complicated by the development purulent sinusitis.

Gum and periodontal disease

To understand the development of diseases in this area, it is necessary to know that the periodontium is a collection of periodontal tissues: gums, bone alveoli, periodontium (morpho-funational complex).

According to the classification adopted by the XVI Plenum of the All-Union Scientific Society of Dentists (1983), the following periodontal diseases were distinguished: gingivitis, periodontitis, dental deposits, periodontal disease, idiopathic progressive periodontolysis, periodontoma.

Gingivitis

Gingivitis- inflammation of the gingival mucosa without violating the integrity of the gingival junction. He can be local and generalized, acute and chronic.

Etiology and pathogenesis. The leading factor in the development of gingivitis are microorganisms (especially associations of streptococci) of dental plaque. The occurrence of local gingivitis (the area of one or more teeth) is associated with a gum injury of a mechanical, physical or chemical nature. Generalized gingivitis occurs, as a rule, with various diseases of infectious, metabolic and endocrine origin in children and young people.

Pathological anatomy. By the nature of the changes There are the following forms of gingivitis: catarrhal, ulcerative, hypertrophic. By degree of involvement parts of the gums in the inflammatory process are distinguished: light, when only the interdental gum (papilla) is affected, and heavy when not only the papilla is affected, but also the marginal and alveolar parts of the gums.

Catarrhal and ulcerative forms gingivitis has an acute and chronic course, hypertrophic- only chronic, although it is preceded by catarrh. At hypertrophic chronic gingivitis,

in addition to massive infiltration of the gum tissue by lymphocytes and plasma cells, a friendly proliferation of collagen fibers and cells of the integumentary epithelium with hyperkeratosis and acanthosis is found. AT period of exacerbation in addition to the appearance of neutrophilic leukocytes in the infiltrate, accumulations of mast cells are found.

Complications and outcomes. Acute local gingivitis, when the cause that caused it, can result in recovery. Acute generalized gingivitis with the elimination of the disease, of which it is a complication, also usually disappears. Chronically current catarrhal, ulcerative and hypertrophic gingivitis is often a pre-stage of periodontitis.

Dental deposits

Deposits on the teeth of foreign masses are observed in the form of either soft white plaque or dense calcareous masses - tartar. AT plaque, consisting of threads of mucus, leukocytes, food debris, etc., microbes find a fertile ground for their development, which contributes to the occurrence and progression of caries. Tartar called deposits on the teeth in the areas of plaque calcium phosphate. Stones form most often in the cervical region (supragingival stones) and in the gum pocket (subgingival stones) spreading along the root. There are several types of stones depending on their density and color: white, brown, gray-green (the most dense). The deposition of stones can contribute to inflammation of the gums, the development of periodontitis and periodontitis.

Periodontitis

Periodontitis is an inflammation of the periodontium with subsequent destruction of the periodontium, bone tissue of the dental partitions with the formation of gingival and periodontal pockets.

By prevalence of the process Distinguish between local and generalized periodontitis. Local periodontitis can be acute and chronic, occurs in people of any age. Generalized periodontitis proceeds chronically, with exacerbation, occurs in people older than 30-40 years, although the onset of its development occurs at a younger age. Depending on the depth of the formed periodontal pocket, light(up to 3.5 mm), middle(up to 5 mm) and heavy(more than 5 mm) degree of periodontitis.

Etiology and pathogenesis. The history of studying the causes and mechanisms of periodontal diseases of various origins, including inflammatory ones, goes back many decades. Theories of the pathogenesis of these diseases (vascular, neurogenic, autoimmune, etc.) were created, which, however, did not reveal all aspects of their development. It is probably more correct to talk about the importance in the etiology and pathogenesis of periodontal diseases,

including periodontitis, a number of local and general factors. To local factors should include: anomalies of bite and development of teeth (their crowding and dystonia), anomalies in the development of soft tissues of the oral cavity (small vestibule, short frenulum of the lips, its incorrect attachment, etc.). General factors are represented by a number of background diseases: endocrine (diabetes mellitus, Itsenko-Cushing's disease, diseases of the genital organs) and nervous (oligophrenia) systems, rheumatic diseases, diseases of the digestive (peptic ulcer, chronic hepatitis), cardiovascular (atherosclerosis, hypertension) systems, metabolic diseases, avitaminosis. Combination of local and general factors creates conditions for the pathogenic impact of associations of microorganisms plaque or tartar, which determines the development gingivitis and the initial stage of periodontitis. At the same time, there are changes in the quantity and quality (viscosity, bactericidal activity) of saliva and oral fluid, on which the formation of both plaque and tartar depends. Of unconditional importance in the development of periodontitis is microangiopathy of various genesis, reflecting the nature of the background disease (common factors), which is associated with an increase in hypoxia, impaired trophism and tissue regeneration, including periodontal disease.

In the stage of pronounced changes destruction periodontal bone tissue associated with inflammation in which many biologically active substances are formed.

This is first of all lysosomal enzymes polymorphonuclear leukocytes and effector cell mediators immune system.

In conclusion, it should be noted that for local form periodontitis, local factors are most important, and for generalized- general factors combined with local ones.

Pathological anatomy. The process begins with inflammation of the gums and manifests itself chronic catarrhal or hypertrophic gingivitis. In the lumen of the gingival sulcus, there are significant accumulations of loose basophilic masses that form above- or subgingival plaque, in which it is possible to distinguish accumulations of microbes, deflated epithelial cells, amorphous detritus, leukocytes. In addition to plaque, they also find dental stone. The epithelium of the marginal gingiva with symptoms of balloon dystrophy and necrosis does not regenerate well and is replaced by oral epithelium. In the connective tissue of the gums, the phenomena of mucoid, fibrinoid swelling develop, vasculitis occurs. Inflammation also captures the alveolar part of the gums. As a result of inflammation of the gums, the dentogingival junction, and then the circular ligament of the tooth, is destroyed, dental pocket, microbes and their toxins penetrate the periodontal gap, where the inflammatory process also begins. The periodontal gap widens. Already at an early stage of periodontitis in the periodontal bone tissue, signs of bone resorption are found: axillary, lacunar and smooth (Fig. 354). The most common type of resorption is lacunar bone resorption, which starts from the region of the edge (crest) of the tooth sockets and is expressed in the appearance of osteoclasts located

flickering in the gaps. This leads to horizontal resorption crest of holes. At vertical resorption osteoclasts and foci of resorption are located along the length of the interdental septum from the side of the periodontium. At the same time, lacunar resorption of bone beams occurs in the body of the jaw bones, which leads to the expansion of the bone marrow spaces. There is a formation periodontal pocket(Fig. 355).

The periodontal pocket is filled with a structureless mass containing colonies of microbes, food debris, a large number of destroyed leukocytes. With exacerbations of the disease, the depth of the pocket increases and the degree of periodontitis is determined by its degree. The outer wall of the pocket and its bottom are formed by granulation tissue, covered and permeated with strands of stratified squamous epithelium (see Fig. 355). In this case, the epithelium reaches the top of the tooth. The granulation tissue contains many neutrophils, plasma cells, macrophages and lymphocytes. From the pocket, especially during exacerbations of the disease, pus is released (alveolar pyorrhea). Over time, osteoporosis develops in the alveolar processes of the jaws, which is very well defined on x-rays.

According to the results of X-ray examination of the jaw bones, 4 degree of resorption bone tissue of the holes: I degree - the decrease in the bone edges of the holes does not exceed 1/4 of the tooth root; II degree - the decrease in the bone edges of the holes reaches half the length of the root; III degree - the edges of the holes are

Rice. 354. Periodontitis. Smooth and lacunar cancellous bone resorption

Rice. 355. Periodontitis. Pathological periodontal pocket lined with stratified squamous epithelium; cellular inflammatory infiltration of periodontal tissue

at the level of 2/3 of the length of the tooth root; IV degree - complete resorption of the bone tissue of the holes, the apex of the root is located in the soft tissues of the periodontium. A tooth devoid of a strengthening apparatus, as it were, is pushed out of its bed.

With periodontitis, resorption of cement is observed in the tooth tissue with the formation of cement and cement-dentine niches. At the same time, new formation of cementum (hypercementosis) and bone trabeculae occurs. Reactive changes (dystrophy, atrophy) develop in the tooth pulp.

Complications and outcomes. Periodontitis leads to loosening and loss of teeth. Atrophy of the alveolar crest of the jaw makes prosthetics difficult. Foci of purulent inflammation in the periodontium can become septic, leading to the development of septicopyemia (see. Sepsis).

periodontal disease

periodontal disease- chronically current periodontal disease of a primary dystrophic nature. It occurs in 4-5% of cases of all periodontal diseases. Often combined with damage to the hard tissues of the tooth of a non-carious nature (enamel erosion, wedge-shaped defects).

Cause periodontal disease is unclear. The background for its development are the same diseases as in periodontitis.

Periodontal disease is characterized gum retraction with cervical exposure, and then tooth root without previous gingivitis and periodontitis. The process develops most often in the area of incisors and canines. In the bone tissue of the alveoli, there is a delay in the change of bone structures, thickening of the trabeculae, strengthening of the line of gluing of osteons, followed by the loss of the usual structure of the bone (foci of eburnation alternate with foci of osteoporosis); dominated by smooth bone resorption. These changes are combined with the defeat microvasculature in the form of sclerosis and hyalinosis of the walls of microvessels with a narrowing of the lumen or its complete obliteration; the capillary network is reduced. There are dystrophic changes in the connective tissue.

Idiopathic progressive periodontal disease

Idiopathic periodontal disease- a disease of unknown nature with a steadily progressive lysis of all periodontal tissues. It occurs in childhood, adolescence, adolescence, combined with neutropenia, Papillon-Lefevre syndrome, insulin-dependent diabetes. There is a rapid formation of gingival and periodontal pockets with alveolar pyorrhea, loosening and loss of teeth within 2-3 years. In children, there is a loss of milk, and then permanent teeth.

Periodontoma

Periodontoma- Tumor and tumor-like diseases of the periodontium. They can be represented by true tumors and tumor-like diseases.

Tumors of the periodontium. They can be represented primarily by many varieties of so-called soft tissue tumors, often benign (see. Tumors). A feature of their course, determined by localization, is frequent injury, ulceration, followed by an inflammatory reaction.

Tumor-like diseases of the periodontium. The most common among them is epulis, gingival fibromatosis is rare.

Epulis(supergingival) - a collective concept that reflects the various stages of tissue growth as a result of chronic irritation of the gums caused by trauma (an artificial poorly fitted crown, filling, roots of a destroyed tooth). The resulting tumor-like formation occurs more often on the gums of incisors, canines, less often premolars, as a rule, from the vestibular surface. It has a mushroom-shaped, sometimes rounded shape, with a diameter of 0.5 to 2 cm, less often more. The epulis is attached by a stalk or wide base to the supraalveolar tissues. It occurs at the age of 20-40 years, more often in women. During pregnancy, their growth may accelerate. The color of the epulis is whitish, reddish, sometimes brownish.

By histological structure isolated angiomatous, fibromatous, giant cell (peripheral giant cell granuloma) epulis. Angiomatous epulis in structure resembles a capillary hemangioma (Fig. 356), fibromatous- hard fibroma. Giant cell epulis (peripheral giant cell granuloma) It consists of connective tissue rich in thin-walled sinusoid-type vessels, with more or less giant osteoclast-type cells and small osteoblast-type cells. There are multiple small foci of hemorrhages, accumulations of hemosiderin grains, therefore, macroscopically, this type of epulis has a brownish appearance. It can form islands of osteoid tissue and primitive bone beams.

Rice. 356. Angiomatous epulis

Allocate also central giant cell reparative granuloma, which is similar in histological structure to a peripheral giant cell granuloma, but is localized in the bone tissue of the alveolus and leads to its rarefaction; its boundaries are clearly defined. Giant cell granulomas (peripheral and central reparative) are often located in the mandible and grow lingually.

Epulises often ulcerate, and then their surface layers are represented by granulation tissue, in which there are many lymphocytes and plasma cells, the bone tissue of the alveoli can undergo marginal resorption, the tooth is loosened. In the epithelium of the mucous membrane covering the epulis, there are reactive changes (parakeratosis, acanthosis, pseudoepitheliomatous hyperplasia).

Fibromatosis of the gums according to clinical manifestations, it resembles hypertrophic gingivitis, but its nature is non-inflammatory. The reason for it has not been established. Education is a proliferation of dense fibrous connective tissue (with a low content of cells and blood vessels) in the form of rollers around the crown of the teeth.

Over time, there is resorption of the interdental septa and the crest of the alveolar process.

Diseases of the jaws

Diseases of the jaw bones varied in etiology, clinical and morphological manifestations. They can be divided into diseases of an inflammatory nature, cysts of the jaw bones, tumor-like diseases and tumors.

Inflammatory diseases

The diseases of this group include osteitis, periostitis, osteomyelitis (odontogenic infection).

Morphogenetically, these diseases are associated with acute purulent apical periodontitis or with exacerbation of chronic apical periodontitis, suppuration of the jaw cysts, and purulent periodontitis.

Ostitis called inflammation of the bone tissue of the jaw outside the periodontium of one tooth; inflammation on the spongy substance of the bone passes through the contact or along the neurovascular bundle. As an independent form, osteitis exists for a very limited time, as periostitis quickly joins.

Periostitis- inflammation of the periosteum. By the nature of the flow it can be acute or chronic, and nature of inflammation - serous, purulent and fibrous. Acute periostitis has a morphology of serous and purulent, chronic- fibrous.

Serous periostitis(previously it was incorrectly called simple periostitis) is characterized by hyperemia, inflammatory edema and moderate neutrophilic infiltration of the periosteum. It usually occurs after an injury. Often turns into purulent periostitis.

Purulent periostitis usually occurs as a complication of purulent periodontitis, when the infection penetrates into the periosteum through the osteon (Havers) and nutritional (Volkmann) channels; inflammation can spread to the periosteum, along the venous pathways from the sockets of the tooth. The focus of purulent inflammation is usually located not in the body, but in the alveolar process of the jaw on one side - external (vestibular) or internal (lingual or palatine). Often, the dense tissue of the periosteum prevents the spread of the purulent process, resulting in the formation of subperiosteal abscess with detachment of the periosteum and accumulation of pus between it and the bone. The formation of a subperiosteal abscess may be accompanied by perifocal edema of the adjacent soft tissues. At the same time, in the cortical part of the jaw, lacunar resorption of bone tissue is observed from the side of the Haversian canals and bone marrow spaces. Purulent periostitis can lead to melting of the periosteum and adjacent soft tissues with fistula formation, opening more often into the oral cavity and less often through the skin of the face.

Chronic fibrous periostitis often occurs with pronounced manifestations of osteogenesis, in connection with which it is called productive, hyperplastic; it is accompanied by compaction of the cortical layer of the bone (ossifying periostitis). In the place of its localization, the bone becomes thickened, somewhat tuberous.

Osteomyelitis- inflammation of the bone marrow of the jaw bones, which is more often observed in the lower jaw, respectively, molars with progressive purulent periodontitis. Osteomyelitis can occur sharply and chronically. It develops, as a rule, when the body is sensitized by bacterial antigens with purulent periodontitis (streptococci, staphylococci, Pseudomonas aeruginosa, coli bacteria). First, purulent inflammation of the bone marrow spaces of the alveolar process develops, and then - the body of the jaw. The bone beams located in this focus undergo lacunar or smooth resorption and become thinner. Subsequently, due to thrombosis of the vessels of the microvasculature, areas of bone tissue necrosis appear, these areas are rejected, and bone sequester. It is surrounded by purulent exudate and is located in the so-called sequester cavity. In chronic course, granulation tissue grows in the preserved bone tissue from the inside, sequester cavity, appears pyogenic membrane, which secretes leukocytes into the sequester cavity. Fibrous connective tissue develops in the outer layers of granulation tissue, forming capsule, delimiting the sequestral cavity from the bone tissue. In this case, purulent fusion of the sequester capsule, bone and periosteum may occur, which leads to the formation of a fistula that opens into the oral cavity or, less often, into the skin. After the release of the sequester and removal of pus, bone regeneration, which leads to the filling of the resulting defect.

Odontogenic infection- a concept that combines diseases of a purulent-inflammatory nature, the development of which is associated with purulent pulpitis or purulent inflammation of the periapical tissues of the tooth. In addition to osteitis, periostitis, osteomyelitis, odontogenic infections include odontogenic purulent regional lymphadenitis, abscesses, phlegmon with different localization in the maxillofacial region, in the soft tissues of the floor of the mouth, tongue and neck.

Complications and outcomes inflammatory diseases of the jaws are diverse. Often there is a recovery. But it should be remembered that any focus of odontogenic infection with a decrease in the body's resistance, the development of immunodeficiency can become septic focus and lead to development odontogenic sepsis(cm. Sepsis). Odontogenic infection contributes to the development phlebitis and thrombophlebitis, among which the most dangerous sinus thrombosis. Possible mediastinitis and pericarditis. When the process is localized in the upper jaw, it is often found odontogenic sinusitis. Chronic osteomyelitis of the jaws can be complicated not only pathological fractures, but also amyloidosis.

Cysts of the jaw bones

Cysts of the jaw bones are the most common lesion. A true cyst is understood as a cavity, the inner surface of which is lined with epithelium, and the wall is represented by fibrous tissue. The cavity contains more often a transparent, sometimes opalescent liquid.

Cyst formation in the jaw bones has a different nature. There are odontogenic and non-odontogenic cysts. Nonodontogenic cysts similar to bone cysts of other localizations. Here, information will only be given on odontogenic cysts. Among these cysts, cysts are of the greatest practical importance. dysontogenetic nature- primordial (keratocyst), follicular (teething cyst), cyst inflammatory origin, which is called radicular (near root).

Primordial cyst (keratocyst) it occurs most often in the region of the angle of the lower jaw or the third molar, sometimes it occurs where the tooth has not developed.

The wall of the cyst is thin, fibrous, the inner surface is lined with stratified squamous epithelium with pronounced parakeratosis, the contents of the cysts resemble cholesteatoma. The cyst can be single- and multi-chambered; islands of odontogenic epithelium are found in its wall. Some patients may have multiple keratocysts, which are combined with other malformations: multiple nevoid basal cell carcinoma, bifurcated rib. After removal, these cysts often recur.

Follicular cyst develops from the enamel organ of an unerupted tooth (toothless cyst). It is most often associated with

second premolar, third molar, mandibular or maxillary canine. The cyst forms in the alveolar margin of the jaws. Its wall is thin, the epithelium lining the cavity is multilayer flat, often flattened. Sometimes there are cells that produce mucus. Keratinization may be seen. The cavity contains a tooth or several teeth, formed or rudimentary.

Radicular cyst- the most common type of odontogenic cyst (80-90% of all jaw cysts). The cyst develops in connection with chronic periodontitis from a complex granuloma and can appear in almost any root of the affected tooth. (periradical cyst). The upper jaw is affected by cysts of this kind 2 times more often than the lower jaw. The diameter of the cysts is from 0.5 to 3 cm. Their inner surface is lined with stratified squamous epithelium without signs of keratinization. The fibrous wall is usually infiltrated with lymphocytes and plasma cells. With an exacerbation of inflammation, the epithelium is hyperplastic and reticular processes are formed, directed into the thickness of the wall and not found in other cysts. Neutrophilic leukocytes appear in the inflammatory infiltrate. In the case of melting of the epithelium, the inner surface of the cyst consists of granulation tissue. The latter can fill the cavity of the cyst. The cyst often suppurates. Accumulations of cholesterol crystals and xanthoma cells are often found in the cyst wall. In children, foci of osteogenesis are often found in the outer parts of the wall. Cysts of the upper jaw can adjoin, push back or penetrate into the maxillary (maxillary) sinus. Exacerbation of inflammation in them may be complicated by the development odontogenic sinusitis. Large cysts cause bone destruction and thinning of the cortical plate. In odontogenic cysts of a dysontogenetic nature, odontogenic tumors, rarely develop cancer.

Tumor-like diseases

To tumor-like diseases of the jaws include fibrous dysplasia, cherubism, and eosinophilic granuloma.

Fibrous dysplasia of the jaw bones- benign tumor-like growth of cellular fibrous tissue no capsule formation with resorption of the pre-existing bone, primitive osteogenesis, accompanied by facial deformity - see fig. 244 (see Diseases of the musculoskeletal system).

Cherubism- family multiple cystic disease of the jaws, manifested in the fact that between the bone beams, a connective tissue rich in cells and vessels grows. Acidophilic material and multinucleated giant cells accumulate around the vessels. Bone beams undergo lacunar resorption. At the same time, primitive bone trabeculae appear in the newly formed connective tissue, surrounded by osteoid and gradually turning into mature bone. The disease begins in early childhood with the appearance of bumpy

foliations in the area of both angles and branches of the lower jaw, less often - the lateral parts of the upper jaw. The face gradually becomes rounded and resembles the face of a cherub - hence the name of the disease.

Interestingly, the process stops by the age of 12 and the bone takes on a normal shape. Cherubism is considered as a type of fibrous dysplasia.

Eosinophilic granuloma(Taratynov's disease) occurs in children and young people in different bones, including the jaw. There are two forms - focal and diffuse. At focal form foci of bone destruction are solitary, perforated, without damage to the alveolar process. At diffuse form the interdental septa of the alveolar process are affected by the type of horizontal resorption. Histologically, the lesion is composed of homogeneous large cells such as histiocytes with a large admixture of eosinophils. The course of eosinophilic granuloma is benign. It belongs to the group of histiocytosis X (see. Tumors of the blood system).

Tumors

Tumors of the jaw bones are divided into non-odontogenic and odontogenic.

Non-odontogenic tumors

All known benign and malignant tumors that develop in other bones can occur in the jaw bones (see Fig. Tumors). It is necessary to pay attention to the most common intraosseous tumor in dental practice, which is called giant cell (osteoclastoma). It accounts for up to 30% of all bone tumors and tumor-like diseases of the jaw bones. It occurs in people aged 11-30 years, more often in women. Its most frequent localization is the lower jaw in the region of premolars. The tumor causes a jaw deformity expressed to some extent, grows for many years, destroys the bone over a considerable distance, as the bone disappears in the tumor itself, along its periphery, new bone formation occurs. The tumor has the appearance of a well-demarcated dense node, on the cut it is red or brown in color with white areas and the presence of small and large cysts.

Histological structure The tumor is very characteristic: its parenchyma consists of a large number of the same type of small oval-shaped mononuclear cells. Among them are giant multinucleated cells, sometimes very numerous (Fig. 357, 358). Free-lying and located outside the capillaries erythrocytes, hemosiderin are also visible, which gives the tumor a brown color. In some places, bone beams are formed among small, mononuclear cells. At the same time, their resorption by multinucleated tumor cells is observed. Thus, in terms of their function, the cells that make up the tumor parenchyma are osteogenic, with small cells of the osteoblast type, and multinucleated cells.

nye - type of osteoclasts. Hence the name of the tumor - osteoblastoclastoma(Rusakov A.V., 1959). The tumor may become malignant.

Deserves special attention Burkitt's tumor or malignant lymphoma (see Tumors of the blood system). In 50% of cases, it is localized in the jaw bones (see Fig. 138), destroys them and grows rapidly, generalization of the tumor is noted.

Odontogenic tumors

The histogenesis of tumors of this group is associated with tooth-forming tissues: enamel organ (ectodermal origin) and dental papilla (mesenchymal origin). As you know, tooth enamel is formed from the enamel organ, odontoblasts, dentin, cement, and dental pulp are formed from the papilla. Odontogenic tumors are rare, but extremely diverse in their structure. These are intramaxillary tumors. Their development is accompanied by deformation and destruction of bone tissue even in the case of benign variants, which constitute the bulk of tumors in this group. Tumors can grow into the oral cavity, accompanied by spontaneous fractures of the jaws. Allocate groups of tumors associated with odontogenic epithelium, odontogenic mesenchyme and having a mixed genesis.

Tumors histogenetically associated with odontogenic epithelium. These include ameloblastoma, adenomatoid tumor, and odontogenic carcinomas.

Rice. 359.Follicular ameloblastoma

Ameloblastoma- a benign tumor with a pronounced local destructive growth. This is the most common form of odontogenic tumor. It is characterized by multifocal destruction of the jaw bone. More than 80% of ameloblastomas are localized in the lower jaw, in the area of its angle and body at the level of the molars. No more than 10% of tumors are localized in the area of the incisors. The tumor most often manifests itself at the age of 20-50 years, but sometimes it also occurs in children. The tumor grows slowly over several years. It occurs with equal frequency in men and women.

There are two clinical and anatomical forms - cystic and solid; the first is common, the second is rare. The tumor is either a dense whitish tissue, sometimes with brownish inclusions and cysts, or a multitude of cysts. Histologically allocate follicular, plexiform (reticulate), acanthomatous, basal cell and granular cell forms. The most common variants are follicular and plexiform forms. Follicular ameloblastoma consists of islands of round or irregular shape, surrounded by odontogenic columnar or cubic epithelium; in the central part it consists of polygonal, stellate, oval cells forming a network (Fig. 359). As a result of dystrophic processes within the islets are often formed cysts. The structure of this form of ameloblastoma resembles the structure of the enamel organ. Plexiform shape The tumor consists of a network of strands of odontogenic epithelium with bizarre branching. Quite often, different histological variants of the structure can occur in one tumor. At acanthomatous form within the islets of tumor cells epi-

dermoid metaplasia with keratin formation. Basal cell form ameloblastoma resembles basal cell carcinoma. At granular cell form the epithelium contains a large number of acidophilic granules. Ameloblastoma with non-radical removal gives relapses.

Adenomatoid tumor most often develops in the upper jaw in the canine region, occurs in the second decade of life, consists of an odontogenic epithelium that forms a duct-like formation. They are located in the connective tissue, often with hyalinosis.

To odontogenic carcinomas, which are rare, include malignant ameloblastoma

and primary intraosseous carcinoma. Malignant ameloblastoma common features of the structure of a benign, but with pronounced atypism and polymorphism of the odontogenic epithelium are inherent. The growth rate is faster, with a pronounced destruction of bone tissue, with the development of metastases in the regional lymph nodes. Under primary intraosseous carcinoma (cancer of the jaw) understand a tumor that has the structure of epidermal cancer, which is believed to develop from islets of the odontogenic epithelium of the periodontal gap (Islets of Malasse) without connection with the epithelium of the oral mucosa. Primary carcinoma of the jaw bones may arise from the epithelium of dysontogenetic odontogenic cysts. Tumor growth is rapid, with severe bone destruction.

Tumors histogenetically associated with odontogenic mesenchyme. They are also varied.

From benign tumors allocate dentin, myxoma, cementum. Dentinoma- a rare neoplasm. On radiographs, it is a well-limited rarefaction of bone tissue. Histologically, it consists of strands of odontogenic epithelium, immature connective tissue, and islands of dysplastic dentin (Fig. 360). Myxoma odontogenic almost never has a capsule, it is characterized by local destructive growth, therefore it often gives relapses after removal. Unlike myxoma of another localization, it contains strands of inactive odontogenic epithelium. Cementoma (cementomas)- a large group of neoplasms with indistinct features. Its indispensable morphological feature is the formation of a cement-like substance with a greater or lesser degree of mineralization (Fig. 361). Allocate benign cementoblastoma, which is found

near the root of a premolar or molar, usually in the lower jaw. Tumor tissue may be soldered to the roots of the tooth. Cementing fibroma- a tumor in which among the fibrous tissue there are rounded and lobulated, intensely basophilic masses of cement-like tissue. rare giant cementoma, which can be multiple and is a hereditary disease.

Odontogenic tumors of mixed genesis. A group of these tumors is represented by ameloblastic fibroma, odontogenic fibroma, odontoameloblastoma and ameloblastic fibroodontoma.

Ameloblastic fibroma consists of islands of proliferating odontogenic epithelium and loose connective tissue resembling the tissue of the dental papilla. This tumor develops in childhood and young age and is localized in the region of premolars. Odontogenic fibroma unlike ameloblastic, it is built from islands of inactive odontogenic epithelium and mature connective tissue. It occurs in people of older age groups. Odontoameloblastoma- a very rare neoplasm that has islands of odontogenic epithelium, as in ameloblastoma, but, in addition, islands of enamel and dentin. Ameloblastic fibroodontoma also occurs at a young age. Histologically, it resembles ameloblastic fibroma but contains dentin and enamel.

Malignant tumors This group includes odontogenic sarcomas (ameloblastic fibrosarcoma, ameloblastic odontosarcoma). Ameloblastic sarcoma in structure it resembles an ameloblastic fibroma, but the connective tissue component is represented by a poorly differentiated fibrosarcoma.

Ameloblastic odontosarcoma- a rare neoplasm. The histological picture resembles ameloblastic sarcoma, but it contains a small amount of dysplastic dentin and enamel.

A number of formations of the jaw bones are considered as malformations - hamartomas, they are called odontomas. They occur more often in the region of the angle of the lower jaw in the place of unerupted teeth. Odontomas usually have a thick fibrous capsule. There are complex and compound odontomas. Complex odontoma consists of dental tissues (enamel, dentin, pulp), randomly located relative to each other. Composite odontoma represents a large number (sometimes up to 200) of small tooth-like formations, where the enamel, dentin and pulp in topography resemble the structure of ordinary teeth.

Diseases of the salivary glands

Diseases of the salivary glands are congenital and acquired (see. diseases of the gastrointestinal tract). To congenital diseases include agenesis, hypoplasia, ectopia, glandular hypertrophy, and accessory glands. A number of diseases are associated with changes in the ducts of the glands: atre-

ductal narrowing, narrowing or ectasia, abnormal branching, wall defects with the formation of congenital fistulas.

Among acquired diseases the most important are inflammation of the salivary glands (sialadenitis), salivary stone disease, gland cysts, tumors and tumor-like diseases.

sialadenitis

Sialoadenitis called inflammation of any salivary gland; mumps- inflammation of the parotid gland. sialadenitis may be primary(independent disease) or more often secondary(complication or manifestation of another disease). One gland or simultaneously two symmetrically located glands can be involved in the process; sometimes there may be multiple lesions of the glands. sialoadenitis flowing sharply or chronically often with exacerbations.

Etiology and pathogenesis. The development of sialoadenitis is usually associated with infection. Primary sialoadenitis, represented by mumps and cytomegaly, is associated with a viral infection (see. childhood infections). Secondary sialoadenitis is caused by a variety of bacteria, fungi. The ways of penetration of infection into the gland are different: stomatogenic (through the ducts of the glands), hematogenous, lymphogenous, contact. Non-infectious nature sialoadenitis develops when poisoned with salts of heavy metals (when they are excreted with saliva).

Pathological anatomy. Acute sialadenitis can be serous, purulent(focal or diffuse), rarely - gangrenous. Chronic sialoadenitis is usually intermediate productive. A special type of chronic sialadenitis with severe lymphocytic infiltration of the stroma observed at dry sjögren's syndrome(cm. diseases of the gastrointestinal tract) and Mikulich's disease in which, unlike dry syndrome, arthritis is absent.

Complications and outcomes. Acute sialoadenitis ends with recovery or transition to chronic. The outcome of chronic sialadenitis is sclerosis (cirrhosis) of the gland with atrophy of the acinar sections, stromal lipomatosis, with a decrease or loss of function, which is especially dangerous in case of systemic damage to the glands (Sjögren's syndrome), as this leads to xerostomia.

Salivary stone disease

Salivary stone disease (sialolithiasis)- a disease associated with the formation of stones in the gland, and more often in its ducts. More often than others, the submandibular gland is affected, parotid stones are rarely formed, and the sublingual gland is almost never affected. Mostly middle-aged men get sick.

Etiology and pathogenesis. The formation of salivary stones is associated with duct dyskinesia, their inflammation, stagnation and alkalization (pH 7.1-7.4) of saliva, an increase in its viscosity, and the ingress of foreign substances into the ducts.

tel. These factors contribute to the precipitation of various salts (calcium phosphate, calcium carbonate) from saliva with their crystallization on an organic basis - a matrix (descended epithelial cells, mucin).

Pathological anatomy. Stones come in different sizes (from grains of sand to 2 cm in diameter), shape (oval or oblong), color (gray, yellowish), consistency (soft, dense). When the duct is obstructed, inflammation occurs or worsens in it - sialodochitis. Developing purulent sialadenitis. Over time, sialoadenitis becomes chronic with periodic exacerbations.

Complications and outcomes. In a chronic course, sclerosis (cirrhosis) of the gland develops.

gland cysts

gland cysts very often occur in the minor salivary glands. Cause they are trauma, inflammation of the ducts, followed by their sclerosis and obliteration. In this regard, in its own way genesis salivary gland cysts should be classified as retention. The size of the cysts is different. A cyst with mucoid content is called mucocele.

Tumors

Tumors of the salivary glands make up about 6% of all tumors found in humans, but in dental oncology they make up a large proportion. Tumors can develop both in large (parotid, submandibular, sublingual) and small salivary glands of the oral mucosa: cheeks, soft and hard palate, oropharynx, floor of the mouth, tongue, lips. The most common tumors of the salivary glands of epithelial origin. In the International Classification of Tumors of the Salivary Glands (WHO), epithelial tumors are represented by the following forms: I. Adenomas: pleomorphic; monomorphic (oxyphilic; adenolymphoma, other types). II. Muco-epidermoid tumor. III. Acinocellular tumor. IV. Carcinoma: adenocystic, adenocarcinoma, epidermoid, undifferentiated, carcinoma in polymorphic adenoma (malignant mixed tumor).

Pleomorphic adenoma- the most common epithelial tumor of the salivary glands, accounting for more than 50% of tumors of this localization. In almost 90% of cases, it is localized in the parotid gland. The tumor is more common in people over 40 years of age, but can occur at any age. It occurs 2 times more often in women than in men. The tumor grows slowly (10-15 years). The tumor is a node of round or oval shape, sometimes bumpy, dense or elastic consistency, up to 5-6 cm in size. The tumor is surrounded by a thin capsule. On section, the tumor tissue is whitish, often mucoid, with small cysts. Histologically the tumor is extremely diverse, for which it received the name pleomorphic adenoma. Epithelial formations have the structure of ducts, solid fields, separate nests, anastomotic

strands interconnected, built from cells of a round, polygonal, cubic, sometimes cylindrical shape. Accumulations of elongated spindle-shaped myoepithelial cells with light cytoplasm are frequent. In addition to epithelial structures, the presence of foci and fields of mucoid, myxoid and chondroid substances (Fig. 362), which is a secretion product of myoepithelial cells that have undergone tumor transformation, is characteristic. In the tumor, foci of stromal hyalinosis may occur, and in epithelial areas - keratinization.

Monomorphic adenoma- a rare benign tumor of the salivary glands (1-3%). It is localized more often in the parotid gland. It grows slowly, has the form of an encapsulated node of a rounded shape, 1-2 cm in diameter, soft or dense consistency, whitish-pinkish or in some cases brownish in color. Histologically allocate adenomas tubular, trabecular structure, basal cell and clear cell types, papillary cystadenoma. Within one tumor, their structure is of the same type, the stroma is poorly developed.

Oxyphilic adenoma(oncocytoma) is built from large eosinophilic cells with fine granularity of the cytoplasm.

Adenolymphoma among monomorphic adenomas, a special place belongs. It is a relatively rare tumor that occurs almost exclusively in the parotid glands and predominantly in older men. It is a clearly demarcated node, up to 5 cm in diameter, grayish-white, lobed, with many small or large cysts. Histological structure characteristically: prismatic epithelium with sharply eosinophilic cytoplasm is located in two rows, forms papillary outgrowths and lines the formed cavities. The stroma is abundantly infiltrated with lymphocytes forming follicles.

Mucoepidermoid tumor- a neoplasm characterized by double differentiation of cells - into epidermoid and mucus

Rice. 362. Pleomorphic adenoma

yawning. It occurs at any age, somewhat more often in women, mainly in the parotid gland, less often in other glands. The tumor is not always clearly demarcated, sometimes rounded or irregular in shape, may consist of several nodes. Its color is grayish-white or grayish-pink, the consistency is dense, cysts with mucous contents are quite often found. Histologically, various combinations of epidermoid-type cells are found, forming solid structures and strands of mucus-forming cells that can line mucus-containing cavities. Cornification is not observed, the stroma is well expressed. Sometimes there are small and dark cells of an intermediate type, capable of differentiating in different directions, and fields of light cells. The predominance of cells of an intermediate type, the loss of the ability to form mucus is an indicator of low tumor differentiation. Such a tumor can have a pronounced invasive growth and give metastases. Signs of malignancy in the form of hyperchromic nuclei, polymorphism and atypism of cells are rare. Some researchers call this tumor mucoepidermoid cancer.

acinar cell tumor(acinous cell) is a rather rare tumor that can develop at any age and have any localization. The cells of the tumor resemble the serous (acinar) cells of the salivary glands, in connection with which this tumor got its name. Their cytoplasm is basophilic, fine-grained, sometimes light. Acinocellular tumors are often well-demarcated, but may also be invasive. The formation of solid fields is characteristic. A feature of the tumor is the ability to metastasize in the absence of morphological signs of malignancy.

Carcinoma (cancer) of the salivary glands varied. The first place among malignant epithelial tumors of the salivary glands belongs to adenocystic carcinoma, which accounts for 10-20% of all epithelial neoplasms of the salivary glands. The tumor occurs in all glands, but especially often in the small glands of the hard and soft palate. It is observed more often at the age of 40-60 years in both men and women. The tumor consists of a dense nodule of small size, grayish color, without a clear border. Histological picture characteristic: small, cubic-shaped cells with a hyperchromic nucleus form alveoli, anastomosing trabeculae, solid and characteristic lattice (cribrose) structures. A basophilic or oxyphilic substance accumulates between the cells, forming columns and cylinders, in connection with which this tumor was previously called cylindroma. Tumor growth is invasive, with characteristic fouling of the nerve trunks; metastasizes predominantly hematogenously to the lungs and bones.

Other types of carcinomas are found in the salivary glands much less frequently. Histological variants are diverse and similar to adenocarcinomas of other organs. Undifferentiated carcinomas have a rapid growth, give lymphogenous and hematogenous metastases.

Tumor-like diseases

Tumor-like diseases of the salivary glands consider lymphoepithelial lesions, sialosis and oncocytosis in adults. They are rare.

Diseases of the lips, tongue, soft tissues of the oral cavity

Diseases of these organs have a different origin: some are congenital, others are acquired, sometimes acquired diseases develop against the background of developmental anomalies. Diseases can be based on various pathological processes: dystrophic, inflammatory, tumor.

This group of diseases consists of cheilitis, glossitis, stomatitis, precancerous changes and tumors.

cheilite

cheilite- inflammation of the lips. The lower lip is affected more often than the upper. Cheilitis can be an independent disease or be combined with lesions of the tongue and oral mucosa. By the nature of the flow There are acute and chronic cheilitis, as well as chronic cheilitis with exacerbation. There are the following clinical and morphological forms cheilitis: exfoliative, glandular, contact, meteorological, actinic and Manganotti cheilitis.

At exfoliative cheilitis only the red border of the lips is affected, characterized by increased desquamation of the epithelium. Runs chronically. Can join acute exudative reaction, then hyperemia, swelling of the lips appear, overlays are formed in the form of crusts. Glandular cheilitis characterized by congenital hypertrophy and heterotopia of small salivary glands and their infection. Contact (allergic) cheilitis occurs when the red border of the lips comes into contact with a wide variety of substances that act as allergens. Immune inflammation occurs, reflecting a delayed-type hypersensitivity reaction (see immunopathological processes).

Meteorological and actinic cheilitis arise as an inflammatory reaction to cold, high humidity, wind, ultraviolet rays. Heilit Manganotti deserves special attention. It occurs in men over 50 years of age and is characterized by damage to the lower lip only. Manifested by erosions in the center of the lip on a brightly hyperemic background with the formation of bloody crusts. Therefore, Manganotti's cheilitis is called abrasive. He is precancerous disease.

Glossitis

Glossitis- inflammation of the tongue. Occurs frequently. Glossitis, like cheilitis, can be an independent disease or be combined with

damage to the oral mucosa. By the nature of the flow it can be acute, chronic, and chronic with exacerbation. Among clinical and anatomical forms glossitis distinguish desquamative, or exfoliative ("geographic language"), and diamond-shaped.

Desquamative (exfoliative) glossitis common, sometimes familial. Characterized by pronounced desquamation of the epithelium with a change in the outlines of foci of desquamation and restoration of the epithelium ("geographical language"). It can often be combined with a folded tongue.

Rhomboid glossitis- chronic, characterized by partial or complete absence of papillae with papillomatous growths in a limited area of the tongue, which has the shape of a rhombus or oval; moreover, this area is located along the midline of the back of the tongue in front of the trough-shaped papillae (“median indurated glossitis”). Cause unknown. Some researchers refer this form of glossitis to developmental anomalies; the role of various microbial flora of the oral cavity is not excluded.

Stomatitis

Stomatitis- inflammation of the mucous membrane of the soft tissues of the oral cavity. This is a fairly common disease. The mucous membrane of the cheeks, the floor of the mouth, soft and hard palate can be affected in isolation and in combination with gingivitis, glossitis, less often - cheilitis.

Stomatitis can be an independent disease, as well as a manifestation or complication of many other diseases. As an independent disease, stomatitis is represented by various clinical and morphological forms.

Guided cause the occurrence of stomatitis, the following groups can be distinguished: 1) traumatic (mechanical, chemical, including medication, radiation, etc.); 2) infectious (viral, bacterial, including tuberculosis and syphilitic, mycotic, etc.); 3) allergic; 4) stomatitis with exogenous intoxications (including professional ones); 5) stomatitis in some somatic diseases, metabolic diseases (endocrine diseases, diseases of the gastrointestinal tract and cardiovascular system, rheumatic diseases, hypo- and beriberi, etc.); 6) stomatitis in dermatoses (pemphigus, Dühring's dermatitis herpetiformis, lichen planus, etc.).

By nature of inflammation stomatitis is catarrhal, catarrhal-desquamative, catarrhal-ulcerative, gangrenous, with the formation of vesicles, blisters, aphthae, foci of para- and hyperkeratosis.

Precancerous changes

The diseases described above (cheilitis, glossitis, stomatitis) in their chronic course can be considered as precancerous conditions,

those. background on which a tumor can develop (see. Tumors). To precancerous changes include leukoplakia, limited hyperkeratosis and keratoacanthoma of the lips, Manganotti cheilitis. The most important among them is leukoplakia.

Leukoplakia(from Greek. leucos- white and french. lake- plate) - dystrophic changes in the epithelium of the mucous membrane with keratinization during its chronic irritation. The course is chronic, first white spots appear on the mucous membrane, and then plaques. Spots and plaques are localized most often on the mucous membrane of the tongue, less often - in other places of the oral mucosa. Plaques usually protrude above the surface of the mucous membrane, their surface may be rough, covered with cracks. Leukoplakia usually occurs in people aged 30-50 and is many times more common in men than in women. It occurs most often on the basis of prolonged irritation from smoking, chewing tobacco, prolonged trauma to the mucous membrane with prostheses and carious teeth (local factors), as well as on the basis of chronically current ulcers of infectious origin (for example, syphilis) or vitamin A deficiency (general factors).

There are two forms of leukoplakia: flat and warty. Histologically at flat shape there is a thickening of the stratified squamous epithelium due to the expansion of the basal and granular layers, the phenomena of parakeratosis and acanthosis. Acanthotic strands of the epithelium are deeply immersed in the dermis, where round cell infiltrates appear. At warty shape the epithelium thickens due to proliferation and expansion of the basal layer. Therefore, the surface of the plaques becomes rough. Massive lymphoplasmacytic infiltrates are found in the dermis.

Risk Factors for Dental Diseases. The position on the risk factors for the occurrence of diseases is the most important in prevention. Its essence lies in the fact that the probability of occurrence of diseases is not the same in different people. People who have risk factors for the disease are more likely to get sick. Risk factors include features of the structure, physiology, heredity of individuals, as well as living conditions, nutrition, life, habits, inclinations of people that can contribute to the development of various diseases.

Identification of risk factors and their elimination in various diseases introduces a number of fundamentally new provisions in the possibilities of prevention. First, the signs are objectified and, according to them, the persons who need prevention in the first place are subjectified. Secondly, the elimination of risk factors makes it possible to eliminate the possibility of diseases with a high degree of probability. Thirdly, work with patients with risk factors can dramatically increase the medical and economic efficiency of prevention, reduce the economic costs of these activities.

Risk factors in various ways participate in certain links in the pathogenesis of diseases, therefore, according to the possibility of a particular disease, they are called cariogenic, periodontitis, etc.

The following indicators can be considered as cariogenic risk factors - close proximity of teeth, their early eruption, viscous saliva, low secretion, the presence of anomalies of the dental system, a high level of reduction of the dental system, low Ca / P-coefficient of enamel, poor oral hygiene, a tendency to the formation of soft plaque, the presence of rheumatism and other severe chronic diseases, toxicosis of pregnancy of the mother, artificial feeding, indiscriminate uncontrolled intake of carbohydrates, chewing laziness.

Risk factors for periodontal disease include: an increased tendency to deposit plaque, a high mineralizing activity of saliva, a tendency to an alkaline reaction of saliva, a low saliva flow rate, its high viscosity, gingival localization of caries, a violation of the closure of the dentition and the normal ratio of the jaws and occlusal contacts , overload and underload of individual sections of the periodontium.

Dental caries and periodontal disease have a number of common risk factors, which allows using the same measures (oral hygiene, exposure to the salivary glands, elimination of anomalies and occlusion deficiencies) to prevent both diseases.

The risk factors for the occurrence of anomalies of the dentoalveolar system include anomalies in the attachment of soft tissues to the alveolar process, defects in the dentition, dysfunction of chewing, swallowing, breathing, delayed abrasion of milk teeth, bad habits of children, violation of the timing and sequence of eruption of permanent teeth, hereditary predisposition, a number of diseases supporting tissues, rickets, etc.

The presence of risk factors does not necessarily lead to disease. Each factor has a certain probability and level of informativeness in relation to the possibility of diseases. For some signs, it is very large, for others it is small, so the ranking of risk factors, their combination for the prevention of various diseases is very important for the development of preventive measures.

Each risk factor can have a specific way to eliminate it, therefore, the definition of risk factors, their quantitative characteristics allow individualizing preventive measures for each patient, depending on the set of existing risk factors.

The approach to prevention from the standpoint of identifying, ranking and eliminating risk factors can dramatically increase the effectiveness of prevention.

Causes of damage to hard tissues of teeth include caries, enamel hypoplasia, pathological abrasion of hard tissues of teeth, wedge-shaped defects, fluorosis, acute and chronic injuries, as well as some hereditary lesions (Fig. 66; see Fig. 7, 8).

These reasons cause defects of the crown part of the tooth of various nature and volume. The degree of damage to hard tissues also depends on the duration of the process, the time and nature of the medical intervention.

Defects in the crowns of the anterior teeth violate the aesthetic appearance of the patient, affect facial expressions, and in some cases lead to a violation of speech. Sometimes, with crown defects, sharp edges are formed that contribute to chronic injury to the tongue and oral mucosa. In some cases, chewing function is also impaired.

Caries is one of the most common dental diseases - progressive destruction of hard tissues of the tooth with the formation of a defect in the form of a cavity. The destruction is based on demineralization and softening of the hard tissues of the teeth.

Pathologically distinguish early and late phases of morphological changes in carious disease of hard tissues of the tooth crown. The early phase is characterized by the formation of a carious spot (white and pigmented), while the late phase is characterized by the appearance of a cavity of various depths in the hard tissues of the tooth (stages of superficial, medium and deep caries).

Pre-surface demineralization of enamel in the early phase of caries, accompanied by a change in its optical properties, leads to the loss of the natural color of the enamel: first, the enamel turns white as a result of the formation of microspaces in the carious focus, and then acquires a light brown tint - a pigmented spot. The latter differs from the white spot in a larger area and depth of the lesion.

In the late phase of caries, further destruction of the enamel occurs, in which, with a gradual rejection of demineralization.

Rice. 67. Reflex connections of the affected areas of the teeth.

bath tissues, a cavity with uneven contours is formed. The subsequent destruction of the enamel-dentin border, the penetration of microorganisms into the dentinal tubules leads to the development of dentinal caries. The proteolytic enzymes and acid released at the same time cause the dissolution of the protein substance and the demineralization of the dentin up to the communication of the carious cavity with the pulp.

With caries and lesions of hard tissues of a non-carious tooth.

character, disorders of nervous regulation are observed. In case of damage to the tissues of the tooth, access is opened to external non-specific stimuli of the nervous apparatus of the dentin, pulp and periodontium, which cause a pain reaction. The latter, in turn, reflexively contributes to neurodynamic shifts in the functional activity of the masticatory muscles and the formation of pathological reflexes (Fig. 67).

Enamel hypoplasia occurs during the period of follicular development of dental tissues. According to M. I. Groshikov (1985), hypoplasia is the result of a perversion of metabolic processes in the rudiments of teeth in violation of mineral and protein metabolism in the body of the fetus or child (systemic hypoplasia) or a cause locally acting on the rudiment of the tooth (local hypoplasia). It occurs in 2-14% of children. Enamel hypoplasia is not a local process that captures only the hard tissues of the tooth. It is the result of a severe metabolic disorder in a young organism. It is manifested by a violation of the structure of the dentin, pulp and is often combined with malocclusion (progenia, open bite, etc.).

The classification of hypoplasia is based on an etiological sign, since hypoplasia of dental tissues of various etiologies has its own specifics, which is usually detected during a clinical and radiological examination. Depending on the cause, hypoplasia of hard tissues of teeth that form simultaneously (systemic hypoplasia) is distinguished; several adjacent teeth that form simultaneously, and more often at different periods of development (focal hypoplasia); local hypoplasia (single tooth).

Fluorosis is a chronic disease caused by excessive intake of fluorine, for example, when its content in drinking water is more than 15 mg / l. It is manifested mainly by osteosclerosis and enamel hypoplasia. Fluorine binds calcium salts in the body, which are actively excreted from the body: depletion of calcium salts disrupts the mineralization of teeth. A toxic effect on the rudiments of teeth is not excluded. Violation of mineral metabolism manifests itself in the form of a variety of fluoride hypoplasia (striation, pigmentation, mottling of enamel, its chipping, abnormal shapes of teeth, their fragility).

Symptoms of fluorosis are represented by morphological changes mainly in the enamel, most often in its surface layer. Enamel prisms as a result of the resorptive process are less tightly adjacent to each other.

In the later stages of fluorosis, areas of enamel with an amorphous structure appear. Subsequently, in these areas, the formation of enamel erosion in the form of specks occurs, the expansion of interprism spaces, which indicates a weakening of the bonds between the structural formations of enamel and a decrease in its strength.

Pathological abrasion of teeth is an increase in time, the loss of hard tissues of the crown of the tooth - enamel and dentin - in certain areas of the surface. This is a fairly common disease of the teeth, occurs in about 12% of people over 30 years of age and is extremely rare at an earlier age. Complete erasure of masticatory tubercles of molars and premolars, as well as partial abrasion of the cutting edges of the anterior teeth in men are observed almost 3 times more often than in women. In the etiology of pathological abrasion of teeth, a prominent place belongs to such factors as the nature of nutrition, the constitution of the patient, various diseases of the nervous and endocrine systems, hereditary factors, etc., as well as the profession and habits of the patient. Reliable cases of increased tooth abrasion are described in thyrotoxic goiter, after extirpation of the thyroid and parathyroid glands, in Itsenko-Cushing's disease, cholecystitis, urolithiasis, endemic fluorosis, wedge-shaped defect, etc.

The use of removable and non-removable prostheses of irregular design is also the cause of pathological abrasion of the surfaces of teeth of various groups, the teeth that are supporting for clasps are especially often erased.

Changes in the pathological abrasion of hard tissues of the crown of the tooth are observed not only in enamel and dentin, but also in the pulp. At the same time, the deposition of replacement dentin is most pronounced, which is first formed in the region of the horns of the pulp, and then along the entire arch of the coronal cavity.

A click defect is formed in the cervical region of the vestibular surface of premolars, canines and incisors, less often than other teeth. This type of non-carious lesion of the hard tissues of the crown of the tooth is usually found in middle-aged and elderly people.

age. An important role in the pathogenesis of the wedge-shaped defect belongs to disturbances in the trophism of the pulp and hard tissues of the teeth. In 8-10% of cases, a wedge-shaped defect is a symptom of periodontal disease, accompanied by exposure of the necks of the teeth.

The currently available data allow us to see in the pathogenesis of the wedge-shaped defect a significant role of both concomitant somatic diseases (primarily the nervous and endocrine systems, the gastrointestinal tract), and the effects of chemical (changes in the organic substance of the teeth) and mechanical (hard toothbrushes) factors. Many authors assign the leading role to abrasive factors.

With a wedge-shaped defect, as with caries, an early stage is distinguished, which is characterized by the absence of a formed wedge and the presence of only superficial abrasions, thin cracks or crevices, detectable only with a magnifying glass. As these depressions expand, they begin to take on the shape of a wedge, while the defect retains smooth edges, a hard bottom, and, as it were, polished walls. Over time, the retraction of the gingival margin increases and the exposed necks of the teeth react more and more sharply to various stimuli. Morphologically, at this stage of the disease, hardening of the enamel structure, obliteration of most dentinal tubules, and the appearance of large collagen fibers in the walls of non-obliterated tubules are revealed. There is also an increase in the microhardness of both enamel and dentin due to increased mineralization process.

Acute traumatic damage to the hard tissues of the crown of the tooth is a fracture of the tooth. Such injuries are mainly exposed to the front teeth, moreover, mainly the upper jaw. Traumatic damage to the teeth often leads to the death of the pulp due to infection. At first, the inflammation of the pulp is acute and is accompanied by profuse pain, then it becomes chronic with a character (n s and pathological phenomena.

The most frequently observed fractures of the teeth in the transverse direction, rarely in the longitudinal. In contrast to dislocation with a fracture, only the broken off part of the tooth is movable (if it remains in the alveolus).

In chronic trauma of hard tissues of the tooth (for example, in shoemakers), spalls occur gradually, which brings them closer to professional pathological abrasion.

Among the hereditary lesions of the hard tissues of the tooth are defective amelogenesis (formation of defective enamel) and defective denganogenesis (violation of the development of dentin). In the first case, as a result of a hereditary disturbance in the development of enamel, a change in its color, a violation of the shape and size of the crown of the tooth, an increased sensitivity of the enamel to mechanical and thermal influences, etc. are observed. The pathology is based on insufficient mineralization of the enamel and a violation of its structure. In the second case, as a result of dentin dysplasia, increased mobility and translucency of both milk and permanent teeth are observed.

The literature describes the Stainton-Capdepon syndrome - a kind of family pathology of the teeth, characterized by a change in the color and transparency of the crown, as well as early onset and rapidly progressing tooth wear and enamel chipping.