Chapter6 Non-carious lesions of teeth

In our country, a number of classifications of non-carious lesions of teeth are known (V.K. Patrikeev; Yu.A. Fedorov, etc.).

In the International Classification of Diseases (ICD X revision, WHO), non-carious dental lesions are presented in the following forms:

K.00.3. Mottled teeth (endemic /fluorous/ mottled enamel /dental fluorosis/; non-endemic mottled enamel /non-fluorotic opacification of the enamel/; unspecified);

K.00.4. Disorders of tooth formation (prenatal, neonatal enamel hypoplasia; aplasia and hypoplasia of cement; dilaceration /enamel crack/, odontodysplasia; Turner tooth; other specified; unspecified);

A 50.512. Hutchinson incisors;

A 50.52. Mulberry-shaped molars;

K.00.5. Hereditary disorders of the tooth structure, not classified elsewhere (incomplete amelogenesis, dentinogenesis, odontogenesis, dentin dysplasia, shell teeth; unspecified);

K.00.8. Other dental development disorders (discoloration during formation due to blood type incompatibility, birth defect biliary system, use of tetracycline; other specified disorders of dental development);

K.03. Other diseases of dental hard tissues:

K.03.0. Increased abrasion (wear) of teeth (occlusal, contact surfaces; other specified; unspecified);

K.03.1. Grinding (abrasive wear) of teeth (caused by tooth powder - wedge-shaped defect, habitual, professional, traditional /ritual/; other specified; unspecified);

K.03.2. Dental erosion (occupational, caused by: persistent regurgitation or vomiting; diet; medications; idiopathic; other specified; unspecified)

K.03.3. Pathological resorption of teeth (external / disturbed /; internal / pink spot/; unspecified);

K.03.6. Deposits on teeth (pigmented plaque - black, green, orange; caused by the habit of using tobacco, chewing betel; white soft deposits; supragingival and subgingival tartar, dental plaque; other specified; unspecified);

K.03.7. Changes in the color of the hard tissues of teeth after eruption (due to the presence of metals and metal compounds, bleeding of the pulp, the habit of chewing betel nut, tobacco; other specified; unspecified);

K.03.8. Other specified diseases of dental hard tissues (sensitive dentin, enamel changes caused by radiation; other specified). Taking into account this classification and domestic clinical classifications, the following division of non-carious lesions of teeth is accepted:

I. Hereditary and congenital lesions of hard dental tissues:

1) anomalies in the size and shape of teeth (fused, spiky teeth, macrodentia, microdentia, invagination of teeth, enamel drop);

2) mottled teeth - endemic mottled enamel (fluorosis);

3) disorders of tooth formation - enamel hypoplasia (prenatal hypoplasia, neonatal hypoplasia, Turner's teeth, Hutchinson's teeth, mulberry-shaped molars, as a result of congenital syphilis);

4) hereditary disorders of the structure of teeth - imperfect enamelo-, dentin- and odontogenesis;

5) other disorders of dental development (discoloration as a result of Rh conflict, malformation of the biliary system, taking tetracycline).

II. Disorders of teething and acquired damage to their hard tissues:

1) violation of teething;

2) increased abrasion, including as a result of the abrasive action of toothpastes, powders, brushes, bad habits, occupational hazards and folk customs;

3) wedge-shaped defect;

4) erosion;

5) change in color of hard tooth tissues after teething;

6) other damage to the hard tissues of the tooth - changes in the enamel as a result of radioactive radiation; dentin hyperesthesia.

III. Dental injuries:

tooth dislocation;

fracture of the tooth crown within the enamel, dentin, opening of the pulp;

tooth root fracture.

In childhood, hereditary and congenital non-carious dental lesions mainly occur:

1) enamel hypoplasia;

2) fluorosis;

3) drug-induced and toxic disorders of the development of dental tissues;

4) hereditary disorders of the development of dental tissues. Non-carious lesions that occur after teething are found much less frequently in children:

1) dental injuries;

2) drug-induced and toxic disorders of the development of dental tissues;

3) increased tooth wear.

Hereditary and congenital lesions of hard dental tissues

Anomalies in the size and shape of teeth are described in section18 " Dental anomalies". This group of hard tissue lesions includes enamel hyperplasia, which manifests itself in the excessive formation of tooth tissue. A synonym for enamel hyperplasia is “enamel drop” or “enamel pearl”. Their origin is associated with the process of differentiation of Hartwig vagina cells into anameloblasts.

Enamel drops are more often found in the area of ​​​​the necks of the teeth, sometimes at the bifurcation of the roots. Their size reaches 2-4 mm in diameter. In the clinic they do not show themselves in any way and are discovered as an unexpected find. Cervical enamel drops are usually found with gingival retraction (see section2) and exposure of the neck of the tooth, the roots can be visible during x-ray examination or after tooth extraction.

Meanwhile, intradental (intradentinal) enamel drops are more common when the doctor, when preparing a carious cavity within the dentin, discovers a more rigid area with a drill.

Only cervical enamel drops are subject to treatment. They need to be ground with a diamond head and this area of ​​the tooth should be polished, and then the patient should be given recommendations for daily applications of phosphate-containing toothpastes for 7-10 days.

Dental fluorosis is an endemic disease caused by fluoride intoxication, resulting from the consumption of drinking water with a high fluoride content during the formation of the dental follicle. One of the early signs of fluorosis is tooth damage. With a significant concentration of fluorine (above 5-10 mg/l), it is also affected bony skeleton humans and animals.

The main source of fluoride is drinking water. The prevalence and intensity of dental fluorosis among the population increases with increasing concentrations of fluoride in water. Thus, with a fluorine content of up to 0.5 mg/l, no changes in dental tissues are observed; at a fluorine concentration of 0.8-1.0 mg/l, mild forms of fluorosis occur in 10-12% of the population; at a concentration of 1.0-1.5 mg/l, fluorosis is observed in 20-30% of the population; with a fluorine content of 1.5-2.5 mg/l - 30-45%; at a fluorine concentration of 2.5-3.0 mg/l - in 80-90% of the population. In areas with hot climates, fluorosis can develop at a fluorine concentration in water of 0.5-0.7 mg/l, which is associated with its increased consumption. The presence of a significant amount of calcium in water reduces the intensity of fluorosis.

Another source of fluoride in the body is food. The fluoride content of foods and beverages depends largely on the concentration in the water used to prepare food and beverages. In food, as well as in water, fluoride is in ionized form. However, food fluoride is less easily absorbed than water-soluble fluoride. Fish (especially cod), parsley, tea, contain large amounts of fluoride. walnuts, liver, beef

Dina, cocoa. The level of fluoride in lamb, veal and oatmeal is quite high.

Another source of fluoride is fluoride-containing toothpastes. Despite the fact that the adsorption of fluoride in the oral cavity is less than 1%, there is evidence of a connection between the frequency of enamel opacities (initial fluorosis) and brushing teeth with fluoride-containing toothpaste in the first two years of life (Sakharova E.B., 2001, etc.).

The exact mechanism of fluorosis is not yet fully understood. The idea of ​​a hematogenous toxic effect of fluoride on anameloblasts during the development of the dental epithelial organ, leading to improper formation of enamel, should be considered more justified.

It is assumed that fluoride, being an enzymatic poison, reduces the activity of phosphatase and, thereby, disrupts the mineralization of enamel. Yu.A. Fedorov et al. (1972) believe that fluorine, when administered orally and even locally, quickly penetrates and blocks and affects the activity of the thyroid gland. It is likely that changes in thyroid function are the most likely explanation for the adverse effects of fluoride on enamel mineralization.

Teeth with fluorosis are called “speckled”, “pockmarked enamel”, “spotted enamel”, “burnt” (Fig. 6.1; 6.2).

Foci of endemic fluorosis are characterized by a decrease in the prevalence and intensity of dental caries. However, research by Koshovskaya V.A. (1975) and Kovalenko L.I. (1977) indicate that the incidence of caries in an endemic focus of fluorosis is influenced not only by fluoride, but mainly by other macro- and microelements contained in drinking water and food products.

The most vulnerable period in terms of the possible development of fluorosis is childhood, namely the period of mineralization of tooth germs (from 3 months to 4 years) and the period of incomplete mineralization of enamel in the first 1-3 years after the eruption of permanent teeth.

While the majority of people living in an endemic focus of fluorosis have significant changes in the dental tissues, some people have only mild lesions. Moreover, in such areas there are children whose teeth are completely healthy. This proves that the severity of dental fluorosis is determined by the degree of sensitivity of the body to fluoride intoxication and its ability to resist this effect.

With fluorosis, symmetrically located teeth are affected, and the degree of manifestation of the disease is usually the same. The most pronounced clinical picture of this disease is observed on the central incisors and first molars, which is associated with calcification of their crowns in the first year of life, when the child’s body is significantly exposed to adverse environmental factors. Teeth, mi-

Rice. 6.1. Dental fluorosis. Erosive form

208 ♦ Dentistry

Rice. 6.2. Dental fluorosis. Chalky-speckled form (according to T.P. Kroll)

whose neuralization occurs at an older age are affected by a milder degree of dental fluorosis.

Depending on the severity of dental changes in endemic fluorosis, the following clinical forms are distinguished (Patrikeev V.K., 1973):

- line form characterized by faint, chalky stripes on the enamel of the anterior teeth of the upper jaw;

- spotted form characterized by the presence of well-defined chalky spots located over the entire surface of the teeth. A special feature of this form of dental fluorosis is that the enamel in the area of ​​the stain is smooth and shiny. Sometimes there is faint light yellow pigmentation;

- chalky (mottled) form manifests itself in the area of ​​all, not just the front teeth, and is clinically very diverse: white shiny and matte spots, areas of pigmentation of spots from light to dark brown. The spots are usually located on the vestibular surface of the front teeth. Sometimes there are small round enamel defects - specks. With this form, there is rapid abrasion of the enamel with exposure of pigmented dentin of a dark brown color;

- erosive form is characterized by more severe damage to teeth and is accompanied by the formation of defects-erosions in the area of ​​chalky altered enamel;

- destructive form characterized by a violation of the shape of the crowns due to erosive destruction and abrasion of hard tissues. The destructive form is observed in areas with increased content fluoride (10-12 mg/l) in drinking water. With this form, the dental tissues are fragile; their breakage and, as a consequence, injury to the oral mucosa are often observed.

Fluorosis of primary teeth is extremely rare (single cases have been described), even in endemic areas, and mainly on molars. This is explained by the ability of the placenta not to allow excess fluoride to pass through to the fetus. Fluorosis of baby teeth is associated with early complementary feeding of infants, or with an increased concentration of fluoride in breast milk.

Morphological changes in teeth affected by fluorosis are determined mainly in the enamel, more often in the surface

nom its layer. The structure of the enamel on the thin section appears to be sharply emphasized, which is explained by the partial resorption of both enamel prisms and the interprismatic substance. As a result of the resorptive process, the enamel prisms themselves adhere less tightly to each other.

The Gunther-Schräger stripes are clearly pronounced, arching and reaching the enamel; the Retzius stripes are clearly visible. The dentin-enamel junction has a jagged shape. The surface layer of enamel has a moiré pattern, which is caused by an increase in interprismatic spaces due to partial resorption of enamel prisms, zones of hypo- and hypermineralization.

Fluorosis at the spot stage is differentiated from caries, which is characterized by a single lesion in areas typical for caries. With fluorosis, the lesions are multiple, located over the entire surface of the tooth crown and appear from the moment teeth erupt. Mild manifestations of fluorosis may have a similar clinical picture to the spotted form enamel hypoplasia. Severe forms of fluorosis, accompanied by the formation of erosions and other defects of the tooth crown, must be differentiated from caries, banal erosion, wedge-shaped defects, etc. (Table 6.1; 6.2).

Treatment. Therapy for fluorosis depends on the stage of the process. For the spotted and streaked form, local treatment, the essence of which consists of bleaching followed by remineralizing therapy, has a positive effect. E.V. Borovsky (1978) recommends bleaching with solutions of inorganic acids.

Recently, they have been trying to replace acid etching of enamel with fluorosis by grinding its surface to 20-70 microns. T.P. Kroll (1990) proposed a method for grinding off fluorous stains using a paste containing hydrochloric acid, carborundum and silicon gel (Fig. 6.3 a, b, c).

In case of erosive and destructive forms of damage, accompanied by a violation of the integrity of the enamel, methods are used to restore the shape and color of the tooth crown. Delayed filling with composite and filling materials is recommended after remineralizing therapy (general and local). Prosthetics with veneers and crowns are also possible.

Non-carious lesions of teeth♦ 209

Table 6.1 Differential diagnosis of caries and non-carious lesions that occur before teeth eruption

Prevention. Preventive measures are divided into collective measures aimed at reducing the fluoride content in drinking water, and individual preventive measures. Reducing the amount of fluoride in drinking water can be achieved by replacing the water source or reducing the content through drinking water purification techniques.

Individual preventive measures should be carried out from the moment the child is born. It is necessary to avoid artificial feeding and early introduction of complementary foods to the child. With the introduction of complementary feeding to a child, the main amount of water in food should be replaced with milk and juices. Additional introduction of vitamin C, D, and calcium supplements into food significantly reduces the manifestations of fluorosis. It is also necessary to remove children from the endemic area for the summer.

Prevention and treatment of dental fluorosis should be carried out comprehensively, taking into account the severity of the lesion, the general condition of the body and the influence of endemic factors. It should begin in early childhood and be carried out

systematically, using all available municipal and individual measures.

The general effect on the body and teeth affected by fluorosis should include:

1) stopping or at least limiting the intake of increased concentrations of fluoride into the child’s body from drinking water and food. For this purpose, it is recommended to use water from a water source with a low fluoride content for drinking and cooking. If this is not possible, partial defluoridation of water is recommended by boiling it for 5-10 minutes and then settling.

The removal of children from the endemic area for the summer period is very important in the prevention of fluorosis. Clinical observations have shown that replacing water sources for 3-4 months annually in the first 8-10 years of a child’s life helps normalize the formation of enamel and significantly reduces the percentage of dental fluorosis;

Table6.2

Differential diagnosis of non-carious lesions

Dentistry

Rice.6.3. Grinding off fluorous spots: a - fluorous spots on the central incisors; b - after sanding off the stains; c - 5 years after grinding (according to T.P. Kroll)

2) weakening the toxic effect of increased concentrations of fluoride on the body in general and dental tissue in particular, by prescribing a rational diet. Restriction in the diet of dishes prepared from sea ​​fish, strongly brewed tea and other fluoride-rich foods. Recommended lean varieties of beef, pork, river fish. Dairy products - low-fat milk, cottage cheese. They are rich in calcium and, thanks to low content fats are better absorbed by the body. Juices made from vegetables and fruits growing in other areas are recommended for drinking;

3) the prescription of medications and specific treatment is carried out by a dentist, taking into account the severity of the lesion and general condition body. Considering the competitive relationship between fluorine and calcium, one of the calcium preparations is prescribed orally: glycerophosphate or calcium lactate in age dosages 1 hour before or 2 hours after meals. To weaken the ulcerogenic effect of calcium, before taking these drugs you need to drink 3-4 sips of warm, sweet, weak tea.

All children living in areas of endemic fluorosis are recommended to take drugs that increase the protective properties and resistance of the body (sodium nucleinate, potassium orotate, tinctures of Eleutherococcus, Schisandra, multivitamins);

Non-carious lesions of teeth do not depend on negative influence microflora on bone tissue. The main causes of pathology are congenital heredity, exposure to toxic substances, or the state of the mother’s body during pregnancy. This group diseases represents wide range pathological deviations of the hard tissues of teeth and the enamel layer of a congenital or acquired nature.

IN modern dentistry It is customary to divide pathological deviations in the hard structures of teeth into three classes:

1. lesions of intrauterine development;
2. lesions after the eruption of molars.

The first class of pathology includes following reasons deviations:

• intrauterine pathology of molar formation;
• abnormal developmental disorder;
• formation of endemic;
• hyperplasia/hypoplasia of the enamel layer.

The second class includes:

• abrasion of crowns;
• plaque and pigmentation;
• acid/radiation tissue necrosis;
• hyperplasia/hypoplasia;
• injury to the crown/root/neck;
• acid erosion.

Non-carious lesions are characterized by varying degrees of distribution: from damage to a single tooth to entire sections of the dentition. They can also include abnormal development molars after eruption:

• crown fracture;
• dislocation/fracture of the neck and root.

Let us consider the symptoms and characteristics of lesions of hard dental structures in detail.

Hypoplasia and hyperplasia

This pathology refers to a defect in the formation of enamel mass due to disruption of metabolic cycles in tissue structures. The protein/mineral cycle, which occurs with deviations, causes irreversible pathological degeneration: underdeveloped enamel persists for life and cannot be restored.

Clinical picture of hypoplasia

This pathology is characterized by the appearance of grooves different sizes, pits and spots with missing enamel. Often grooves and rounded pits appear simultaneously on one molar. Non-carious lesions are located parallel to the chewing part and cover the entire surface of the tooth.

There are three types of hypoplasia:

• focal odontodysplasia - pathology of adjacent molars;
• systemic hypoplasia - pathology of several molars;
• local hypoplasia - damage to a single molar.

Focal pathology occurs in healthy babies. This type of disease is characterized by a reduction in the crown due to insufficiency of the enamel layer. The crowns have a yellowish coating and are rough. At the moment, the etiology of the deviation has not been identified.

Systemic is characterized by a deficiency of mineralization of all teeth or several molars of one period of formation. The pathology is provoked by a violation of metabolic cycles in the mother’s body during gestation or a violation of the baby’s diet after birth, or it is a consequence past infection. TO this disease may result from the mother taking tetracyclines during pregnancy or administering the medication to the child.

Hypoplasia also occurs in children:

• with congenital allergies;
• premature;
• due to hemolytic jaundice;
• due to birth trauma.

Hypoplasia permanent molars occurs due to an unbalanced diet and serious illnesses experienced by the baby:

• rickets;
• ARVI;
• brain disorders;
• gastrointestinal pathologies;
• pathology of the endocrine system;
• other serious illnesses.

Pathology in the formation of molars is observed in the first year of a baby’s life, when any disruption of metabolic cycles as a result of diseases can affect the formation of bone and enamel structures. Hypoplasia affects individual molars, however, with repeated somatic diseases the pathology spreads to the remaining teeth.

Hyperplasia

It is a point localization of excess amount of dental tissue due to disruption of metabolic cycles during the formation of molars. Hyperplasia looks like pearly (enamel) drops on the surface of the crown.

Endemic fluorosis

Non-carious lesions of this type are formed due to an excess of fluoride in tap water. Fluorosis is the localization of chalky inclusions on the surface of the enamel. Constant fluoride intoxication provokes changes in the enamel mass, as a result of which it loses its natural gloss and protective properties.

There are 4 degrees of fluorosis:

• weak - single inclusions, difficult to distinguish during visual inspection;
• medium - the spots acquire a yellowish tint, the lesion covers half of the tooth crown and spreads to several teeth at once;
• moderate - the lesion covers the dentition, is localized on most of the dental crowns and is characterized by pronounced pigmentation;
• severe damage - in this case, multiple spots merge into large lesions, characterized by severe abrasion and deformation of the teeth.

Important! Fluorosis is curable. Therapeutic measures are carried out by the dentist, however, to prevent the re-development of fluorosis, it is necessary to replace fluoride water with purified water and take care of proper metabolism.

Non-carious lesions in the form of abnormalities in the structure of the teeth

Developmental anomalies include several congenital factors:

• incorrect localization of molar primordia;
• abnormal formation bone tissue jaws;
• fusion of the roots of adjacent molars.

Jaundice in newborns can also lead to an anomaly due to Rh conflict between mother and fetus. However, this pathology affects only baby teeth, causing changes in the color of the enamel.

Note! Treatment of babies with tetracycline after six months leads to permanent molars turning yellow.

““ is also considered an anomaly. This pathology is formed due to the accumulation of tetracycline in the dental tissue. Not even large number the injected medicine turns the enamel yellow. A feature of this pathology is the color change of the crown from yellow to gray/brown under the influence of daylight.

Congenital abnormalities

Pathology data concerns abnormal development dentin. Treatment of pathology is carried out by masking the affected teeth orthodontic structures from various materials - metal, plastic, porcelain. When teeth are lost, dentures are prescribed.

Pigmentation and plaque

Pigmentation (staining of the dental crown) can be caused by several factors:

• consequences of serious illnesses;
• consequences of taking aggressive medications;
• due to pulp necrosis.

Temporary pigmentation also appears as a result of eating certain foods (blueberries, carrots), rinsing oral cavity medicines. Constant pigmentation is present in smokers: the enamel turns yellowish, sometimes brown.

Plaques can be soft or hard. When plaque hardens, it is referred to as tartar. Deposits of a loose consistency appear as a result of unscrupulous sanitation of the oral cavity or disease of the gum tissue. A person with healthy gums and a correct bite does not have deposits on their teeth. When the oral cavity is neglected, loose plaque hardens and turns into tartar.

Erasing

Erasure of the chewing plane is present in all people to varying degrees. Pathological abrasion was recorded in 11% of people and is formed by several factors:

• body constitution and heredity;
• pathology of metabolic cycles;
• defects in the functioning of the endocrine system;
• deviations in the functioning of the nervous system;
• some chronic diseases;
• quality of drinking water (increased mineralization);
• eating excess amounts of berries/fruits.

Pathological abrasion is caused by additional load when chewing due to the loss of a dentition or several molars, incorrectly selected dentures, and defects in tissue structures. Work in enterprises where there are a large number of mechanical particles in the air can also lead to abrasion.

There are three levels of washability:

• at the level of the enamel layer;
• at the level of the enamel-dentin layer;
• loss of 2/3 parts of the crown.

Teeth can wear down horizontally and vertically, sometimes mixed horizontal-vertical abrasion of the surface occurs.

Wedge-shaped defect

Non-carious lesions of this type are common among patients with problematic gums - periodontal disease. A wedge-shaped defect is characterized by exposure of the neck of the tooth. Dentists agree that the cause of the pathology is the presence of internal diseases:

• central nervous system;
• endocrine system;

The presence of these diseases affects the health of the periodontium, which, in turn, causes exposure of the neck of the teeth. Pathology can affect single teeth, but multiple lesions of periodontal tissues are more common.

Hard tissue erosion

It is considered a pathological decrease in the hard structures of the teeth. Sometimes the enamel itself becomes thinner, sometimes the enamel decreases along with the dentin. Some scientists believe that non-carious lesions of hard tooth tissues are caused by the abuse of juices and pulp of citrus fruits. Also the cause of the pathology are some internal ailments:

• endocrine abnormalities;
• neuropsychiatric disorders;
• violation of salt metabolism, etc.

Acid erosion can occur with an unhealthy diet dominated by acidic foods, frequent vomiting and improper use of medications.

Necrosis

This pathology can provoke the loss of single molars or all the patient’s teeth. A type of necrosis of solid structures is cervical necrosis, which can occur with certain metabolic cycle disorders. This disease often occurs in pregnant women. The disease is characterized by the formation of chalky streaks and thinning of the enamel coating on the affected surface.

Necrosis can form when:

• exposure (radiation);
• exposure to organic acids (acid);
• taking medications for Achilles gastritis (mild).

If dental care is not taken properly, caries forms in the affected areas. At active process pathological changes the enamel of the entire surface is loosened and dentin is exposed. When the enamel layer is lost, teeth become sensitive to temperature changes and other irritants.

Injury

A fall or careless chewing of rough food can cause injury. After an impact, you can lose one or more teeth at once. The consequences of an impact injury are:

• bruised/dislocated tooth;
• root/neck/crown fracture;
• fracture of a section of the crown;
• trauma to the molar bud in children;
• combined defeat.

Hyperesthesia

This pathology is characterized by increased sensitivity of dentin to force, chemical or temperature effects. A person experiences pain while drinking water and brushing his teeth. Hypersensitivity may occur when:

• exposure of dentin canals;
• transmission of stimulus impulses through tooth cement.

In addition, heightened sensitivity may appear due to the close location of the nerve roots to the surface of the tooth, which is due to the constitution of the structure. It is more common with carious lesions of dental tissue, pathological abrasion, and thinning of the enamel.

Hereditary pathology

These deviations are characterized pathological form mutation that is independent of environment. All hereditary pathologies can be divided into two classes:

1. chromosomal;
2. genetic

Gene mutations are transmitted along a related line and are characterized by the constancy of clinical manifestations. The class of gene pathology includes:

• defective dentinogenesis;
• defective odontogenesis;
• defective amelogenesis;
• discalorite.

Defective dentinogenesis forms three degrees of deviations:

• translucent bone, weak enamel;
• high bone fragility and abrasion of the crown, discoloration of the enamel coating;
• unusual shape and pigmentation of teeth: dome-shaped crowns, opalescent enamel color.

Enamel pathology is expressed in a reduced mass of the layer (hypoplasia), insufficient calcification (hypocalcification), and pathological structuring of apatite crystals in the enamel mass.

With imperfect odontogenesis, molars are distinguished by a gray tint, increased abrasion and fragility of the enamel surface. Amelogenesis imperfecta is characterized by a defect in the enamel mass: the surface of the crown has either partial or complete absence coverings.

With discoloration, the natural color of the enamel is disturbed. The color depends on the prerequisites for the formation of the disease:

• Rh conflict of blood groups of mother and baby;
• incompatibility of parental blood;
• pathology of the biliary system;
• porphyria (pathology of the metabolic cycle of pigment cells);
• treatment with tetracycline drugs during pregnancy.

Hereditary pathologies cannot be cured; in dentistry, cosmetic restoration is used - covering with crowns, veneers, etc.
(votes: 1, average: 5.00 out of 5)