Generalized periodontitis mkb 10. Catarrhal gingivitis

Periodontitis- inflammation of the entire complex of periodontal tissues, characterized by progressive destruction of the periodontal and bone tissue of the alveoli, and accompanied by the formation of pathological periodontal pockets.

Code for the international classification of diseases ICD-10:

K05.2
K05.3

Causes

Etiology. The most important local etiological factors include the microflora of the oral cavity (Porphyromonas gingivalis, Peptostreptococcus, Fusobacterium nucleatum, Veillonella parvula, etc.), dental deposits, anomalies in the position of the teeth, occlusion and others. Common disorders include diseases of the gastrointestinal tract, endocrine and nervous systems, metabolic disorders, and vitamin imbalances. Bad habits can contribute to periodontal damage.
Pathogenesis. Periodontitis always preceded by inflammation of the gingival margin (gingivitis). In the course of the development of the pathological process, there is a violation of the epithelial attachment of the gums to the tooth, destruction of the ligamentous apparatus, resorption of the bone tissue of the alveolar process. A periodontal pocket is formed, which constantly deepens, reaching the apex of the root. Progressive resorption of the alveolar bone leads to pathological tooth mobility. The destruction of the ligamentous apparatus of the tooth is accompanied by an overload of individual teeth or groups, and traumatic occlusion occurs. With generalized periodontitis, there is a gradual destruction of the entire complex of periodontal tissues, which ultimately ends with the loss of teeth.
Classification. Acute, chronic, aggravated periodontitis (including abscess formation), remission are isolated along the course. According to the severity of the process, mild, moderate, severe periodontitis is distinguished, in terms of prevalence - localized and generalized.

Symptoms (signs)

Clinical manifestations. They are mainly due to the severity and prevalence of the disease.
... Localized periodontitis. It is characterized by aching pain, bleeding and severe swelling of the gums. Limited destructive inflammatory process in the area of one or more teeth (up to 5 teeth). Examination with a periodontal probe from all four sides of the affected teeth reveals a violation of the periodontal attachment and periodontal pockets of various depths with purulent discharge or with granulations. Mobility of teeth of varying degrees appears. With exacerbations of the process, there is a sharp soreness of the gums and alveolar part of the mucous membrane, painful percussion of the tooth, difficulty in eating and brushing teeth. If the outflow of purulent contents through the periodontal pocket is difficult, a periodontal abscess may form.
... Generalized periodontitis. The initial stage is characterized by bleeding, swelling of the gums, pain in the gum area, bad breath and shallow periodontal pockets, mainly in the interdental area. In the developed stage of periodontitis, multiple pathological periodontal pockets of various depths appear - with serous - purulent contents with chronic or abundant purulent contents with an exacerbated course of the disease. According to the depth of these periodontal pockets, I, II, III degrees of the disease are distinguished. The mobility of the teeth develops, and then traumatic occlusion is formed. Characterized by an abundance of soft plaque, over - and subgingival dental plaque. Exposure of the necks and roots of the teeth can be accompanied by hyperesthesia. Retrograde pulpitis sometimes occurs. A chronic progressive course can give exacerbations, accompanied by pain of a spontaneous nature. Abscesses and fistulas form one after the other at intervals of several days. In parallel, there are changes in the general state of the body - a rise in body temperature, weakness, malaise. There is an increase and soreness of regional lymph nodes. The state of remission is characterized by a dense pale pink gum, possibly exposing the roots of the teeth. There are no dental deposits and discharge from the pockets.

Diagnostics

Diagnostics. In addition to clinical data, radiography (panoramic or orthopantomography) is of great importance. With localized periodontitis, destruction and foci of directed resorption along the tooth root are revealed. At the initial stage of the generalized process, a compact plate is determined at the tops of the interdental septa, the expansion of the periodontal gap in the cervical region. The developed stage is characterized by resorption of the interdental septa with a decrease in the height of the alveolar process and the formation of bone pockets; detect foci of osteoporosis. In the remission stage, there are no signs of active destruction of the interdental septa on the X-ray, the bone tissue is dense.
Differential diagnosis... Chronic gingivitis. Periodontal disease. Periostitis and osteomyelitis of the jaw.

Treatment

TREATMENT
Local treatment
... It must start with a thorough removal of dental plaque, especially subgingival, using a sclera (Pieson - master - 400). It includes the whole range of local influences: medication, orthopedic and physiotherapy. Eliminate local causes that lead to the development of inflammation. For a longer contact of drugs with periodontal tissues, gingival dressings or forms with prolonged action are used.
... Of particular importance are surgical methods (curettage, gingivitomy, flap operations, etc.) performed on the gums and bone tissue, which are aimed at removing granulations, eliminating periodontal pockets, restoring bone defects in the alveolar ridge, etc. Surgical intervention is recommended to be combined with drugs, contributing to the regeneration of periodontal tissues (keratoplasty). Teeth with mobility are splinted. It is imperative to remove teeth that have no functional value. To avoid overloading the existing / remaining teeth, direct prosthetics are recommended.
... Physical therapy can be varied, including exposure to ultrasound and low-intensity laser radiation. Hydrotherapy in the form of irrigation of the oral cavity with water saturated with carbon dioxide has not only a therapeutic effect, but also improves oral hygiene.

General treatment is mainly carried out with exacerbations of chronic generalized periodontitis and in the presence of severe general somatic pathology (hereditary neutropenia, type 1 diabetes, etc.). It includes: broad-spectrum antibiotics, desensitizing and sedatives, immunotropic drugs (imudon, xymedon). Sometimes hormone therapy and drugs that affect mineral metabolism (thyrocalcitonin) are prescribed. General treatment is combined with specific therapy for a general disease and vitamin therapy.
Prophylaxis... Timely treatment of gingivitis. Thorough oral hygiene. It is advisable to use spa factors (balneo - and peloid therapy). Physicochemical properties of mineral waters, therapeutic mud and climatotherapy have a healing effect on the oral cavity and the entire body.

ICD-10. K05.2 Acute periodontitis. K05.3 Chronic periodontitis.

The complex of therapeutic measures should be planned by a dentist. This means that when diagnosed with periodontitis, treatment with folk remedies is an additional method of combating the disease, but in no way a substitute for surgical and therapeutic methods.
If periodontitis was detected at an early stage of development, then the course of treatment consists of professional teeth cleaning, removal of calculus and polishing of the tooth surface. The crown and root are treated with special brushes, which are treated with fluorine-containing protective compounds. Cured dental plaque is removed by mechanical treatment or ultrasound. In especially advanced cases, doctors use curettage - a procedure for removing deposits using special hooks.
If the depth of the dental "pockets" exceeds 5 mm, surgery is recommended for patients. The main goal of the operation is to eliminate cavities, stop tissue resorption and do everything possible to ensure that the tooth regains stability. Elimination of pathological mobility is performed using temporary splints or permanent prostheses.
Since both generalized periodontitis and chronic periodontitis are infectious and inflammatory diseases, specialists usually prescribe effective antibiotics for patients. Tetracycline or lincomycin is preferred. In addition, patients should take care of strengthening the immune system and increasing the body's defenses. For this, both common vitamin and mineral complexes are used, as well as special means - immunocorrectors. Of course, periodontitis treatment is not complete without timely filling of diseased teeth, occlusion correction and correction of other local risk factors.
Treatment with folk remedies.
Traditional medicine recipes can only help in the early stages of the disease. With the development of the inflammatory process, you should immediately consult a doctor and do not abuse self-medication. Now, here are the most common recipes:
6 grams of dry lingonberry leaves are poured with a glass of boiled water and boiled for 20 minutes over low heat. Then the broth is cooled and filtered. Rinse your mouth with medicine every 2-3 hours;
2 teaspoons of calendula flowers are brewed in 2 glasses of boiled water. The product is used to rinse the mouth every 3-4 hours;
With severe bleeding of the gums, it will be useful to rinse your mouth with a tincture of blackberry leaves;
St. John's wort decoction helps against periodontitis. 2 tablespoons of the herb are poured over with 2 cups of boiling water and cooked over low heat for 5 minutes. The broth must be infused for 4 hours, then strain and use for rinsing the mouth 3 times a day.

Basic concepts and provisions of the topic:

Gingivitis- This is an inflammation of the gums, caused by the unfavorable effect of local or general factors, proceeding without violating the integrity of the periodontal junction and without destructive processes in other structures of the periodontium.

Classification of gingivitis ICD-10, 1997

Acute gingivitis: K05.0

exception: acute pericoronitis (K05.22), acute necrotizing ulcerative gingivitis - Vincent (A69.10), herpetic gingivostomatitis (B00.2X)

Chronic gingivitis (K05.1):

K05.10 - simple marginal;

K05.11 - hyperplastic;

K05.12 - ulcerative, excl. necrotizing ulcerative gingivitis (A69.10).

Classification of gingivitis

(adopted at the StAR periodontal congress, 2001)

Forms: catarrhal, ulcerative, hypertrophic.

Course: acute, chronic.

Phases (stages) of the process: exacerbation, remission.

Prevalence of the process: localized, generalized.

Severity for hypertrophic gingivitis only:

Light (gingival hypertrophy does not exceed 1/3 of the length of the tooth crown);

Medium (gingival hypertrophy up to 1/2 of the length of the tooth crown);

Severe (gingival hypertrophy more than 1/2 or covers the entire tooth).

Forms of hypertrophic gingivitis: edematous, fibrous.

Etiology. The gum is a borderline structure through which the periodontal complex interacts with the external environment. Normally, at clinically healthy gums, directly under the epithelial attachment to the tooth, one can see a small accumulation of lymphocytes and macrophages that penetrate into the gingival fluid in response to the action of microorganisms growing on the surface of the mucous membrane and teeth. At the same time, there are no clinical signs of gum inflammation. These cells are absent only in exceptional cases. Then talk about "Completely intact" gums.

Inflammation of the periodontal tissues is a response to the damaging effect of microbial agents in dental plaque. The surface of the macroorganism (skin) and organs in contact with the external environment (gastrointestinal tract, vagina) is inhabited by saprophytic microflora. Normally, there is a dynamic balance between macro and microorganisms. Inflammation occurs when their interaction is disturbed, caused by a change in the quantitative or qualitative composition of microflora or a decrease in local or general factors of specific or nonspecific protection.

The virulence of microorganisms is determined by their ability to:

1. Attach to host tissues, form colonies and penetrate directly into tissues (invasion), avoiding or neutralizing the host's defense mechanisms.

2. Cause tissue destruction by direct exposure to toxins and enzymes and indirectly - as a result of the development of chronic inflammation and immunopathological reactions.

Dental plaque (structured dental plaque) is visually determined one to two days after stopping brushing the teeth in the form of accumulations of white or slightly pigmented dental plaque, which is most pronounced in places where self-cleaning of the tooth surface with a current of saliva, movements of the oral cavity organs and a food lump (cervical part of the tooth, interdental spaces).

Natural and iatrogenic factors contribute to the increased accumulation of plaque. Natural factors include tartar. The first foci of mineralization appear on the inner surface of the microbial biofilm in four to eight hours. By the 14th day, a full-fledged tartar is formed. It should be noted that the stone itself does not cause an inflammatory response, but its porous and very rough surface is always covered with a layer of soft plaque; the rough surface of exposed roots also retains plaque; cervical caries, root caries; bite pathology (tight, dystopic position of the teeth) does not allow adequate hygienic care; oral breathing - self-cleaning of the oral cavity and the action of protective factors contained in saliva are impaired.

Iatrogenic factors include: overhanging edges of fillings and artificial crowns; orthodontic equipment; rough surface of fillings, temporary artificial crowns.

The plaque formation process goes through three main stages:

1. Formation of a pellicle, which is a protein-polysaccharide film formed from components of saliva and gingival fluid. The enamel pellicle plays an important role as a biological protective barrier.

2. Despite this, it is its receptors that provide the primary adhesion of microorganisms to the resulting dental plaque. As a rule, this is a gram-positive flora that is constantly present in the oral cavity - cocci, a small number of rods ( Streptococcus sanguis, Actinomyces viscosus etc). Adhesion is carried out due to the structural elements of the shell of microorganisms (fimbriae, cilia, adhesion proteins).

3. At this stage, the number of microorganisms increases, the microbial mass builds up, an anaerobic environment is created in the deep layers. Conditions are formed for the secondary colonization of more aggressive gram-negative flora ( Prevotella intermedia, Porphyromonas gingivalis, Fusobacterium nucleatum). These microorganisms themselves cannot carry out the initial colonization of the pellicle, but they are able to selectively interact with the already attached and multiplied gram-positive flora when a sufficient amount of substrate appears for their growth and the oxygen content in the deep layers of the plaque decreases.

Microorganisms secrete toxins (leukotoxin), enzymes (collagenase, hyaluronidase), metabolites (fatty acids, amino acids, indole), which have a direct damaging effect. Of great importance are endotoxins (lipopolysaccharides - components of the outer membrane of gram-negative bacteria), which cause the activation of the complement system, the Hageman factor, and have a cytotoxic effect on fibroblasts that induce bone resorption.

Periodontal pathogenic microorganisms ( Actinobacillus аctinomycetemcomitans, Porphyromonas gingivalis) are able to penetrate into the periodontal tissue (invasion) as a result of erosion of the epithelial lining of the periodontal sulcus (periodontal pocket) between the cells, or penetrating directly through the cell membrane.

In response to damage, inflammation develops - this is a defensive reaction aimed at destroying or isolating microorganisms. Long-term exposure to microorganisms leads to the chronicity of the inflammatory process, as a result of which the mechanisms aimed at destroying bacterial pathogens lead to the destruction of the periodontal tissues. Active components of the complement system - enzymes, free radicals, cytokines, immune complexes - become damaging factors against the background of impaired microcirculation and rheological properties of blood, reduced antioxidant protection.

The effect of the microbial factor is aggravated by: occlusive trauma, mechanical trauma; genetic structural features; chemical agents, radiation. Occlusal trauma in itself does not cause inflammation of the gums, it promotes the spread of the inflammatory process from the gum tissue to all periodontal tissues.

The congenital features of periodontal structures that aggravate the effect of the microbial factor include: pathology of soft tissue attachment in the vestibule, thinned mucosa; thinning of the cortical plate; the ratio of the length of the roots and the crown of the tooth; root divergence angle; the size of the tongue.

Mechanical trauma can be caused by: deep bite, traumatic hygienic care of the oral cavity, trauma during dental manipulations (application of a rubber dam, installation of a separation matrix, strip treatment, traumatic removal), removable dentures.

Chemical damage occurs due to: aggressive antiseptic and anti-inflammatory drugs, misuse of drugs, dental procedures (bleaching, devitalizing paste), smoking (toxic effects, changes in microflora, ischemia, damage to local protective factors).

Congenital and acquired disorders of immunity, violations of nonspecific factors of the body's defense contribute to the development of the inflammatory process.

Common predisposing factors: age, stress, heredity (cyclic neutropenia, increased IL-1 reactivity); endocrine disorders (diabetes mellitus, pregnancy); autoimmune diseases; hematological disorders (leukopenia, thrombocytopenia, sickle cell anemia); nutritional deficiency (vitamin deficiency); medicines (antihypertensive drugs, anticonvulsants). The presence of these factors increases the risk of developing periodontal disease and worsens their prognosis.

Bacterial colonization triggers inflammatory and destructive processes, and the effect of this effect largely depends on general and local factors of protection of the macroorganism.

The development of periodontal diseases occurs only if the force of the influence of pathogenic factors of the adaptive-protective capabilities of the periodontal tissues is exceeded or when the reactivity of the organism decreases.

With an increase in the intensity of exposure to external pathogenic factors, the amount of lymphomacrophage elements in the connective tissue stroma of the gums increases. Segmented leukocytes and plasma cells appear. There is a destruction of the fibrillar structures of the gums and cellular elements. Although the epithelial attachment is preserved, it is displaced apically. The dentogingival groove deepens, the epithelium of the groove becomes thinner.

After the elimination of the microbial agent, vascular, tissue and cellular structures return to their normal state. If the damaging agent is not completely destroyed, the inflammation becomes chronic. There is a depolarization of the main substance under the action of hyaluronidase, under the action of collagenase and elastase, collagen is destroyed, regeneration processes are disrupted, and pathological granulation tissue is formed. Under conditions of a decrease in pH, the formation of osteoclasts is activated, which actively lyse bone tissue.

Mechanisms aimed at destroying bacterial pathogens lead to the destruction of the periodontal tissues. The active components of the complement system (enzymes, free radicals, cytokines, immune complexes) against the background of impaired microcirculation and rheological properties of blood, reduced antioxidant protection, become damaging factors.

Periodontium- a complex of tissues surrounding the tooth (gum, circular tooth ligament, alveolar bone and periodontium), closely related anatomically and functionally.

WHO proposes “to include all pathological processes occurring in it as periodontal diseases. They can be limited to any one component of the periodontium (gingivitis), affect some or all of its structures ”(WHO, technical report series No. 207. Periodontal disease. Geneva, 1984). These recommendations are consonant with those that are common in our country and abroad.

Classification

In November 1983, at a meeting of the XVI Plenum of the Board of the All-Union Society of Dentists, a classification of periodontal diseases was adopted, which also corresponds to the tasks of pediatric dentistry, which is more widely used than international (ICD-10).

Gingivitis- inflammation of the gums, caused by the unfavorable effect of general and local factors and proceeding without violating the integrity of the periodontal attachment.
1. Forms: catarrhal, hypertrophic, ulcerative.
2. Course: acute, chronic, exacerbated, remission.
Periodontitis- inflammation of the periodontal tissues, which is characterized by progressive destruction of the periodontal ligament and bone.
1. Course: acute, chronic, exacerbated (including abscess), remission.
2. Severity: mild, moderate, severe.
3. Prevalence: localized, generalized.
Periodontal disease- dystrophic lesion of the periodontium.
1. Course: chronic, remission. Severity: mild, moderate, severe. Prevalence: generalized.
Idiopathic diseases with progressive lysis of periodontal tissues (Papillon-Lefebvre syndrome, X-histiocytosis, akatalasia, neutropenia, agammaglobulinemia, etc.).
Periodontomas are tumor and tumor-like processes of the periodontium.

International classification of periodontal diseases (ICD-10, 2004)

K 05. Gingivitis and periodontal disease.
K 05. Acute gingivitis.

Excluded: gingivostomatitis caused by the herpes simplex virus (Herpes simplex) (BOO.2), acute necrotizing ulcerative gingivitis (A 69.1).

K 05.1. Chronic gingivitis.
K 05.2. Acute periodontitis.

Excluded: acute apical periodontitis (K 04.4), periapical abscess (K 04.7) with a cavity (K 04.6).

K 05.3. Chronic periodontitis.
K 05.4. Periodontal disease.
By 05.5. Other periodontal diseases.
By 05.6. Unspecified periodontal disease.
K 06. Other changes in the gums and edentulous alveolar ridge.

Excluded: atrophy of the edentulous alveolar margin (K 08.2).

Gingivitis:
- NOS (K 05.1);
- acute (K 05.0);
- chronic (K 05.1).
- K 06.0. Gum recession.
K 06.1. Gingival hypertrophy.
K 06.2. Lesions of the gums and edentulous alveolar margin due to trauma.
K 06.8. Other specified changes in the gingiva and edentulous alveolar ridge.
By 06.9. Unspecified change in gingiva and edentulous alveolar ridge.

Clinical forms periodontal disease in children have many differences from similar conditions in adults.

This is explained primarily by the fact that all pathological processes caused by different reasons develop in a child in growing, developing and rebuilding tissues that are morphologically and functionally immature, and because of this, they can respond inadequately and non-identically to similar stimuli and causal factors that cause the disease. periodontal disease in adults.

In addition, of great importance in the pathogenesis of the development of the disease is the possibility of disproportions in the growth and maturation of immature structures, which can arise both within the system (tooth, periodontium, alveolar bone, etc.) and in structures and systems that provide and adapt the entire body to external conditions from birth to old age.

All this causes juvenile chronic gingivitis, periodontitis and periodontomas, which arise as a result of temporary transient functional juvenile hypertension, juvenile disorders of carbohydrate metabolism (juvenile diabetes, diencephalic syndrome, etc.).

Previously, it was believed that periodontal disease does not occur either in childhood or adolescence. According to Kantorovich (1925), periodontal disease (periodontitis) up to 18 years of age is not observed even with particularly unfavorable general and local conditions, and up to 30 years of age is very rare. Currently, a number of observations confirm that all forms of periodontal disease can occur already in childhood.

In the dental department of the pediatric faculty in Prague, cases of periodontal lesions were observed in the presence of temporary teeth with not yet formed roots. There are two forms of periodontal lesions, which differ from each other clinically. Both forms begin with gingivitis. In some cases, the process develops very slowly: extensive lesions of the periodontal tissues occur only at an older age, in others, the destruction of the periodontium has been noted for several months. The authors attribute this to primary periodontal inferiority.

Three groups of children were studied: 1) preschoolers; 2) schoolchildren; 3) children suffering from diathesis. In the 1st group, 44 children were examined 3 times - at 4, 5 and 6 years of age. In 24.3% of them, gingivitis was diagnosed once, in 3.5% - 2 times. In 1.26% of children, the disease was diagnosed in all 3 groups. In the 2nd group (500 children) there were schoolchildren of 10-12 years old. They were examined once. The incidence of gingivitis increased with age. A more rapid course is observed in 10-14-year-old children with diabetes. If in young children there is a direct dependence of gingivitis on anomalies and oral hygiene, then in the period preceding puberty, the number of anomalies decreases, and the number of gingivitis increases. In 10-year-old patients with diabetes, gingivitis was found in 37.1% of cases, in 14-year-olds - in 73.8%. In childhood, quite often, early gingivitis ends with the formation of pockets, bone resorption and loosening of the teeth. In addition to inflammatory processes, there is also a uniform atrophy of the dental alveoli and gums, as well as periodontitis associated with the degeneration of the periodontal and with the displacement of the teeth.

Periodontal disease that occurs in childhood differs in some respects from this disease in adults. This difference is explained by the peculiarity of the metabolism in children, the differences in the anatomical structure of the developing and already formed periodontium.

Recognition periodontal disease in a temporary bite is complicated by the fact that loosening of the teeth, which is the most obvious symptom, is difficult to differentiate from the process of resorption during the physiological change of teeth. Due to the fact that in temporary teeth the course of periodontal disease in most cases is slow, protracted, since temporary teeth fall out in 6-10 years even under intact conditions, the clinic usually pays attention only to pronounced, severe forms. Mild cases are considered early loss of deciduous teeth.

The importance of recognizing periodontal disease in childhood is explained by the fact that in most cases it accompanies some general disease of the body. As a symptom of anemia, hypovitaminosis, malnutrition, metabolic disease or endocrine disease, and sometimes diseases of the hematopoietic system, well-recognized and characteristic changes are also manifested in the periodontium. A correctly diagnosed periodontal disease draws the doctor's attention to a possibly latent general disease. In the case of periodontal disease of deciduous teeth, the same changes can be expected with the development of permanent teeth. Therefore, pediatric dentists sometimes have to deal with the timely recognition and careful treatment of periodontal diseases.

Causes of periodontal disease

The child reacts to harmful influences faster and sharper than adults. The cure of the disease as a result of the significant regenerative capacity of the young organism is faster and more perfect. The occurrence of periodontal disease in childhood can be reduced to both local causes and general diseases of the body.

The concept of "childhood" includes the age from the beginning of the eruption of a temporary tooth until the end of the change of teeth. Acute marginal periodontitis occurs in children more often than in adults. In the area of temporary molars, the process extends, as a rule, to the level of root bifurcation. The inter-root septum is melted. Children are characterized by phlegmonous infiltration of the gingival papilla.

There are three forms of periodontal disease:

accidental, caused by local irritating factors;
symptomatic, in which periodontopathy accompanies lesions of other organs;
idiopathic, the cause of which has not been established.

The reason for the first form in a temporary bite is the same as in a permanent one: dental deposits, carious defects in the neck of the tooth, irritating prosthetic structures. Symptomatic periodontopathy occurs with keratoma of the hands and feet with neurosis. Nevertheless, the connection between ectodermal dysplasias and periodontopathy cannot be considered firmly established. In children (as in adults), this form is associated with hormonal disorders, blood diseases, Mongolism, and Fallot's tetralogy. It is believed that with the introduction of immunohematological reactions, the diagnosis of periodontal diseases will improve and the symptomatic group will further decrease.

While a change in the body creates a predisposition to disease, local causes are the factors that cause disease. In the body throughout life, the formation and destruction of bone occurs constantly. In healthy adults, these two processes are in balance. In a developing young organism, bone formation predominates. Its death occurs only if, for any reason, bone destruction begins to prevail. As a result of significant resistance and regenerative capacity of the body in childhood and during puberty, the effect of local factors causing the disease is usually less pronounced than in adults. Various general changes in the body are of great importance.

So, the development of periodontitis is more often observed with metabolic disorders, blood circulation, endocrine system, alimentary disease or with severe vitamin deficiencies.

Local factors

Of the local factors causing the disease, a certain role is played by gingivitis as well as occlusal articulation anomalies. Although gingivitis at a young age is quite common, but the inflammatory process relatively rarely leads to the death of periodontal tissue, bone resorption develops only in the case of widespread, severe ulcerative stomatitis or recurrent chronic gingivitis.

Gingivitis causes the formation of tartar. In children, tartar deposition is relatively rare, with very poor oral hygiene or in connection with certain diseases (diabetes, congenital heart disease). Discoloration of the coronal part of the teeth and the formation of plaques are often observed. The discoloration takes place in the cervical part of the crown of the tooth from the vestibule of the oral cavity and manifests itself in the form of delimited dark brown, greenish or pink spots, they can only be removed by strong friction.