Catarrhal gingivitis. Gingivitis Periodontal diseases according to ICD 10

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2015

Acute gingivitis (K05.0), Chronic gingivitis (K05.1)

Dentistry

general information

Short description

Recommended
Expert advice
RSE at the RVC "Republican Center"
healthcare development"
Ministry of Health
and social development
Republic of Kazakhstan
dated October 15, 2015
Protocol No. 12

Protocol name: Gingivitis

Gingivitis- inflammation of the gums, caused by the adverse effects of local and general factors and occurring without compromising the integrity of the dentogingival junction.

Protocol code:

ICD-10 code(s):
K05. Gingivitis and periodontal diseases
K05.0 Acute gingivitis
K05.1 Chronic gingivitis

Abbreviations used in the protocol:
PMA-papillary-marginal-alveolar index

Date of protocol development/revision:2015

Protocol users: dentist, therapist, endocrinologist, hematologist.

Assessment of the degree of evidence of the recommendations provided.

Table - 1. Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to relevant population.
WITH	Cohort or case-control study or controlled trial without randomization with low risk of bias (+). Results that can be generalized to the relevant population or RCTs with very low or low risk of bias (++ or +) whose results cannot be directly generalized to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best pharmaceutical practice.

Classification

Clinical classification:

Classification of periodontal diseases,approved forXVI PlenumeBUnion Scientific Society of Dentists in 1983 :

I. Gingivitis- inflammation of the gums, caused by the adverse effects of local and general factors and occurring without compromising the integrity of the dentogingival junction.
By form: catarrhal, ulcerative, hypertrophic.

According to the course: acute, chronic, aggravated.

II. Periodontitis- inflammation of periodontal tissue, characterized by progressive destruction of the periodontium and bone of the alveolar process of the jaws.
By severity: light, medium, heavy.
According to the course: acute, chronic, exacerbation, abscess, remission.
By prevalence: localized, generalized.

III. Periodontal disease- dystrophic periodontal disease.
By severity: light, medium, heavy.
According to the course: chronic, remission.
By prevalence: generalized.

IV. Idiopathic diseases with progressive lysis of periodontal tissue (periodontolysis) - Papillon-Lefevre syndrome, neutropenia, agammaglobulinemia, uncompensated diabetes mellitus and other diseases.

V. Periodontomas - tumors and tumor-like diseases (epulis, fibromatosis, etc.).

Diagnostics

List of diagnostic measures:

Basic (mandatory) diagnostic examinations performed on an outpatient basis:
1. collection of complaints and medical history;
2. general physical examination (visual examination of the condition of the gums (color, consistency, shape of the interdental papillae, size, configuration of the gingival margin, deformation, thickening, thinning, palpation of regional lymph nodes, gingival margin, horizontal percussion of the teeth, determination of tooth mobility, probing of the integrity of the dentogingival attachments).

Additional diagnostic examinations performed on an outpatient basis:
1. Determination of the hygienic index according to Green-Vermillion;
2. Carrying out the Schiller-Pisarev test;
3. Determination of the gingivitis index RMA;
4. Orthopantomography or panoramic radiography;
5. General detailed blood test;
6.Biochemical study (determination of glucose in blood serum);
7. Immunological study (determination of cytokines IL-8, IL-2, IL-4, IL-6 in blood serum by ELISA method, determination of cytokines interferon-alpha in blood serum by ELISA method);

Instrumental studies:
· Probing - the integrity of the periodontal attachment in all clinical forms of gingivitis in the area of all teeth of the upper and lower jaw is not compromised.
· Schiller-Pisarev test - detects the presence of inflammation in the gums. During the inflammatory process, glycogen accumulates in the epithelial cells of the mucous membrane, and the gums become stained with iodine-containing solutions from light brown to dark brown. The Schiller-Pisarev test for gingivitis is positive.
· Determination of the gingivitis index PMA - PMA (papillary-marginal-alveolar) index is determined in the area of all teeth of the upper and lower jaw, characterizing the prevalence and intensity of the inflammatory process. When the index value is up to 25%, there is a mild degree of gingivitis, up to 50% is a moderate degree of gingivitis, and more than 50% is a severe degree of gingivitis.
· Determination of the Green-Vermillion hygienic index. The Green-Vermillion hygienic index characterizes the presence of soft and hard dental plaque. The value of the Green-Vermillion hygienic index increases with gingivitis.
· X-ray changes in the bone tissue of the alveolar process with gingivitis are absent. Orthopantomography or panoramic radiography is necessary for differential diagnosis from generalized periodontitis.

Indications for consultation with specialists:
· Consultation with an endocrinologist - in case of endocrine pathology (diabetes mellitus, hyperfunction of the thyroid gland and adrenal cortex), there is a more active course of the inflammatory process in the gums, which is associated with the underlying endocrine disease. Complex treatment with the participation of an endocrinologist is required.
· Consultation with a hematologist - in case of blood diseases (leukemia, agranulocytosis, aplastic anemia), catarrhal, ulcerative and hypertrophic processes in the gums are symptomatic. Consultation with a hematologist is necessary both for differential diagnosis and for complex treatment with the participation of a hematologist.
- Consultation with a gastroenterologist - chronic catarrhal gingivitis, as a rule, is accompanied by chronic diseases of the gastrointestinal tract, which requires complex treatment with the participation of a gastroenterologist.

Laboratory diagnostics

Laboratory research:
general detailed blood test; carried out for the purpose of differential diagnosis from symptomatic catarrhal, ulcerative and proliferative processes in the gums associated with blood diseases (leukemia, agranulocytosis, aplastic anemia, thrombocytopenic purpura). In case of blood diseases, a detailed blood test contains changes in indicators corresponding to the blood disease;
· biochemical study (determination of glucose in blood serum)
The course of gingivitis in patients with diabetes is active and progressive, the blood glucose level is above 6 mmol/l.
According to indications:
· immunological research; determination of cytokines IL-8, IL-2, IL-4, IL-6 in blood serum by ELISA method, determination of cytokines interferon-alpha in blood serum by ELISA method.
The ratio of pro-inflammatory and anti-inflammatory cytokines changes

Differential diagnosis

Differential diagnosis.

Table - 3. Differential diagnosis of various clinical forms of gingivitis.

№	A form of gingivitis.	The disease with which to differentiate	General clinical signs	Distinctive clinical features
1.	Chronic catarrhal gingivitis.	Mild chronic periodontitis.	Cyanotic, swelling of the gingival margin; upon probing, bleeding is detected.	With periodontitis, there is a violation of the integrity of the dentogingival attachment, periodontal pockets with a depth of 3-3.5 mm are determined. Exposure of the necks in the area of individual teeth. The radiograph shows resorption of the cortical plate of the apexes of the interalveolar septa, osteoporosis and a decrease in the height of the interalveolar septum within 1/3 of the root length.
2.	Hypertrophic gingivitis, fibrous form.	Fibromatosis of the gums.	Increasing the size, changing the configuration of the gingival margin.	Overgrowth of the gingival margin with fibromatosis not only from the vestibular, but also from the oral surface, affects not only the marginal, but also the alveolar gum. In some cases, the bone tissue of the alveolar process is affected.
3.	Hypertrophic gingivitis, edematous form.	Leukemic infiltration of the gums in leukemia.	Deformation of the gingival margin, change in gum configuration.	General clinical signs of leukemia are disturbances in general condition, changes in general blood count.
4.	Ulcerative gingivitis.	Acute leukemia.	General condition disorders - malaise, weakness, increased body temperature. Necrotic changes in the gingival margin, bad breath.	In acute leukemia - pallor of the mucous membrane, hemorrhages, necrotic changes in the gingival margin against the background of a non-inflamed mucous membrane. Changes in general blood test. Ineffectiveness of treatment, duration of the disease.
5	Ulcerative gingivitis.	Agranulocytosis.	Pain, ulcerative-necrotic changes in the gingival margin.	For agranulocytosis, there is a history of taking medications and radiation exposure. Necrotic changes not only in the gums, but also in other areas of the oral mucosa. Changes in general blood test. Ineffectiveness of treatment, duration of the disease.
6	Ulcerative gingivitis.	Ulcerative-necrotizing gingivostomatitis of Vincent.		Necrotic changes not only in the gingival margin, but also in other areas of the oral mucosa. Fusobacteria and Vincent's spirochetes are found in areas of necrosis.
7	Ulcerative gingivitis.	Drug-induced ulcerative necrotic stomatitis.	Pain, ulcerative-necrotic changes in the gingival margin. General condition disorders.	For drug-induced necrotizing ulcerative stomatitis, there is a history of taking medications. Necrotic changes not only in the gingival margin, but also in other areas of the oral mucosa. Positive laboratory test results indicating sensitization of the body.

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Treatment

Treatment goals:

elimination of the inflammatory process in the gums, preventing further progression of the inflammatory process and its spread to surrounding tissues.

Treatment tactics: The choice of treatment method depends on the nosological form of gingivitis. When treating a patient, the following principles should be observed: individual approach, complexity, systematicity, consistency and activity. Treatment is carried out on an outpatient basis.

Treatment plan for a patient with chronic catarrhal gingivitis.[ A. B]
1. Hygiene training with supervised brushing of teeth;
2. Antiseptic treatment of the oral cavity (oral baths, rinses, applications to the gums);
3. Removal of supragingival dental plaque in 1-2 visits, followed by antiseptic treatment of the oral cavity;
4. Sanitation of the oral cavity with the elimination of local irritating factors (overhanging fillings, sharp edges of teeth, improperly formed contact point, selective grinding of the bite);
5. Physiotherapy using physical factors that improve the trophism of periodontal tissues, normalize metabolic processes and microcirculatory circulation;
6. Treatment of general somatic pathology by internists of the appropriate profile.

Treatment plan for a patient with ulcerative gingivitis. [A. B] .
1. For symptoms of moderate to severe intoxication, consultation with an internist is required with the prescription of general treatment: rational nutrition, vitamin therapy, antibiotics, sulfonamides, transfusion of detoxification drugs, symptomatic treatment - antipyretic and analgesic drugs.
2. Pain relief;
3. Antiseptic treatment of the oral cavity;
4. Removal of soft plaque from the oral, contact, vestibular surfaces of teeth in the affected area;
5. Repeated antiseptic treatment of the oral cavity;
6. Removal of necrotic plaque using proteolytic enzymes (trypsin, chymopsin, chymotrypsin, etc. in the form of applications for 15-20 minutes);
7. Carrying out antibacterial therapy in the form of applications of antibacterial drugs;
8. Keratoplasty preparations 3-5-7 days after rejection of necrotic masses in the form of applications (carotoline, solcoseryl, methyluracil ointment, rose hip oil, sea buckthorn oil, vitamin A, etc.).

Treatment plan for a patient with hypertrophic gingivitis (edematous form). [A. B] .
1. Antiseptic treatment of the oral cavity (3% hydrogen peroxide solution, 0.06% chlorhexidine solution, 1% etonium solution, 0.02% furacillin solution, etc.);
2. Removal of dental plaque;
3. Repeated antiseptic treatment of the oral cavity;
4. Carrying out antimicrobial, anti-inflammatory and decongestant therapy (0.5% chlorophyllipt solution, 1% dioxidine solution, 0.25% salvin solution, 1% sanguiritrin solution, maraslavin, polyminerol, plantain juice, etc.);
5. Carrying out sclerosing therapy (if decongestant therapy is ineffective) - injection of 0.1-0.2 ml of 40% glucose solution, 0.25% calcium chloride solution into hypertrophied papillae);
6. Physiotherapy (electrophoresis, phonophoresis with heparin, 5% potassium iodide solution, lidase, ronidase, for a course of 3 to 8 procedures);
7. Treatment of general somatic pathology by internists of the appropriate profile .

Treatment plan for a patient with hypertrophic gingivitis (fibrous form). [A. B] .
1. If sclerotherapy therapy is ineffective, surgical excision of the hypertrophied gums (simple gingivectomy, cryodestruction, diathermocoagulation) with subsequent formation of the gingival margin;
2. Treatment of general somatic pathology by internists of the appropriate profile .

14.1 Non-drug treatment: Mode III. Table No. 15

14.2 Drug treatment:

14.2.1 Drug treatment provided on an outpatient basis:

Table - 4. Medicines for local and general treatment.

Name of the drug (INN)	Release form	Method of drug administration	Single dose	Frequency of application	Duration of treatment
Local treatment
Potassium permanganate	0.1% solution	Rinsing Washing between teeth		Mouth rinse after eating. Irrigation of the lesion	5-7 days
Hydrocortisone acetate, oxytetracycline hydrochloride	ointment	Applications to the lesion		Once a day when treating the lesion	3-4 days before acute inflammatory phenomena subside
Sodium heparin, benzocaine, benzyl nicotinate	ointment	Applications to the lesion	The ointment is applied in a thin layer onto a gauze or cotton swab for application.	Once a day during treatment.	5-7 days until the swelling of the gum tissue disappears
Metronidazole	Tablets 0.25 g	Powdering powder of the lesion	The tablet is crushed to a fine powder. Powder is applied to the affected area	Once a day when treated for 5-7 days	5-7 days before the removal of exudation phenomena
General treatment
Tinidazole	Pills	Per os	0.5 g.	2 times a day	5 days
Ibuprofen	Pills	Per os	0.2 g	3-4 times a day	Until clinical improvement

Drugs (active ingredients) used in treatment

Hospitalization

Indications for hospitalization: No

Information

Sources and literature

Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health of the Republic of Kazakhstan, 2015
1. List of used literature: 1. Bayakhmetova A.A. Periodontal diseases. – Almaty, 2009. -169 p. 2. Diagnostics in therapeutic dentistry: Textbook / T.L. Redinova, N.R. Dmitrakova, A.S. Yapeev, etc. - Rostov n/D.: Phoenix, 2006. -144 p. 3. Zazulevskaya L.Ya. Practical periodontology. – Almaty, 2006. -348 p. 4. Lutskaya I.K. Dentistry Guide. – Rostov n/d.: Phoenix, 2002. -544 p. 5. Therapeutic dentistry: A textbook for students of medical universities / Ed. E.V. Borovsky. - M.: “Medical Information Agency”, 2004. 6. Therapeutic dentistry: Textbook / Ed. Yu.M. Maksimovsky. – M.: Medicine, 2002. -640 p. 7. Kornman KS. Mapping the pathogenesis of periodontitis: A new look. J Periodontol 2008;79(Suppl. 8):1560-1568. Stroke 2004;35:2020-2023.

Information

List of protocol developers with qualification information:
1) Esembaeva Saule Serikovna - Doctor of Medical Sciences, Professor , Director of the Institute of Dentistry of KazNMU;
2) Aliya Aldashevna Bayakhmetova - Doctor of Medical Sciences, KazNMU, Head of the Department of Therapeutic Dentistry;
3) Tuleutaeva Raikhan Yesenzhanovna - Candidate of Medical Sciences, Associate Professor of the Department of Pharmacology and Evidence-Based Medicine of the Russian State University at the State Medical University, Semey.

Disclosure of no conflict of interest: No

Reviewers:
1) Mazur Irina Petrovna - Doctor of Medical Sciences, National Medical Academy of Postgraduate Education named after. P.L. Shubik, Institute of Dentistry, Department of Dentistry, professor;
2) Zhanalina Bakhyt Sekerbekovna - Doctor of Medical Sciences, Professor, RSE at the University of West Kazakhstan State Medical University named after. M. Ospanova”, Head of the Department of Surgical Dentistry and Pediatric Dentistry.

Indication of the conditions for reviewing the protocol: revision of the protocol after 3 years and/or when new diagnostic and/or treatment methods with a higher level of evidence become available.

Attached files

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Basic concepts and provisions of the topic: is an inflammation of the gums caused by the adverse effects of local or general factors, occurring without compromising the integrity of the periodontal junction and without destructive processes in other periodontal structures.

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;

Basic concepts and provisions of the topic:

K05.11 – hyperplastic;

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

(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 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., directly under the epithelial attachment to the tooth you can see a small accumulation of lymphocytes and macrophages penetrating into the gingival fluid in response to the action of microorganisms growing on the surface of the mucous membrane and teeth. However, there are no clinical signs of gum inflammation. These cells are absent only in exceptional cases. Then they talk about "absolutely intact" gum.

Inflammation of periodontal tissues is a response to the damaging effects of microbial agents on dental plaque. The surface of the macroorganism (skin) and organs in contact with the external environment (gastrointestinal tract, vagina) is populated by saprophytic microflora. Normally, there is a dynamic balance between macro- and microorganisms. Inflammation occurs when their interaction is disrupted, caused by a change in the quantitative or qualitative composition of the 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 through 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 teeth in the form of accumulations of white or slightly pigmented dental plaque, most pronounced in places where self-cleaning of the tooth surface with saliva flow, movements of the oral cavity and food bolus (cervical part of the tooth, interdental spaces).

Natural and iatrogenic factors contribute to increased plaque accumulation. Natural factors include: tartar. The first foci of mineralization appear on the inner surface of the microbial biofilm after four to eight hours. By the 14th day, full-fledged tartar has 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 traps plaque; cervical caries, root caries; bite pathology (close, dystopic position of teeth) does not allow adequate hygienic care; mouth 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 process of plaque formation goes through three main stages:

1. Formation of a pellicle, which is a protein-polysaccharide film formed from the 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 ensure the primary adhesion of microorganisms in the forming 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 increases, and an anaerobic environment is created in the deep layers. Conditions are created for secondary colonization of more aggressive gram-negative flora ( Prevotella intermedia, Porphyromonas gingivalis, Fusobacterium nucleatum). These microorganisms cannot themselves carry out the initial colonization of the pellicle, but are able to selectively interact with already attached and multiplied gram-positive flora when a sufficient amount of substrate appears for their growth and a decrease in the oxygen content in the deep layers of the plaque.

Microorganisms secrete toxins (leukotoxin), enzymes (collagenase, hyaluronidase), metabolites (fatty acids, amino acids, indole), which have a direct damaging effect. Endotoxins (lipopolysaccharides - components of the outer membrane of gram-negative bacteria) are important, causing activation of the complement system, Hageman factor, having a cytotoxic effect on fibroblasts, inducing bone tissue resorption.

Periodontopathogenic microorganisms ( Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis) are able to penetrate into periodontal tissue (invasion) as a result of erosion of the epithelial lining of the periodontal groove (periodontal pocket) between the cells, or penetrating directly through the cellular membrane

In response to damage, inflammation develops - this is a protective reaction aimed at destroying or isolating microorganisms. Long-term exposure to microorganisms leads to chronicity of the inflammatory process, as a result of which 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 - against the background of impaired microcirculation and rheological properties of the blood, reduced antioxidant protection, become damaging factors.

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

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

Mechanical trauma can be caused by: deep bite, traumatic hygienic care of the oral cavity, trauma during dental procedures (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, improper use of medications, dental procedures (whitening, devitalizing paste), smoking (toxic effects, changes in microflora, ischemia, damage to local protective factors).

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

General 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); medications (hypertensive drugs, anticonvulsants). The presence of these factors increases the risk of developing periodontal diseases and worsens their prognosis.

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

The development of periodontal diseases occurs only when the influence of pathogenic factors exceeds the adaptive and protective capabilities of periodontal tissues or when the reactivity of the body decreases.

With increasing intensity of exposure to external pathogenic factors, the number of lymphomacrophage elements in the connective tissue stroma of the gums increases. Segmented leukocytes and plasma cells appear. The fibrillar structures of the gums and cellular elements are destroyed. The epithelial attachment, although preserved, is displaced more apically. The dentogingival groove deepens, the epithelium of the groove becomes thinner.

After eliminating the microbial agent, vascular, tissue and cellular structures return to normal. If the damaging agent is not completely destroyed, the inflammation becomes chronic. Depolarization of the main substance occurs 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 decreasing 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. Active components of the complement system (enzymes, free radicals, cytokines, immune complexes) against the background of impaired microcirculation and rheological properties of the blood, reduced antioxidant protection become damaging factors.

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

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

Classification

In November 1983, at the 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 the international one (ICD-10).

Gingivitis- inflammation of the gums, caused by the adverse effects of general and local factors and occurring without violating the integrity of the dentogingival attachment.
1. Forms: catarrhal, hypertrophic, ulcerative.
2. Course: acute, chronic, aggravated, remission.
Periodontitis- inflammation of periodontal tissue, which is characterized by progressive destruction of the periodontal ligament and bone.
1. Course: acute, chronic, aggravated (including abscess), remission.
2. Severity: mild, moderate, severe.
3. Prevalence: localized, generalized.
Periodontal disease- dystrophic periodontal disease.
1. Course: chronic, remission. Severity: mild, moderate, severe. Prevalence: generalized.
Idiopathic diseases with progressive lysis of periodontal tissue (Papillon-Lefevre syndrome, X-histiocytosis, acatalasia, 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 diseases.
K 05. Acute gingivitis.

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

By 05.1. Chronic gingivitis.
By 05.2. Acute periodontitis.

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

By 05.3. Chronic periodontitis.
By 05.4. Periodontal disease.
By 05.5. Other periodontal diseases.
By 05.6. Periodontal disease, unspecified.
K 06. Other changes in the gingiva and edentulous alveolar margin.

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

Gingivitis:
- NOS (K 05.1);
- acute (K 05.0);
- chronic (K 05.1).
- By 06.0. Gum recession.
By 06.1. Gingival hypertrophy.
By 06.2. Lesions of the gums and edentulous alveolar margin caused by trauma.
By 06.8. Other specified changes in the gingiva and edentulous alveolar margin.
By 06.9. Changes in the gingiva and edentulous alveolar margin, unspecified.

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

This is explained primarily by the fact that all pathological processes, caused by various reasons, develop in a child in growing, developing and restructuring tissues that are morphologically and functionally immature, and because of this they can react inadequately and differently to similar stimuli and causative 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 disproportion in the growth and maturation of immature structures, which can arise both within the system (tooth, periodontium, alveolar bone, etc.), and in the 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 periodontal disease, which arise as a result of temporary transient functional juvenile hypertension, juvenile carbohydrate metabolism disorders (juvenile diabetes, diencephalic syndrome, etc.).

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

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

Three groups of children were studied: 1) preschoolers; 2) schoolchildren; 3) children suffering from diathesis. In group 1, 44 children were studied 3 times - at 4, 5 and 6 years of age. In 24.3% of them, gingivitis was diagnosed 1 time, in 3.5% - 2 times. The disease was diagnosed in 1.26% of children in all 3 groups. In the 2nd group (500 children) there were schoolchildren aged 10-12 years. 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 diabetic patients, gingivitis was detected in 37.1% of cases, in 14-year-old patients - in 73.8%. In childhood, quite often early gingivitis ends with the formation of pockets, bone resorption and loosening of teeth. In addition to inflammatory processes, uniform atrophy of the dental alveoli and gums occurs, as well as periodontitis associated with periodontal degeneration and tooth displacement.

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

Recognition periodontal diseases in temporary occlusion is complicated by the fact that loosening of teeth, which is the most obvious symptom, is difficult to differentiate from the process of resorption during physiological change of teeth. Due to the fact that in temporary teeth the course of periodontal disease in most cases is slow and protracted, since temporary teeth even under intact conditions fall out within 6-10 years, the clinic usually pays attention only to pronounced, severe forms. Milder cases are considered to be early loss of primary 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 or endocrine disease, and sometimes a disease of the hematopoietic system, well-recognized and characteristic changes also appear on the periodontium. Correctly diagnosed periodontal disease draws the doctor's attention to a possibly hidden general disease. In the case of periodontal disease in primary teeth, the same changes can be expected during the development of permanent teeth. Therefore, pediatric dentists sometimes have to engage in timely recognition and thorough treatment of periodontal diseases.

Causes of periodontal disease

Children react to harmful influences faster and more sharply than adults. The cure of the disease as a result of the significant regenerative ability of the young organism occurs faster and more completely. The occurrence of periodontal diseases 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 to the end of the change of teeth. Acute marginal periodontitis is observed in children more often than in adults. In the area of temporary molars, the process usually extends to the level of root bifurcation. The interroot septum melts. Children are characterized by phlegmonous infiltration of the gingival papilla.

There are three forms of periodontopathy:

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 plaque, carious defects in the area of the tooth neck, irritating prosthetic structures. Symptomatic periodontopathy occurs with keratoma of the hands and feet due to neurosis. However, the connection between ectodermal dysplasia and periodontopathy cannot be considered firmly established. In children (as in adults), this form is associated with hormonal disorders, blood diseases, mongolism and tetralogy of Fallot. 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 changes in the body create a predisposition to disease, local causes are the factors that cause disease. Bone formation and destruction occur constantly in the body throughout life. In healthy adults, these two processes are in a state of equilibrium. In the developing young organism, bone formation predominates. Its death occurs only if, for some reason, bone destruction begins to predominate. As a result of the 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.

Thus, the development of periodontitis is more often observed in cases of metabolic disorders, circulatory disorders, endocrine system disorders, nutritional diseases or severe vitamin deficiencies.

Local factors

Of the local factors causing the disease, a certain role is played by gingivitis, as well as occlusal-articulatory anomalies. Although gingivitis at a young age is quite common, 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 deposits are observed relatively rarely, with very poor oral hygiene or in connection with certain diseases (diabetes, congenital heart disease). Often there is a change in the color of the crown of the teeth and the formation of plaques. The discoloration occurs in the cervical part of the tooth crown 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.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2015

Acute periodontitis (K05.2), Chronic periodontitis (K05.3)

Dentistry

general information

Short description

Recommended
Expert advice
RSE at the RVC "Republican Center"
healthcare development"
Ministry of Health
and social development
Republic of Kazakhstan
dated October 15, 2015
Protocol No. 12

Protocol name: Periodontitis

Periodontitis- inflammation of periodontal tissue, characterized by progressive destruction of the periodontium and bone of the alveolar process of the jaws. .

Protocol code:

ICD-10 code(s):
K05. Gingivitis and periodontal diseases
K05.2 Acute periodontitis
K05.3 Chronic periodontitis

Abbreviations used in the protocol: No

Date of protocol development/revision:2015

Protocol users: dentist, therapist, endocrinologist, hematologist.

Assessment of the degree of evidence of the recommendations provided.

Table - 1. Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to relevant population.
WITH	Cohort or case-control study or controlled trial without randomization with low risk of bias (+). Results that can be generalized to the relevant population or RCTs with very low or low risk of bias (++ or +) whose results cannot be directly generalized to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best pharmaceutical practice.

Classification

Clinical classification:

Classification of periodontal diseases,approved forXVI PlenumeBUnion Scientific Society of Dentists in 1983 :

III. Periodontal disease- dystrophic periodontal disease.
By severity: light, medium, heavy.
According to the course: chronic, remission.
By prevalence: generalized.

V. Periodontomas - tumors and tumor-like diseases (epulis, fibromatosis, etc.).

Clinical picture

Symptoms, course

Diagnostic criteria for diagnosis[ 1- 12]

Complaints and anamnesis:

Table - 2. Data of complaints and anamnesis

№	Nosology	Complaints	Anamnesis
1.	Acute periodontitis	acute spontaneous pain, bleeding gums.	Newly placed permanent filling, artificial crown, orthodontic appliance
2.	Chronic generalized mild periodontitis	periodic occurrence of bleeding gums, usually when brushing teeth and eating hard foods, sometimes bad breath, discomfort in the gums, itching, burning
3.	Chronic generalized moderate periodontitis	bleeding of the gums when brushing teeth, almost constant when biting food, changes in the color and appearance of the gums, mobility of individual teeth, changes in their position in the dental arch	There is a chronic general somatic pathology, most often diseases of the gastrointestinal tract, endocrine, and nervous systems.
4.	Chronic generalized severe periodontitis	pain when eating, sometimes independent pain not associated with eating, changes in the position of the teeth, the appearance of gaps between the teeth, tooth loss, periodic appearance of ulcers.	There is a chronic general somatic pathology, most often diseases of the gastrointestinal tract, endocrine, and nervous systems.
5.	Exacerbation of chronic generalized periodontitis	pain in the gums, in the jaws, intensifying when the teeth are closed, due to “swelling of the gums,” suppuration from under it, difficulty eating, soreness of the lymph nodes.	There is a chronic general somatic pathology, most often diseases of the gastrointestinal tract, endocrine, and nervous systems. Recently suffered acute viral diseases, psycho-emotional stress, exacerbation of concomitant general somatic pathology.
6.	Remission of chronic generalized periodontitis	No complaints.	There is a chronic general somatic pathology, most often diseases of the gastrointestinal tract, endocrine, and nervous systems. There are indications of pain and bleeding in the past, tooth mobility and difficulty chewing food.

Physical examination.

ABOUTsevere localized periodontitis.
Vivid hyperemia of the gums, swelling, bleeding and pain when touched in the area of 1 to 3 teeth. Palpation of the gingival margin is painful. Percussion of teeth is painful.

Xmild chronic generalized periodontitis.
Congestive venous hyperemia and swelling of the mucous membrane of the gingival margin. Exposure of the necks and upper third of the roots of the teeth. There are supra- and subgingival dental deposits. Palpation of the gums is painless. Percussion of teeth is painless.

Xmoderate chronic generalized periodontitis.
Cyanosis of the mucous membrane of the gingival margin, interdental papillae, changes in the configuration of the gingival papillae, and in some areas thinning of the mucous membrane of the gingival margin. When probed, the gums bleed. There are supragingival and subgingival dental deposits. Exposure within ½ of the roots of the teeth. The mobility of individual teeth of I, less often II degree, traumatic occlusion is determined. Palpation of the gums is painless. Percussion of teeth is painless.

Xsevere chronic generalized periodontitis.
Cyanotic appearance of the mucous membrane of the gingival margin, interdental papillae, changes in the configuration of the gingival papillae, in some areas thinning of the mucous membrane of the gingival margin and deformation of the gums. Abundant supragingival and subgingival dental plaque. Exposure of more than ½ of the roots of the teeth, exposure of the bifurcations and trifurcations of the teeth. Some teeth have II-III degree of pathological mobility. Fan-shaped displacement of teeth, rotation around an axis, and traumatic occlusion are expressed. Palpation of the gums is painless. Percussion of teeth is painless.

Exacerbation of chronic generalized periodontitis.
Congestive venous hyperemia of the gingival mucosa with areas of bright hyperemia and edema, bleeding and pain when touched, release of serous-purulent exudate when pressing on the gingival margin. The necks and roots of the teeth are exposed to varying degrees, corresponding to the severity of the process. Palpation of the gums is painful. Horizontal percussion of individual teeth is painful.

Remission of chronic generalized periodontitis.
The mucous membrane of the gums is pale pink, the gingival margin tightly covers the surfaces of the tooth crowns. Exposure of the necks and roots of the teeth, depending on the severity of the process. Palpation of the gums is painless. Percussion of teeth is painless.

Diagnostics

List of diagnostic measures:

Basic (mandatory) diagnostic examinations performed on an outpatient basis: ( Activities that have a major role in making a diagnosis at the amb. level are indicated)
1. collection of complaints and medical history;
2. general physical examination: visual examination of the condition of the gums (color, consistency, shape of interdental papillae, size, configuration of the gingival margin, deformation, thickening, thinning); palpation of regional lymph nodes, gingival margin, percussion of teeth, determination of tooth mobility, probing of the dentogingival attachment, determination of the depth of periodontal pockets.

Additional diagnostic examinations performed on an outpatient basis:
1. Determination of the hygienic index according to Green-Vermillion;
2. Carrying out the Schiller-Pisarev test;
3. Determination of the periodontal Russell index;
4. Orthopantomography or panoramic radiography;
5. General detailed blood test;
6.Biochemical study (determination of glucose in blood serum)
7. Immunological study (determination of cytokines IL-8, IL-2, IL-4, IL-6 in blood serum by ELISA method, determination of cytokines interferon-alpha in blood serum by ELISA method)

Instrumental studies:
· Probing - the integrity of the periodontal attachment in chronic generalized periodontitis is impaired, periodontal pockets are determined, the depth of which reaches 3-3.5 mm in mild cases, up to 5 mm in moderate cases, and more than 5 mm in severe cases.
· Schiller-Pisarev test - detects the presence of inflammation in the gums. During the inflammatory process, glycogen accumulates in the epithelial cells of the mucous membrane, and the gums are stained with an iodine-containing solution from light brown to dark brown, depending on the intensity of the inflammatory process in the gums. The Schiller-Pisarev test for periodontitis is positive.
· Determination of the periodontal index according to Russell. Russell's periodontal index characterizes the severity of the inflammatory-destructive process in the periodontium. As the process becomes more severe, the periodontal index values increase. When the periodontal index value is up to 1.0 - mild periodontitis, up to 4.0 - moderate periodontitis, up to 8.0 - severe periodontitis.
· Determination of the Green-Vermillion hygienic index. The Green-Vermillion hygienic index characterizes the presence of soft and hard dental plaque. The value of the Green-Vermillion hygienic index increases with periodontitis.
· Panoramic radiography or orthopantomography of the jaws. With periodontitis, changes are detected in the bone tissue of the alveolar process that correspond to one or another degree of severity of the process. In case of mild periodontitis, the expansion of the periodontal gap in the cervical region of the teeth, the destruction of the compact plate of the apexes of the interdental septa, and osteoporosis of the apexes of the interalveolar septa within 1/3 of the root length are determined radiologically. With moderate periodontitis, a mixed uneven type of destruction of the bone tissue of the alveolar process is determined, reaching up to 1/2 the length of the root in the area of individual teeth. In severe periodontitis, a mixed, uneven type of destruction of the bone tissue of the alveolar process is revealed, reaching more than 1/2 the length of the root in the area of individual teeth, with the formation of bone pockets along the entire length of the root.

Indications for consultation with specialists:
· Consultation with an endocrinologist - in case of endocrine diseases, changes in the bone tissue of the jaws are noted, characteristic of this endocrine pathology, against the background of which a more active course of the destructive process is observed. Complex treatment with the participation of an endocrinologist is required.
· Consultation with a hematologist - ulcerative-necrotic processes in the gums, gingival hypertrophy, leukemic infiltration of periodontal tissues observed in blood diseases (leukemia, agranulocytosis, aplastic anemia) require the participation of a hematologist both in the diagnosis and in the complex treatment of this category of patients.
· Consultation with a gastroenterologist - chronic generalized periodontitis is usually accompanied by chronic diseases of the gastrointestinal tract, which requires complex treatment with the participation of a gastroenterologist.

Laboratory diagnostics

Laboratory research:
· General detailed blood test - carried out for the purpose of differential diagnosis from symptomatic catarrhal, ulcerative and proliferative processes in periodontal tissues associated with blood diseases (leukemia, agronulocytosis, aplastic anemia, thrombocytopenic purpura). In case of blood diseases, a detailed blood test shows changes in indicators corresponding to the blood disease.
· Biochemical study (determination of glucose in blood serum) - the course of periodontitis in patients with diabetes mellitus is active and progressive, with diabetes mellitus the blood glucose level is above 6 mmol/l.
According to indications: -immunological study;
· Immunological study (determination of cytokines IL-8, IL-2, IL-4, IL-6 in blood serum by ELISA method, determination of cytokines interferon-alpha in blood serum by ELISA method).
The ratio of pro-inflammatory and anti-inflammatory cytokines changes.

Differential diagnosis

Differential diagnosis.

Table - 3. Differential diagnosis of periodontitis

№	Periodontitis	The disease with which it is differentiated	General clinical signs	Distinctive clinical features
1.	Mild chronic periodontitis.	Chronic catarrhal gingivitis.	Cyanotic, swelling of the gingival margin; upon probing, bleeding is detected.	With periodontitis, there is a violation of the integrity of the dentogingival attachment, periodontal pockets up to 3.5 mm are determined. Exposure of the necks in the area of individual teeth. An orthopantomogram shows resorption of the cortical plate of the apices of the interalveolar septa, osteoporosis and a decrease in the height of the interalveolar septa within 1/3 of the length of the roots.
2.	Periodontitis of varying severity in remission.	Periodontal disease of varying severity.	Exposure of the necks and roots of the teeth, depending on the severity.	With periodontal disease, there is uniform exposure of the necks and roots of the teeth, there is no tooth mobility even with significant exposure of the roots. On the orthopantomogram, in contrast to periodontitis, there is a uniform decrease in the height of the interdental septa, the integrity of the cortical plates of the apexes of the interdental septa is not damaged, osteosclerosis.
3.	Acute localized periodontitis	Acute catarrhal gingivitis	Pain, bleeding when touching the gums, pronounced hyperemia and swelling of the gum mucosa	In acute periodontitis, the process is localized, there is a causative local factor, a violation of the integrity of the periodontal attachment is determined with the formation of a periodontal pocket. X-ray changes in the bone tissue of the alveolar process, corresponding to the severity of the process.
4.	Exacerbation of mild chronic generalized periodontitis	Exacerbation of chronic catarrhal gingivitis.	Hyperemia and swelling of the gums, bleeding and pain when touched	during exacerbation of mild chronic generalized periodontitis, probing reveals periodontal pockets up to 3.5 mm deep. Exposing the necks of the teeth. An orthopantomogram shows resorption of the cortical plate of the apices of the interalveolar septa, osteoporosis and a decrease in the height of the interalveolar septa within 1/3 of the length of the roots.

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Treatment

Treatment goals:

prevent further progression of the inflammatory-destructive process in periodontal tissues, achieve remission and stabilization of the process.

Treatment tactics: The choice of treatment method depends on the severity of the inflammatory-destructive process in the periodontium. When treating a patient, the following principles should be observed: individual approach, complexity, systematicity, consistency and activity.

Treatment plan for a patient with periodontitis [A. B]
1. Hygiene training with supervised brushing of teeth;
2. Sanitation of the oral cavity with the elimination of local irritating factors;
3. Local and general drug treatment (treatment of symptomatic gingivitis, pathogenetic effect on the inflammatory process in the periodontium);
4. Elimination of periodontal pockets using surgical methods (closed and open curettage, gingivotomy, gingivectomy, flap surgery with osteoplasty, etc.)
5. Temporary splinting, selective grinding of the bite, rational prosthetics;
6. Physiotherapeutic methods of treatment.

Non-drug treatment: Mode III. Table No. 15

Drug treatment:

Table - 4. Medicines for local and general treatment.

Name of the drug (INN)	Release form	Method of drug administration	Single dose	Frequency of application	Duration of treatment
Local treatment
Potassium permanganate	0.1% solution	Rinsing Washing between teeth		Mouth rinse after eating. Irrigation of the lesion	5-7 days
Hydrocortisone acetate, oxytetracycline hydrochloride	ointment	Applications to the lesion		Once a day when treating the lesion	3-4 days before acute inflammatory phenomena subside
Sodium heparin, benzocaine, benzyl nicotinate	ointment	Applications to the lesion	The ointment is applied in a thin layer onto a gauze or cotton swab for application.	Once a day during treatment.	5-7 days until the swelling of the gum tissue disappears
Metronidazole	Tablets 0.25 g	Powdering powder of the lesion	The tablet is crushed to a fine powder. Powder is applied to the affected area	Once a day when treated for 5-7 days	5-7 days before the removal of exudation phenomena
General treatment
Doxycycline	Pills	Per os	0.1 g	According to the scheme (on the first day 0.2 g 2 times a day, subsequently 0.1 g 2 times a day)	10 days
Tinidazole	Pills	Per os	0.5 g.	2 times a day	5 days
Ibuprofen	Pills	Per os	0.2 g	3-4 times a day	Until clinical improvement

Other types of treatment:

Other types of treatment provided on an outpatient basis:

Physiotherapeutic treatment:

1. Phototherapy.

Infrared radiation
Local ultraviolet irradiation.
Infrared radiation
Laser therapy (quantum therapy).
Bioptron

2. D.C.
Electrophoresis.

3. Alternating electric current.
Darsonvalization.
UHF therapy.
Centimeter therapy (CMT)
Decimeter therapy (DMW)

4. Ultra tone therapy.

5. Magnetotherapy.

6. Magnetic laser therapy

7. Massage.
Acupressure.
Vacuum massage.
Vibromassage

8. Paraffin therapy

9. Ozocerite treatment.

10. Therapeutic use of native mud

Surgical intervention:

Surgical intervention provided on an outpatient basis: open and closed curettage, simple and radical gingivectomy.

Surgical intervention provided in an inpatient setting: No

Indicators of treatment effectiveness.
Remission and stabilization of the inflammatory-destructive process in periodontal tissues.

Drugs (active ingredients) used in treatment

Hospitalization

Indications for hospitalization: No

Prevention

Preventive actions:
· oral hygiene, correction of fillings and dentures
elimination of defects of occlusion and articulation,
· plastic surgery for improper attachment of the frenulum of the lips and tongue with a small vestibule of the oral cavity.
· timely sanitation of the oral cavity,
restoration of dental defects,
· correction of malocclusions.
· prevention of general somatic diseases.

Further management: Dispensary observation. In the presence of general somatic diseases four times a year, in the absence - twice a year.

Information

Sources and literature

Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health of the Republic of Kazakhstan, 2015
1. List of used literature: 1. Bayakhmetova A.A. Periodontal diseases. – Almaty, 2009. -169 p. 2. Diagnostics in therapeutic dentistry: Textbook / T.L. Redinova, N.R. Dmitrakova, A.S. Yapeev, etc. - Rostov n/D.: Phoenix, 2006. -144 p. 3. Zazulevskaya L.Ya. Practical periodontology. – Almaty, 2006. -348 p. 4. Lutskaya I.K. Dentistry Guide. – Rostov n/d.: Phoenix, 2002. -544 p. 5. Therapeutic dentistry: A textbook for students of medical universities / Ed. E.V. Borovsky. - M.: “Medical Information Agency”, 2004. 6. Therapeutic dentistry: Textbook / Ed. Yu.M. Maksimovsky. – M.: Medicine, 2002. -640 p. 7. Kornman KS. Mapping the pathogenesis of periodontitis: A new look. J Periodontol 2008;79(Suppl. 8):1560-1568. Stroke 2004;35:2020-2023.

Information

List of protocol developers with qualification information:
1) Esembaeva Saule Serikovna - Doctor of Medical Sciences, Professor, Director of the Institute of Dentistry of KazNMU;
2) Bayakhmetova Aliya Aldashevna - Doctor of Medical Sciences of KazNMU, Head of the Department of Therapeutic Dentistry;
3) Tuleutaeva Raikhan Yesenzhanovna - Candidate of Medical Sciences, Associate Professor of the Department of Pharmacology and Evidence-Based Medicine of the Russian State University at the Petropavlovsk State Medical University in Semey.

Disclosure of no conflict of interest: No

Reviewers:
1) Mazur Irina Petrovna - Doctor of Medical Sciences, National Medical Academy of Postgraduate Education named after. P.L. Shubik, Institute of Dentistry, Department of Dentistry, professor;
2) Zhanalina Bakhyt Sekerbekovna - Doctor of Medical Sciences, Professor, RSE at WKGMU named after. M. Ospanova”, Head of the Department of Surgical Dentistry and Pediatric Dentistry.

Attached files

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

Classification

Gingivitis- inflammation of the gums, caused by the adverse effects of general and local factors and occurring without violating the integrity of the dentogingival attachment.
1. Forms: catarrhal, hypertrophic, ulcerative.
2. Course: acute, chronic, aggravated, remission.
Periodontitis- inflammation of periodontal tissue, which is characterized by progressive destruction of the periodontal ligament and bone.
1. Course: acute, chronic, aggravated (including abscess), remission.
2. Severity: mild, moderate, severe.
3. Prevalence: localized, generalized.
Periodontal disease- dystrophic periodontal disease.
1. Course: chronic, remission. Severity: mild, moderate, severe. Prevalence: generalized.
Idiopathic diseases with progressive lysis of periodontal tissue (Papillon-Lefevre syndrome, X-histiocytosis, acatalasia, 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 diseases.
K 05. Acute gingivitis.

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

By 05.1. Chronic gingivitis.
By 05.2. Acute periodontitis.

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

By 05.3. Chronic periodontitis.
By 05.4. Periodontal disease.
By 05.5. Other periodontal diseases.
By 05.6. Periodontal disease, unspecified.
K 06. Other changes in the gingiva and edentulous alveolar margin.

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

Gingivitis:
- NOS (K 05.1);
- acute (K 05.0);
- chronic (K 05.1).
- By 06.0. Gum recession.
By 06.1. Gingival hypertrophy.
By 06.2. Lesions of the gums and edentulous alveolar margin caused by trauma.
By 06.8. Other specified changes in the gingiva and edentulous alveolar margin.
By 06.9. Changes in the gingiva and edentulous alveolar margin, unspecified.

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

Causes of periodontal disease

There are three forms of periodontopathy:

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

Thus, the development of periodontitis is more often observed in cases of metabolic disorders, circulatory disorders, endocrine system disorders, nutritional diseases or severe vitamin deficiencies.

Local factors