Chronic generalized periodontitis ICD. Catarrhal gingivitis. Get treatment in Korea, Israel, Germany, USA

Basic concepts and provisions of the topic:

Periodontitis – an inflammatory disease accompanied by destructive destruction of all periodontal tissues.

The prevalence of inflammatory periodontal diseases in our country reaches 95% and higher.

Classification of periodontitis according to ICD-10 (1997):

Acute periodontitis (K05.2):

K05.20 – periodontal (periodontal) abscess of gingival origin without fistula;

K05.21 – periodontal (periodontal) abscess of gingival origin with a fistula.

Chronic periodontitis (KO5.3):

K05.30 – localized;

K05.31 – generalized;

K05.32 – chronic pericoronitis;

K05.33 – thickened follicle (papillary hypertrophy).

Classification of periodontitis

(Periodontological Congress StAR, 2001)

Course: chronic, aggressive.

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

The severity of periodontitis is determined by three symptoms:

Degree of resorption bone tissue.

The depth of the periodontal pocket.

Mobility of teeth.

Severity:

mild – periodontal pockets no more than 4 mm, resorption of bone tissue of the interradicular septum up to 1/3 of the length of the roots, no pathological mobility;

medium – pockets from 4 to 6 mm, resorption of bone tissue of the septa by 1/3-1/2 of the length of the roots, pathological mobility of grades I-II.

severe – pocket depth more than 6 mm, resorption of bone tissue of the septa more than ½ the length of the roots, pathological mobility grade II-III.

Prevalence of the process: localized (focal), generalized.

Acute periodontitis is observed extremely rarely; it is often local in nature and develops as a result of acute mechanical trauma to the periodontium.

Etiology of periodontitis. The leading etiological factor of periodontitis, according to domestic and foreign researchers, is the microflora of dental plaque formed on the pellicle of the tooth in the area of ​​the periodontal sulcus. The pathogenic influence of microflora may be associated with a change in its composition due to excessive accumulation in dental plaque. In these cases, predominantly gram-negative microorganisms, fusobacteria, and spirochetes appear. IN last years In dental plaque, which causes inflammation and destruction of periodontal tissue, the role of so-called associations of potentially aggressive microflora is noted: Actinobacillus, Actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsytus, Spirochete,Prevotella intermedia, Campilobacter rectus, Eubacteriuv nodatum, Treponema denticola, Streptococcus intermedius, Peptostreptococcus micros, Fusobacterium nucleaum, Eikenella corrodens.

There are a number of local and common factors risks contributing to the occurrence of periodontitis. Factors causing periodontal overload: occlusal pathology (crowding of teeth), supracontacts, traumatic “knots”, parafunctional habits (teeth clenching, bruxism), defects in prosthetics and fillings. Factors that cause ischemia of periodontal tissue are short frenulums of the tongue and lips, impaired attachment of the frenulums of the tongue, lips and cords, and a shallow vestibule of the mouth. Poor hygiene oral cavity, gingival carious cavities predispose to the development of periodontitis. Congenital structural features of the periodontium: thin, low-keratinized gums, insufficient thickness of the alveolar bone, convex contour of the dental arch, often combined with convexity of the roots.

Common diseases associated with disruption of adaptation processes: chronic emotional stress, endocrine diseases, urolithiasis, gastrointestinal ulcer, systemic osteoporosis and other somatic pathologies.

All of these factors, disrupting the periodontal protective system, create the prerequisites for the pathogenic influence of microflora on periodontal tissue and, first of all, on the periodontal attachment, inflammation and destruction of which is the beginning of periodontitis.

Pathogenesis. Features of the influence of dental plaque on the development of periodontitis:

Active influence of proteolytic enzymes, which, acting on the intercellular connections of the attachment epithelium, lead to an increase in its permeability;

In addition, acting on the organic substance of the epithelial attachment, enzymes change the colloidal state and contribute to the disruption of the connection between the epithelium and tooth enamel;

Endotoxins produced by anaerobic bacteria damage cells, connective tissue formations and the ground substance. They can activate the complement system, kinins and other inflammatory mediators, causing immune responses - humoral and cellular, promoting the development of soft tissue inflammation with subsequent destruction of alveolar bone tissue;

Biologically secreted during inflammation active substances(histamine, serotonin) affect the cell membranes of blood vessels - precapillaries and capillaries. Biologically active substances activate the release of blood cells, activate mast and plasma cells, lymphocytes;

Pathogenic microflora, having antigenic properties and exerting a sensitizing effect, leads to increased alteration and the formation of autoantigens, which cause lysis of the circular ligament of the tooth and bone tissue. At the same time, new tissue antigens are released, which aggravate the course of periodontitis.

Main pathogenetic mechanisms development of chronic periodontitis:

1. Damage to cells and intercellular matrix, collagen structures due to the release of lysosomal enzymes by polymorphonuclear leukocytes.

2. Release of plasma and cellular inflammatory mediators.

3. Disruption of the microcirculatory bed and, as a result, an increase in vascular-tissue permeability.

4. Deterioration of the trophism of periodontal tissues leads to disruption of oxygen supply to tissues and changes in energy processes that ensure cell viability. In these cases, primitive methods of energy production are included using peroxide and free radical oxidation with the formation of a large amount of highly toxic products: superoxide anion, malonaldehyde, etc.

As periodontitis develops, a periodontal pocket is formed, this is associated with the destruction of the periodontal attachment, its ulceration and the growth of the epithelium into the underlying connective tissue, the destruction of the connective tissue attachment and collagen structures of the circular ligament of the tooth. As a result of lysis of these structures, granulation tissue is formed, infiltrated with macrophages, plasma cells and lymphocytes. In the mechanism of periodontal pocket formation, hard subgingival dental deposits play a significant role.

Subsequently, inflammatory resorption of alveolar bone tissue is observed against the background of osteoclast activation. At the same time, the activity of osteoblasts is suppressed, that is, osteogenesis is disrupted, so bone tissue is replaced by granulation tissue. This is how a periodontal pocket is formed and complete destruction of the supporting-retaining apparatus of the tooth occurs, which ultimately leads to tooth loss.

Basic concepts and provisions of the topic:

Gingivitis 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;

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 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 border structure through which the periodontal complex interacts with the external environment. Normally, with clinically healthy gums, 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 effect 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 hygiene 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 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.

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

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.).

Clinical picture

Symptoms, course

Diagnostic criteria making a diagnosis[ 1- 12]

Complaints and anamnesis:

Table - 2. Data of complaints and anamnesis

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 gingival mucosa is pale Pink colour, 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 (required) diagnostic examinations carried out 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. With a periodontal index value of up to 1.0 -mild degree 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 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 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 periodontitis

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

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, you should follow the following principles: 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 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. Medications for local and general treatment.

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 the 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 with 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

1. Minutes of meetings Expert Council RCHR MHSD RK, 2015
   1. List of used literature: 1. Bayakhmetova A.A. Periodontal diseases. – Almaty, 2009. -169 p. 2. Diagnostics in therapeutic dentistry: Tutorial/ 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 : 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. 8. Axelsson P, Nystrom B, Lindhe J. The long-term effect of a plaque control program on tooth mortality, caries, and periodontal disease in adults.Results after 30 years of maintenance. J ClinPeriodontol 2004;31:749-757. 9. Van der Velden U, Abbas F, Armand S, et al. Java project on periodontal diseases. The natural development of periodontitis: Risk factors, risk predictors, and risk determinants. J ClinPeriodontol 2006;33:540-548. 10. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr. Microbial complexes in subgingival plaque. J ClinPeriodontol 1998;25:134-144. 11. Van Dyke TE. The management of inflammation in periodontal disease. J Periodontol 2008;79:1601-1608. 12. Van Dyke TE, Sheilesh D. Risk factors for periodontitis. J IntAcadPeriodontol 2005;7:3-7. 13. American Academy of Periodontology. Diabetes and periodontal diseases (position paper). J Periodontol 2000;71:664-678. . 14. Lalla E, Kaplan S, Chang SM, et al. Periodontal infection profiles in type 1 diabetes. J ClinPeriodontol 2006;33:855-862. . 15. Kornman KS, Crane A, Wang HY, et al. The interleukin-1 genotype as a severity factor in adult periodontal disease. J ClinPeriodontol1997;24:72-77. 16. Loos B. G. Systemic markers of inflammation and periodontitis. J Periodontol 2005;76:2106-2115. 17. Noack B, Genco RJ, Trevisan M, et al. Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol2001;72:1221-1227. 18. Paraskevas S, Huizinga JD, Loos BG. A systematic review and meta-analyses on C-reactive protein in relation to periodontitis. J ClinPeriodontol 2008;35:277-290. 19. Pussinen PJ, Alfthan G, Rissanen H, et al. Antibodies to periodontal pathogens and stroke risk. Stroke 2004;35:2020-2023. 20. Tu YK, Tugnait A, Clerehugh V. Is there a temporal trend in the reported treatment efficacy of periodontal regeneration? A meta-analysis of randomized-controlled trials. J ClinPeriodontol 2008;35:139-146. 21. Berkey CS, AntczakBouckoms A, Hoaglin DC, Mosteller F, Pihlstrom BL. Multiple-outcomes meta-analysis of treatments for periodontal disease. J Dent Res 1995;74:1030-1039. 22. Hung HC, Douglass CW. Meta-analysis of the effect of scaling and root planning, surgical treatment, and antibiotic therapy on periodontal probing depth and attachment loss. J ClinPeriodontol 2002;29:975-986. 23. Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP, Dyer JK. Long-term evaluation of periodontal therapy: I. Response to 4 therapeutic modalities. J Periodontol 1996;67:93-102. 24. Lutskaya I.K., Martov V.Yu. Medicines in dentistry. –M.: Med.lit., 2007. -384 p. 25. Muravyannikova Zh.G. Dental diseases and their prevention. – Rostov n/d: Phoenix, 2007. -446 p.

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 RSE at PKhVSMU Semey.

Disclosure of no conflict of interest: No

Reviewers:
1) Mazur Irina Petrovna - Doctor of Medical Sciences, National medical Academy 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.

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 more high level evidence.

Attached files

Attention!

• By self-medicating, you can cause irreparable harm to your health.
• The information posted on the MedElement website and in the mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" cannot and should not replace a face-to-face consultation with a doctor. Be sure to contact medical institutions if you have any diseases or symptoms that bother you.
• Choice medicines and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body.
• MedElement website and mobile applications"MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are solely information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders.
• The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.

K05 Gingivitis and periodontal diseases

K05.0 Acute gingivitis

K05.00 Acute streptococcal gingivostomatitis

K05.08 Other specified acute gingivitis

K05.1 Chronic gingivitis

K05.10 Chronic gingivitis. Simple marginal

K05.11 Chronic gingivitis. Hyperplastic

K05.12 Chronic gingivitis. Ulcerative

K05.13 Chronic gingivitis. Desquamative

K05.18 Other specified chronic gingivitis

K05.19 Chronic gingivitis, unspecified

Classification of acute ulcerative gingivitis according to ICD-10.

Block: Other diseases caused by spirochetes

A69.10 Acute necrotizing ulcerative gingivitis (fusospirochetal gingivitis), (Vincent gingivitis)

Catarrhal gingivitis.( K05.10 Simple marginal gingivitis)

In the clinic it occurs mainly in the form of chronic inflammation or its exacerbations. Acute is usually a symptom of an acute respiratory infection.

The prevalence of catarrhal gingivitis largely depends on etiological factors. Localized gingivitis occurs when there are local causes. The manifestation of generalized catarrhal gingivitis is associated with a change in the body’s reactivity in diseases of the gastrointestinal tract, hormonal disorders(thyroid and gonads), infectious diseases and etc.

The clinical picture of catarrhal gingivitis is caused by morphological changes occurring in the epithelium and the underlying tissue. connective tissue. In the epithelium, areas of desquamation, edema, signs of parakeratosis and acanthosis, and an increase in acid glycosaminoglycans and glycogen are detected. In the spinous layer of the epithelium, the protein content decreases and the RNA content is sharply reduced.

In the connective tissue there is chronic inflammation: edema, hyperemia, stasis, accumulation of lymphocytes and plasma cells.

Biochemical changes are observed in the structure of the main substance, indicating a decrease in the activity of redox enzymes. The epithelial attachment is not disrupted.

The clinical picture of catarrhal gingivitis depends largely on its severity, which is associated with the degree of involvement of the gums in the pathological process.

Mild gingivitis is characterized by damage to the interdental gums, moderate severity - interdental and alveolar gums, and severe gingivitis - damage to the entire gum, including the alveolar.

With mild chronic catarrhal gingivitis, patients usually do not go to the doctor. Subsequently, patients complain of bleeding gums when brushing teeth, eating solid food, a burning sensation, and swelling in the gums. The general condition of the patients was not impaired.

Upon examination, hyperemia and swelling of the gums are detected, the gingival margin loses its scalloped contour.

An instrumental examination determines bleeding gums, soft plaque and the presence of supragingival tartar. When a periodontal probe is inserted into the periodontal sulcus, there is no violation of the integrity of the periodontal junction, and there is no periodontal pocket. The symptom of bleeding is positive.

At additional methods examination, a positive Schiller-Pisarev test is determined. The hygiene index value is more than 1.0, PMA is more than "0". The resistance of capillaries during the Kulazhenko vacuum test is reduced.

The oxygen tension in the gums (polarographic method) is reduced in chronic catarrhal gingivitis. The rheoparodontographic curve reveals changes in its shape, indicating either pronounced dilatation of the vascular wall, which is better prognostically, or the configuration of the curve indicates constriction of the vascular wall. There are no changes in the apexes of the interdental septa on the radiograph.

Clinical tests that identify preclinical signs of gingivitis are very important, as this will allow for prevention clinical manifestation gingivitis. These tests primarily include the manifestation of the symptom of bleeding during probing of the periodontal sulcus, the study of the composition and amount of periodontal fluid, etc. It should be taken into account that the morphological signs of inflammation are determined even in clinically intact gums.

Hypertrophic gingivitis ( K05.11 Chronic hyperplastic gingivitis)

It can manifest itself in two forms: edematous and fibrous forms.

In the etiopathogenesis of hypertrophic gingivitis, hormonal changes (adolescent gingivitis, pregnant gingivitis), medication intake (contraceptives, diphenin, etc.), and blood diseases (leukemic reticulosis) are of significant importance. In the etiology of localized hypertrophic gingivitis, local factors are important: malocclusions (deep, open, cross), abnormalities in the position of teeth (crowding, supernumerary teeth), eruption defects.

Morphologically, the edematous form of hypertrophic gingivitis, in addition to swelling of the epithelium and the basic substance of the connective tissue, an increase in acid glycosaminoglycans, is characterized by dilation and proliferation of capillaries, which creates an increase in gum mass. Abundant and varied cellular infiltration is observed (leukocytes, plasma and mast cells, lymphocytes).

Clinically, with the edematous form of hypertrophic gingivitis, patients, in addition to complaints of bleeding gums when eating and brushing their teeth, complain of a cosmetic defect associated with an increase in the volume of the gums. Hypertrophic gingivitis in which gum hypertrophy does not exceed 1/3 of the length of the tooth crown is called mild. Moderate hypertrophic gingivitis is characterized by more pronounced gum deformation - up to 1/2 of the tooth crown. in severe cases, the gum covers 2/3 or the entire crown of the tooth.

Objectively, the edematous form of hypertrophic gingivitis is characterized by enlarged gums, a glossy bluish surface, bleeding when probing the periodontal sulcus, sometimes when touched, and the formation of false periodontal pockets. Epithelial attachments are not broken.

The fibrous form of hypertrophic gingivitis is morphologically characterized by keratinization of the epithelium like parakeratosis, its thickening and proliferation into the depths of the connective tissue. In the stroma, proliferation of fibroblasts and coarsening and proliferation of collagen structures, thickening of the walls of blood vessels, and rare foci of inflammatory infiltration are observed. The epithelial attachment is not broken. This form of gingivitis usually does not bother patients at the beginning of the disease. As it develops (moderate and severe), patients are concerned about the growth of gums and cosmetic defects. Objectively, deformation of the gums is detected, which has a pale pink color, dense with a lumpy surface. There is no bleeding, false periodontal pockets are identified.

Ulcerative gingivitis is a destructive form of inflammation, in the etiopathogenesis of which a significant role is played by a change in the reactivity of the body and, consequently, a decrease in the resistance of the gums to autoinfection of the oral cavity (especially to gram-negative bacteria, fusospirochetosis).

This condition may be preceded by acute respiratory disease. stressful situations, hypothermia. plays a provocative role poor hygiene oral cavity and tartar, the presence of multiple carious cavities, difficult eruption of wisdom teeth.

Ulcerative gingivitis characterized acute pain, bleeding gums, difficulty eating, general malaise, fever. Upon examination, the gums have a grayish color, the gingival papillae are necrotic, and there is an abundance of soft plaque.

The severity of ulcerative gingivitis is determined not only by the degree of gum damage (interdental, marginal or alveolar), but also by the severity general intoxication, (increase in body temperature, changes in peripheral blood: leukocytosis, accelerated ESR, shift to the left).

When diagnosing ulcerative gingivitis, one must be wary of excluding blood diseases (leukemia, agranulocytosis), which are very characterized by ulcerative necrotic lesions of the gums.

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

Code by international classification diseases ICD-10:

• K05.2
• K05.3

Causes

Etiology. To the most important local etiological factors include oral microflora (Porphyromonas gingivalis, Peptostreptococcus, Fusobacterium nucleatum, Veillonella parvula, etc.), dental plaque, anomalies in the position of teeth, bite, and others. Common disorders include diseases of the gastrointestinal tract, endocrine and nervous systems, metabolic disorders, and vitamin imbalance. Can contribute to periodontal damage bad habits.
Pathogenesis. Periodontitis always preceded by inflammation of the gingival margin (gingivitis). During the development of the pathological process, a violation of the epithelial attachment of the gum to the tooth occurs, destruction of the ligamentous apparatus, and resorption of the bone tissue of the alveolar process. A periodontal pocket is formed, which constantly deepens, reaching the root apex. Progressive resorption of alveolar bone leads to pathological tooth mobility. Destruction of the ligamentous apparatus of the tooth is accompanied by overload of individual teeth or groups, and traumatic occlusion occurs. With generalized periodontitis, gradual destruction of the entire complex of periodontal tissues occurs, which ultimately ends in tooth loss.
Classification. According to the course, acute, chronic, aggravated periodontitis (including abscess formation), and remission are distinguished. Based on the severity of the process, they distinguish between mild, moderate, and severe periodontitis; according to its prevalence, localized and generalized.

Symptoms (signs)

Clinical manifestations. They are mainly determined by the severity and prevalence of the disease.
. Localized periodontitis. Characterized by aching pain, bleeding and severe swelling of the gums. Limited destructive inflammatory process in the area of ​​one or several teeth (up to 5 teeth). Examination with a periodontal probe on all four sides of the affected teeth reveals a violation of the periodontal attachment and periodontal pockets of varying depths with purulent discharge or granulations. Tooth mobility of varying degrees appears. With exacerbations of the process, there is a sharp pain in 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 can form.
. Generalized periodontitis. For initial stage characterized by bleeding, swelling of the gums, painful sensations in the gum area, bad breath and shallow periodontal pockets, mainly in the area of ​​​​the interdental spaces. In the developed stage of periodontitis, multiple pathological periodontal pockets of varying depths appear - with serous-purulent contents in chronic cases or abundant purulent contents in aggravated course of the disease. Based on the depth of these periodontal pockets, I, II, III degree diseases. Mobility of teeth develops, and subsequently traumatic occlusion is formed. Characterized by an abundance of soft dental plaque, supra- and subgingival dental plaque. Exposure of the necks and roots of the teeth may be accompanied by hyperesthesia. Sometimes there are retrograde pulpitis. A chronic progressive course can lead to exacerbations accompanied by pain of a spontaneous nature. Abscesses and fistulas form one after another at intervals of several days. Parallel changes occur general condition body - rise in body temperature, weakness, malaise. Enlargement and tenderness of regional lymph nodes are observed. The state of remission is characterized by dense gums of a pale pink color, possibly exposing the roots of the teeth. There is no dental plaque or discharge from pockets.

Diagnostics

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

Treatment

TREATMENT
Local treatment
. It must begin with a thorough removal of dental plaque, especially subgingival plaque, using a scaler (Pieson - master - 400). It includes the whole range of local effects: medication, orthopedic and physiotherapeutic. Eliminate local causes that led to the development of inflammation. For longer contact of drugs with periodontal tissues, gingival dressings or forms with a prolonged action are used.
. Special meaning acquire surgical methods(curettage, gingivitomy, flap operations, etc.) performed on the gum and bone tissue, which are aimed at removing granulations, eliminating periodontal pockets, restoring defects in the bone tissue of the alveolar process, etc. Surgical intervention is recommended to be combined with drugs that promote the regeneration of periodontal tissue ( keratoplasty). Teeth that have mobility are splinted. It is mandatory 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 ultrasound and low-level 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 They are mainly carried out during exacerbations of chronic generalized periodontitis and in the presence of severe general somatic pathology (hereditary neutropenia, type 1 diabetes, etc.). It includes: antibiotics wide range actions, desensitizing and sedatives, immunotropic drugs (imudon, xymedon). Sometimes prescribed hormone therapy and drugs that affect mineral metabolism(thyrocalcitonin). General treatment is combined with specific therapy general illness and vitamin therapy.
Prevention. Timely treatment of gingivitis. Careful oral hygiene. It is advisable to use resort factors (balneotherapy and peloid therapy). Physico - Chemical properties 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.