Catarrhal gingivitis. Catarrhal gingivitis Other treatments

Treatment of acute catarrhal gingivitis comes down to identifying the etiological factor and treating the underlying disease. Local therapy is aimed at anesthetizing the gum mucosa, reducing swelling, and preventing secondary infection.
When treating acute inflammation of the oral mucosa in children, it is advisable to use herbal remedies that have enveloping properties (decoction of mallow leaves, sage, marshmallow root) and capillary-strengthening properties. Phenolic compounds of plant origin - flavonoids - are recommended as capillary-strengthening agents. The resistance of capillary walls mainly depends on the condition of the cells and fibers of the connective tissue located around the vessels. During an acute inflammatory process, the permeability and strength of capillaries change. Phenolic compounds with P-vitamin activity act on the permeability and strength of vascular-tissue barriers. Vitamin C has the same effect, but, unlike P-vitamin phenolic compounds that have P-vitamin activity, it does not protect the basic substance of connective tissue from the effects of hyaluronidase, but stimulates the formation of collagen.
Phenolic compounds have the properties of antagonists of inflammatory mediators - serotonin, bradykinin, prostaglandins.
It is advisable to use plant phenolic compounds for the treatment of inflammatory lesions of the oral mucosa of various origins, since they have a milder effect compared to steroidal anti-inflammatory drugs, are non-toxic, and even with long-term use do not have harmful side effects, which allows them to be widely used in children. The anti-inflammatory effect manifests itself mainly during the exudative phase; they have a much weaker effect on the proliferative phase of inflammation.
In case of acute inflammation of the gums, astringents of plant origin containing tannins are widely used. The anti-inflammatory effect of tannins is due to the formation of insoluble compounds with proteins - albuminates - when exposed locally to the mucous membrane. The film of precipitated protein protects the nerve endings from irritation by decay products, which reduces pain.
In addition, these substances cause a narrowing of pathologically dilated vessels, thicken their walls, reduce permeability and, consequently, the exudation of fluid and swelling, i.e., they reduce the severity of the exudative phase of inflammation. The consequence of compaction of biological membranes (lysosome walls, cell membranes) is a decrease in the release of inflammatory mediators - histamine, proteases, nucleases. The weakening of inflammation may be associated with the effect of these substances on the cellular components of inflammation - immunological mechanisms, processes of cell reproduction. Sage leaf, romazulan, chamomile flowers, serpentine rhizome, galascorbine are used.
Treatment of chronic catarrhal gingivitis begins with sanitation of the oral cavity and teaching the child to brush his teeth. Remove soft and hard dental deposits.
Taking into account the child’s age, recommendations are given on the selection of a toothbrush and oral hygiene products. It is important to familiarize yourself with the child’s diet and diet and talk about the need to eat hard foods (vegetables, fruits in their natural form), which will provide sufficient functional load on the masticatory apparatus and cleanse the teeth of soft plaque. Due to these measures, inflammation is often eliminated.
If gum inflammation persists, then additional anti-inflammatory therapy is carried out using non-steroidal anti-inflammatory drugs or herbal remedies, physiotherapy, and treatment by an orthodontist if indicated.
Among the physiotherapeutic methods of treatment for chronic catarrhal gingivitis, hydrotherapy with carbon dioxide is prescribed for 10 minutes daily or every other day, for a course of treatment of 10-15 sessions; electrophoresis of a 1% solution of galascorbine or a 5% solution of ascorbic acid, a 4% solution of nicotinic acid, for which intraoral electrodes are used. The duration of electrophoresis depends on the individual's tolerance to the current. The course of treatment is 10 sessions, prescribed daily or every other day.

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 causal factors that cause the disease periodontal disease in adults.

In addition, of great importance in the pathogenesis of the development of the disease is the possibility of 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 disease 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 well 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.

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 according to the international classification of diseases ICD-10:

K05.2
K05.3

Reasons

Etiology. 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, occlusion, and others. Common disorders include diseases of the gastrointestinal tract, endocrine and nervous systems, metabolic disorders, and vitamin imbalance. Bad habits can contribute to periodontal damage.
Pathogenesis. Periodontitis always preceded by inflammation of the gingival margin (gingivitis). During the development of the pathological process, there is a violation of the epithelial attachment of the gum to the tooth, 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. It is 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 from 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. The initial stage is characterized by bleeding, swelling of the gums, pain in the gum area, bad breath and shallow periodontal pockets, mainly in the interdental 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, degrees of the disease are distinguished: I, II, III. Tooth mobility 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 retrograde pulpitis occurs. 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. At the same time, changes in the general condition of the body occur—a rise in body temperature, weakness, and 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, radiography (panoramic or orthopantomography) is of great importance. 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.
. Of particular importance are surgical methods (curettage, gingivitomy, flap operations, etc.) performed on the gums and bone tissue, which are aimed at removing granulations, eliminating periodontal pockets, restoring defects in the bone tissue of the alveolar process, etc. Surgical intervention is recommended to be combined with drugs, promoting 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: broad-spectrum antibiotics, desensitizing and sedatives, immunotropic drugs (imudon, xymedon). Sometimes hormonal therapy and drugs that affect mineral metabolism (thyrocalcitonin) are prescribed. General treatment is combined with specific therapy for the general disease and vitamin therapy.
Prevention. Timely treatment of gingivitis. Careful oral hygiene. It is advisable to use resort factors (balneotherapy and peloid therapy). The physical and chemical properties of mineral waters, therapeutic mud and climatotherapy have a healing effect on the oral cavity and the entire body.

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

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

ICD-10 CODE
K05.0
K05.09. Acute catarrhal gingivitis.
K05.10. Chronic catarrhal gingivitis.
Among other forms of gingivitis, catarrhal is the most common - in almost 90% of cases.

ETIOLOGY
Inflammation of the gums in catarrhal gingivitis is nonspecific and develops clinically and morphologically in the same way as in other organs and tissues.
Causal factors: microbial; mechanical, chemical, physical trauma, etc. Currently, the leading importance of microbial plaque (microbial plaque, or biofilm) in the etiology of catarrhal gingivitis is generally recognized. Under the influence of microbial plaque toxins, an initial acute inflammation, or acute catarrhal gingivitis, develops after 3-4 days. The vast majority of patients do not turn to specialists due to the short-term, mildly or asymptomatic course of the acute phase. In this regard, the clinical significance of this form is insignificant. After 3-4 weeks, the inflammation takes on a chronic nature with all clinical and morphological signs. This is chronic catarrhal gingivitis.
A microbial plaque is a structural formation on the secondary cuticle of tooth enamel (pellicle), tightly connected to it. Initially, more than 75% of it consists of aerobic microorganisms, or saprophytes: streptococci, staphylococci, actinomycetes, etc. Later, anaerobes (fusobacteria, treponemes, amoebas, trichomonas, etc.) begin to predominate.
The main reason for the formation of microbial plaque is unsatisfactory tooth brushing. Violation of their natural self-cleaning, changes in the amount of saliva secreted and its quality, mouth breathing, the predominance of carbohydrates and soft foods in the diet, gingival carious cavities - these are the local factors that increase the accumulation of microorganisms and, accordingly, their influence.
To realize the damaging potential of microbial accumulations, the state of the body’s defenses, its immune status, which is subject to change and weakening under the adverse influence of not only general diseases of the body, but also environmental factors, nutrition, and taking certain medications (immunosuppressants, cytostatics, etc.) is important. .
Thus, gingivitis develops only when the main etiological factor (microbial) finds appropriate conditions in the patient’s body.

PATHOGENESIS
The mechanism of pathological changes in the gums can be briefly presented as follows. The stage of early inflammation is characterized by the penetration into the gum tissue of a large number (up to 70% of the total number of cells) of small and medium-sized lymphocytes, as well as polymorphonuclear leukocytes, macrophages, plasma and mast cells. Therefore, the morphological feature of the early stage of inflammation is precisely dense small cell infiltrates with a predominance of lymphocytes in the preparations.
In healthy gums, T-lymphocytes numerically predominate over B-lymphocytes in all its zones.
In chronic periodontitis, numerous B lymphocytes and plasma cells are found in the gums. The more severe the disease, the higher the content of B-lymphocytes and plasma cells producing IgG, IgA, IgM.
Morphologically, the phase of established inflammation is characterized by the predominance of plasma cells in the cellular infiltrate, which reflect the immune response to damage.
At the stage of established inflammation, a picture of a mixed infiltrate is observed, consisting of polymorphonuclear leukocytes, small and medium-sized lymphocytes, and large plasma cells. This indicates that a pattern of chronic and acute inflammation is simultaneously observed in the tissues.
The main difference between the progressive inflammation phase is that plasma cells make up up to 80% of all exudate cells. This indicates the chronicity of inflammation and the active involvement of immune mechanisms of inflammation. Plasma cells are the final stage of development of B lymphocytes; they provide humoral immunity through the active production of immunoglobulins. In periodontal lesions, the number of plasma cells increases in proportion to the severity of the process and the degree of tissue destruction.

CLINICAL PICTURE, DIAGNOSTICS
Characteristic signs of catarrhal gingivitis:
- the disease is detected in children and adolescents or young people;
- the gums are hyperemic, swollen, either in the area of all teeth or several teeth;
-dental gingival junction is preserved;
- depending on the intensity of inflammation, different degrees of bleeding are noted, but a probe test for bleeding is always positive;
- there is non-mineralized dental plaque and (or) tartar;
- on the radiograph there are no signs of destruction of the interalveolar septa;
-the general condition of patients is usually not disturbed, with the exception of acute and exacerbation of chronic catarrhal gingivitis. As a rule, the cause is either trauma (including due to incorrect manufacturing of otropedic structures) or chemical damage. It usually occurs in children due to a sharp increase in the pathogenic effect of a microbial plaque, subject to a significant decrease in the activity of local and general defense factors, usually due to a viral or other infection (ARVI, influenza, etc.), so it is rightly regarded as an almost natural complication of these and a number of other common diseases. The acute stage lasts from 3 to 7 days. If the child recovers, acute inflammation either goes away completely or becomes chronic. In adults, chronic catarrhal gingivitis as an independent form is rare.
Complaints with catarrhal gingivitis are very scarce. In most cases, patients do not suspect the presence of the disease for a long time, since the onset of gingivitis is usually not accompanied by significant pain and other unpleasant symptoms. The main symptom is bleeding gums, but patients usually cope with this themselves: they either stop brushing their teeth altogether, or start using a soft brush, rinsing the mouth with herbal infusions, etc. Since in most cases bleeding either spontaneously or under the influence of measures taken stops or significantly decreases, patients rarely consult a doctor on their own. Treatment is usually recommended by a dentist. Sometimes bad breath causes you to consult a specialist.
Clinical and laboratory diagnostic methods
To objectify the local status of catarrhal gingivitis, several indicators are used. The amount of microbial plaque is determined by the size of its accumulation in the cervical area - according to the Silness-Loe index (Silness J., Loe H., 1964) (Fig. 14-4) or according to the hygienic simplified Green-Vermillion index (Green J.C., Vermillion J.R., 1967). The intensity of inflammation is determined using the papillary-marginal-alveolar index (Shour J., Massler M., 1947, modified by Parma C., 1960) or the Muhlemann bleeding index (Muhlemann H.R., 1971, modified by Cowell J., 1975), ( Fig. 14-5) using the so-called probe test.

For practicing doctors, these indicators are sufficient. For scientific purposes, it is of interest to study the state of the microvasculature of the gums using vital microscopy, rheoparodontography, and laser Doppler flowmetry; oxygen tension (pO2) in the gum - by polarography; quantitative and qualitative composition of gingival fluid.
Clinical analysis in the blood does not reveal specific changes characteristic of catarrhal gingivitis. Only the study of capillary blood of the gums makes it possible to identify certain changes already in the initial stages of inflammation (increased content of polymorphonuclear leukocytes, immunoglobulins, interleukins, complement protein fractions, etc.) compared with indicators of peripheral blood. However, this is of no interest to practitioners.
Radiological changes in bone tissue in the early stages of gingivitis are absent (the compact lamina of the interdental septa is preserved). However, when the process becomes chronic or worsens, small foci of osteoporosis are identified in the apices of the interdental septa, which usually disappear after treatment or on their own in case of remission.
Catarrhal chronic gingivitis is differentiated from hypertrophic (its edematous form), mild periodontitis, manifestations of some dermatoses on the gums - LP, pemphigus, etc.
TREATMENT
Treatment of patients with chronic catarrhal gingivitis should include, first of all, elimination of the main cause of inflammation - dental plaque -
using a set of hand tools (Fig. 14-6) or ultrasonic devices (Fig. 14-7). This should always be carried out under local anesthesia, after preliminary treatment of the oral cavity with antiseptic solutions [Listerine℘, furacilin♠, chlorhexidine, asepta (rinsing), etc.]. Then it is necessary to eliminate local factors that contribute to increased accumulation of plaque; restore contact points, fill cervical cavities, mainly using light-curing composites or ceramic inlays.
It is imperative not only to teach the patient the rules of brushing teeth, but also to monitor the patient’s ability to perform them. Using dyes to indicate plaque, the patient is shown microbial accumulations before cleaning and poorly cleaned areas remaining after cleaning. Hygiene products are individually recommended: toothbrushes, floss, irrigators, interdental brushes, stimulants, as well as pastes and rinses containing medicinal additives. Monitoring of compliance with oral hygiene rules is carried out during the first week of each visit, and then once a week for a month. During the treatment process, it is advisable, after brushing the teeth, to prescribe the patient to rinse with solutions of Listerine℘, chlorhexidine, Asepta in a concentration of 0.05 to 0.3% for 1 minute 2 times a day for no more than 7-10 days.

Professional oral hygiene is complemented by thorough polishing of the tooth surface with special pastes containing abrasives, using brushes, plastic heads and a mechanical tip. After completion of treatment, to consolidate the therapeutic results, toothpastes containing antiseptics such as triclosan, chlorhexidine, enzymes or other anti-inflammatory agents are recommended (see chapter “Oral Hygiene”). In this case, chlorine-based pastes should be used for no more than 3 weeks, and then regular hygienic pastes should be recommended to patients for a month. It is very important to remember that it is undesirable to use red or burgundy pastes that mask the first sign of inflammation - bleeding gums.
If, even after professional hygienic treatment, hyperemia and swelling of the gums persist, then medications should be used to influence specific manifestations. As a rule, these are anti-inflammatory drugs that normalize vascular permeability and eliminate tissue swelling, i.e. acting on the pathogenetic mechanisms of the inflammatory reaction: prostaglandin inhibitors (3% acetylsalicylic, indomethacin, butadione ointments, etc.), that is, non-steroidal anti-inflammatory drugs that do not reduce tissue resistance to infection; antioxidants and antihypoxants - mexidol-gel♠, troxevasin, heparin ointment. In order to normalize the processes of collagen formation and tissue metabolism, along with the listed therapeutic dressings and therapeutic and prophylactic pastes and rinses, the administration of vitamin complexes is justified. It is advisable to minimize soft, sugar-rich foods and sticky foods to avoid increased accumulation of bacterial plaques. However, it should be remembered that this does not matter provided that the patient brushes his teeth thoroughly after eating.
Only after normalization of the gum condition, in order to improve and restore metabolic processes in the gums, it is possible to prescribe digital automassage of the gums, hydromassage, and recommend increasing the chewing load by eating solid food (carrots, apples, etc.). For persons predisposed to increased accumulation of plaque and tartar, rinsing is recommended. At least twice a year, patients must undergo a preventive examination, during which, if necessary, they undergo professional hygiene treatment and be sure to repeat the rules of brushing their teeth.
Timely diagnosis and adequate treatment of catarrhal gingivitis, subject to motivated oral care, usually provide a cure without residual effects and prevent the transition of the inflammatory process to another form - periodontitis.
Exacerbation of chronic catarrhal gingivitis is characterized by pronounced clinical manifestations and subjective sensations of patients. In this case, there may be complaints of pain in the gums, general malaise due to intoxication. Objectively, inflammatory phenomena in the gums are intensely expressed: the gums are hyperemic, swollen and at the same time cyanotic, bleed sharply even from an air stream, hyperemic, submandibular lymph nodes can be enlarged and painful. Possible increase in body temperature. Without therapeutic interventions, the symptoms of acute inflammation, depending on the general condition, can persist for 7-10 days and then disappear on their own.
Treatment in the acute stage is aimed at eliminating the acute inflammatory reaction and associated pain and intoxication. Antibacterial, antiseptic painkillers, anti-inflammatory (ketorolac, etc.), sometimes hyposensitizing [clemastine (tavegil♠), chloropyramine (suprastin♠), mebhydrolin (Diazolin♠), etc.] agents are prescribed. The patient is not recommended to eat spicy, irritating foods during this period.
Local anti-inflammatory interventions are of primary importance: treatment with effective antimicrobial and antiseptic drugs both before removing dental plaque and after removing it (to avoid toxicemia). Under local application anesthesia using 5% lidocaine gel, dental plaque is removed as atraumatically as possible. At the first stage, a gel is applied to the gums, which includes the most etiologically substantiated drugs: metronidazole and chlorhexidine. After this gel, you can apply a gel that contains diclofenac. To prolong the therapeutic effect, applied ointments or medicinal mixtures are covered with one of the Diplen-denta medicinal films containing antiseptics, anti-inflammatory, antimicrobial drugs, and analgesics.
The listed interventions are carried out not only to eliminate the acute inflammatory reaction, but also in the treatment of chronic catarrhal gingivitis. However, in the acute phase, traumatic manipulations are strictly prohibited, and tooth brushing should be replaced with antiseptic rinses. Only after the symptoms of acute inflammation have been eliminated can you begin to fully carry out professional hygienic treatment and the entire necessary range of treatment.