Acute gingivitis is an inflammation of the gums that occurs with a pronounced clinic without violating the integrity of the dental joint. With catarrhal gingivitis, the gum becomes edematous, hyperemic. There is a burning sensation, bleeding. Ulcerative gingivitis is characterized by the development of ulceration sites, the gingival margin acquires a pitted appearance, covered with a gray coating. Diagnostics includes anamnesis collection, clinical examination, instrumental and laboratory research methods. For the purpose of etiotropic treatment of acute gingivitis, the following measures are indicated: professional oral hygiene, the appointment of antimicrobial therapy, the elimination of local irritating factors.
ICD 10
K05.0 Acute gingivitis
Meaning
Acute gingivitis is a disease that occurs due to the involvement of gum tissues in the inflammatory process, proceeds with the preservation of the integrity of the dental epithelial attachment. Female and male representatives are equally susceptible to the development of the disease. Pathology is diagnosed much less often than chronic. Most often, desquamative gingivitis is detected in girls during puberty. Ulcerative gingivitis is more common in men under the age of 30. In addition to primary form caused by the association of conditionally pathogenic microorganisms of the oral cavity, symptomatic gingivitis is also diagnosed in dentistry, signaling blood diseases, pathology of the endocrine system, dysfunction of the gastrointestinal tract.
Causes
The leading role in the occurrence belongs to the infectious factor. Abundant periodontopathogenic microflora, located in the dental plaque, has a pronounced damaging effect on periodontal tissue. Multiple carious cavities, dental deformities, malocclusion – all these local factors create favorable conditions for the accumulation of plaque and the development of the inflammatory process. However, the bacterial model of etiopathogenesis of acute gingivitis must be considered in combination with individual reactions of the body.
The microbial factor can be realized only in conditions of inadequate immune protection. Common predisposing conditions that reduce the reactivity of the body and contribute to the development of acute gingivitis include infectious diseases, diseases of the endocrine system, bad habits, stressful situations. Most often, with this disease, an increased content of actinomycetes is detected in plaque. A direct correlation between the severity of the clinic and the quantitative content of Actinomyces viscosus has been proved.
The leukotoxin produced by pathogens causes neutrophil lysis, as a result of which blood cells lose their protective properties. Endotoxins, penetrating through the intact epithelium of the gum, activate the complement system, stimulate the production of biologically active substances, under the influence of which signs of disease develop: edema, hyperemia, bleeding. Due to the exit of shaped elements outside the vascular wall, microcirculation disorder is aggravated. Disorders of blood flow, increased vascular permeability are the leading link in the inflammatory response.
The pathogenetic mechanism of the development of the ulcerative form is based on an immunocomplex reaction of type 3, as a result of which superficial vasculitis occurs, the blood flow rate decreases, which contributes to the triggering of thrombosis reactions. This eventually leads to the development of ischemia and necrosis. The desquamative form occurs as a result of changes in the hormonal background during puberty.
Classification
According to the nature of the course , acute gingivitis is divided into the following forms:
- Light. The lesion is localized in the area of the interdental papillae.
- Midle. The pathological process involves not only the interproximal papillae, but also the marginal edge.
- Heavy. Pathological changes are detected throughout the gingival mucosa, including in its alveolar part.
According to the prevalence of the inflammatory process, acute gingivitis can be localized (covers the mucosa in the area of 4 teeth) and generalized. Catarrhal, desquamative and ulcerative forms of acute gingivitis are most often diagnosed.
Symptoms
In acute catarrhal gingivitis, patients complain of pain, burning, swelling of the gums, bad breath. During the examination, a brightly hyperemic gum is detected. The relief of the gingival margin changes, the papillae acquire a domed shape. Bleeding can be provoked not only by brushing teeth, but also by eating hard food. During the examination of the oral cavity in patients with acute gingivitis, it is possible to establish a causal relationship between the occurrence of the inflammatory process and local irritating factors: the presence of hard and soft deposits, caries, anomalies of attachment of the frenules, malocclusion pathologies.
Desquamative gingivitis is a form of catarrhal inflammatory process. It is manifested by pronounced hyperemia of the gums, swelling, burning, bleeding. Areas of epithelial peeling are detected on the gum. With the ulcerative form of acute gingivitis, body temperature rises, well-being worsens, and performance decreases. Patients complain of mucosal soreness. Unpleasant sensations are intensified even with a slight touch of the tongue to the affected area. In acute ulcerative gingivitis, ulceration zones are detected in the oral cavity, covered with gray-green layers on top. The pathological process may involve the interproximal papillae, the marginal edge, as well as the alveolar part of the gum.
Diagnostics
The diagnosis of “acute gingivitis” is based on the collected anamnesis, physical examination data, and the results of additional research methods. During the examination for catarrhal gingivitis, the dentist reveals a hyperemic, edematous gum. Papillae are tense, bleed with a light touch. The integrity of the dental epithelial attachment in acute gingivitis is preserved, there are no periodontal pockets. With the desquamative form of acute gingivitis, along with swelling and bleeding in the gum area, areas of peeling of the surface epithelium are diagnosed.
Ulcerative gingivitis is characterized by the formation of ulceration. There is a pitted gingival margin, the interproximal gaps gape. Regional lymph nodes in patients with ulcerative form of acute gingivitis are enlarged. The Schiller-Pisarev test for acute gingivitis is positive. After applying iodine-containing preparations, the color of the mucosa changes from light yellow to dark brown. The intensity of staining correlates with the severity of inflammation. The PMA index for acute gingivitis is positive. When the interdental papillae are affected, PMA is 25%, when the marginal part of the gum is involved in the pathological process, PMA is 50%. If the PMA index is greater than 50%, this indicates the presence of inflammatory changes in the area of the alveolar gum.
During the assessment of the level of hygiene in acute gingivitis, high figures of Green-Vermillion indicators are revealed, which indicates an unsatisfactory hygiene index. There are no pathological changes in the bone tissue of the alveolar process on the sighting X-ray and orthopantomogram. With the ulcerative form of acute gingivitis, using bacterioscopic examination, it is possible to detect an increased content of fusobacteria and spirochetes in the surface layer of the mucosa along with the resident microflora of the oral cavity. Deeper tissues contain an exceptionally pure culture of fusispirillary symbiosis. During bacterioscopy in patients with catarrhal form of acute gingivitis, an increased number of actinomycetes is detected.
It is necessary to differentiate acute gingivitis of infectious origin not only with periodontitis, but also with a secondary inflammatory process that develops in blood diseases, pathologies of the endocrine system, disorders of the functioning of the gastrointestinal tract. To exclude symptomatic acute gingivitis, consultations of narrow specialists are indicated: a hematologist, an endocrinologist, a gastroenterologist.
Treatment
Acute gingivitis requires complex treatment. During the first visit, professional oral hygiene is performed. Manual curettes and ultrasonic scalers are used to remove hard and soft dental deposits. Cleaning procedures are carried out under constant irrigation of the mucosa with antiseptic solutions. At the final stage, polishing of teeth is shown to prevent subsequent retention of plaque. Etiotropic therapy of acute gingivitis includes the use of chlorine-containing agents, derivatives of nitrofurans, oxidants. Preparations with antibacterial action are prescribed in the form of rinses, irrigation.
In acute gingivitis, herbal remedies are also widely used, which have a pronounced antiseptic and anti-inflammatory effect. In the absence of positive dynamics, the use of drugs from the group of nonsteroidal anti-inflammatory drugs is indicated. After the relief of inflammation in acute gingivitis, the oral cavity is sanitized, local irritating factors are eliminated. Therapy of desquamative gingivitis is carried out in a similar way to the algorithm of treatment of catarrhal inflammatory process. Keratoplasty is used to accelerate tissue regeneration in the desquamative form of acute gingivitis.
Treatment of ulcerative gingivitis includes measures aimed at analgesia of the affected tissues, antiseptic treatment of the oral cavity. Necrolytic preparations based on proteolytic enzymes are used to eliminate necrotic layers. A good effect can be achieved by combining antibiotics with corticosteroids, proteolytic enzymes. In order to accelerate the recovery processes in acute gingivitis, agents are prescribed to stimulate epithelialization. In case of violation of the general condition, antibiotics, anti-inflammatory, antiprotozoal drugs are used for oral administration.
With timely detection and complex treatment of acute gingivitis in 95% of cases, it is possible to stop the inflammatory process and prevent the development of complications. Only in 5% of cases there is a progression of acute gingivitis with the appearance of destructive changes, the appearance of signs of periodontitis.
Literature
- Chronic Gingivitis: The Prevalence of Periodontopathogens and Therapy Efficiency / M. Igic, L. Kesic, V. Lekovic, M. Apostolovic, D. Mihailovic, L. Kostadinovic, J. Milasin // Eur J Clin Microbiol Infect Dis. — 2012; 31(8): 1911-1915.link
- Brook I. Microbiology and management of periodontal infection // Gen. dent.- 2003; 51(5):424-428.
- Nair S., Faizuddin M., Dharmapalan J. Role of autoimmune responses in periodontal disease //Autoim. Dis.-2014;2014:596824.
- Sharma C.G., Pradeep A.R. Anti-neutrophilcytoplasmic autoantibodies: a renewed paradigm in periodontal diseasepathpgenesis? // J.Periodontol.- 2006; 77(8): 1304-13.
- Socransky S.S., Haffajee A.D. The bacterial etiology of destructive periodontal disease: current concepts // J. Periodontal. – 1992. – 63.- Suppl.4. – P. 322-331.
