Definition:
It includes Necrotizing gingivitis (NG), necrotizing periodontitis (NP), and necrotizing stomatitis (NS). They are the most severe inflammatory periodontal disorders caused by plaque bacteria. The necrotizing diseases usually run an acute course and therefore the term acute is often included in the diagnoses. They are rapidly destructive and debilitating conditions.NG:is an inflammatory destructive gingival condition, characterized by ulcerated and necrotic papillae and gingival margins resulting in a characteristic punched-out appearance. the lesions are only involving gingival tissue with no loss of periodontal attachment.
NP:it is the disease which results in loss of attachment; the lesions are confined to the periodontal tissues including gingiva, periodontal ligament and alveolar bone. NS: it is the lesion in which there is further progression of lesion to include tissue beyond the mucogingival junction.
Progression of lesion and Clinical characteristics:
In early phases of the disease lesions are typically confined to the top of a few interdental papillae. The first lesions are often seen interproximally in the mandibular anterior region, but they may occur in any interproximal space.The ulcers are covered by a yellowish white or grayish slough, which has been termed “pseudomembrane”. It consists primarily of fibrin and necrotic tissue with leukocytes, erythrocytes, and masses of bacteria.
Removal of the sloughed material results in bleeding and ulcerated underlying tissue becomes exposed.
The necrotizing lesions develop rapidly and are painful, but in the initial stages, when the necrotic areas are relatively few and small, pain is usually moderate. Severe pain is often the chief reason for patients to seek treatment.
Bleeding is readily provoked.This is due to the acute inflammation and necrosis with exposure of the underlying connective tissue. Bleeding may start spontaneously as well as in response to even gentle touch.
In regions where lesions first appear, there are usually also signs of pre-existing chronic gingivitis. Usually the papillae swell rapidly and develop a rounded contour; this is particularly evident in the facial aspect.
The zone between the marginal necrosis and the relatively unaffected gingiva usually exhibits a well demarcated narrow erythematous zone, sometimes referred to as the linear erythema. This is an expression of hyperemia due to dilation of the vessels in the gingival connective tissue in the periphery of the necrotic lesions.
The lesions are seldom associated with deep pocket formation, because extensive gingival necrosis often coincides with loss of crestal alveolar bone.
The gingival necrosis develops rapidly and within a few days the involved papillae are often separated into one facial and one lingual portion with an interposed necrotic depression, a negative papilla, between them.
The central necrosis produces considerable tissue destruction and a regular crater is formed. At this stage of the disease, the disease process usually involves the periodontal ligament and the alveolar bone and loss of attachment is now established.
Along with the papilla destruction, the necrosis usually extends laterally along the gingival margin at the oral and/or facial surfaces of the teeth and merges to form a continuous necrotic area.
The attached gingiva becomes reduced in width as the result of disease progression.
The palatal and lingual marginal gingiva is less frequently involved than the corresponding facial area.
Frequently, gingiva of semi-impacted teeth and in the posterior maxillary region is affected.
Progression of the interproximal process often results in destruction of most interdental alveolar bone.
In more advanced cases, pain is often considerable and may be associated with a markedly increased salivary flow. As a result of pain it is often difficult for the patients to eat and a reduced food intake may be criticalto HIV-infected patients because they may already lose weight in association with their HIV infection.
The disease progression may be rapid and result in necrosis of small or large parts of the alveolar bone. Such a development is particularly evident in severely immune compromised patients including HIV seropositive individuals. The necrotic bone, denoted a sequestrum, is initially irremovable but after some time becomes loosened, where after it may be removed with forceps. A sequestrum may involve interproximal bone or adjacent facial and oral cortical bone.
NS may result in extensive denudation of bone, resulting in major sequestration with the development of oro-antral fistula and osteitis.
Swelling of the regional lymph nodes may occur in NPD but is particularly evident in advanced cases. Such symptoms are usually confined to the submandibular lymph nodes.
Fever and malaise is not a consistent characteristic of NPD.
The oral hygiene in patients with NPD is usually poor. Moreover, brushing of teeth and contact with the acutely inflamed gingiva is painful. Therefore, large amounts of plaque on the teeth are common, especially along the gingival margin.
A thin, whitish film sometimes covers parts of the attached gingiva. This film is a characteristic finding in patients who have neither eaten nor performed oral hygiene for days. It is composed of desquamated epithelial cells and bacteria in a meshwork of salivary proteins. The film is easily removed.
The lesions in HIV-seropositive patients may not be associated with large amounts of plaque and calculus. Thus, the disease activity in these patients sometimes shows limited correlation with etiologic factors as determined by the amount of bacterial plaque. Further, lesions of NPD in HIV-seropositive patients have sometimes been revealed in gingival tissue affected by Kaposi’s sarcoma.
Diagnosis:
Clinical findings.Histopathological examination is not pathognomonic for NG, and biopsy is certainly not indicated in the heavily infected area.
Differential diagnosis:
HistopathologyHistopathologically, NG lesions are characterized by ulceration with necrosis of epithelium and superficial layers of the connective tissue and an acute, nonspecific inflammatory reaction.
Microbiology
Microbial samples from NPD lesions have demonstrated a constant and a variable part of the flora. The “constant flora” primarily contained Treponema sp., Selenomonas sp., Fusobacterium sp., and B. melaninogenicusssintermedius (Prevotella intermedia), and the “variable flora” consisted of a heterogeneous array of bacterial types. Although the characteristic bacterial floras of spirochetes and fusobacteria have been isolated in large numbers from the necrotic lesions in several studies, their presence is not evidence of a primary etiologic importance. Their presence could equally well result from secondary overgrowth.Predisposing factors:
Presence of Systemic diseases.
HIV infection.
Malnutrition.
Poor oral hygiene, pre-existing gingivitis and history of previous NPD.
Psychologic stress and inadequate sleep.
Smoking and alcohol use.
Young age.
Caucasian background.
Treatment:
Acute phase treatment: The aims of the acute phase treatment are;
Elimination of disease activity as manifest by ongoing tissue necrosis developing laterally and apically.
Avoiding the pain and general discomfort which may severely compromise patient food intake.
The treatment will include:
Scaling should be attempted, as thoroughly as the condition allows. Ultrasonic scaling may be preferable to the use of hand instruments. With minimal pressure against the soft tissues.
Patients should be instructed in substituting tooth brushing with chemical plaque control in such areas until healing is accomplished.
Hydrogen peroxide (3%) is used for debridement in necrotic areas and as a mouth rinse (equal portions 3% H2O2 and warm water). It has been thought that the apparently favorable effects of hydrogen peroxide may be due to mechanical cleaning, and the influence on anaerobic bacterial flora through the liberation of oxygen.
Twice daily rinsing with a 0.2% chlorhexidine solution is a very effective adjunct to reduce plaque formation.
Supplementary treatment with metronidazole 250 mg three times daily has been found effective against spirochetes and is the first choice in the treatment of NPD. Antibiotics such as penicillins and tetracyclines are also effective. Topical application of antibiotics is not indicated in the treatment of NPD, because intralesional bacteria are frequent, and topical application does not result in sufficient intralesional concentration of antibiotics.