Necrotizing periodontal disease

Lindhe 2015

1. Necrotizing Periodontal Disease

2. Nomenculture Necrotizing gingivitis (NG), necrotizing periodontitis (NP ), and necrotizing stomatitis (NS) are the most severe inflammatory periodontal disorders caused by plaque bacteria . They are rapidly destructive and debilitating, and they appear to represent various stages of the same disease process . “ ulceromembranous gingivitis ”, “acute necrotizing ulcerative gingivitis ” (ANUG), “Vincent’s gingivitis” or “Vincent’s gingivostomatitis”, “necrotizing gingivostomatitis ”, and “trench mouth”

3. Vincent first described the mixed fusospirochetal microbiota of so‐called “Vincent’s angina”, characterized by necrotic areas in the tonsils (Vincent 1898). A similar mixed microbiota has been isolated from NG lesions , but Vincent’s angina and NG usually occur independently of each other, and should be regarded as separate disease entities .

4. NS has features in common with the far more serious cancrum oris , also denoted noma . This is a destructive and necrotizing , frequently mortal , stomatitis in which the same mixed fusospirochetal flora dominates. It occurs almost exclusively in certain developing countries, mostly in children suffering from systemic diseases including malnutrition. It has been suggested that cancrum oris always develops from pre‐existing NG and this connection has been supported by similarities between the microflora of NG and that of noma .

5. Prevalence After World War II, the prevalence of NPD declined substantially and in industrialized countries NPD is now rare (<0.05%) It occurs most often in young adults . In developing countries, the prevalence of NPD is higher than in industrialized countries, and the disease frequently occurs in children .

6. NP was found in 1% of 200 HIV‐seropositive individuals in Washington, DC, a prevalence that may not be so different from that in the general population . A prevalence similar to that in the general population has been particularly true since the introduction of highly active antiretroviral therapy ( HAART ), which has resulted in a declining incidence and prevalence of oral conditions associated with HIV infection

7. NPD was more prevalent among HIV‐infected intravenous drug users than among HIV‐infected non‐intravenous drug users. Also, mean probing depth and clinical attachment level were significantly higher in the former group.

8. Clinical characteristics NG is characterized by ulcerated and necrotic papillae and gingival margins , giving a punched‐out appearance . The ulcers are covered by a yellowish–white or grayish slough , which has been termed a “ pseudomembrane ”. However, the sloughed material has no coherence , and bears little resemblance to a membrane. It consists primarily of fibrin and necrotic tissue with leukocytes, erythrocytes, and masses of bacteria . Consequently , the term is misleading and should not be used.

9. 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 seeking treatment. Bleeding is readily provoked on removal of the sloughed material and exposure of the ulcerated underlying connective tissue. Bleeding may also start spontaneously as well as in response to even gentle touch .

10. 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 .

11. In regions where lesions first appear, there are usually also signs of pre‐existing chronic gingivitis , but the papillae are not always edematous at this stage and gingival stippling may be maintained . Usually , however, the papillae rapidly swell and achieve a rounded contour , and 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

12. A characteristic and pronounced foetor ex ore is often associated with NPD, but can vary in intensity and in some cases is not very noticeable. Strong foetor ex ore is not pathognomonic of NPD as it can also be found in other pathologic conditions of the oral cavity such as chronic destructive periodontal disease.

13. 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. The diagnosis of the disease process is consequently NP.

14. Along with the papilla destruction, the necrosis usually extends laterally along the gingival margin . Necrotic areas originating from neighboring interproximal spaces frequently merge to form a continuous necrotic area.

15. Superficial necrotic lesions only rarely cover a substantial part of the attached gingiva , which becomes reduced in width as the result of the 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 are affected

16. Progression of the interproximal process often results in destruction of most interdental alveolar bone In the more advanced cases, pain is often considerable and may be associated with a markedly increased salivary flow . 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 immunocompromised patients , including HIV‐seropositive individuals.

17. NS When the necrotic process progresses beyond the mucogingival junction, the condition is denoted NS. The severe tissue destruction characteristic of this disease is related to the seriously compromised immune functions typically associated with HIV infection or malnutrition Importantly , it may be life threatening. NS may result in extensive denudation of bone, resulting in major sequestration with the development of an oroantral fistula and osteitis

18. Swelling of lymph nodes 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, but the cervical lymph nodes may also be involved. In children with NPD , swelling of lymph nodes and increased bleeding tendency are often the most pronounced clinical findings

19. 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 It is composed of desquamated epithelial cells and bacteria in a meshwork of salivary proteins . It is easily removed.

20. In general, the clinical characteristics of NPD in HIV‐seropositive patients do not essentially differ from those in HIV‐seronegative patients. However, 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

21. if inadequately treated or left untreated, the acute phase may gradually subside . The symptoms then become less unpleasant for the patient, but the destruction of the periodontal tissues continues, although at a slower rate , and the necrotic tissues do not heal completely. Such a condition has been termed chronic necrotizing gingivitis , or periodontitis in the case of attachment loss. Although the characteristic ulcerative , necrotic areas of the acute phase usually disappear, acute exacerbations with intervening periods of quiescence may also occur. In recurrent acute phases, subjective symptoms again become more prominent and necrotic ulcers reappear.

22. Several adjoining interdental craters may fuse, resulting in total separation of facial and oral gingivae, which form two distinct flaps.

23. Differential diagnosis

24. Oral mucosal diseases that have been confused with NPD include desquamative gingivitis, benign mucous membrane pemphigoid, erythema multiforme exudativum , streptococcal gingivitis, and gonococcal gingivitis.

25. In some forms of leukemia , especially acute leukemia, necrotizing ulcers may occur in the oral mucosa and are not infrequently seen in association with the gingival margin, apparently as an exacerbation of an existing chronic inflammatory condition. In acute leukemia the gingiva often appears bluish–red and edematous with varying degrees of ulceration and necrosis. Generally , the patient has more marked systemic symptoms than with ordinary NPD, but can for a while feel relatively healthy. The dentist should be aware of the possibility that leukemias show such oral manifestations, which require medical examination of the patient; biopsy is usually not indicated.

26. Host response and predisposing factors Systemic diseases Poor oral hygiene, pre‐existing gingivitis, history of previous necrotizing periodontal diseases Psychological stress and inadequate sleep Smoking and alcohol use Caucasian ethnicity Young age

27. Treatment

28. Acute phase treatment The aim of acute phase treatment is to eliminate disease activity as manifest by ongoing tissue necrosis laterally and apically. A further aim is to avoid pain and general discomfort which may severely compromise food intake.

29. At the first consultation, 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, ultrasonic cleaning may accomplish the removal of soft and mineralized deposits. The continuous water spray combined with adequate suction usually allows good visibility. How far it is possible to proceed with debridement at the first visit usually depends on the patient’s tolerance of pain during instrumentation . Obviously , toothbrushing in areas with open wounds does not promote wound healing. Therefore , patients should be instructed in substituting toothbrushing with chemical plaque control in such areas until healing is accomplished.

30. Hydrogen peroxide (3%) is still used for debridement in necrotic areas and as a mouth rinse (equal portions of 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 of the liberated oxygen

31. Twice‐daily rinsing with a 0.2% chlorhexidine solution is a very effective adjunct to reduce plaque formation , particularly when toothbrushing is not performed . It also assists self‐performed oral hygiene during the first weeks of treatment . For an optimal effect of this medicament , it should be used only in conjunction with and in addition to systematic scaling and root planing . The chlorhexidine solution does not penetrate subgingivally and the preparation is readily inactivated by exudates, necrotic tissues, and masses of bacteria .

32. In some cases of NPD, the patient’s response to debridement is minimal or his/her general health is affected to such an extent that the supplementary use of systemic antibiotics or chemotherapeutics is indicated . This also applies to patients with malaise, fever , and lassitude . The choice of drug aims at a direct action on bacteria which are the cause of the inflammatory process in NPD.

33. Supplementary treatment with metronidazole 250 mg t.i.d . has been found to be effective against spirochetes and appears to be the first choice in the treatment of NPD. The adjunctive use of metronidazole in HIV‐associated NPD is reported to be extremely effective in reducing acute pain and promoting rapid healing. Acute pain usually disappears after a few hours.

34. Antibiotics such as penicillins and tetracyclines are also effective. Penicillin 1 mIU t.i.d should be used as an adjunct to scaling until the ulcers are healed. Topical application of antibiotics is not indicated in the treatment of NPD, because intralesional bacteria are frequent, and topical application does not result in a sufficient intralesional concentration of antibiotics.

35. Usually, in HIV‐infected patients antibiotic prophylaxis as an adjunct to scaling does not appear to be necessary. Bacteria recovered from venipuncture 15 minutes after scaling were not detectable in samples obtained at 30 minutes. Neither does removal of sequestra always appear to require antibiotic cover. HIV‐infected patients are susceptible to candidal infections and if oral candidosis is present or occurs throughout the period of antibiotic treatment, treatment with appropriate antimycotic drugs such as miconazole may be necessary.

36. 1. Patients with NPD should be seen almost daily as long as the acute symptoms persist. Appropriate treatment alleviates symptoms within a few days. Thereafter the patient should return in approximately 5 days . 2. Systematic subgingival scaling should be continued with increasing intensity as the symptoms subside . 3. Correction of restoration margins and polishing of restorations and root surfaces should be completed after healing of the ulcers. When the ulcerated areas are healed, the local treatment is supplemented with oral hygiene instruction and patient motivation . Instruction in gentle but effective toothbrushing and approximal cleaning is mandatory.

37. The formerly necrotic areas are healed and the gingival craters are reduced in size, although some defects usually persist. In such areas, bacterial plaque readily accumulates and the craters, therefore, predispose to recurrence of NPD or to further destruction because of a persisting chronic inflammatory process , or both. These sites, therefore, may require surgical correction.

38. Shallow craters can be removed by simple gingivectomy , while the elimination of deep defects may require flap surgery. Treatment of NPD has not been completed until all gingival defects have been eliminated and optimal conditions for future plaque control have been established. Due to delayed healing in HIV‐infected patients, periodontal surgery is not recommended in these patients. Instead, intensive approximal cleaning is necessary to prevent recurrence of disease.

39. Thanks for attention