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

17.  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.

19. 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

20. 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

22.  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.

23.  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

24.  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.

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

26. Differential diagnosis

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

28.  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.

29. 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

30. Treatment

31. 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.

32.  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.

33.  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

34.  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.

35.  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.

36.  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.

37.  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.

38.  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.

39.  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.

40.  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.

41.  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.

42. Thanks for attention