necrotizing periodontal diseases ,its prevalance , clinical features ,diagnosis,differential diagnosis,histopathology,microbiology,host response predisposing factors and treatment

1. Dr RINKY TRIPATHI

2. INTRODUCTION
 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 (Horning & Cohen 1995).

3. Vincent first described the mixed fusospirochetal microbiota of
so‐called “Vincent’s angina”, characterized by necrotic areas in
the tonsils (Vincent 1898).

4. PREVALANCE
 NPD can be observed in all age groups It occurs most often in
young adults
 Their exist geographic differences in the age distribution.
 Among human immunodeficiency virus (HIV)‐infected
individuals, the disease seems to occur slightly more often.
 In developing countries, the prevalence of NPD is higher than
in industrialized countries, and the disease frequently occurs in
children.
 India, 54–68% of NPD cases occurred in children below 10
years of age (Migliani & Sharma 1965).

5. CLINICAL CHARACTERISTICS
 Development of lesions
NG is an inflammatory, destructive gingival condition
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”.

6.  It consists primarily of fibrin and necrotic tissue with
leukocytes, erythrocytes, and masses of bacteria.
 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.

8.  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.

9.  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. In regions where lesions first appear, ther
are usually also signs of pre‐existing chronic

10.  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.
 A characteristic and pronounced foetor ex ore is often
associated with NPD.

11. Interproximal craters
 The lesions are seldom associated with deep pocket formation,
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.

13.  Progression of the interproximal process often results in
destruction of most interdental alveolar bone

14. Sequestrum formation
 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.

15. 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.
Fever and malaise
 Fever and malaise is not a consistent characteristic of NPD.

16. Oral hygiene
 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, whitishfilm
sometimes covers parts of the attached gingiva

17. Diagnosis
The diagnosis of NG, NP, and NS is based on clinical
findings.
The patient has usually noticed pain and bleeding from
the gingiva, particularly upon touch.
The histopathology of the necrotizing diseases is not
pathognomonic for NG,and biopsy is certainly not
indicated in the heavily infected area.

18. DIFFERENTIAL DIAGNOSIS
NPD may be confused with other diseases of the oral
mucosa.
Primary herpetic gingivostomatitis (PHG) is often
frequently mistaken for NPD (Klotz 1973).
The important differential diagnostic criteria for the two
diseases are:

20. Primary herpetic gingivostomatitis
The ulcers affect the gingival margin but
are not primarily interdental papillae. A
circular ulcer of the gingiva of the second
premolar is highly suggestive of the
diagnosis.

21.  Oral mucosal diseases that have been confused with NPD
include desquamative gingivitis, benign mucous membrane
pemphigoid, erythema multiforme exudativum, streptococcal
gingivitis, and gonococcal gingivitis. All of these are clinically
quite distinct from NPD.

22. HISTOPATHOLOGY
 Histopathologically, NG lesions are characterized by ulceration
with necrosis of the epithelium and superficial layers of the
connective tissue and an acute, non‐specific inflammatory
reaction.
 The histologic findings demonstrate the formation of regular
layers with certain characteristics (Listgarten 1965)
 At the ultrastructural level, bacteria of varying sizes and forms,
including small, medium‐sized and large spirochetes, have
been revealed between the inflammatory cells, the majority of
which are neutrophilic granulocytes.

23. Electron micrograph showing
a phagocytosing neutrophil close to
the surface of a sequestrum , covered
by numerous microorganisms including
spirochetes and rods (R).

24. Microbiology
Microorganisms isolated from necrotizing lesions
•Microbial samples from NPD lesions have demonstrated that
there is a constant and a variable part of the flora.
•The “constant flora” primarily contained Treponema spp.,
Selenomonas spp., Fusobacterium spp.,andPrevotella intermedia,
and the “variable flora” consisted of a heterogeneous array of
bacterial types
(Loesche et al. 1982; Ramos et al. 2012).

25. Pathogenic potential of microorganisms
•The capacity of the microorganisms to invade the host tissues.
•The bacteria isolated from necrotizing lesions, spirochetes and
fusiform bacteria can invade the epithelium.
•The spirochetes can also invade the vital connective tissue
(listgarten 1965).
•The pathogenic potential is further substantiated by the fact
that both fusobacteria and spirochetes can liberate endotoxins
(mergenhagen Et al. 1961; kristoffersen & hofstad 1970).

26. Endotoxins
Direct effect
Indirect
effect

27. Host response and predisposing factors
Systemic
disease
Psychological
stress and
inadequate
sleep
Smoking
and alcohol
Poor oral
hygiene
Caucasian
ethnicity
Young age
malnutrition

28. Treatment
The treatment of the NPD is divided into two phases:
.
Maintenance phase
treatmentAcute phase

29. Acute phase treatment
Aim of
acute phase
treatment
Systemic
antibiotics
chemical
plaque
control
Eliminate
disease
activity
Avoid pain and
discomfort
comporising food
intake

30. Maintenance phase treatment
surgical correction
•Simple gingivectomy
• The elimination of deep defects may require flap
surgery

31. THANK YOU