Necrotising periodontal diseases, Necrotising periodontal diseases as a manifestation of systemic diseases. By Dr. Ritam Kundu, MDS PGT, Dr. R. Ahmed Dental College & Hospital, Kolkata, India.

2. • Introduction:
• Necrotizing ulcerative gingivitis (NUG) , necrotizing ulcerative
periodontitis(NUP), necrotizing stomatitis (NS) are the most
severe inflammatory periodontal disorders caused by plaque
bacteria.
• They are rapidly destructive & debilitating & represents
various stages of same disease process (Horning & Cohen
1995).
1986 – Necrotizing ulcerative gingivoperiodontitis
1989 – NUP ( World workshop of Clinical Periodontics )
1999 – Classification of Periodontal Diseases – NUG & NUP , included under
the broader classification of Necrotizing Ulcerative Periodontal Diseases

3. A distinction
between these
diseases has
not always
been made in
the literature

4. • Ulceromembranous gingivitis
• Trench mouth (Pickard 1973)
• Vincent’s gingivostomatitis
• Phagedenic gingivitis
• Fusospirallary periodontitis
• Plaut-Vincent stomatitis

5. • Fourth century BC, Xenophon mentioned that Greek soldiers were
affected with “sore mouth” and foul-smelling breath
• In 1778, John Hunter described the clinical findings and
differentiated ANUG from scurvy and chronic destructive
periodontal disease
• ANUG occurred in epidemic form in the French army in the 19th
century

6. • In 1886, Hersch, a German pathologist, discussed
some of the features associated with the disease
such as enlarged lymph nodes, fever, malaise and
increased salivation
• In 1890s, Plaut and Vincent described the disease
and attributed its origin to fusiform bacilli and
spirochetes

7.  NUG often occurs in groups in an epidemic form.
 During world war I & II “ epidemics “ broke out among the allied
troops. Epidemic like outbreaks have also occurred among civilian
populations.
 In developing countries, the prevalence of NPD is higher than in the
industrialized countries, & the disease frequently affects the
children.
 In India, 54- 68 % of NPD cases occurred in children below 10 yrs of
age.( Migliani& Sharma 1965; Pindborg et al 1996).
 NUG occurs at all ages, with the highest incidence reported
between ages 20 & 30 yrs & ages 15 -20 yrs.

8. • The disease seems to occur slightly more among HIV infected
individuals. Studies among groups of HIV infected individuals have
revealed prevalence of NPD between 0 & 27.7%. (Holmstrup &
Westergaard1994; Reichart et al 2003).
• NP was found in 1% of 200 HIV seropositive individuals (Riley et al
1992) & the prevalence may not in fact, differ from much of the
general population ( Drinkard et al 1991 );This is particularly true
after introduction of antiretroviral therapy. HAART resulted in
decline of incidence & prevalence of oral conditions associated with
HIV
• Among HIV+ individuals, NPD is more in intravenous drug abusers
than non-intravenous drug abusers. ( Ranganathan et al, 2012)

9. Clinical features - Oral signs
• NG – an inflammatory destructive gingival condition, characterized by
ulcerated and necrotic papilla and gingival margins. Punched out crater
like depressions at the crest of the interdental papillae is a characteristic
feature.
• The surface of the craters is covered by a gray pseudomembranous
slough. The sloughed material has little coherence and is composed of
fibrin, necrotic tissue, RBC,WBC, Bacteria.
• Linear erythema demarcating marginal necrosis and the relatively
unaffected zone
• In some cases the lesions are denuded of the surface
pseudomembrane, exposing the gingival margin which is red, shiny, &
hemorrhagic. The characteristic lesion may progressively destroy the
gingiva & underlying periodontal tissues.

10. Initial punched out lesion

11. • Spontaneous gingival hemorrhage or pronounced bleeding
after the slight stimulation are characteristic clinical signs.
• A characteristic & pronounced foetor ex ore is often
associated with this disease . Although it is not always very
noticeable.
• Increased salivation.
• The palatal/lingual gingiva
Is less frequently involved
than the facial gingiva
• Frequently gingiva of
partially impacted tooth are
also affected.

12. In NUP:
Progression of the interproximal lesion often results in destruction of the
interdental alveolar bone.
Sequestrum formation: necrosis of a small or large part of the alveolar bone,
which is denoted as sequestrum. The bone fragment is initially immovable, later
on it becomes loose. Sequestrum involves interproximal as well as facial or
palatal cortical bone.
Involvement of the alveolar mucosa : NS
In severe malnutrition or immunocompromised individual as in HIV, the necrotic
process progresses beyond the mucogingival junction affecting the alveolar
mucosa.
It may result in extensive denudation of the bone – leading to major
sequestration – with the development of oroantral fistula and osteitis.

13. Oral Symptoms
• The lesion is extremely sensitive to touch, & the patient may
often complains of a constant radiating, gnawing pain that is
often intensified by eating spicy or hot foods & chewing.
• There is metallic foul taste & an excessive amount of pasty
saliva.

14. Extra oral & systemic signs & symptoms
 In mild & moderate stages of disease
Local lymphadenopathy & slight elevation in temperature.
 In severe cases
High fever, increased pulse rate, leucocytois, loss of appetite &
general lassitude.
 Systemic reactions are more severe in children.
 Insomnia, constipation, gastro-intestinal disorders, headache, &
mental depression sometimes accompany the condition.
 In very rare cases, severe squeal such as gangrenous stomatitis
& noma have been described.

15. CLINICAL COURSE OF THE DISEASE BY PINDBORG et al
Stage 1: Erosion of only
tip of interdental papilla
Stage 2: marginal gingiva affected and
complete loss of interdental papilla
Stage 3: Involving attached gingiva Stage 4: Exposure of bone

16. Stages of oral necrotizing disease – by
Horning & Cohen
• Stage 1- necrosis of the tip of the interdental papilla.
• Stage 2- necrosis of entire papilla
• Stage 3- necrosis extending to the gingival margin.
• Stage 4- necrosis extending to the attached gingiva.
• Stage 5– necrosis extending to labial & buccal mucosa.
• Stage 6- necrosis exposing alveolar bone.
• Stage 7– necrosis perforating skin of cheek.

17. ETIOLOGY
It includes,
• Role of microorganism
• Role of host response
• Predisposing factors includes
1. Local predisposing factor
2. Systemic predisposing factor

18. ROLE OF BACTERIA
• Plaut & Vincent introduced the concept that NUG is caused by
specific bacteria ; fusiform bacillus & spirochetal organism.
• Loesche et al described a predominant constant flora & a variable
flora associated with NUG. The constant flora is composed of
prevotella intermedia, treponema sp, selenomonas sp, &
fusobacterium sp. The variable flora consists of heterogeneous
array of bacterial types.
• The bacteriologic findings have been supported by immunologic
data from Chung et al. - reported increased antibody titers for
spirochetes & P.intermedia in NUG patients compared with titers
in those with chronic gingivitis & healthy controls.

19. • Borrelia, gram positive cocci, b-hemolytic streptococci &
Candida albicans have been isolated from the lesions of HIV
associated NUP.(Reichart & Schiodt 1989).
• It has also been proposed that human cytomegalovirus may
play a role in the pathogenesis of NPD. (Sabiston 1986).

20. Pathogenic potential of microorganism
• An important aspects in the pathogenesis is the capacity of the
microorganism to invade the host tissues.
• Among the bacteria isolated from necrotizing lesions, spirochetes &
fusobacterium can in fact invade the epithelium. (Heylings 1967).
• The spirochetes can also invade the vital connective tissue
(Lisgarten 1965).
• The pathogenic potential is further substantiated by the fact that
both fusobacterium & spirochetes can liberate endotoxins
(Kristoffersen et al).

21. • Gram negative bacteria liberate endotoxins in close contact with
connective tissue. Endotoxins may produce tissue destruction
both by direct toxic effects & indirectly by activating & modifying
tissue responses of the host.(Wilton & Lehner 1980)
• Indirectly endotoxins contribute to tissue damage in several
ways;
– They can function as antigens & elicit immune reactions.
– They can activate compliment directly through the alternative
pathway & thereby liberate chemotoxins.

22. • Fusobacterium & Spirochetes are found in moderate numbers of
other oral diseases, as well as in apparently healthy mouths
suggests that predisposing factors are essential to the development
of NUG.
• The disease has never been produced experimentally in either
human beings or animals simply by oral inoculation of materials
from lesion in patients with disease. (Schwartz & Grossman).
• King also attempted to produce disease in his own mouth by
inoculation of infected material but he was unsuccessful even after
traumatizing gingiva & the organism promptly disappeared.
• But he did show characteristic signs of ANUG however after he
became ill with several colds, a short time later.

23. ROLE OF HOST RESPONSE
• Regardless of whether specific bacteria are implicated in the
etiology of NUG, the presence of these organism is insufficient
to cause the disease.
• The role of an impaired host response in NUG has long been
recognized.
• It is particularly evident for HIV-infected patients that the
disease is associated with diminished host resistance; among
other predisposing factors, the basic mechanism may include
altered host immunity.
• Changes in leukocyte function & the immune system have been
observed.(Johnson & Engle et al)

24. • NUG is not found in well nourished individuals with a fully
functional immune system. All the predisposing factor for NUG
is associated with immunosuppresion.
• Cohen et al described a depression in host defense mechanism
particularly in PMN.
• Total leukocyte count have been found to be similar for
patients & controls. Patients with NG shows marked depression
in polymorphonuclear leukocyte chemotaxis & phagocytosis as
compared with control individuals.
• Reduced proliferation of peripheral blood lymphocytes has also
been found in those patients.
• It was also suggested that elevated levels of blood steroids
may account for the reduced chemotactic & phagocytic
responses.

25. LOCAL PREDISPOSING FACTORS
• It includes poor oral hygiene, preexisting gingivitis , injury to
gingiva, & smoking
• It may also occur in disease free mouth, it most often occurs
superimposed on preexisting chronic gingival disease &
periodontal pockets.
• Areas of gingiva traumatized by opposing teeth in malocclusion –
may predispose to NUG.
• Pindborg et al – 98% of his patients with NUG were smokers &
that the frequency of disease increases with an increase exposure
to smoke.

26. Systemic predisposing factors
• It includes
– nutritional deficiency (malnutrition),
– debilitating diseases,
– fatigue caused by chronic sleep deficiency,
– psychological stress,
– immunodeficiency,
– other health habits like alcohol & drug abuse.

27. MALNUTRITION
• Malnutrition results in lowered tissue resistance - most common
public health problem affecting children who are most often
affected by NPD. (Enwonwu 1985, 1994).
• Malnutrition is characterized by marked tissue depletion of the
key antioxidant nutrients, & impaired acute phase reactions to
the infections. This is due to impairment in the production &
cellular action of cytokines.
• Malnutrition – defective mucosal integrity, hormonal imbalance.
• Malnutrition usually involves concomitant deficiencies of several
essential macro & micronutrients, & therefore has the potential
to adversely influence the prognosis of periodontal infections.
(Enwonwu 1994).

28. Debilitating disease
• Debilitating systemic disease may predispose the patient to the
development of NUG.
• It includes chronic disease ( eg. Syphilis, cancer), severe
gastrointestinal disorders such as ulcerative colitis, blood
dyscracias (anemia , leukemia) & acquired immunodeficiency
syndrome.
• Nutritional deficiency resulting from debilitating disease may be
an additional pre disposing factor.
• Ulceronecrotic lesions appear in the gingival margins of hamsters
exposed to total body irradiation.(Mayo J et al)

29. PSYCHOSOMATIC FACTORS
 Psychological factors appear to be important in the etiology of
NUG.
 The disease often occur with association with stressful situation
(Induction in to armed forces, examination periods, emotional disorders, patients
feeling inadequate at handling life situations).
 Cohen – Cole et al – psychiatric disturbance and the impact of
negative life events may lead to activation of hypothalamic-
pituitary adrenal axis resulting in elevation of cortisol levels.
 Reduced gingival microcirculation & salivary flow - depressed
neutrophil & lymphocyte functions which facilitate bacterial
invasion & damage.(Johnson et al)

30. • The mechanisms whereby psychological factors create or
predispose to gingival damage have not been established, but
alterations in digital & gingival capillary response suggestive
of increased autonomic nervous activity have been
demonstrated in patients with ANUG.

31. Smoking
• The relationship between tobacco usage & NPD appears to be
complex.
• Smokers in general poorer oral hygiene than the non smokers.
• Smoking could lead to increased disease activity by influencing
host response & tissue reactions. As examples, smokers have
depressed numbers of T- helper lymphocytes, & tobacco smoke
can also impair chemotaxis and phagocytosis of oral & peripheral
phagocytes.( Lannan et al 1992, Selby et al 1992)
• Nicotine- induced secretion of epinephrine resulting in gingival
vasoconstriction – possible mechanism by which smoking may
influence tissue susceptibility.( Bergstrom & Preber 1986)

32. HIV infection
• HIV infection attacks the T- helper cells of the body, causing
drastic change in the T-helper (CD4+)/T-suppressor(CD8+) ratio
with severe impairment of the host resistance to infection.
• Depleted T- helper lymphocyte counts correlate closely with the
occurrence of NG as demonstrated in the study of 390 US HIV
seropositive soldiers (Thompson et al 1992).
• In HIV-positive patients, NPD are more frequent and show
faster progression, although no differences have been detected
between the characteristics of the disease in HIV-negative and
HIV-positive patients. It has been suggested that HIV-positive
patients have a higher tendency for recurrence and a
diminished response to both mechanical and/or
pharmacological periodontal treatment Novak Mj (1999)

33. HISTOPATOLOGICAL FEATURE
 Histopathologically, NG lesions is characterized by ulceration with
necrosis of epithelium & superficial layers of the connective tissue
& an non specific inflammatory reaction.
 The surface epithelium is destroyed & replaced by a meshwork of
fibrin, necrotic epithelium, PMNs & various types of
microorganism. This appears clinically as the surface
pseudomembrane.
 Below this necrotic pseudomembrane, the epithelium is
edematous, & the individual cells exhibit varying degrees of
hydropic degeneration.

34. • The underlying connective
tissue is extremely hyperemic
with numerous engorged
capillaries & dense infiltration
of PMNs. This acutely inflamed
zone appears clinically as the
linear erythema.
• Numerous plasma cells may
appear in the periphery of the
infiltrate. This is interpreted as
an area of established chronic
gingivitis on which acute lesion
is superimposed.

35. RELATION OF BACTERIA TO THE CHARACTERISTIC
LESION
• The light microscope & the electron microscope have been
used to study the relationship of bacteria to the characteristic
lesion of NUG.
LISGARTEN(1965) described the following four zones which blend
with each other & may not all be present in every case;
• Zone1 – bacterial zone
• Zone 2 – neutrophil rich zone
• Zone 3 – necrotic zone
• Zone 4 – zone of spirochetal infiltration

36. Electron micrograph demonstrating phagocytosing (N)neutrophil close to the
surface of a sequestrum, numerous spirochetes and rods.

37. DIAGNOSIS
• The diagnosis of NG, NP, NS is based on clinical findings as
described above.
• The histopathology of the necrotizing disease is not
pathognomonic of NG & biopsy is not certainly indicated.
• Bacterial studies are useful in the differential diagnosis of NUG
& specific infections of oral cavity.

38. Diagnostic essentials for NUG
• Lesions are painful.
• Lesions are gingival ulcers, punched out crater like of
interdental papilla & may involve marginal gingiva.
• Non essential clinical features of NUG the
absence which does not preclude the
diagnosis of NUG
• Pseudomembrane of sloughed necrotic debris & bacteria
covering the ulcerated area.
• Foetor ex ore.
• Fever, malaise & lymphadenopathy

39. Differential diagnosis
• Herpetic gingivostomatitis
• Desquamative gingivitis
• Streptococcal gingivostomatitis
• Apthous stomatitis
• Candidiasis
• Agranulocytosis
• Gonococcal gingivostomatitis
• Tuberculous gingival lesion

40. Important characteristics for differential
diagnosis between NPD & PHG
NPD PHG
Etiology Bacteria Herpes simplex virus
Age 15-30 Frequently children
Site Interdental papilla. Rarely outside
the gingiva
Gingiva and entire oral mucosa
Symptoms •Ulcerations and necrotic tissue
and a yellowish –white plaque
•Fetor ex ore
•Moderate Fever may occur
•Multiple vesicles which disrupt,
leaving small round fibrin covered
ulcerations
•Fetor ex ore
•Fever
Duration 1-2 days if treated 1-2weeks
Contagious - +
Immunity - Partial
Healing Destruction of periodontal tissue
remains
No permanent destruction

41. TREATMENT
• The treatment of necrotizing periodontal disease is divided into
two phases,
1)acute phase treatment
2)maintenance phase treatment
ACUTE PHASE TREATMENT
• The aim is to eliminate the disease activity as manifest by
ongoing tissue necrosis developing laterally & apically.
• It is also to avoid pain & general discomfort which may severely
compromise food intake.

42. FIRST VISIT
• General examination of the patient
• The oral cavity is examined for the characteristic feature of NUG, its
distribution & possible involvement of oropharyngeal region.
• Oral hygiene is evaluated with special attention to the presence of
pericoronal flaps, periodontal pockets & local factors.
• History taking – H/o present illness, diet, socio-economic
background, diet, smoking, chances of HIV infection, stress,
profession.
Treatment during initial visits includes,
• It is mainly confined to the acutely involved areas
• After application of topical anesthetics, the pseudomembrane &
non attached surface debris is removed using a moistened cotton
pellet.

43. • After the area is cleansed with warm water
supragingival calculus is removed using ultrasonic
scalers.
• Subgingival scaling & curettage is contraindicated at
this time.
• Procedures such as extractions or periodontal surgery
are postponed until the patient has been symptom free
for 4 weeks, to minimize the likelihood of exacerbating
the acute symptoms.
• Patients with moderate or severe NUG & local
lymphadenopathy or systemic signs or symptoms are
placed on an antibiotic regimen.

44. • First Choice : Metronidazole(250 mg) * TID (Loesche et
al 1982)
• Other antibiotics such as Amoxycillin(500mg) in every 6
hours for 10 days or erythromycin (500mg every 6 hrs)
are used.
• The adjunctive use of metronidazole in HIV associated
NPD is reported to be extremely effective in reducing
acute pain & promoting rapid healing.(Scully et al).
• Topical application of antibiotics is not indicated in the
treatment of NPD because intralesional bacteria are
frequent &topical application does not results in
sufficient intralesional concentration of antibiotics.

45. • Hydrogen peroxide & other oxygen releasing agents
also have a long standing tradition in the treatment
of NPD.
• Hydrogen peroxide (3%) is used for debridement in
necrotic areas & as a mouth rinse (equal portions 3%
H2O2 & warm water).
• Favorable effects of hydrogen peroxide may be due
to mechanical cleaning,& the influence on anaerobic
bacterial flora of the liberated oxygen. (Macphee &
Cowley 1981).
• Further adjunctive local Oxygen therapy of NPD
showed a more rapid clinical restitution with less
periodontal destruction than in a group without
oxygen therapy. (Gaggl et al 2006)

46.  Twice daily rinsing with a 0.2% chlorhexidine solution is a very effective
adjunct to reduce plaque formation, when particularly tooth brushing is not
performed. It also assists self performed oral hygiene during the first weeks of
treatment.
 Appropriate treatment alleviates symptoms with in few days.(5 days)
 Physical rest advised.
 Brushing instructions
Second visit
 Systematic subgingival scaling should be continued with increasing intensity as
the symptoms subside.
 Correction of restoration margins
 Polishing of restorations & root surfaces should be completed after healing of
ulcers.
 When ulcerated areas are healed local treatment is supplemented with oral
hygiene & patient motivation.

47. • Third Visit:
• Approximately 5 days after 2nd visit
• Patient counseling : Nutrition, Smoking cessation
• H2O2 rinse discontinued
• CHX maintained for 2-3 weeks
• Maintenance Therapy
Suspected seropositive NPD patients, who are unaware of
their serostatus , should be referred to the physicians.

48. Supportive systemic treatment
• In addition to systemic antibiotics, supportive treatment
consists of copious fluid consumption & administration of
analgesics for relief of pain.
• Bed rest is necessary for the patients with systemic
complication such as high fever, malaise, anorexia & general
debility.

49. Nutritional supplements
The rationale for the nutritional supplements in the treatment of
NUG is based on the following;
• 1) lesions resembling those of the ANUG have been produced
experimentally in animals with nutritional deficiencies.
• 2) isolated clinical studies report fewer recurrences when local
treatment of NUG is supplemented with vitamin B & vitamin C.
(Linghorne WJ et al)
• And hence nutritional supplements may be indicated along with
local treatment to ward off deficiencies of these vitamins.

50. MAINTENANCE PHASE TREATMENT
On further visits,
• When the acute phase treatment has been completed, necrosis
& acute symptoms in NPD have disappeared.
• The formerly necrotic areas are healed & the gingival craters are
reduced in size, although some defects usually persists.
• Bacterial plaque accumulates & therefore may predispose to
recurrences of NPD or to further destruction because of a
persisting chronic inflammatory process or both.
• These sites therefore requires surgical correction.

51. • Shallow craters can be removed by simple gingivectomy, while
the elimination of deep defects may require flap surgery.
• Treatment of NG is not completed until all gingival defects
have been eliminated & optimal conditions for future plaque
control have been established.
• Elimination of predisposing factors is also very important to
prevent recurrences.

52. Persistent or recurrent cases
• Adequate local therapy with optimal home care will resolve most
cases of NUG. If it persists despite therapy or recurs , the patient
should be revaluated with the focus on the following factors,
• Reassessment of differential diagnosis to rule out the disease that
resembles NUG.
• Underlying systemic disease that cause immunosuppresion.
• Inadequate local therapy.
• Inadequate compliance