Necrotising Periodontal Diseases

Necrotising periodontal disease 

Etiology 
  • NUG //  NUP //  Necrotising stomatitis – lesion spread to the tissues beyond mucogingival junction // Cancrum oris/noma – extensive destruction of face and jaw. Seen in malnourish

NUG starts of first as a gingivitis first. Then spirochaetes and further ppt factors will lead to NUG

Primary causative factors : 

-Opportunistic bacteria (Fusospirochaetes,Fusiform, Spirochaetes : treponema pallidum,Prevotella intermedia) NUG is a gram -ve anaerobic infection 

These bacteria are present in normal gingivitis also

Precipitating factors:

-pre existing gingivitis, injury to gingiva 

-Smoker (decrease host response by decreasing T lymphocytes and impairs chemotaxis and phagocytosis of neutrophils) 

-Stress(high prevalence in developing countries)

-Immunosuppression (DM, leukemia, anaemia, AIDS, pregnancy) NUG seen in apparently young healthy adults → suspect HIV → examine mouth to look for HIV signs → counselling, HIV test

-Malnutrition

-Poor oral hygiene

-Low socioeconomic status (healthcare not easily accessible, low education, more stressful)

-Previous history of NUG 

Epidemiolo Young adults (<30)
Presentation Clinical symptoms of NUG : 

-halitosis/foetor oris, metallic taste, white pasty saliva 

-bleeding gum when i get up 

-radiating gnawing pain and extreme sensitivity to touch/ sensation of teeth being wedged apart

-fever, malaise lymphadenopathy, don’t feel like eating, insomnia, constipation, GI disease 

Clinical signs of NUG : 

-punched out interdental papilla with crater like formation and grayish white pseudomembrane slough 

-marginal gingiva will get affected by the adjacent interdental papilla (moth eaten appearance) 

-bleeding of marginal gingiva on retraction of lips /slightest stimulation

-mostly affects the anterior region 

-absence of pockets in NUG (cause requires a viable junctional epithelium to have pocket formation) 

-interproximal crater develop with loss of interdental bone and s/t bone sequestra

 -Tip of interdental papilla → marginal gingiva affected and whole of IDP loss → attached gingiva → bone

D/D  -NUG (occurs in young adults (rare in children) presence of ulcerations, located more in anterior gingiva area, spontaneous pain)

-herpetic gingivostomatitis (occurs in children , presence of pinhead vesicles, more diffuse, no whitish pseudomembrane, no punched out IDP, pain only on touching, no fetid odour)

-Desquamative gingivitis/ pemphigus (borders are irregular, nikolsky sign, immunofluorescence, presence of systemic manifestation)

-Diphtheria (seen in tonsillar area and pharyngeal area) 

NUP : involve periodontal attachment and bone loss 
Microscopic findings Can take swab of pseudomembrane area, but not from highly infected areas. 

Zone seen in electron microscope findings. These zones blend with each other. 

Zone 1 : bacterial zone (most superficial zone composed of various bacteria, including small, medium and large types of spirochaetes) 

Zone 2 : neutrophil rich zone (below the bacterial later, got dense agg of PMN leucocytes, neutrophils with bacteria including spirochetes of various types) 

Zone 3 : necrotic zone (consisting of lytic and dead tissue cells, remnants of CT fragments, collagen fibres and numerous spirochaetes)

Zone 4 : spirochaete infiltration zone:  presence of well preserved tissue infiltrated with medium and large size spirochetes w/o other microorganism 

Pathogenesis of periodontal disease : capacity of microorganism to invade the tissues 

Decrease oral immunity and defective mucosal integrity. 

Spirochaetes can invade the CT in larger extent, release endotoxin 

Direct effect :can release enzyme that directly can cause direct lysis of CT. 

Indirect effect : activates cells (lymphocytes, macrophages), releasing products and cause self destruction of host. It also activates complement system, causing damage to host tissue.

Mx  In the first visit,

  • Complete evaluation (get PMHx with illness, living status, employment, stress, nutritional status, smoking, hours of rest, occupation)
  • Look for E/O and I/O examination 
  • Apply topical anaesthetic gel for 2 minutes, use a cotton pellet to remove the pseudomembrane. Then, flush area with warm water 
  • Remove superficial plaque and calculus +- LA using ultrasonic scalers cause they got flushing action (do supragingival scaling) 
  • Rinse every 2 hours (equal mixture of 3% hydrogen peroxide and warm water (provide O2 to fight anaerobes)
  • Rinse 0.2% chlorhex x 10ml 2x daily for antiplaque 
  • Antibiotics (Metronidazole 200mg TDS 3 days) – only with fever, lymphadenopathy. Pink book say penicillin are also effective
  • Analgesics (ibuprofen) 
  • Palliative (rest, hydration, soft diet,) 
  • OHI (Brush tooth surface only with gentle pressure, not on the damaged gums. X floss) 

#Subgingival scaling and curettage C/I in 1st visit (can lead to bacteraemia and can extend the bacteria into deeper tissues) Extractions and perio surgery C/I for at least 1 month (cause can exacerbate the lesion) 

2nd visit (After 1 – 2 days)

  • Assess if condition improved. (pain is less,  pseudomembrane will be gone but gingival margin still red)
  • Can perform subgingival scaling 

3rd visit (After 5 days) 

  • Assess condition again (symptom free, some erythema still present) 
  • OHI 
  • Remove ppt factor to prevent recurrence (smoking, nutrition → take balanced diet,stress mx) → behavioural counselling and dietary counselling 
  • Can stop hydrogen peroxide but continue chlorhexidine for 2 weeks 
  • Repeat SnP if needed

4-6 weeks, 

-check pt maintenance, oral hygiene 

-if the gums have receded and if tooth appears longer, can do surgery. 

-gingivectomy in persistent craters (rare) 

3 months 

  • For periodic recall
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