Gingivitis and Periodontal Disease Flashcards
(41 cards)
Anatomy of the Periodontium in children compared to adults
- More red
- Lower prevalence of periodontal disease: Junctional epithelium is thicker -> Less permeable to toxins -> More resistant to inflammation
- Enhanced rate of progression of periodontal disease
Why is gingiva in children more red?
Increased vascularity of marginal gingiva and thinner epithelium
Why is there a lower prevalence of periodontal disease in children?
Junctional epithelium is thicker -> Less permeable to toxins -> More resistant to inflammation
Why is there an enhanced rate of progression of periodontal disease?
PDL space is wider, less fibrous, and more vascular. Alveolar bone has larger marrow spaces, greater vascularity and fewer trabeculae
Criteria for Gingival Health
Probing attachment loss: No
Probing pocket depths ≤ 3mm
Bleeding on probing: <10%
No radiographic bone loss
Criteria for Gingivitis
Probing attachment loss: No
Probing pocket depths ≤ 3mm
Bleeding on probing: ≥10%
No radiographic bone loss
Describing Gingivitis
Extent: Localised or generalised
Severity: Mild, moderate or severe
e.g. Generalised moderate gingivitis, biofilm-induced, intact periodontium
Examples of modifying factors
- Systemic factor
- Sex steroid hormones
- Hyperglycemia - Local factors
- Dental plaque biofilm retention factors - Drug-induced gingival enlargements
Drugs associated with gingival enlargement
Phenytoin, cyclosporine, nifedipine
Clinical characteristics of drug-induced gingival enlargement
Higher prevalence in younger age groups
More often in anterior
Proposed pathophysiology of drug-induced gingival enlargement
- Increase inflammatory cytokines
- Increase fibroblasts
- Increase collagen accumulation
Management of drug-induced gingival enlargement
- Plaque control
- Control inflammation
- Alternate drug choice
- Surgical intervention
Complication of drug-induced gingival enlargement
Retained primary teeth
Examples of mechanically induced gingival trauma
Self-inflicted or habitual: Nails, toys, toothpicks, zips
Etiology of Primary Herpetic Gingivostomatitis
HSV-1
Clinical Characteristics of Primary Herpetic Gingivostomatitis
- Prodrome of 2-4 days: Fever, malaise, headaches, cervical lymphadenopathy
- Generalised gingival inflammation, vesicles that rupture into ulcers.
- Resolves in 10-14 days
Management of Primary Herpetic Gingivostomatitis
- Oral acyclovir within first 72 h
- Symptomatic care: Anti-pyretics, hydration advice, soft diet
- Chlorhexidine mouthwash to prevent secondary infection
- Review 7-10 days later
Complication of Primary Herpetic Gingivostomatitis
Meningitis, encephalitis
Differential Diagnosis of Primary Herpetic Gingivostomatitis
- HFMD
- Herpangina
Predisposing factors of Necrotizing Periodontal Disease
Impaired host immune system: HIV, stress, malnutrition
Clinical Features of Necrotizing Periodontal Disease
- Necrosis and ulceration in interdental papillae
- Pseudomembrane formation
- Gingival bleeding
- Halitosis
- Pain
Treatment of Necrotizing Periodontal Disease
- Scale away superficial plaque and calculus
- Reduce stress, remove overhanging margins
- Gingival flap surgery if needed
Complications of Necrotizing Periodontal Disease
Progress to necrotizing ulcerative periodontitis or spread as necrotizing stomatitis or noma
What is the implicated infecting agent in early onset periodontitis?
A.actinomycetemcomitans