24.2 Plaque-Induced and Non-Plaque-Induced Gingival Disease

3. Dental Plaque-Induced Gingivitis vs Non-Plaque-Induced Lesions

Dental Plaque-Induced Gingivitis

Dental plaque-induced gingivitis is an inflammatory lesion resulting from bacterial biofilm interactions with the host immune-inflammatory response, remaining strictly confined to the gingiva without extending apically into the periodontal ligament, root cementum, or alveolar bone. It is completely reversible upon professional debridement and effective personal plaque removal.

• Plaque Biofilm Alone: Primary bacterial succession initiating inflammatory vascular dilatation, neutrophil extravasation, and connective tissue degradation.
• Mediated by Systemic Risk Factors:
  • Sex Steroid Hormones: Puberty, menstrual cycle, pregnancy (pregnancy gingivitis and pyogenic granuloma driven by elevated progesterone and oestrogen increasing capillary permeability and gingival exudate), and oral contraceptives.
  • Hyperglycaemia: Exaggerated gingival inflammation in uncontrolled diabetic patients despite moderate plaque scores.
  • Haematological Malignancies: Leukaemic gingival enlargement and spontaneous bleeding due to leukaemic blast cell infiltration and secondary thrombocytopenia.
  • Smoking: Exerts profound local and systemic immunosuppression; blunts clinical signs of inflammation (reduced bleeding and erythema) despite high microbial burden.
  • Malnutrition: Scurvy (hypovitaminosis C) compromising prolyl and lysyl hydroxylase in collagen synthesis, yielding swollen, bleeding, friable gingival tissues.
• Mediated by Local Plaque-Retentive Factors: Overhanging restorative margins, subgingival margins, crowding, enamel pearls, and root grooves that impede plaque removal.
• Drug-Induced Gingival Enlargement (DIGE):
  • Anticonvulsants: Phenytoin (~50% prevalence).
  • Immunosuppressants: Ciclosporin (~30% prevalence; exacerbated when combined with calcium channel blockers).
  • Calcium Channel Blockers: Amlodipine, nifedipine, diltiazem, verapamil (~10–20% prevalence).
  • Pathophysiology: Altered intracellular calcium flux in gingival fibroblasts, leading to impaired collagenase activity, accumulation of extracellular matrix ground substance (glycosaminoglycans), and fibroblastic hyperplasia.

Non-Plaque-Induced Gingival Diseases and Conditions

These conditions do not resolve with plaque removal alone, although plaque accumulation often secondary exacerbates the inflammatory presentation:

1. Genetic / Developmental Disorders: Hereditary gingival fibromatosis (autosomal dominant or recessive; diffuse, firm, non-haemorrhagic, dense collagenous enlargement covering the crowns of teeth).
2. Specific Bacterial Infections: Necrotizing ulcerative gingivitis (Treponema denticola, Prevotella intermedia, fusobacteria); Neisseria gonorrhoeae, Treponema pallidum (syphilitic mucous patches), Mycobacterium tuberculosis.
3. Specific Viral Infections: Primary Herpetic Gingivostomatitis (HSV-1: high pyrexia, cervical lymphadenopathy, diffuse painful vesicular eruptions on gingiva and oral mucosa rupturing into shallow ulcers; treated with aciclovir if within 72 hours, analgesia, hydration); Varicella-zoster (unilateral dermatomal vesicles/ulcers); Coxsackievirus (Herpangina, Hand-foot-and-mouth disease).
4. Fungal Infections: Candida albicans (pseudomembranous, erythematous candidiasis); Linear Gingival Erythema (distinct 2–3 mm continuous fiery red marginal band observed characteristically in immunocompromised / HIV-seropositive individuals, resistant to conventional scaling).
5. Immune-Mediated Mucocutaneous Disorders:
   • Oral Lichen Planus (OLP): T-cell mediated autoimmune destruction of basal keratinocytes; manifests as desquamative gingivitis, fine reticular Wickham's striae, or painful erosions.
   • Mucous Membrane Pemphigoid (MMP): Autoantibodies against hemidesmosomal basement membrane antigens (BP180, laminin-332); presents with subepithelial bullae, positive Nikolsky sign, and desquamative gingivitis; risks ocular cicatrization and blindness.
   • Pemphigus Vulgaris: Autoantibodies against desmoglein-3; intraepithelial acantholysis, flaccid bullae that rupture immediately leaving raw, bleeding erosions; positive Nikolsky sign.
6. Reactive Processes (Epulides):
   • Fibrous Epulis: Dense collagenous reactive hyperplasia to local chronic irritation.
   • Pyogenic Granuloma (Pregnancy Epulis): Exuberant endothelial proliferation with rich vascularity; bleeds profusely on touch.
   • Peripheral Giant Cell Granuloma: Multinucleated osteoclast-like giant cells in a vascular stroma; originates from the periosteum or PDL; characteristic purplish-red hue; causes superficial cup-shaped alveolar bone resorption.

Recognising the Non-Plaque-Induced Lesions

The importance of this category is that the lesions do not respond to improved plaque control, so failure to recognise them leads to repeated, futile hygiene phase therapy. The examinable groups are infections — primary herpetic gingivostomatitis, necrotising gingivitis, candidosis; immune and inflammatory conditions — lichen planus, pemphigoid, pemphigus, erythema multiforme, plasma cell gingivitis, orofacial granulomatosis; reactive processes — the epulides; neoplasia — squamous cell carcinoma and, importantly, leukaemic infiltration; genetic conditions — hereditary gingival fibromatosis; endocrine and metabolic influences; traumatic lesions — chemical, thermal and physical, including toothbrush trauma and factitious injury; and gingival pigmentation.

The reasoning examiners want is pattern recognition. Gingival changes that are desquamative, that affect the attached gingiva diffusely and that do not correlate with plaque distribution suggest a vesiculobullous or lichenoid disease requiring biopsy. Gingival changes that are localised, rapidly growing and ulcerated suggest neoplasia and require urgent referral. Gingival swelling that is generalised, boggy and associated with spontaneous bleeding, pallor and lymphadenopathy suggests acute leukaemia and is a same-day medical referral.

A useful discipline at the chair is to ask, at every review, whether the gingival appearance is proportionate to the plaque present. Where inflammation greatly exceeds the deposits, the differential widens immediately to the non-plaque-induced lesions, to a drug-influenced enlargement, to a haematological cause and to an undiagnosed systemic condition, and the next step is investigation rather than a further round of hygiene instruction.