Gingivitis
Reversible gingival inflammation — the most prevalent oral disease and precursor to periodontitis
Prevalence: Affects 70–90% of the global population at some point; universal in populations with inadequate oral hygiene
Overview
Gingivitis is a reversible inflammatory condition of the gingiva caused by bacterial plaque biofilm accumulation at the gingivo-dental junction. It is the most common oral disease globally, with survey data showing clinical signs in the majority of adults examined in most countries regardless of socioeconomic status.
The 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases redefined gingivitis within a comprehensive classification framework, distinguishing plaque-induced gingivitis (most common) from non-plaque-induced gingival conditions (viral, bacterial, fungal, genetic, neoplastic, traumatic, or systemic causes).
Gingivitis is clinically significant not merely as a disease in itself, but as the obligatory precursor to periodontitis — the irreversible, bone-destroying progression. All periodontitis begins as gingivitis, though not all gingivitis progresses to periodontitis. Identifying and treating gingivitis is therefore primary prevention for the most common cause of adult tooth loss.
Etiology
Plaque-induced gingivitis is caused by supragingival and subgingival bacterial biofilm. The transition from healthy gingival flora to a dysbiotic, pro-inflammatory biofilm occurs within 10–21 days of cessation of oral hygiene. Classic gingivitis induction experiments (Löe et al., 1965) demonstrated complete reproducibility and reversibility of this process.
Local factors that promote plaque retention and thereby increase gingivitis susceptibility: calculus (mineralized plaque providing rough retention surface), overhanging restorations, ill-fitting crowns and dentures, orthodontic appliances, carious lesions, gingival anatomy variations, and mouth breathing causing gingival desiccation.
Systemic modifying factors amplify the gingival response to plaque: hormonal changes (pregnancy gingivitis from progesterone-driven capillary proliferation, puberty gingivitis, oral contraceptive-associated gingivitis); medications inducing gingival overgrowth (phenytoin, cyclosporin, calcium channel blockers — nifedipine, amlodipine); diabetes mellitus; hematological disorders (leukemia presenting as gingival hyperplasia); malnutrition especially vitamin C deficiency (scurvy).
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Pathogenesis
Initial lesion (0–4 days): bacterial products activate Toll-like receptors on gingival fibroblasts and keratinocytes, triggering IL-8 and other chemokines. Neutrophils migrate through junctional epithelium into the gingival crevice (sulcus). Complement activation, vasodilation, and increased vascular permeability occur. No clinical signs yet.
Classification
Plaque-Induced Gingivitis on Intact Periodontium
Most common form; caused by bacterial plaque; fully reversible with treatment
Gingivitis Mediated by Systemic/Local Risk Factors
Exaggerated response to plaque due to hormones, medications, systemic disease
Clinical Manifestations
The clinical hallmarks of gingivitis are: erythema (redness from increased vascularity and vasodilation), edema (puffiness, loss of the sharp, knife-edged gingival margin), and bleeding on probing (BOP). BOP is the most sensitive clinical indicator of gingival inflammation — healthy gingiva does not bleed on probing with normal force (25g).
Diagnosis
Clinical diagnosis is made using the plaque index (or control record), gingival index, and BOP percentage. The Löe-Silness Gingival Index scores 0–3 for erythema, edema, and bleeding tendency. A BOP score >25% indicates generalized gingivitis requiring intervention.
Treatment Protocol
Non-Surgical Periodontal Therapy (Step 1)
Eliminate plaque biofilm and calculus; modify risk factors
Prognosis
Plaque-induced gingivitis has an excellent prognosis with treatment — complete resolution of gingival inflammation within 2–4 weeks of effective oral hygiene combined with professional debridement. This resolution is one of the most predictable treatment outcomes in dentistry.
Prevention
- Twice-daily toothbrushing with fluoride toothpaste using modified Bass technique
- Daily interdental cleaning (flossing or interdental brushes) — removes plaque from gingival embrasures
Interactive Quiz
Test your understanding of Gingivitis.
Q1. What is the MOST sensitive clinical indicator of gingival inflammation?
3D Pathology Description
Comparative 3D cross-section split view: healthy gingivae (left) vs. established gingivitis (right). Healthy: dense collagen fiber bundles (white fibrous strands) running from root cementum to alveolar bone (dentogingival, alveologingival groups); thin junctional epithelium tightly adapted to tooth surface; blood vessels (red tubes, normal caliber); minimal inflammatory cells; stippled surface texture. Gingivitis: dilated blood vessels (larger red tubes with increased branching showing neovascularization); edematous ground substance (blue-tinged fluid spaces between collagen fibers); collagen degradation near junctional epithelium (reduced fiber density); junctional epithelium thickened, ulcerated pockets; plasma cells and lymphocytes as small colored spheres; neutrophils migrating through epithelium toward sulcus. Animate the transition over 21 days in time-lapse: plaque biofilm accumulating (brown layer on tooth surface), vessel dilation, inflammatory cell infiltration, collagen degradation. Include BOP indicator: probe entering inflamed sulcus triggers animation of bleeding from vessels. Show measurement of sulcus depth: 2mm (normal) vs 3mm (gingivitis with pseudo-pocket).