Etiology
Etiology
Periapical (dentoalveolar) abscess arises from pulp necrosis. Mixed anaerobic flora — Fusobacterium nucleatum, Prevotella, Porphyromonas, Peptostreptococcus — colonize the necrotic pulp and produce virulence factors enabling tissue invasion. Gram-positive facultatives (viridans streptococci) initiate infection; gram-negative anaerobes sustain and spread it.
Periodontal abscess originates from the periodontal pocket — acute exacerbation of periodontal disease, often triggered by foreign body impaction, subgingival scaling without adequate drainage, or acute apical extension of a narrow-mouthed pocket obstructed by food debris.
Pericoronal abscess (pericoronitis) develops in soft tissue around a partially erupted tooth (most commonly the mandibular third molar), where the operculum creates a stagnant space harbouring bacteria. Masticatory trauma to the operculum triggers acute exacerbation.
Systemic risk factors markedly increase both incidence and severity: diabetes mellitus (impaired neutrophil function, poor wound healing), immunosuppression (organ transplant, chemotherapy, HIV), bisphosphonate use (medication-related osteonecrosis), and hematological malignancies.