Pathogenesis
Pathogenesis
Pus formation begins when neutrophil influx overwhelms local tissue. Neutrophil-derived enzymes (elastase, MPO, collagenase) destroy surrounding connective tissue, and the resulting liquefactive necrosis creates a pus-filled cavity — the abscess. The cavity wall is initially thin and friable; over days it becomes walled off by granulation tissue (chronic abscess) or ruptures.
Spread occurs along paths of least resistance — fascial planes, between muscle layers, and through cancellous bone. The mandibular molar region is the most common source of life-threatening spread because the root apices lie below the attachment of mylohyoid muscle; pus can spread directly into the submandibular, sublingual, and submental spaces (Ludwig's angina territory).
Maxillary abscesses typically spread buccally (thin buccal cortex) into the buccal space, or palatally into the palatal space. Maxillary molars with apices above buccinator may spread into the infratemporal or masticator space, threatening the parapharyngeal space and ultimately the mediastinum via the carotid sheath (descending necrotizing mediastinitis).
Systemic response to severe spreading infection includes fever, leukocytosis, and in advanced cases SIRS (systemic inflammatory response syndrome) criteria — tachycardia, tachypnea, temperature >38.3°C or <36°C, elevated WBC >12,000. Septicemia occurs when bacteria breach lymphatic/vascular barriers.