Avascular necrosis (AVN), also known as avascular necrosis of bone, is a pathological condition in which necrotic changes develop in bone tissue as a result of interrupted blood supply. The condition most commonly affects the epiphyses of long bones, where disruption of vascular perfusion leads to progressive collapse and structural destruction of bone architecture. Three recognized forms are primary avascular necrosis, secondary avascular necrosis, and dysbaric osteonecrosis. Prevalence data are not established in the available packet.

Clinical manifestations arise from the structural consequences of bone ischemia, including progressive epiphyseal collapse, joint deformity, and loss of normal joint function. The hip, knee, shoulder, and ankle are among the most commonly affected sites. Standardized phenotypic data from clinical registries are not available in this packet; symptom profile and severity vary based on anatomical location, lesion size, and underlying cause.

Avascular necrosis results from interruption of bone blood supply. Secondary avascular necrosis arises from identifiable exposures or conditions, including corticosteroid use, excessive alcohol consumption, trauma, hemoglobinopathies such as sickle cell disease, and coagulation disorders. Dysbaric osteonecrosis occurs following rapid ambient pressure changes in divers and caisson workers. No genetic determinants are specified in the available data for this condition.

Diagnosis is established through clinical evaluation and imaging. Magnetic resonance imaging is the most sensitive modality for early detection, identifying characteristic signal changes within affected bone before structural collapse occurs. Plain radiography and computed tomography evaluate the extent of structural changes in later-stage disease. Staging frameworks based on imaging and clinical findings guide disease severity assessment.

No pharmacological agent is specifically approved for avascular necrosis. Seventy-two active clinical trials are investigating pharmacological, surgical, and other interventional strategies. Active investigation includes bisphosphonate pharmacotherapy and joint implant systems, with approaches varying by disease stage and affected site.

The natural history is variable and depends on disease site, extent of involvement, and presence of underlying comorbidities. Progressive joint destruction may occur as necrotic bone fails to remodel, potentially leading to significant functional impairment. Three subtypes—primary, secondary, and dysbaric—may have differing prognostic trajectories. Population-level outcome data are not available in this packet.

Seventy-two active clinical trials are registered for avascular necrosis. The published literature base includes 240 classified articles spanning reviews, meta-analyses, and 56 case reports, reflecting an active investigational landscape across etiologies and treatment approaches.