From Silent Ischemia to Hip Collapse: A Critical and Integrative Literature Review of Avascular Necrosis of the Femoral Head in Early Adulthood, With Emphasis on Etiopathogenesis Risk Factors, Early Clinical Recognition, Disease Progression and Homoe

Avascular necrosis of the femoral head (AVNFH), also termed osteonecrosis of the femoral head (ONFH), is a potentially progressive disorder characterized by compromised intraosseous circulation, osteocyte death, structural failure of the femoral head, and eventual secondary degenerative arthritis. Its clinical importance is particularly pronounced in early adulthood because the disease may affect individuals during their most productive years and may ultimately necessitate hip arthroplasty at a relatively young age. The transition from apparently silent ischemia to symptomatic disease and structural collapse is often clinically subtle, creating a critical window during which early recognition and appropriate staging may influence management. The pathogenesis of ONFH is increasingly understood as a multifactorial process involving vascular compromise, endothelial dysfunction, intravascular coagulation, altered lipid metabolism, marrow adipogenesis, intraosseous pressure, impaired osteogenesis, apoptosis, inflammatory mechanisms, and mechanical failure. Corticosteroid exposure and excessive alcohol consumption remain major non-traumatic associations, while autoimmune disease, haematological disorders, metabolic abnormalities, smoking, transplantation, decompression sickness, trauma, and idiopathic disease constitute additional pathways. Importantly, disease progression is not determined solely by the presence of necrosis; lesion size, anatomical location, weight-bearing involvement, and subchondral fracture substantially influence the probability of collapse. Early symptoms may be absent or nonspecific, commonly presenting as groin, hip, buttock, or referred thigh pain with restricted internal rotation. Conventional radiography may remain normal during early disease, whereas magnetic resonance imaging (MRI) can identify marrow abnormalities before radiographic changes become apparent. A meta-analysis reported pooled MRI sensitivity and specificity of approximately 93% and 91%, respectively, for early ONFH. This review critically examines ONFH from etiopathogenesis through clinical progression and discusses the potential conceptual role of homoeopathic individualisation as a complementary, patient-centred framework, while emphasising that homoeopathic prescribing should not substitute for MRI-based diagnosis, orthopaedic assessment, risk-factor modification, or established joint-preserving and reconstructive interventions. Classical homoeopathic principles emphasise individualised assessment and the totality of characteristic symptoms; however, contemporary clinical evidence demonstrating that individualised homoeopathic treatment reverses femoral-head necrosis or prevents collapse remains insufficient.