NEUROVASCULAR ANATOMY OF THE FEMORAL HEAD AND HISTOPATHOLOGICAL CORRELATES IN AVASCULAR NECROSIS: A HISTOLOGICAL STUDY

Abstract

Background: Avascular necrosis (AVN) of the femoral head is a debilitating orthopedic condition, often leading to progressive hip collapse and the need for arthroplasty in relatively young patients. Its pathogenesis is strongly linked to the unique vascular architecture of the femoral head, which relies on terminal end-arterial supply with minimal collateralization. Despite advances in imaging, histological studies exploring microvascular and neurovascular architecture remain limited.

Objective: To investigate the neurovascular anatomy of the femoral head using histological techniques and to characterize the histopathological changes underlying AVN.

Methods: Twenty-four human cadaveric femoral heads (12 male, 12 female; age range 25–68 years) were harvested within 48 hours of death. Samples were fixed, decalcified, sectioned, and stained with hematoxylin–eosin (H&E) for cellular detail, Masson’s trichrome for connective tissue, and immunohistochemistry (IHC) with CD34 for endothelial cells and neurofilament protein (NFP) for nerve fibers. Six AVN specimens retrieved during arthroplasty were analyzed for comparison. Microvascular density (MVD) was quantified in superior, anterior, inferior, and posterior regions of the femoral head. Statistical analysis was performed using Student’s t-test and ANOVA, with p<0.05 considered significant.

Results: In normal specimens, retinacular arteries were the predominant contributors to intraosseous circulation, entering obliquely through the femoral neck and branching into subchondral terminal networks. MVD was significantly higher in the superior (18.6 ± 3.1 vessels/HPF) and anterior regions (17.9 ± 2.7) compared with inferior (12.1 ± 2.3) and posterior regions (11.7 ± 2.5; p<0.05). Thin NFP-positive nerve fascicles consistently accompanied arteries, suggesting neurovascular regulation. AVN specimens demonstrated hallmark histopathological features including empty osteocyte lacunae, marrow adipocyte necrosis, disrupted trabecular integrity, and fibrovascular ingrowth. CD34 staining revealed significant reduction in MVD (7.2 ± 2.0 vs. 15.8 ± 3.0 vessels/HPF in controls; 42% reduction, p<0.01).

Conclusion: The femoral head depends on a precarious terminal vascular network without significant collateralization, predisposing it to ischemic injury. Neurovascular coupling may influence perfusion regulation. AVN is characterized by profound microvascular rarefaction and trabecular collapse, supporting the hypothesis that microvascular compromise and dysregulation are central to its pathogenesis. These insights may inform vascular-preserving surgical strategies and early therapeutic interventions.