The molecular connections between apoptosis, autophagy, inflammatory processes, and vascular compromise in femoral head necrosis (FHN) that is induced by hormones were examined quantitatively. With microvascular damage, hormone-induced FHN, particularly that brought on by prolonged glucocorticoid exposure, was complicated and rapidly progressing. The research aimed to clarify how pathological processes that lead to femoral head structural deterioration were aggravated by vascular compromise, which decreased blood perfusion and induced hypoxia. Case-control, experimental cohort, and clinical methods were all used in a multi-tiered quantitative design. The mechanistic analytical study used imaging data, clinical biomarker profiling, and molecular assays to evaluate cellular and tissue changes. Excel, SPSS 25, and IBM SPSS-26 were used to analyse the data. 1,239 people were found using multi-centre retrospective cohort sampling, while the final sample size was 649. Verified ARCO staging, complete biomarker profiles, documented glucocorticoid prescription, and MRI FHN were required for admission. After removing missing data and complicating comorbidities, 95.4% of eligible patients were included in the final analytical sample. Participants were split up into several subgroups for the purpose of precise mechanistic mapping. According to the research, the development and course of hormone-induced FHN depended on vascular compromise. Through mitochondrial dysfunction, a prolonged hypoxic microenvironment brought on by decreased perfusion activated intrinsic apoptotic pathways. Autophagy, a protective mechanism, becomes dysregulated after extended glucocorticoid exposure, either moving towards maladaptive autophagic cell death or diminishing its recycling function. The findings validated the theory that in individuals exposed to hormones, vascular compromise accelerated necrotic transformation and acquired effects on hormone-induced FHN.