Is COVID-19 infection an independent etiologic factor in osteonecrosis development beyond corticosteroid exposure?

An increased incidence of non-traumatic osteonecrosis has been reported during the COVID-19 pandemic. Corticosteroid therapy, particularly dexamethasone, has often been implicated as a major risk factor. However, emerging evidence suggests that the pathogenesis of osteonecrosis in COVID-19 patients may extend beyond corticosteroid exposure.

COVID-19 infection itself may serve as an independent etiologic factor in osteonecrosis, with virus-induced pathogenic mechanisms synergizing with corticosteroid exposure to heighten risk, even at lower doses and shorter treatment durations.

This review synthesizes available literature on COVID-19, corticosteroid therapy, and osteonecrosis pathogenesis. Evidence from clinical observations, mechanistic studies, and prior models of corticosteroid-induced osteonecrosis were examined to identify overlapping and distinct pathways contributing to disease development.

Findings indicate that COVID-19 and corticosteroids converge on common pathogenic pathways-lipid dysregulation, impaired bone homeostasis, endothelial dysfunction, and coagulopathy. COVID-19 additionally promotes osteonecrosis through cytokine storm-driven inflammation. The combined effects of viral infection and corticosteroid therapy amplify disease risk, explaining reported cases of osteonecrosis even under reduced corticosteroid exposure.

COVID-19 may represent an independent etiologic factor for osteonecrosis, with intrinsic viral effects potentiating the impact of corticosteroids. Recognition of this dual risk underscores the need for preventive and therapeutic strategies tailored to COVID-19-associated osteonecrosis.