Differential risk of autoimmune disorders in non-traumatic osteonecrosis: clue to pathogenesis

Non-traumatic osteonecrosis is a frequent complication in patients with autoimmune disorders, though its prevalence varies markedly depending upon the type of disorder. Understanding the causes of this difference can help uncover the underlying pathophysiology of osteonecrosis and guide the development of effective preventive and therapeutic strategies.

In this perspective study, we reviewed available databases, including PubMed, Cochrane Library, Scopus, and Web of Science, to explore why the risk of osteonecrosis varies among different autoimmune disorders. Is this variation primarily due to the disease's pathophysiology, the use of medications such as corticosteroids, or a combination of both? If both factors are involved, what is the extent of each contribution in this context?

Non-traumatic osteonecrosis is often induced by an interaction between disease pathophysiology and corticosteroid use. In patients with different autoimmune disorders but an identical history of corticosteroid use, the risk of osteonecrosis is influenced by how the underlying pathophysiology compromises bone health. In autoimmune disorders with multiple adverse effects on bone, such as SLE (systemic lupus erythematosus), there is a much higher risk of osteonecrosis compared to disorders with minimal impact on bone health, such as celiac disease and MS (multiple sclerosis).