Osteonecrosis of the femoral head (ONFH) is a disabling disease characterized by the disruption of the blood supply to the femoral head, leading to the apoptosis and
necrosis of bone cells and subsequent joint collapse.
Total hip arthroplasty is not optimal since most patients are young. Multiple risk factors contribute to
osteonecrosis, including
glucocorticoid (GC) usage, excessive alcohol intake,
hypercholesterolemia, and smoking. Continuous stimulation by many variables causes a chronic inflammatory milieu, with clinical repercussions including endothelial dysfunction, leading to
thrombosis, coagulopathy, and poor angiogenesis. Immune cells are the primary regulators of
inflammation. Innate and adaptive immune cells interact with endothelial cells to hinder the regeneration and repair of bone lesions. An in-depth examination of the pathological drivers of ONFH reveals that endothelial dysfunction may be a major cause of
osteonecrosis. Understanding the involvement of endothelial dysfunction in the chronic
inflammation of
osteonecrosis could aid in the development of possible
therapies. This review summarizes the role of endothelial cells in
osteonecrosis and further explains the pathophysiological mechanism of endothelial dysfunction in this disease from the perspective of
inflammation to provide new ideas for the treatment of
osteonecrosis.