Accumulative cell stress: the multifactorial etiology of idiopathic osteonecrosis.
Most cases of idiopathic osteonecrosis are caused by many factors and rarely by an instantaneous, sudden, or solitary phenomenon. The cells in bony tissues become progressively sick or ill and therefore stressed. Depending on the condition, the cell sickness may intensify as the underlying disease progresses or as other factors are added that further decompensate the cells to the point at which they can no longer maintain cellular equilibrium. In many diseases, the final stress that overwhelms the cell is a course of corticosteroid therapy that could cause necrosis by several mechanisms, including increased stores of marrow fat, fat embolization, intraosseous hypertension, and a direct cellular toxic effect (see Fig. 3). The reasons why bone cells within the femoral head and condyles, humeral head, and certain other anatomic locations are especially susceptible remain obscure. However, in each of these sites, the blood supply enters from one direction only, and this relative ischemia could limit the reparative abilities of the cells.
D000305:Adrenal Cortex Hormones / Q000502:physiology; D000818:Animals; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D016030:Kidney Transplantation; D010011:Osteocytes / Q000502:physiology*; D010020:Osteonecrosis / Q000209:etiology / Q000503:physiopathology*; D013312:Stress, Physiological / Q000503:physiopathology*
D000305:Adrenal Cortex Hormones; D007166:Immunosuppressive Agents