Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA 95616, USA.
Clin Rev Allergy Immunol. 2011 Aug;41(1):102-13. doi: 10.1007/s12016-010-8217-z.
The pathophysiology of non-traumatic osteonecrosis is more complex than that of traumatic osteonecrosis, and corticosteroid-induced osteonecrosis presents the greatest challenge because of the multiple effects of corticosteroids on multi-system pathways; these pathways include the effects of corticosteroids on osteoblast differentiation, osteoblast and osteoclast apoptosis, lipid metabolism, coagulation pathways, and calcium metabolism. These pathways are frequently interrelated with each other, which makes the pathogenesis even more difficult to understand. Host factors and underlying disease have been shown to play a significant role in the risk of developing osteonecrosis, and our understanding of the pathogenesis must be able to explain why some patients are at greater risk than others. Identification of genetic variants that convey additional risk will also help to personalize the way we deliver care, both in the prevention and treatment of osteonecrosis. Further understanding of the intricate immunologic and genetic pathways contributing to osteonecrosis is at the forefront of research and may soon lead to viable and less invasive non-surgical therapeutic strategies.
非创伤性骨坏死的病理生理学比创伤性骨坏死更为复杂，而皮质类固醇诱导性骨坏死则带来了最大的挑战，因为皮质类固醇对多系统途径具有多种影响；这些途径包括皮质类固醇对成骨细胞分化、成骨细胞和破骨细胞凋亡、脂代谢、凝血途径和钙代谢的影响。这些途径经常相互关联，这使得发病机制更难以理解。宿主因素和基础疾病已被证明在发生骨坏死的风险中起重要作用，我们对发病机制的理解必须能够解释为什么有些患者比其他患者风险更大。鉴定出传递额外风险的遗传变异也将有助于我们以个性化的方式提供护理，无论是在预防还是治疗骨坏死方面。对导致骨坏死的复杂免疫和遗传途径的进一步了解是研究的前沿领域，可能很快就会带来可行且侵入性较小的非手术治疗策略。
