Department of Orthopedic Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Chin Med J (Engl). 2012 Jan;125(1):134-9.
To review the recent developments in the mechanisms of glucocorticoids induced osteonecrosis of femoral head (ONFH) and introduce a new theory of ONFH.
Both Chinese- and English-language literatures were searched using MEDLINE (1997 - 2011), Pubmed (1997 - 2011) and the Index of Chinese-language Literature (1997 - 2011).
Data from published articles about mechanisms of glucocorticoids induced ONFH in recent domestic and foreign literature were selected. Data extraction Data were mainly extracted from 61 articles which are listed in the reference section of this review.
Glucocorticoids are steroid hormones secreted by the adrenal cortex that play a pivotal role in the regulation of a variety of developmental, metabolic and immune functions. However, high dose of exogenous glucocorticoids usage is the most common non-traumatic cause of ONFH. Glucocorticoids can affect the metabolisms of osteoblasts, osteoclasts, bone marrow stromal cells and adipocytes which decrease osteoblasts formation but increase adipocytes formation and cause ONFH finally.
Glucocorticoids affect the differentiation of mesenchymal stem cells, through activating or inhibiting the related transcript regulators of osteogenesis and adipogenesis. At last, the size and volume of mesenchymal stem cells derived adipocytes will increase amazingly, but the osteoblasts will be decreased obviously. In the meantime, the activity of the osteoclasts will be activated. So, these mechanisms work together and lead to ONFH.
综述糖皮质激素诱导性股骨头坏死(ONFH)机制的研究进展,并提出股骨头坏死的新理论。
应用计算机检索 MEDLINE(1997-2011 年)、PubMed(1997-2011 年)及中国生物医学文献数据库(1997-2011 年),同时手检相关会议论文集和综述。
纳入糖皮质激素诱导性股骨头坏死机制的国内外研究文献,对资料进行初审,选择符合标准的文献。
糖皮质激素是由肾上腺皮质分泌的甾体激素,在调节多种发育、代谢和免疫功能方面发挥着关键作用。然而,大剂量外源性糖皮质激素的应用是导致股骨头坏死的最常见的非创伤性原因。糖皮质激素可以影响成骨细胞、破骨细胞、骨髓基质细胞和脂肪细胞的代谢,减少成骨细胞的形成,增加脂肪细胞的形成,最终导致股骨头坏死。
糖皮质激素通过激活或抑制成骨和脂肪生成相关的转录调节因子,影响间充质干细胞的分化。最终,间充质干细胞来源的脂肪细胞的大小和体积会显著增加,而成骨细胞则明显减少。同时,破骨细胞的活性也会被激活。这些机制共同作用导致股骨头坏死。