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非典型股骨骨折和颌骨骨坏死的病理生理学。

Pathophysiology of atypical femoral fractures and osteonecrosis of the jaw.

机构信息

Cambridge University Hospitals NHS Foundation Trust, Cambridge, CB2 0QQ, UK.

出版信息

Osteoporos Int. 2011 Dec;22(12):2951-61. doi: 10.1007/s00198-011-1804-x. Epub 2011 Oct 14.

DOI:10.1007/s00198-011-1804-x
PMID:21997225
Abstract

In recent years, atypical femoral fractures and osteonecrosis of the jaw have emerged as potential complications of long-term bisphosphonate therapy; osteonecrosis of the jaw has also been reported in patients receiving high doses of denosumab. The pathophysiology of both conditions is poorly defined, and the underlying mechanisms are likely to differ. The initiation of atypical fractures in the lateral femoral shaft suggests that reduced tensile strength, possibly secondary to alterations in the material properties of bone resulting from low bone turnover, may be an important pathogenetic factor. Osteonecrosis of the jaw is characterised by infection, inflammation, bone resorption and bone necrosis, but the sequence in which these occur has not been established. However, the observation that bone resorption occurs in close proximity to microbial structures suggests that infection may be the most important trigger, often as a result of dental disease. Other possible pathogenetic factors include suppression of bone turnover, altered immune status and adverse effects of bisphosphonates on the oral mucosa.

摘要

近年来,非典型股骨骨折和颌骨骨坏死已成为长期使用双膦酸盐治疗的潜在并发症;接受高剂量地舒单抗治疗的患者也有颌骨骨坏死的报告。这两种情况的病理生理学尚未明确,潜在机制可能不同。股骨外侧干骺端非典型骨折的发生提示,张力强度降低,可能是由于低骨转换导致骨的材料特性改变所致,这可能是一个重要的发病因素。颌骨骨坏死的特征是感染、炎症、骨吸收和骨坏死,但尚未确定这些过程的发生顺序。然而,观察到骨吸收发生在微生物结构附近表明,感染可能是最重要的触发因素,通常是由于牙科疾病。其他可能的发病因素包括骨转换抑制、免疫状态改变以及双膦酸盐对口腔黏膜的不良影响。

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The effect of long-term alendronate treatment on cortical thickness of the proximal femur.长期阿伦膦酸钠治疗对股骨近端皮质厚度的影响。
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