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破骨细胞血管生成抑制作用可能在双膦酸盐相关性颌骨骨坏死的发生发展中起作用。

Angiogenic suppression of osteoclasts may play a role in developing bisphosphonate-related osteonecrosis of the jaw.

机构信息

State Key Laboratory of Oral Disease, Sichuan University, Renmin South Avenue, Chengdu 610041, Sichuan Province, PR China.

出版信息

Med Hypotheses. 2011 Mar;76(3):347-9. doi: 10.1016/j.mehy.2010.10.036. Epub 2010 Nov 12.

Abstract

Since it was firstly reported in 2003, a large number of cases have been published concerning bisphosphonate-related osteonecrosis of the jaw (BRONJ). It has generated great interest in the medical and research communities yet remains an enigma, given its unknown pathogenesis. Many hypotheses concerning the underlying pathophysiology are discussed, including two most popular hypotheses: bone remodeling suppression and angiogenesis suppression, but none of them could explain all the unique characters of BRONJ. Bisphosphonates are potent osteoclast inhibitors, and recent studies revealed that osteoclasts were important for bone angiogenesis. Therefore, we hypothesize that bisphosphonates could inhibit osteoclast stimulation of angiogenesis, which plays an important role in developing BRONJ. Our hypothesis could help to explain some unintelligible characters of BRONJ, and deserves further studies.

摘要

自 2003 年首次报道以来,已经有大量关于双膦酸盐相关性颌骨骨坏死(BRONJ)的病例发表。由于其发病机制不明,这在医学和研究界引起了极大的兴趣。目前已经讨论了许多关于潜在病理生理学的假说,包括两个最流行的假说:骨重建抑制和血管生成抑制,但没有一个能够解释 BRONJ 的所有独特特征。双膦酸盐是有效的破骨细胞抑制剂,最近的研究表明破骨细胞对于骨血管生成很重要。因此,我们假设双膦酸盐可能抑制破骨细胞对血管生成的刺激,这在 BRONJ 的发生发展中起着重要作用。我们的假设可以帮助解释 BRONJ 的一些难以理解的特征,值得进一步研究。

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