Interleukin-1 and bone metabolism: a review.

Interleukin-1 and bone metabolism: a review.
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Interleukin-1 和骨代谢:综述。

DOI:
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发表时间:
1993
期刊:
The Journal of Periodontology
影响因子:
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通讯作者:
D. Tatakis
D. Tatakis
中科院分区:
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文献类型:
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作者:
D. Tatakis

文献摘要

被引文献

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本文综述了白细胞介素-1(IL-1)对骨代谢的影响以及IL-1与牙周病的关系。IL-1是一种有效的细胞因子,对包括骨在内的许多组织的代谢具有显著影响。几项体外和体内研究已经确定了IL-1的强效骨吸收作用。研究表明,IL-1抑制骨形成,尽管它在某些条件下可以刺激骨形成。成骨细胞是表达IL-1受体并对IL-1应答的骨细胞。IL-1对成骨细胞的作用包括刺激前列腺素形成和调节几种蛋白质(细胞因子、酶、酶抑制剂、基质蛋白等)的基因表达。成骨细胞也产生IL-1,表明IL-1在骨中的自分泌/旁分泌功能。IL-1已被证明与其他全身和局部的骨因子相互作用。这些相互作用调节IL-1对骨的作用。IL-1对骨代谢的影响,沿着其他观察,提示IL-1可能参与骨疾病的发病机制。来自体内和体外研究的证据表明,IL-1是牙周组织破坏的重要因素。牙周病细菌刺激IL-1产生的能力,牙周病组织中IL-1水平升高的检测,以及IL-1对牙周组织细胞的影响,为牙周病的发病机制提供了一个合理的事件序列。最后,还讨论了旨在控制IL-1作用的治疗方式。
This review discusses the effects of interleukin-1 (IL-1) on bone metabolism and the evidence implicating IL-1 in periodontal disease. IL-1 is a potent cytokine with significant effects on the metabolism of many tissues, including bone. Several in vitro and in vivo studies have established the potent bone-resorbing effect of IL-1. Studies have indicated that IL-1 inhibits bone formation, although it can stimulate formation under certain conditions. Osteoblastic cells are the bone cells expressing IL-1 receptors and responding to IL-1. IL-1 effects on osteoblastic cells include stimulation of prostaglandin formation and modulation of gene expression of several proteins (cytokines, enzymes, enzyme inhibitors, matrix proteins, etc.). Osteoblastic cells also produce IL-1, suggesting an autocrine/paracrine function of IL-1 in bone. IL-1 has been shown to interact with other osteotropic factors, both systemic and local. These interactions modulate the effects of IL-1 on bone. The IL-1 effects on bone metabolism, along with other observations, suggest that IL-1 may be involved in the pathogenesis of bone diseases. Evidence from in vivo and in vitro studies suggests that IL-1 is an important factor in periodontal tissue breakdown. The ability of periodontopathic bacteria to stimulate IL-1 production, the detection of elevated IL-1 levels in periodontally-diseased tissues, and the effects of IL-1 on cells of the periodontium provide a plausible sequence of events in the pathogenesis of periodontal disease. Finally, therapeutic modalities aimed to control the actions of IL-1 are also discussed.