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肿瘤坏死因子与骨重塑

TNF and Bone Remodeling.

作者信息

Zhao Baohong

机构信息

Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY, USA.

Graduate Program in Biochemistry, Cell and Molecular Biology, Weill Cornell Graduate School of Medical Sciences, New York, NY, USA.

出版信息

Curr Osteoporos Rep. 2017 Jun;15(3):126-134. doi: 10.1007/s11914-017-0358-z.

Abstract

PURPOSE OF REVIEW

The mechanisms involved in the TNF-mediated deregulated bone remodeling are little appreciated. This review will discuss and summarize the impact of TNF, Notch, and RBP-J signaling on bone remodeling.

RECENT FINDINGS

The integrity of the adult skeleton undergoes constant and dynamic remodeling throughout life to maintain a proper bone homeostasis, which is achieved by the essential tight control of coupling between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. The studies in this field include not only the differentiation and function of osteoblasts and osteoclasts, but also the mechanisms that simultaneously control both cell types during bone remodeling. Chronic inflammation is one of the most evident and common pathological settings that often leads to deregulated bone remodeling. The resounding success of TNF blockade therapy has demonstrated a key role for TNF in inflammation and the pathogenesis of inflammatory bone resorption associated with diseases such as rheumatoid arthritis and periodontitis. Recent studies have highlighted the function of Notch and RBP-J signaling in both physiological and TNF-mediated inflammatory bone remodeling.

摘要

综述目的

肿瘤坏死因子(TNF)介导的骨重塑失调所涉及的机制鲜为人知。本综述将讨论并总结TNF、Notch和RBP-J信号通路对骨重塑的影响。

最新研究发现

成年骨骼的完整性在一生中经历持续且动态的重塑,以维持适当的骨稳态,这通过对破骨细胞介导的骨吸收和成骨细胞介导的骨形成之间耦合的严格控制来实现。该领域的研究不仅包括成骨细胞和破骨细胞的分化与功能,还包括骨重塑过程中同时控制这两种细胞类型的机制。慢性炎症是最明显且常见的病理情况之一,常导致骨重塑失调。TNF阻断疗法的巨大成功已证明TNF在炎症以及类风湿关节炎和牙周炎等疾病相关的炎症性骨吸收发病机制中起关键作用。最近的研究突出了Notch和RBP-J信号通路在生理和TNF介导的炎症性骨重塑中的作用。

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