硬化蛋白-沉默的破骨者

Q3 Dentistry
ROSHNİ, K B , SHETTY, Neetha J , GİRİDHAR KAMATH, Deepa
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引用次数: 0

摘要

牙周炎是一种高发的牙周炎症性疾病,由于宿主防御与牙周病致病菌的差异导致了牙周炎的发生。疾病的持续发展导致宿主免疫反应失调,可能导致组织和骨骼破坏,最终导致牙齿脱落。对骨代谢的解释已经加强,作为鉴定硬化蛋白及其功能的骨量调节。首先,骨细胞表达硬化蛋白,一种已知抑制骨形成的SOST基因。参与骨稳态的典型Wnt通路被Sclerostin显著抑制。它被认为是通过改变OPG和RANKL的比例导致骨的吸收。现就硬化蛋白的特点、作用方式及在牙周病中的意义作一综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sclerostin - The silent bone breaker
A disparity between host defense and periodontopathogens leads to periodontitis, which is an inflammatory disease of the periodontium of high prevalence. The dysregulated host immune response brought on by the disease’s ongoing progression may result in tissue and bone destruction, which ultimately leads to tooth loss. Interpretation of bone metabolism has enhanced as a result of the identification of sclerostin and its function as a bone mass regulator. Primarily, osteocytes express sclerostin, an SOST gene known to inhibit formation of bone. The canonical Wnt pathway involved in bone homeostasis, is significantly suppressed by Sclerostin. It is thought to result in resorption of bone by altering the ratio of OPG and RANKL. Characteristics, mode of action and significance of sclerostin in periodontal diseases are discussed in this review.
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来源期刊
Cumhuriyet Dental Journal
Cumhuriyet Dental Journal Dentistry-Dentistry (all)
CiteScore
0.40
自引率
0.00%
发文量
0
审稿时长
8 weeks
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