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骨桥蛋白缺失小鼠的细胞外牙骨质和牙周附着缺失。

Deficiency in acellular cementum and periodontal attachment in bsp null mice.

机构信息

National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

J Dent Res. 2013 Feb;92(2):166-72. doi: 10.1177/0022034512469026. Epub 2012 Nov 26.

Abstract

Bone sialoprotein (BSP) is an extracellular matrix protein found in mineralized tissues of the skeleton and dentition. BSP is multifunctional, affecting cell attachment and signaling through an RGD integrin-binding region, and acting as a positive regulator for mineral precipitation by nucleating hydroxyapatite crystals. BSP is present in cementum, the hard tissue covering the tooth root that anchors periodontal ligament (PDL) attachment. To test our hypothesis that BSP plays an important role in cementogenesis, we analyzed tooth development in a Bsp null ((-/-)) mouse model. Developmental analysis by histology, histochemistry, and SEM revealed a significant reduction in acellular cementum formation on Bsp (-/-) mouse molar and incisor roots, and the cementum deposited appeared hypomineralized. Structural defects in cementum-PDL interfaces in Bsp (-/-) mice caused PDL detachment, likely contributing to the high incidence of incisor malocclusion. Loss of BSP caused progressively disorganized PDL and significantly increased epithelial down-growth with aging. Bsp (-/-) mice displayed extensive root and alveolar bone resorption, mediated by increased RANKL and the presence of osteoclasts. Results collected here suggest that BSP plays a non-redundant role in acellular cementum formation, likely involved in initiating mineralization on the root surface. Through its importance to cementum integrity, BSP is essential for periodontal function.

摘要

骨唾液蛋白(BSP)是一种存在于骨骼和牙齿矿化组织中的细胞外基质蛋白。BSP 具有多功能性,通过 RGD 整联蛋白结合区域影响细胞附着和信号转导,并通过成核羟基磷灰石晶体作为矿化沉淀的正调节剂发挥作用。BSP 存在于牙骨质中,牙骨质是覆盖牙根的硬组织,锚定牙周韧带(PDL)附着。为了验证我们的假设,即 BSP 在牙骨质形成中发挥重要作用,我们在 Bsp 缺失((-/-))小鼠模型中分析了牙齿发育。通过组织学、组织化学和 SEM 的发育分析表明,在 Bsp(-/-)小鼠磨牙和切牙根部的无细胞牙骨质形成显著减少,沉积的牙骨质矿化不足。Bsp(-/-)小鼠牙骨质-PDL 界面的结构缺陷导致 PDL 分离,可能导致切牙错位的发生率较高。BSP 的缺失导致 PDL 逐渐失去组织,上皮向下生长显著增加,随年龄增长而增加。Bsp(-/-)小鼠表现出广泛的根和牙槽骨吸收,这是由 RANKL 增加和破骨细胞的存在介导的。这里收集的结果表明,BSP 在无细胞牙骨质形成中发挥非冗余作用,可能参与启动牙根表面的矿化。通过对牙骨质完整性的重要性,BSP 对牙周功能至关重要。

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