Mineralization defects in cementum and craniofacial bone from loss of bone sialoprotein.
Mineralization defects in cementum and craniofacial bone from loss of bone sialoprotein.
复制标题
DOI：
10.1016/j.bone.2015.05.007
复制
发表时间：
2015-09
期刊：
影响因子：
4.1
通讯作者：
Somerman, M. J.
中科院分区：
文献类型：
--
作者：
Foster, B. L.;Ao, M.;Willoughby, C.;Soenjaya, Y.;Holm, E.;Lukashova, L.;Tran, A. B.;Wimer, H. F.;Zerfas, P. M.;Nociti, F. H., Jr.;Kantovitz, K. R.;Quan, B. D.;Sone, E. D.;Goldberg, H. A.;Somerman, M. J.
骨唾液蛋白（BSP）是一种多功能的细胞外基质蛋白，存在于矿化组织中，包括骨、软骨、牙根牙骨质（无细胞和细胞类型）和牙本质。为了明确BSP在这些组织生物矿化过程中的作用，我们分析了牙骨质形成、牙本质形成和骨形成Bsp基因敲除小鼠和野生型（WT）对照组在发育期颅面骨中（膜内和软骨内）（纳塔尔1-60天; dpn）通过组织学、免疫组织化学、不脱钙组织化学、显微计算机断层扫描（microCT）、扫描电子显微镜（SEM），透射电子显微镜（TEM）和定量PCR（qPCR）。通过von Kossa和Goldner三色染色在1和14 dpn评估，肺泡、下颌骨和颅骨中的膜内骨化区域呈现延迟矿化和类骨质积聚。此外，Bsp−/−小鼠在早期时间点（1 dpn）的颅缝尺寸增加。免疫染色和PCR表明，成骨细胞标志物，osterix，碱性磷酸酶，骨桥蛋白在Bsp空下颌骨相比，WT不变。通过组织学、SEM和TEM观察，Bsp−/−小鼠磨牙缺乏功能性脱细胞牙骨质形成，随后Sharpey胶原纤维插入牙根结构的损失。Bsp−/−小鼠牙槽骨和下颌骨在早期（1和14 dpn）具有相等或更少的破骨细胞，然而，RANKL免疫染色和mRNA增加，在后期（26和60 dpn）发现破骨细胞样细胞数量显著增加（2-5倍），对应于磨牙进入咬合后观察到的牙周破坏和严重牙槽骨吸收。在Bsp−/−小鼠磨牙中，牙本质形成未受干扰，矿化没有延迟，牙本质尺寸没有改变，成牙本质细胞标记物没有差异。在Bsp−/−小鼠中，未发现颅底软骨内骨化缺陷，颅面形态不受影响。这些分析证实了BSP在颅面骨的牙骨质形成和膜内骨化过程中的关键作用，而颅底的软骨内骨化受到的影响最小，BSP−/−磨牙的牙本质形成正常。BSP缺失对牙齿和颅面组织矿化的不同影响表明BSP的作用存在局部差异和/或与位点特异性因素的相互作用尚未确定。
Bone sialoprotein (BSP) is a multifunctional extracellular matrix protein found in mineralized tissues, including bone, cartilage, tooth root cementum (both acellular and cellular types), and dentin. In order to define the role BSP plays in the process of biomineralization of these tissues, we analyzed cementogenesis, dentinogenesis, and osteogenesis (intramembranous and endochondral) in craniofacial bone in Bsp null mice and wild-type (WT) controls over a developmental period (1-60 days post natal; dpn) by histology, immunohistochemistry, undecalcified histochemistry, microcomputed tomography (microCT), scanning electron microscopy (SEM), transmission electron microscopy (TEM), and quantitative PCR (qPCR). Regions of intramembranous ossification in the alveolus, mandible, and calvaria presented delayed mineralization and osteoid accumulation, assessed by von Kossa and Goldner's trichrome stains at 1 and 14 dpn. Moreover, Bsp−/− mice featured increased cranial suture size at the early time point, 1 dpn. Immunostaining and PCR demonstrated that osteoblast markers, osterix, alkaline phosphatase, and osteopontin were unchanged in Bsp null mandibles compared to WT. Bsp−/− mouse molars featured a lack of functional acellular cementum formation by histology, SEM, and TEM, and subsequent loss of Sharpey's collagen fiber insertion into the tooth root structure. Bsp−/− mouse alveolar and mandibular bone featured equivalent or fewer osteoclasts at early ages (1 and 14 dpn), however, increased RANKL immunostaining and mRNA, and significantly increased number of osteoclast-like cells (2-5 fold) were found at later ages (26 and 60 dpn), corresponding to periodontal breakdown and severe alveolar bone resorption observed following molar teeth entering occlusion. Dentin formation was unperturbed in Bsp−/− mouse molars, with no delay in mineralization, no alteration in dentin dimensions, and no differences in odontoblast markers analyzed. No defects were identified in endochondral ossification in the cranial base, and craniofacial morphology was unaffected in Bsp−/− mice. These analyses confirm a critical role for BSP in processes of cementogenesis and intramembranous ossification of craniofacial bone, whereas endochondral ossification in the cranial base was minimally affected and dentinogenesis was normal in Bsp−/− molar teeth. Dissimilar effects of loss of BSP on mineralization of dental and craniofacial tissues suggest local differences in the role of BSP and/or yet to be defined interactions with site-specific factors.
登录
查看更多内容
影响因子：
7.6
作者：
Gericke A;Qin C;Sun Y;Redfern R;Redfern D;Fujimoto Y;Taleb H;Butler WT;Boskey AL
通讯作者：
Boskey AL
DOI：
10.1002/ar.a.20308
发表时间：
2006-03-01
期刊：
ANATOMICAL RECORD PART A-DISCOVERIES IN MOLECULAR CELLULAR AND EVOLUTIONARY BIOLOGY
影响因子：
--
作者：
Bloom, MW;Murakami, S;Duke, PJ
通讯作者：
Duke, PJ
影响因子：
2.9
作者：
Fisher, LW;Fedarko, NS
通讯作者：
Fedarko, NS
影响因子：
4.1
作者：
Baht, Gurpreet S.;O'Young, Jason;Goldberg, Harvey A.
通讯作者：
Goldberg, Harvey A.
影响因子：
3.7
作者：
Bouleftour W;Boudiffa M;Wade-Gueye NM;Bouët G;Cardelli M;Laroche N;Vanden-Bossche A;Thomas M;Bonnelye E;Aubin JE;Vico L;Lafage-Proust MH;Malaval L
通讯作者：
Malaval L