Department of Oral and Maxillofacial Surgery, School of Dentistry, University of Alabama at Birmingham, Birmingham, AL, USA.
M.D. Anderson Cancer Center, University of Texas, Houston, TX, USA.
J Bone Miner Res. 2018 Jun;33(6):1126-1140. doi: 10.1002/jbmr.3401. Epub 2018 Mar 24.
The Sp7/Osterix transcription factor is essential for bone development. Mutations of the Sp7 gene in humans are associated with craniofacial anomalies and osteogenesis imperfecta. However, the role of Sp7 in embryonic tooth development remains unknown. Here we identified the functional requirement of Sp7 for dentin synthesis and tooth development. Sp7-null mice exhibit craniofacial dysmorphogenesis and are completely void of alveolar bone. Surprisingly, initial tooth morphogenesis progressed normally in Sp7-null mice. Thus the formation of alveolar bone is not a prerequisite for tooth morphogenesis. Sp7 is required for mineralization of palatal tissue but is not essential for palatal fusion. The reduced proliferative capacity of Sp7-deficient ectomesenchyme results in small and misshapen teeth with randomly arranged cuboidal preodontoblasts and preameloblasts. Sp7 promotes functional maturation and polarization of odontoblasts. Markers of mature odontoblast (Col1a, Oc, Dspp, Dmp1) and ameloblast (Enam, Amelx, Mmp20, Amtn, Klk4) are barely expressed in incisors and molar tissues of Sp7-null mice. Consequently, dentin and enamel matrix are absent in the Sp7-null littermates. Interestingly, the Sp7 expression is restricted to cells of the dental mesenchyme indicating the effect on oral epithelium-derived ameloblasts is cell-nonautonomous. Abundant expression of Fgf3 and Fgf8 ligand was noted in the developing tooth of wild-type mice. Both ligands were remarkably absent in the Sp7-null incisor and molar, suggesting cross-signaling between mesenchyme and epithelium is disrupted. Finally, promoter-reporter assays revealed that Sp7 directly controls the expression of Fgf-ligands. Together, our data demonstrate that Sp7 is obligatory for the differentiation of both ameloblasts and odontoblasts but not for the initial tooth morphogenesis. © 2018 American Society for Bone and Mineral Research.
Sp7/Osterix 转录因子对于骨骼发育是必需的。人类 Sp7 基因突变与颅面异常和骨发育不全有关。然而,Sp7 在胚胎牙齿发育中的作用尚不清楚。在这里,我们确定了 Sp7 对牙本质合成和牙齿发育的功能要求。Sp7 基因敲除小鼠表现出颅面发育不良,并且完全缺乏牙槽骨。令人惊讶的是,Sp7 基因敲除小鼠的初始牙齿形态发生正常进展。因此,牙槽骨的形成不是牙齿形态发生的前提。Sp7 对于腭组织的矿化是必需的,但对于腭融合不是必需的。Sp7 缺陷的中胚层的增殖能力降低导致牙齿小且畸形,具有随机排列的立方前成牙本质细胞和前成釉细胞。Sp7 促进成牙本质细胞的功能成熟和极化。成熟成牙本质细胞(Col1a、Oc、Dspp、Dmp1)和成釉细胞(Enam、Amelx、Mmp20、Amtn、Klk4)的标志物在 Sp7 基因敲除小鼠的切牙和磨牙组织中几乎不表达。因此,Sp7 基因敲除小鼠的牙本质和釉质基质缺失。有趣的是,Sp7 的表达仅限于牙齿间质细胞,表明对口腔上皮来源的成釉细胞的影响是细胞非自主性的。在野生型小鼠发育中的牙齿中,大量表达 Fgf3 和 Fgf8 配体。这两种配体在 Sp7 基因敲除小鼠的切牙和磨牙中都明显缺失,表明中胚层和上皮之间的交叉信号传递被破坏。最后,启动子报告基因分析表明 Sp7 直接控制 Fgf 配体的表达。总之,我们的数据表明 Sp7 对于成釉细胞和成牙本质细胞的分化是必需的,但对于初始牙齿形态发生不是必需的。