Popowics T, Foster B L, Swanson E C, Fong H, Somerman M J
Department of Oral Biology, University of Washington School of Dentistry, Seattle, Wash. 98195, USA.
Cells Tissues Organs. 2005;181(3-4):248-57. doi: 10.1159/000091386.
Significant progress has been seen in research aimed at regeneration of the disease-damaged periodontium. Our own strategy has been to approach periodontal tissue development (i.e. root, cementum, periodontal ligament, and bone) as a source for the identification of key regulators of cellular processes that may be applicable to periodontal tissue repair. Specifically, enamel-like molecules, bone morphogenetic proteins (BMPs), and phosphates have been investigated for their role in altering gene expression and cell functions in follicle cells, periodontal ligament cells, and cementoblasts. Amelogenin, leucine-rich amelogenin peptide, and tyrosine-rich amelogenin peptide have been found to similarly affect cementoblast gene expression and cementoblast-mediated mineralization in vitro; however, these enamel-like factors do not increase cell proliferation as has been observed in cells treated with Emdogain (Biora AB, Malmö, Sweden), an enamel matrix derivative. BMP-2 has been found to promote differentiation of follicle cells into a cementoblast/osteoblast phenotype, and BMP-3 is being investigated as a negative regulator of mineralization. The increased ratio of phosphate to pyrophosphate in the local region during root development has been found to significantly enhance the extent of cementum formation in animal models. Furthermore, phosphate has been identified as a regulator of cementoblast SIBLING (small integrin-binding ligand N-linked glycoprotein) gene expression in vitro. These investigations of candidate factors for periodontal regeneration have uncovered mechanisms regulating gene expression and cell function in cells controlling the behavior of periodontal tissues (i.e. follicle cells, periodontal cells, and cementoblasts) and offer new directions to consider for clinical repair of periodontal defects.
在旨在使受损牙周组织再生的研究中已取得显著进展。我们自己的策略是将牙周组织发育（即牙根、牙骨质、牙周韧带和牙槽骨）作为一个来源，以识别可能适用于牙周组织修复的细胞过程的关键调节因子。具体而言，已对类釉质分子、骨形态发生蛋白（BMP）和磷酸盐在改变卵泡细胞、牙周韧带细胞和成牙骨质细胞的基因表达和细胞功能方面的作用进行了研究。已发现釉原蛋白、富含亮氨酸的釉原蛋白肽和富含酪氨酸的釉原蛋白肽在体外同样会影响成牙骨质细胞的基因表达和成牙骨质细胞介导的矿化；然而，这些类釉质因子不会像用釉基质衍生物Emdogain（瑞典马尔默的Biora AB公司）处理的细胞那样增加细胞增殖。已发现BMP-2可促进卵泡细胞分化为成牙骨质细胞/成骨细胞表型，并且正在研究BMP-3作为矿化的负调节因子。已发现在牙根发育过程中局部区域磷酸盐与焦磷酸盐的比例增加可显著提高动物模型中牙骨质形成的程度。此外，磷酸盐在体外已被确定为成牙骨质细胞SIBLING（小整合素结合配体N-连接糖蛋白）基因表达的调节因子。这些对牙周再生候选因子的研究揭示了在控制牙周组织行为的细胞（即卵泡细胞、牙周细胞和成牙骨质细胞）中调节基因表达和细胞功能的机制，并为牙周缺损的临床修复提供了新的思考方向。
