Institute of Molecular Biology and Genetics, University of Valladolid, and Spanish Research Council, Valladolid, Spain.
J Periodontol. 2010 Jul;81(7):1064-74. doi: 10.1902/jop.2010.090678.
BACKGROUND: Periodontitis is a chronic inflammatory condition that leads to the destruction of the tooth-supporting tissues. Its treatment includes the arrest of the inflammatory process and, in some circumstances, the restoration of the lost anatomy and function, including the formation of new cementum, periodontal ligament (PDL), and bone. With this goal, we investigated the effects of low concentrations of 17beta-estradiol on human cementoblast proliferation and its possible regenerative potential in vivo. METHODS: Human cementum-derived cells obtained from a healthy human premolar were isolated and characterized by immunocytochemistry. Cell proliferation assays were performed to test the effects of 100 nM 17beta-estradiol and enamel matrix derivative (EMD). Three-wall intrabony periodontal defects were created in beagle dogs. After 1 month of plaque accumulation, 0.225 mg 17beta-estradiol impregnated in a collagen sponge was applied to randomly selected defects (test group), whereas a collagen sponge impregnated in a culture medium was applied to the control group. After 3 months, specimens were obtained, and tissue regeneration was assessed by histometric analysis. RESULTS: Cells spreading out from human tooth-layer explants were able to form cell colonies, produce a mineral matrix, and express osteocalcin, indicating they were cementoblast-like cells. In contrast, PDL fibroblasts did not express osteocalcin. 17beta-estradiol, but not EMD, increased the rate of human cementoblast cell proliferation in vitro by 2.5-fold. Histometric results from the treated periodontal defects revealed that 17beta-estradiol promoted the formation of 2.94 mm of new cementum, (45% of the defects) compared to 1.54 mm of new cementum in the control group (28% of the defects). Furthermore, the test group showed an inhibition of epithelial downgrowth and a gain of new connective tissue attachment. CONCLUSION: 17beta-estradiol promoted human cementoblast cell proliferation in vitro and periodontal regeneration in an experimental periodontitis model.
背景：牙周炎是一种慢性炎症性疾病，导致牙齿支持组织的破坏。其治疗包括炎症过程的抑制，以及在某些情况下，恢复丢失的解剖结构和功能，包括新的牙骨质、牙周韧带（PDL）和骨的形成。为此，我们研究了低浓度 17β-雌二醇对人成牙骨质细胞增殖的影响及其在体内的可能再生潜能。
方法：从健康人前磨牙中分离出人牙骨质源性细胞，并通过免疫细胞化学进行鉴定。进行细胞增殖实验以测试 100 nM 17β-雌二醇和釉基质衍生物（EMD）的作用。在比格犬的三壁骨内牙周缺损中创建 3 个月的菌斑堆积。在应用胶原海绵浸渍 0.225 mg 17β-雌二醇（实验组）或胶原海绵浸渍培养基（对照组）前 1 个月，随机选择缺损部位进行处理。3 个月后，获取标本，通过组织学分析评估组织再生情况。
结果：从人牙层外植体上扩散的细胞能够形成细胞集落、产生矿化基质并表达骨钙素，表明它们是成牙骨质细胞样细胞。相比之下，PDL 成纤维细胞不表达骨钙素。17β-雌二醇而非 EMD 可使体外人成牙骨质细胞增殖率增加 2.5 倍。经处理的牙周缺损的组织学结果显示，与对照组（缺损的 28%）相比，17β-雌二醇促进了 2.94mm 的新牙骨质形成（缺损的 45%）。此外，实验组还显示出抑制上皮向下生长和获得新的结缔组织附着。
结论：17β-雌二醇促进了体外人成牙骨质细胞增殖和实验性牙周炎模型中的牙周再生。
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