ULTRASTRUCTURE OF EXPERIMENTAL PERIODONTITIS

我们计划进行免疫细胞化学研究，以定位纤维连接蛋白(FN) 正常Beagle牙周组织中I型和III型胶原(Col I、Col III)的表达 并确定它们在结扎诱导和 自然发生的牙周炎。我们将测量FN、第一列和第三列 并将这些水平与炎症相关联，如 通过光镜、电子显微镜和免疫细胞化学测定。vbl.使用 同样的方法，我们将研究胶原酶的抑制效果 米诺环素对牙周沟FN、Col I、Col III水平的影响 流体。我们预计将显示监控FN、I列和III列 牙周沟液是测量正在进行的组织的准确方法 毁灭。如果小猎犬的研究证明是令人鼓舞的，我们将开始 在人类身上也进行了类似的研究。在一个相关项目中，我们将使用 用免疫细胞化学方法检测牙周组织中FN的存在 斑块和结石。 我们将继续对穿透和放射自显影进行研究 小分子代谢物在牙龈上皮细胞中的掺入 至牙周沟区。我们希望确定细胞间的 沟通和胞质内运输是一条重要的途径。 牙龈上皮。初步研究结果表明，进一步的研究 看起来很有价值。在这笔赠款的任期内，我们进行了 胶原蛋白分泌和成纤维细胞结构的大量基础研究。 我们建议通过定位成纤维细胞来继续这些重要的研究 通过荧光显微镜观察富含应力纤维的抗肌动蛋白和 带有抗波形蛋白抗体的中间丝。我们还将检查 纤维连接蛋白的分布与纤维神经丛发育的关系 通过电子显微镜免疫细胞化学观察先前区域的接触情况 经光学显微镜鉴定为富含应力纤维的部位 发展。我们希望将它们的存在与抵抗压力联系起来。 在牙周结缔组织中。体外研究也在计划中。 进一步评价牙周韧带的极性和运动性 成纤维细胞与应力纤维的存在和分布 和纤维连接蛋白。

We plan to conduct immunocytochemical studies to localize fibronectin (FN) and collagen types I and III (Col I, Col III) in normal beagle periodontium and to determine changes in their distribution during ligature-induced and naturally-occurring periodontitis. We will measure FN, Col I, and Col III in gingival sulcular fluid and correlate these levels with inflammation as determined by light and electron microscopy and immunocytochemistry. Using the same methods, we will study the effect of inhibiting collagenase with minocycline on the level of FN, Col I, and Col III in gingival sulcular fluid. We expect to show that monitoring FN, Col I, and Col III in gingival crevicular fluid can be an accurate way to measure ongoing tissue destruction. If the beagle studies prove encouraging, we will begin similar investigations in humans. In a related project, we will use immunocytochemical methods to investigate the presence of FN in gingival plaque and calculus. We will continue autoradiographic studies of the penetration and incorporation into gingival epithelial cells of small metabolites applied to the gingival sulcular area. We hope to determine whether cell-to-cell communication and intracytoplasmic transport is a significant pathway in gingival epithelium. Preliminary findings suggest that further studies appear worthwhile. During the tenure of this grant, we have conducted numerous and basic studies of collagen secretion and fibroblast structure. We propose to continue these important studies by localizing fibroblasts rich in stress fibers by fluorescent microscopy with anti-actin and intermediate filaments with anti-vimentin antibodies. We will also examine the distribution of FN in relation to the development of fibronexus contacts by electron microscopy immunocytochemistry in areas previously identified by light microscopy to be sites rich in stress fiber development. We hope to correlate their presence with resistance to stress in the periodontal connective tissues. In vitro studies are also planned to further evaluate the polarity and locomotion of periodontal ligament fibroblasts in relation to the presence and distribution of stress fibers and fibronectin.