STUDY OF ADHESIN FROM Aggregatibacter actinomycetemcomitans LOCAL ISOLATE ON ALVEOLAR BONE DESTRUCTION IN AGGRESSIVE PERIODONTITIS DISEASE

R. D. Ridwan, Tuti Kusumaningsih, Sidarningsih, Soetjipto
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Abstract

Adhesion is a powerful survival mechanism as well as a virulence mechanism for bacterial pathogens. Bacterial adhesin is a media for bacteria to invade the host. Bacterial adhesin,is a medium for bacteria to invade the host. Baterial adhe-sion, moreover, is depend on the ligand interaction as a signaling mediator that will influence the invasion process and increase pro and anti-inflammatory due tob the influence of the receptors of innate immune response. Aggregatibacter actimycetemcomitans (A.actinomycetemcomitan) have many virulence factors that may result in tissue and alveolar bone damage. One of the virulence factors is adhesin that can be isolated from the fimbriae. This research purposed to analyze the ability of adhesin protein from A.actinomycetemcomitan that cause the destruction of alveolar bone. Thus, the number of osteoblasts and osteoclasts as well as osteocalcin expression can be used as a marker of damage on the alveolar bone of Wistar rats. The research was conducted through several processes. First, the adhesin of A.actinomycetemcomitan with a molecular weight (MW) of 24 kDa is induced into Wistar rats. Next, to determine the number of osteoblasts and osteoclasts performed, hematoxylin eosin staining is conducted. Meanwhile, to determine osteocalcin expression performed, immunohistochemical techniques is used. This research shows the decreasing of the number of osteoblasts and increasing of the number of osteoclasts in the treatment groups induced by adhesin proteins, A. actinomycetemcomitans + adhesin protein, and A.actinomycetemcomitan compared those in the control group. It also shows the increasing of osteocalcin expressions on the alveolar bone of Wistar rats in the groups induced by adhesin proteins, A. actinomycetemcomitans + adhesin protein, and A. actinomycetemcomitans than those in the control group. It can be concluded that the adhesin protein of A. actinomycetemcomitans plays an important role in the destruction of alveolar bone through the reduction of the number of osteoblasts, the increasing of the number of osteoclasts and oste-ocalcin expression in aggressive periodontitis.
放线菌局部分离黏附素对侵袭性牙周炎牙槽骨破坏作用的研究
粘附是细菌病原体的一种强大的生存机制,也是一种毒力机制。细菌黏附素是细菌侵入宿主的媒介。细菌黏附素,是细菌侵入宿主的媒介。此外,细胞粘附依赖于配体相互作用,作为一种信号介质,它将影响入侵过程,并由于先天免疫反应受体的影响而增加促炎和抗炎。放线菌聚集菌(a.a actinomycetemcomitans)有许多毒力因子可导致组织和牙槽骨损伤。其中一个毒力因子是粘连素,它可以从菌毛中分离出来。本研究旨在分析放线菌胞杆菌黏附蛋白对牙槽骨破坏的作用。因此,成骨细胞和破骨细胞的数量以及骨钙素的表达可以作为Wistar大鼠牙槽骨损伤的标志。这项研究是通过几个过程进行的。首先,将分子量为24 kDa的放线菌黏附素诱导Wistar大鼠。接下来,通过苏木精伊红染色来确定成骨细胞和破骨细胞的数量。同时,采用免疫组化技术测定骨钙素的表达。本研究显示,与对照组相比,粘附素蛋白、放线菌蛋白+粘附素蛋白、放线菌蛋白诱导的各处理组成骨细胞数量减少,破骨细胞数量增加。黏附素蛋白、放线菌+黏附素蛋白、放线菌诱导组Wistar大鼠牙槽骨骨钙素的表达均高于对照组。由此可见,放线菌黏附蛋白在侵袭性牙周炎中通过降低成骨细胞数量、增加破骨细胞数量和骨钙素表达,对牙槽骨的破坏起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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