Tokutomi Fumiaki, Wada-Takahashi Satoko, Sugiyama Shuta, Toyama Toshizo, Sato Takenori, Hamada Nobushiro, Tsukinoki Keiichi, Takahashi Shun-suke, Lee Masaichi Chang-il
Department of Oral Science, Graduate School of Dentistry, Kanagawa Dental University, 82 Inaoka-cho, Yokosuka, Kanagawa 238-8580, Japan.
Department of Infection Control, Division of Microbiology, Graduate School of Dentistry, Kanagawa Dental University, Kanagawa, Japan.
Arch Oral Biol. 2015 Jun;60(6):911-8. doi: 10.1016/j.archoralbio.2015.02.012. Epub 2015 Feb 21.
Porphyromonas gingivalis (P. gingivalis) is one of the prominent periodontal pathogens and is the most important bacteria involved in the onset and exacerbation of periodontitis. P. gingivalis is an anaerobic, Gram-negative coccobacillus that plays a role in the progression of periodontal disease by promoting alveolar bone resorption. The aim of the present study was to examine P. gingivalis-induced osteoclastic bone resorption in the stroke-prone spontaneously hypertensive rat (SHRSP), in which oxidative stress induced by reactive oxygen species (ROS) is increased. In the present study, we used animals orally challenged with P. gingivalis as a chronic inflammation model. Horizontal bone loss around the maxillary molars was assessed morphometrically. Animals were divided into four groups: (1) P. gingivalis-non-infected Wister Kyoto Rat (WKY), (2) orally challenged with P. gingivalis WKY (WKY + Pg), (3) P. gingivalis-non-infected SHRSP, and (4) orally challenged with P. gingivalis SHRSP (SHRSP + Pg). Alveolar bone resorption was significantly increased in the orally challenged with P. gingivalis groups, and was accelerated in the SHRSP group. Histological analysis revealed that the infiltration of inflammatory cells was absent in all groups. However, the infiltration of osteoclasts was observed in the SHRSP + Pg and SHRSP groups. We examined P. gingivalis-induced alveolar bone loss in both the SHRSP and WKY. The results obtained demonstrated that P. gingivalis-induced alveolar bone loss would be involved in hypertension and stroke animal model, such as SHRSP and/or periodontal disease.
牙龈卟啉单胞菌（P. gingivalis）是主要的牙周病原体之一，也是参与牙周炎发生和加重的最重要细菌。牙龈卟啉单胞菌是一种厌氧革兰氏阴性球杆菌，通过促进牙槽骨吸收在牙周疾病进展中发挥作用。本研究的目的是在易中风自发性高血压大鼠（SHRSP）中检测牙龈卟啉单胞菌诱导的破骨细胞性骨吸收，在该模型中由活性氧（ROS）诱导的氧化应激增加。在本研究中，我们使用经牙龈卟啉单胞菌口服攻击的动物作为慢性炎症模型。通过形态计量学评估上颌磨牙周围的水平骨丢失。动物分为四组：（1）未感染牙龈卟啉单胞菌的京都Wistar大鼠（WKY），（2）经牙龈卟啉单胞菌口服攻击的WKY（WKY + Pg），（3）未感染牙龈卟啉单胞菌的SHRSP，以及（4）经牙龈卟啉单胞菌口服攻击的SHRSP（SHRSP + Pg）。在经牙龈卟啉单胞菌口服攻击的组中牙槽骨吸收显著增加，并且在SHRSP组中加速。组织学分析显示所有组均无炎症细胞浸润。然而，在SHRSP + Pg和SHRSP组中观察到破骨细胞浸润。我们在SHRSP和WKY中均检测了牙龈卟啉单胞菌诱导的牙槽骨丢失。获得的结果表明牙龈卟啉单胞菌诱导的牙槽骨丢失与高血压和中风动物模型如SHRSP和/或牙周疾病有关。
