Kumar Purnima S, Griffen Ann L, Moeschberger Melvin L, Leys Eugene J
Section of Peridontology, College of Dentistry, The Ohio State University, Columbus, Ohio 43218, USA.
J Clin Microbiol. 2005 Aug;43(8):3944-55. doi: 10.1128/JCM.43.8.3944-3955.2005.
Most studies of the bacterial etiology of periodontitis have used either culture-based or targeted DNA approaches, and so it is likely that pathogens remain undiscovered. The purpose of this study was to use culture-independent, quantitative analysis of biofilms associated with chronic periodontitis and periodontal health to identify pathogens and beneficial species. Samples from subjects with periodontitis and controls were analyzed using ribosomal 16S cloning and sequencing. Several genera, many of them uncultivated, were associated with periodontitis, the most numerous of which were gram positive, including Peptostreptococcus and Filifactor. The genera Megasphaera and Desulfobulbus were elevated in periodontitis, and the levels of several species or phylotypes of Campylobacter, Selenomonas, Deferribacteres, Dialister, Catonella, Tannerella, Streptococcus, Atopobium, Eubacterium, and Treponema were elevated in disease. Streptococcus and Veillonella spp. were found in high numbers in all samples and accounted for a significantly greater fraction of the microbial community in healthy subjects than in those with periodontitis. The microbial profile of periodontal health also included the less-abundant genera Campylobacter, Abiotrophia, Gemella, Capnocytophaga, and Neisseria. These newly identified candidates outnumbered Porphyromonas gingivalis and other species previously implicated as periodontopathogens, and it is not clear if newly identified and more numerous species may play a more important role in pathogenesis. Finally, more differences were found in the bacterial profile between subjects with periodontitis and healthy subjects than between deep and shallow sites within the same subject. This suggests that chronic periodontitis is the result of a global perturbation of the oral bacterial ecology rather than a disease-site specific microbial shift.
大多数关于牙周炎细菌病因的研究都采用了基于培养或靶向DNA的方法，因此很可能仍有未被发现的病原体。本研究的目的是利用与慢性牙周炎和牙周健康相关的生物膜进行非培养定量分析，以鉴定病原体和有益菌种。使用核糖体16S克隆和测序对牙周炎患者和对照组的样本进行分析。有几个属与牙周炎相关，其中许多属无法培养，数量最多的是革兰氏阳性菌，包括消化链球菌属和丝状杆菌属。巨球形菌属和脱硫球菌属在牙周炎中有所增加，弯曲菌属、栖瘤胃普雷沃菌属、脱铁杆菌属、戴阿李斯特菌属、卡顿菌属（学名：Catonella）、坦纳菌属、链球菌属、阿托波菌属、真杆菌属和密螺旋体属的几个菌种或系统型在疾病中有所增加。在所有样本中都发现了大量的链球菌属和韦荣球菌属，它们在健康受试者的微生物群落中所占比例明显高于牙周炎患者。牙周健康的微生物谱还包括含量较少的弯曲菌属、营养缺陷菌属、孪生球菌属、二氧化碳嗜纤维菌属和奈瑟菌属。这些新鉴定出的菌种数量超过了牙龈卟啉单胞菌和其他先前被认为是牙周病原体的菌种，目前尚不清楚新鉴定出的数量更多的菌种是否可能在发病机制中发挥更重要的作用。最后，牙周炎患者与健康受试者之间的细菌谱差异比同一受试者的深部和浅部位点之间的差异更大。这表明慢性牙周炎是口腔细菌生态系统整体紊乱的结果，而不是疾病部位特异性的微生物变化。
