Relationship of Bacteria to the Etiology of Periodontal Disease
Relationship of Bacteria to the Etiology of Periodontal Disease
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细菌与牙周病病因的关系
DOI：
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发表时间：
1970
期刊：
影响因子：
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通讯作者：
S. Socransky
中科院分区：
文献类型：
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作者：
S. Socransky
引言在介绍人类牙周病的细菌病因学的讨论，这是值得讨论的一些独特的问题面临的调查。首先，牙周病是一种多种形式的慢性疾病。如果支撑牙根的牙槽骨长度约为20 mm，在20年内丢失，骨破坏的速度平均约为1 mm/年，或小于1 mm/月的十分之一。破坏不可能以恒定的速度发生，但可能会有恶化和缓解的时期。牙周破坏的缓慢速度和区分牙周病活动性的困难联合收割机使疾病决定因素的证明复杂化。研究牙周病细菌病因的第二个问题是宿主抵抗力的变化。“一种对一个人造成严重破坏的有害刺激可能对另一个人几乎没有影响。当这个问题与微生物群的复杂性相结合时，很难将病原学作用分配给任何生物体。第三个问题是缺乏良好的动物模型系统。目前使用的每种动物模型系统都有一定的缺点。所有人共同的一个主要缺点是存在与人类微生物群不同的驻留口腔微生物群。由于这种差异，在动物中获得的结果不能直接转移到人身上。此外，在许多情况下，动物的固有微生物群似乎阻止了人类口腔微生物在试验动物口腔中的建立。微生物学家面临的第四个问题是人类牙周袋中微生物的复杂性。通常可以从该地点分离出大约50个或更多物种的大量微生物群。许多分离物很难培养，因为它们对大气中的氧气敏感，或者依赖于其他细菌或活的哺乳动物细胞提供的不寻常的生长要求。最后，人类牙周病可能是一种单一病因的疾病，其临床变异主要是由于宿主反应的差异。或者，“牙周病”可以是一组具有不同病因的疾病。在后一种情况下，牙周病是影响器官系统的许多疾病的集合术语。这类似于使用“肺部疾病”作为一个包含性术语来涵盖由肺炎球菌、结核杆菌、葡萄球菌等引起的感染。如果牙周病是一组疾病，那么在复杂的、持续存在的微生物群中挑选出病原体将是一项具有挑战性的任务。本报告的目的是（1）引用细菌在牙周病病因学中发挥作用的证据，（2）指出人类牙龈缝隙区域微生物的性质，（3）讨论确定哪些微生物可能导致牙周病的尝试，（4）指出牙周破坏的一些潜在机制。
Introduction In introducing a discussion of the bacterial etiology of human periodontal disease, it is worthwhile to discuss some of the unique problems confronting the investigator. First, periodontal disease is a chronic disease in many of its forms. If the alveolar bone supporting a tooth root that is approximately 20 mm in length were lost in 20 years, the rate of bone destruction would average approximately 1 mm/year, or less than one tenth of 1 mm/month. It is unlikely that destruction would occur at a constant rate, but there would probably be periods of exacerbation and remission. The slow rate of periodontal destruction and the difficulty in distinguishing periodontal disease activity combine to complicate the demonstration of determinants of the disease. A second problem in studying the bacterial etiology of periodontal disease is variation in host "resistance." A noxious stimulus that causes severe destruction in one individual might have little or no effect in another individual. When this problem is coupled with the complexity of the microbiota, it becomes difficult to assign an etiologic role to any organism. A third problem is the lack of a good animal model system. Each animal model system currently in use has certain drawbacks. A major drawback common to all is the presence of a resident oral microbiota that is different from the human microbiota. Because of this difference, results obtained in animals are not directly transferrable to man. In addition, in many instances the indigenous microbiota of the animals appears to prevent the establishment of human oral organisms in the oral cavity of test animals. A fourth problem facing the microbiologist is the complexity of the microbiota inhabiting the human periodontal pocket. A great number of microbiota of perhaps 50 or more species can be commonly isolated from this site. Many of the isolates are difficult to cultivate because of a sensitivity to atmospheric oxygen or a dependence on unusual growth requirements provided by other bacteria or living mammalian cells. Finally, periodontal disease in humans could be a disease of single etiology with clinical variations that are principally due to differences in host response. Or alternatively, "periodontal disease" could be a group of diseases with differing etiology. In the latter instance, periodontal disease is a collective term for a number of diseases affecting an organ system. This is analogous to using "lung disease" as an inclusive term to cover infections caused by pneumococci, tubercle bacilli, staphylocci, and so on. If periodontal disease is a group of diseases, the sorting out of the etiologic agents in a complex, continually present microbiota would be a challenging task. The purpose of the present report is to (1) cite evidence that bacteria play a role in the etiology of periodontal disease, (2) indicate the nature of the microorganisms that reside in the human gingival crevice region, (3) discuss attempts to determine which of these organisms may be responsible for periodontal disease(s) and, (4) indicate some potential mechanisms of periodontal destruction.