Löe H
Int Dent J. 1983 Jun;33(2):119-26.
Modern periodontal therapy is based on the fundamental realization that accumulation of bacterial plaque at the gingival margin causes the incipient lesion in periodontal disease. Without interference, most lesions will progress to involve deeper parts of the periodontium. Recent research has revealed that dental plaque comprises a multitude of bacteria in various combinations with a variety of pathogenic potentials, that supragingival plaque is significantly different from the subgingival variety and that particular bacterial species are associated with different periodontal disease states. However, studies have not yet clearly defined a group of bacteria, much less one species, that is responsible for the different forms of periodontal disease. Therefore, the concept of specific pathogenesis is still not ready for clinical application in the prevention and treatment of these diseases, and dental plaque must be dealt with as an entity. Investigators have failed to demonstrate local or systemic factors, other than local aggregates of micro-organisms, that cause gingivitis and periodontitis. As in any other infections, the pathological events and final outcome are determined by the relationship between the microflora and host resistance. Presently, there are no known means by which the host factors can be manipulated to enhance the defense of the periodontium. Therefore, the only rationale for the clinical management of periodontal diseases is to interfere with the microbiological events. Since it is known that gingivitis precedes periodontitis, the only useful approach to preventing the development of periodontitis is to control gingivitis. The treatment of moderate and severe periodontitis also focuses on the elimination of subgingival bacteria and inhibition of recolonization. The target for this is the root surface, which must be detoxified. Surgical elimination of periodontal pockets is still a valid approach to the treatment of the advanced periodontal lesion but only in so far as it provides access to the subgingival accumulations of plaque. The key to success in periodontal therapy is to prepare the tooth surfaces in such a way as to make them biologically acceptable to the gingival tissues. This may be achieved with or without gaining surgical access.
牙龈边缘细菌菌斑的积聚导致牙周疾病的初期病变。如果不加以干预,大多数病变会进展至累及牙周组织的更深部位。最近的研究表明,牙菌斑由多种具有不同致病潜力组合的细菌组成,龈上菌斑与龈下菌斑显著不同,并且特定的细菌种类与不同的牙周疾病状态相关。然而,研究尚未明确界定出一组细菌,更不用说一种细菌,能导致不同形式的牙周疾病。因此,特定发病机制的概念仍未准备好应用于这些疾病的预防和治疗临床中,牙菌斑必须作为一个整体来处理。研究人员未能证明除微生物局部聚集外的局部或全身因素会导致牙龈炎和牙周炎。与任何其他感染一样,病理事件和最终结果取决于微生物群与宿主抵抗力之间的关系。目前,尚无已知方法可操控宿主因素来增强牙周组织的防御能力。因此,牙周疾病临床管理的唯一基本原理是干扰微生物学事件。由于已知牙龈炎先于牙周炎,预防牙周炎发展的唯一有效方法是控制牙龈炎。中度和重度牙周炎的治疗也侧重于消除龈下细菌并抑制再定植。其目标是牙根表面,必须对其进行解毒。手术消除牙周袋仍是治疗晚期牙周病变的有效方法,但前提是它能提供进入龈下菌斑积聚部位的途径。牙周治疗成功的关键是以使牙龈组织在生物学上可接受的方式处理牙面。无论是否通过手术进入,都可以实现这一点。