Williams Ray C
Department of Periodontology, School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
J Periodontol. 2008 Aug;79(8 Suppl):1552-9. doi: 10.1902/jop.2008.080182.
Throughout the 20th century, an understanding of the role of causative bacteria and the susceptible host in the initiation and progression of periodontal disease(s) has emerged from the research efforts of scientists and clinicians worldwide. Over time, specific bacterial types, such as Porphyromonas gingivalis, were discovered and shown to be important in the cause of periodontal disease. At the same time, inflammatory mediators, such as prostaglandins and interleukins, and enzymes, such as matrix metalloproteinases, were discovered and found to be important participants in the destruction of periodontal tissues. Acquired and inherited environmental risk factors began to emerge that could explain, in part, the susceptibility of individuals to periodontal disease. The discovery of antibiotics, beginning with sulfanilamide, penicillin, and streptomycin, led to additional strategies for managing periodontal disease. With the discovery of the mechanism of action of aspirin, scientists began to develop new strategies for treating diseases that focused on controlling inflammation. Thus, host-modulating therapies emerged for the management of periodontal disease through the control of inflammation. At the end of the 20th century, an old concept in medicine and dentistry reappeared: that the infection and inflammation of periodontal disease in the mouth could reach distant sites via the bloodstream. Apparently oral disease could, in fact, contribute to systemic diseases, such as atherosclerosis, diabetes, and adverse outcomes in pregnancy. This concept of the oral health-general health connection is now supported by sound and rational evidence-based observations. Clearly, the 21st century has arrived with a new understanding of the nature of periodontal diseases based on a notable era of discovery. There is a promising future for preventing and treating this common and troubling condition that affects not just the mouth but also the whole body.
在整个20世纪,通过全球科学家和临床医生的研究努力,人们对致病细菌和易感宿主在牙周疾病发生和发展中的作用有了认识。随着时间的推移,发现了特定的细菌类型,如牙龈卟啉单胞菌,并证明其在牙周疾病病因中很重要。同时,还发现了炎症介质,如前列腺素和白细胞介素,以及酶,如基质金属蛋白酶,并发现它们是牙周组织破坏的重要参与者。后天和遗传的环境风险因素开始出现,这在一定程度上可以解释个体对牙周疾病的易感性。从磺胺类药物、青霉素和链霉素开始的抗生素发现,带来了治疗牙周疾病的其他策略。随着阿司匹林作用机制的发现,科学家们开始制定新的疾病治疗策略,重点是控制炎症。因此,通过控制炎症出现了宿主调节疗法来治疗牙周疾病。在20世纪末,医学和牙科领域一个古老的概念再次出现:口腔中牙周疾病的感染和炎症可通过血液循环到达远处部位。显然,口腔疾病实际上可能导致全身性疾病,如动脉粥样硬化、糖尿病以及妊娠不良结局。口腔健康与全身健康联系的这一概念现在得到了合理且基于证据的观察结果的支持。显然,21世纪带着基于一个显著发现时代对牙周疾病本质的新认识到来了。预防和治疗这种不仅影响口腔而且影响全身的常见且令人困扰的疾病有着光明的未来。