The pathogenesis of human periodontitis: an introduction.

The pathogenesis of human periodontitis was placed on a rational footing for the first time by Page & Schroeder in 1976 (7). Although the details were scanty, the general principles and the overall conclusions reached in that article, which became a citation classic, are still largely acceptable today. An enormous amount has been learned about all aspects of human periodontitis, including its pathogenesis, since 1976. Several reviews of the pathogenesis have been written during that time (1, 3-6, 9-11), but with one possible exception (4), no publication has summarized currently available data and organized it into a relatively complete and rational picture. There are good reasons for this. Whereas the amount of information available in 1976 was limited and all relevant information could be accommodated in a single lengthy article, this is no longer the case. Although much of the detail is still missing, a far more complete and compelling picture of the pathogenesis is now emerging. Indeed, it is possible to approach the pathogenesis not only from the cellular level as was done in 1976 but to extend the story to the molecular level and to some extent to the genetic level. A staggering amount of information is available about the pathogenesis of human periodontitis. The information derives from a broad range of fields and disciplines, and much of it is highly specialized. We enthusiastically accepted the invitation to lead the effort to create a volume of PERIODONTOLOGY 2000 devoted completely to the pathogenesis of human periodontitis. Such a volume provides sufficient space for an inclusive, highly integrated result and, equally important, it provides the opportunity to include many of the world’s experts, whose collective efforts far surpass those that could have been achieved by any one or two individuals. Even with this format, we could not be all-inclusive, and many recognized experts could not be included. Our goals for this volume are to provide chapters that collectively present the current understanding of the pathogenesis of periodontitis in a userfriendly manner. Although the individual chapters are intended to be able to stand alone, they are all highly interrelated and integrated and the total is far greater than the sum of the parts. We have chosen the final chapter as a discussion section in which we summarize highlights of all the chapters, emphasize broad concepts, make clinical application where appropriate, speculate based on the data and point out future directions of the field. Experts agree that human periodontitis is initiated and perpetuated by a small group of predominantly gram-negative, anaerobic or microaerophilic bacteria that colonize the subgingival area. Indeed, at the 1996 World Workshop on Clinical Periodontics, the relevant working group concluded (2) that most human periodontitis is caused by Porphyrornonas gingivalis, Bacteroides forsythus and Actinobacillus actinornyceterncornitans. During the 1970s and 1980s, great strides were made in elucidating the infectious nature of human periodontitis; in the 1990s we have come to realize that, although bacteria are essential, they are insufficient for the disease to occur. Host factors such as inheritance, tobacco smoking and various other risk factors may even outweigh the bacteria as determinants of whether the disease occurs and of the severity of clinical outcome. These observations have led to major changes in ideas and concepts about pathogenesis, prevention and treatment. Over the past 10 to 15 years, substantial new information has been obtained about how these bacteria cause the formation of periodontal pockets, conversion of junctional epithelium to pocket epithelium and destruction of the alveolar bone and connective tissues of the gingiva and periodontal ligament. Bacteria mostly cause the observed tissue destruction indirectly, and they do so by activating various components of the host defense systems in such a manner that destruction ensues. It is enigmatic that the same host systems that provide protection and de-