Ten years have passed since a paradigm shift in the pathogenesis of periodontitis was proposed by Page & Kornman (16). A plethora of research papers has since revised our previous concepts in this field. In particular, important information has appeared on cellular, molecular and genetic aspects of destructive periodontal disease. Recent conceptual and technical advances have provided us with further insights into the infectious agents and the characteristics of the host immune response in periodontal diseases. The information gained may help to improve our ability to diagnose and treat such diseases. In 1997, a symposium at North Carolina Chapel Hill entitled ÔPeriodontal diseases and human health: New edition in periodontal medicineÕ advanced the notion that oral infections may have powerful and multiple influences on the occurrence and severity of systemic conditions and diseases (27). Since then, numerous publications in dental and medical journals have focused on the relationship between periodontal disease and systemic conditions, especially cardiovascular diseases, diabetes and respiratory pathosis. Progress in this field within the last few years has been tremendous. ÔPeriodontal disease and coronary heart disease: a reappraisal of the exposureÕ (1), ÔHigh serum antibody levels to Porphyromonas gingivalis predict myocardial infarctionÕ (19), ÔAntibodies to periodontal pathogens and stroke riskÕ (18), ÔEarly carotid atherosclerosis in subjects with periodontal diseasesÕ (26), ÔGender differences in the relationship between periodontal disease tooth loss, and atherosclerosisÕ (3), ÔPeriodontal disease and biomarkers related to cardiovascular diseasesÕ (7), ÔPeriodontal disease and mortality in type 2 diabetesÕ (22) and ÔOral bacteria in the occluded arteries of patients with Buerger diseaseÕ (6), are titles of recently published articles in medical journals, which have identified a positive correlation between periodontal disease and systemic diseases. Stamm (27) mentioned that practitioners of obstetrics, cardiovascular disease and periodontics are collaborating in scientific progress in ways not previously imagined. Recently, it has been suggested that herpesviruses comprise an important source for triggering periodontal tissue destruction. Herpesvirus infections may initiate or accelerate periodontal breakdown via their ability to stimulate cytokine release from host cells, or they might impair host defense mechanisms, resulting in heightened virulence of resident periodontopathic bacteria (24). In the light of the potential importance of mammalian viruses in periodontal diseases (23–25), a discussion of virally induced host responses is also included in this volume. Microbial antigens and virulence factors elicit an immediate inflammatory and immune response from the host. The host reacts to microbial insults by producing cytokines, eicasonoids, kinins, complement activation products and matrix metalloproteinases. Some of these inflammatory mediators participate in periodontal ligament and bone destruction. In turn, the inflammatory response is regulated by genetic and environmental modifiers. As reported by Page et al.(17), bacteria are essential in, but not sufficient to cause, periodontitis, and host factors, such as heredity, and environmental factors, such as smoking, are important determinants of periodontal disease occurrence and severity. Bacteria may cause periodontal tissue destruction indirectly by activating various components of the host defense system. When activated, these host systems may provide protection at the cost of some level of periodontal destruction. Periodontal researchers have extensively studied …