Immunological mechanisms have been implicated in the pathogenesis of periodontal disease for over 25 years. Studies throughout the 1970s established that advanced forms of the disease were dominated by B-cells/plasma cells while early and putative stable forms of the disease were dominated by T-cells/lymphocytes. Based on these observations, a model of disease was put forward which highlighted a possible T-cell/macrophage immunoregulatory imbalance being involved in disease pathogenesis. Studies throughout the 1980s have supported such a concept although the precise nature of this imbalance remains elusive. At the same time, clinical studies have established that patient susceptibility may be of overriding importance in determining disease outcome. In this context therefore, factors which influence this susceptibility should be fundamental in determining periodontal disease activity. These factors may include genetic variation between individuals in the way in which they respond to periodontopathic bacteria upon which environmental factors would be superimposed. These environmental factors would include anything that altered the balance between the host and the parasite and may be as diverse as recent viral infections resulting in T-cell anergy or physical and mental stress. Recent studies have shown that in elite atheletes, physical stress during training and competition leads to a suppression of mucosal immunity as evidenced by a reduction in salivary IgA. The subsequent effect of these environmental factors at the level of the periodontium, however, remains to be determined.