A novel hypothesis concerning the mechanisms of activation, and of control, of periodontal bone loss.

Chronic inflammatory periodontitis fulfills the classical definition of an infectious disease in that it is a disease of the host caused by the activities of one or more parasites. Typically, the etiology of an infectious disease has been defined as the specific microbe which incites the disease process, even though the quality and nature of host responses to the pathogen may underlie much of the pathology seen. This approach in the study of the etiology of chronic periodontitis has not resulted in the identification of a single 'periodontopathogen', but rather is leading to the realization that multiple sets of microbes may induce the same endpoint, albeit some possibly more efficiently than others. The premise of this paper is that a different view of the literature in the area, with the primary emphasis on the mechanisms of damage and resistance to periodontitis, reveals a probable commonality, rather than a plethora of diseases. The concept of a mechanism-based etiology, rather than of a microbe-based one, deserves consideration for this complex, host-parasite interaction. The novel hypothesis presented here is that the common virulence factor of chronic periodontitis is lipopolysaccharide (LPS), that the central damaging mediator is a cyclooxygenase product of arachidonic acid (probably prostaglandin E2), and that the critical resistance mechanism that limits disease activity is the effective, peripheral neutralization of LPS by emigrated polymorphonuclear neutrophils.