Inflammatory and immunological aspects of the pathogenesis of human periapical lesions

As summarized in Fig. 1, present studies indicate that multiple mechanisms are involved in the pathological changes that are associated with human periapical lesions. They include specific immunological reactions as well as nonspecific mediators of inflammation such as vasoactive amines, kinins, complement fragments, and arachidonic acid metabolites. Mechanical injury to the periapical tissue is likely to initiate the release of nonspecific mediators of inflammation. In addition, continuous egress of antigens from a pathologically involved root canal into the periapical tissue can result in one or a combination of various types of immunological reaction. Present data indicate that the arachidonic metabolites and the complement system play an important role in bone resorption associated with human periapical lesions. Because of complex interactions between the various components of inflammatory effector systems, the dominance of any one substance or reaction in the pathogenesis of human periapical lesions may be difficult to establish.