PERIAPICAL INFLAMMATORY RESPONSES AND THEIR MODULATION

Periapical inflammatory responses occur as a consequence of bacterial infection of the dental pulp, as a result of caries, trauma, or iatrog enic insult. Periapical inflammation stimulates the formation of granu lomas and cysts, with the destruction of bone. These inflammatory resp onses are complex and consist of diverse elements. Immediate-type resp onses-including vasodilatation, increased vascular permeability, and l eukocyte extravasation-are mediated by endogenous mediators, including prostanoids, kinins, and neuropeptides, Non-specific immune responses -including polymorphonuclear leukocyte and monocyte migration and acti vation, and cytokine production-are elicited in response to bacteria a nd their products. Interleukin-1 and prostaglandins in particular have been implicated as central mediators of periapical bone resorption. C hronic periapical inflammation further involves specific T- and B-cell -mediated anti-bacterial responses, and activates a network of regulat ory cytokines which are produced by Th1- and Th2-type T-lymphocytes. V arious naturally occurring and genetically engineered models of immuno deficiency are beginning to help elucidate those components of the imm une system which protect the pulpal/periapical complex. Both specific and non-specific responses interface with and are regulated by the neu ral system. The modulation of these responses by immune response modif iers, cytokine antagonists, and other novel therapeutic agents is disc ussed. As an experimental model, periapical inflammation has many adva ntages which permit it to be used in studies of microbial ecology and pathogenesis, host response, neuroimmunology, and bone resorption and regeneration.