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These inflammatory responses are complex and consist of diverse elements. Immediate-type responses-including vasodilatation, increased vascular permeability, and leukocyte extravasation-are mediated by endogenous mediators, including prostanoids, kinins, and neuropeptides. Non-specific immune responses-including polymorphonuclear leukocyte and monocyte migration and activation, and cytokine production-are elicited in response to bacteria and their products. Interleukin-1 and prostaglandins in particular have been implicated as central mediators of periapical bone resorption. Chronic periapical inflammation further involves specific T- and B-cell-mediated anti-bacterial responses, and activates a network of regulatory cytokines which are produced by Th 1- and Th2-type T-lymphocytes. Various naturally occurring and genetically engineered models of immunodeficiency are beginning to help elucidate those components of the immune system which protect the pulpal\/periapical complex. Both specific and non-specific responses interface with and are regulated by the neural system. The modulation of these responses by immune response modifiers, cytokine antagonists, and other novel therapeutic agents is discussed. 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