Authors: Torabinejad M, Eby WC, Naidorf IJ.
Title: Inflammatory and immunological aspects of the pathogenesis of human periapical lesions.
Journal: J Endod
Date: Nov 1985
Citation: 11(11):479-88
Category: Endodontic Biology, Histology and Physiology
Evidence-based Ranking: 5
Purpose/ Objectives: To review concepts regarding mediators and mechanisms involved in the pathogenesis of human periapical lesions.

Discussion: Pathological changes associated with human periapical lesions of pulpal origin are the result of activation of nonspecific inflammatory reactions as well as specific immunological responses. Trauma to the periapical tissue and rupture of blood vessels can activate intrinsic and exsinsic pathways of the clothing system. Contact of the Hageman factor with collagen basement membrane or endotoxins in perapical tissues can activate the kinin system which contribute to the inflammatory process and its consequences such as swelling and pain in periapical lesion. Activation of the complement system in periapical tissues can contribute to bone resorption either by destruction of the bone or by inhibition of new bone formation. The activated complement system can also stimulate phospholipids metabolism and cause release of lipids from cell membrane, which provides a source for the prostaglandin precursor, arachidonic acid. In addition to the production of the nonspecific inflammatory mediators, the host has a number of defensive mechanisms that are acquired by specific interaction with invading antigens. This acquired immunity is the result of learning by the lymphoid cells, which have specialized receptors for foreign materials.

Author’s Conclusion: Multiple mechanisms are involved in the pathological changes that are associated with human periapical lesions. Because of complex interactions between the various components of inflammatory systems, the dominance of any one substance or reaction in the pathogenesis of human periapical lesions may be difficult to establish.