Healing of Periapical Lesions - Biologic Mediators

Biologic Mediators

There are a number of active biologic mediators that have been implicated in promoting apical resorption. Matrix metalloproteinases (MMPs), which are endogenous zinc-dependent catabolic enzymes, are primarily responsible for the degradation of much of the tissue matrices built on such architecturally important substances as collagen and proteoglycan core proteins. Their biologic activities have been extensively researched and reviewed, and their importance in the pathogenesis of apical periodontitis is obvious. Furthermore, concentrations of IgG antibodies have been found to be nearly five times higher in lesions of apical periodontitis than in uninflamed oral mucosa.

Prostaglandins, specifically PGE2 and PGI2, are important in inflammation and have been implicated in promoting apical resorption. This is because neutrophils, which are rich sources of PGE2, are present when the majority of rapid bone loss occurs during the initial stages of apical periodontitis. It has been illustrated clinically that parenteral administration of indomethacin, an inhibitor of cyclooxygenase, can act to suppress resorption of apical hard tissue.

The predominant mechanism of bone resorption in a periapical lesion, as in the rest of the body, is the performed by osteoclasts. In the periapical lesion, mediators that are normally produced primarily only by osteoblasts are released by many other cells as well, overstimulating proosteoclasts. As a result, these begin to proliferate and several cells fuse to form multinucleated giant cells capable of spreading over the infected, injured site and cause resorption of the periapical alveolar bone.