Proinflammatory mediators related to orthodontically induced periapical root resorption in rat mandibular molars.

Abstract

The early phase of orthodontic tooth movement involves acute inflammatory response that may induce bone resorption. The aim of this study was to localize and quantify cells in the periodontium expressing proinflammatory mediators during orthodontically induced periapical root resorption of the rat mandibular molars. The levels of proinflammatory cytokines interleukin-1 (IL-1) α and β, tumor necrosis factor-α (TNF-α), inflammatory enzymes cyclooxygenase (COX) 1 and 2, and their product prostaglandin E2 (PGE2) in the root resorption site were compared to those in the corresponding area of the untreated periodontal ligament (PDL) of physiologically drifting teeth. Continuous heavy orthodontic force was applied to the mandibular first molar for 8 and 15 days while in occlusion to induce root resorption. Frozen sections including root resorption lacunae were analyzed for the activity of non-specific esterase (NSE) and tartrate-resistant acid phosphatase (TRAP) by enzyme histochemistry and for the expression of IL-1α, IL-1β, TNF-α, COX-1, COX-2, and PGE2 by immunohistochemistry. The active root resorption lacunae had significantly more TRAP-positive multinucleated odontoclasts, whereas the number of NSE-positive cells of the monocyte-macrophage lineage did not differ from that in the control PDL. Several types of periodontal cells exhibited a significant increase in the expression of IL-1α, IL-1β, TNF-α, COX-2, and PGE2 in the root resorption zone, while COX-1 was rarely detected. These data suggest that proinflammatory mediators expressed in periodontal cells may synergistically promote apical root resorption in response to continuous heavy mechanical force applied to teeth.