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In this study, it was suggested that OPG and RANKL are involved in alveolar bone remodeling during orthodontic tooth movement. We examined RANKL localization and osteoclast induction in periodontal tissues during experimental movement of incisors in OPG\u2010deficient mice. To produce orthodontic force, an elastic band was inserted between the upper right and left incisors for 2 or 5 days, and the dissected maxillae were examined for cytochemical and immunocytochemical localization of tartrate\u2010resistant acid phosphatase (TRAP), vacuolar\u2010type H<jats:sup>+<\/jats:sup>\u2010ATPase, and RANKL. Compared to wild\u2010type OPG (+\/+) littermates, TRAP\u2010positive multinucleated cells were markedly induced in the periodontal ligament (PDL) on the compressed side and in the adjacent alveolar bone of OPG\u2010deficient mice. These multinucleated cells exhibited intense vacuolar\u2010type H<jats:sup>+<\/jats:sup>\u2010ATPase along the ruffled border membranes. Because of accelerated osteoclastic resorption in OPG\u2010deficient mice, alveolar bone was severely destroyed and partially perforated at 2 and 5 days after force application. In both wild\u2010type and OPG\u2010deficient mice, RANKL expression became stronger at 2 and 5 days after force application than before force application. There was no apparent difference in intensity of RANKL expression between OPG (+\/+) littermates and OPG\u2010deficient mice. In both wild\u2010type and OPG\u2010deficient mice, expression of RANKL protein was detected in osteoblasts, fibroblasts, and osteoclasts mostly located in resorption lacunae. These results suggest that during orthodontic tooth movement, RANKL and OPG in the periodontal tissues are important determinants regulating balanced alveolar bone resorption. 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