The osteoclast is the major cellular agent of bone resorption. Hormonal stimulation of bone resorption is indirect and depends on the osteoblastic function. Protease production is the final common pathway through which osteoblastic cells initiate osteoclastic resorption. Exposition of the mineralised matrix and contact with the osteoclasts always comes before resorption, regardless of the stimulating agent involved in the resorption process. In orthodontic conditions, production and activation of osteoclasts may be attained through different ways. Inflammation subsequent to tissue damage and bioelectric perturbations associated to alveolar bending can be considered as two major events which may lead to increase bone resorption and orthodontic tooth displacement. The precise transduction mechanism of an orthodontic force into cellular resorbing activity is still obscure.