Tooth movement is induced by bone remodeling during orthodontic treatment. Bone remodeling is regulated by various cytokines. Especially interleukin-1 (IL-1β), a cytokine present in periodontal ligaments of experimentally moved teeth, elicits bone resorption. In these processes, IL-1 -induced bone resorption is mediated by interleukin-6 (IL-6) and granulocyte macrophage-colony stimulating factor (GM-CSF) secreted from osteoblasts. Periodontal ligament cells, which function as an anchorage for tooth, lie between alveolar bone and cementum. Therefore cytokines produced in the periodontal ligament (PDL) cells may also directly affect alveolar bone resorption in orthodontic tooth movement. Here I have examined whether PDL cells empress IL-1β, interleukin-6 (IL-6) and granulocyte macrophage-colony stimulating factor (GM-CSF) mRNA and secrete those cytokines in response to IL-1β. Finally I have investigated whether IL-6 produced from PDL cells induces osteoclast formation in mouse bone marrow cell cultures. The expression of mRNA was estimated by polymerase chain reaction (PCR). The concentration of cytokines was quantified using enzyme linked immunosorbent method and the osteoclasts in bone marrow cultures were identified by tartrate resistant acid phosphatase (TRAP) stain. As results of these studies, IL-1β stimulated the expression of IL-1β, IL-6 and GM-CSF mRNA in PDL cells. 0.05 ng/ml IL-1β also induced maximum production of IL-6 and GM-CSF in these cells. After an addition of IL-1β (0.05 ng/ml), IL-6 production increased from 2 hours to 8 hours and GM-CSF production also increased from 4 hours to 8 hours. IL-6 (100 ng/ml) increased the number of TRAP positive multinucleated cells in the presence of soluble interleukin-6 receptor (sIL-6R, 100 ng/ml). These results suggest that IL-1β may stimulate alveolar bone resorption by inducing IL-6 and GM-CSF production in PDL cells which enhance osteoclast differentiation and IL-6 enhances osteoclast formation in the presence of sIL-6R. And this process by IL-1 β may be closely associated with alveolar bone resorption induced by orthodontic force.