SYNOPSIS
In Orthodontic therapy, osteoclast precursors such as monocytes and macrophages migrate from vessels into the periodontium and then differentiate into osteoclasts, causing bone resorption. Focal adhesion kinase (FAK) is a 125-kDa non-receptor type tyrosine kinase that localizes to focal adhesions. FAK is involved in osteoclastic bone resorption. Vascular cell adhesion molecule-1 (VCAM -1) is bound to VLA-4(very late antigen-4) which is kind of the α₄ β1-integrin, and recruits monocytic osteoclast progenitors and elevates local osteoclast activity.
In our present study we focused on VCAM-1 /α₄ integrin-mediated the differentiation into osteoclasts and found that this type of the differentiation was medi-ated through FAK. RAW267.4 expressed both α₄ integrins, and it was reported that expression of α₄ integrin and its counterreceptor, VCAM-1, was not enhanced in response to receptor activator of NF-B ligand (RANKL). Neutralizing antibodies against integrin α₄ effectively inhibit the differentiation into osteoclasts and phosphorylation of FAK. These findings establish VCAM-1 regulate the differentiation into osteoclasts in bone.

Key words: osteoclast, FAK, VCAM-1, RANKL