Bone remodeling is required for orthodontic tooth movement, and it is essential to clarify the mechanisms. In bone remodeling mechanism, the differentiation into osteoclasts is an important role. It is known that Focal adhesion kinase (FAK) is activated by chemokines, cytokines and engagement with β-1 integrin. Fibronectin is decreased in chronically inflamed connective tissue, such as periodontitis. Focal adhesion kinase (FAK) is a 125-kDa non-receptor type tyrosine kinase that localizes to focal adhesions. FAK is involved in osteoclast bone resorption. Fibronectin is bound to α4 β1-integrin and α5 β1-integrin.In our present study we focused on fibronectin / integrin-mediated the differentiation into osteoclasts and found that this type of the differentiation was mediated through FAK. RANKL stimulation did not enhance the expression of α₄, α₅ and β1-integrin. Fibronectin inhibited RANKL-induced osteoclasts differentiation in RAW264.7 cells. Fibronectin induced the phosphorylation of FAK. These findings establish fibronectin regulate the differentiation into osteoclasts in bone.