LAUSR

Considering the high rate of osteoclast‐related diseases worldwide, research targeting osteoclast formation/function is crucial. In vitro, we demonstrated that chitooligosaccharide (CS) dramatically inhibited osteoclastogenesis as well as osteoclast function dose‐dependently. CS suppressed osteoclast‐specific genes expression during osteoclastogenesis. Furthermore, we found that CS attenuated receptor activator of nuclear factor kappa B ligand (RANKL)‐mediated mitogen‐activated protein kinase (MAPK) pathway involving p38, erk1/2, and jnk, leading to the reduced expression of c‐fos and nuclear factor of activated T cells c1 (NFATc1) during osteoclast differentiation. In vivo, we found CS protected rats from periodontitis‐induced alveolar bone loss by micro‐computerized tomography and histological analysis. Overall, CS inhibited RANKL‐induced osteoclastogenesis and ligature‐induced rat periodontitis model, probably by suppressing the MAPK/c‐fos/NFATc1 signaling pathway. Therefore, CS may be a safe and promising treatment for osteoclast‐related diseases.