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An anti‐c‐Fms antibody inhibits osteoclastogenesis in a mouse periodontitis model
Author(s) -
Kimura K,
Kitaura H,
Fujii T,
Ishida M,
Hakami ZW,
TakanoYamamoto T
Publication year - 2014
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12117
Subject(s) - rankl , periodontitis , bone resorption , osteoclast , dental alveolus , resorption , medicine , endocrinology , chemistry , antibody , acid phosphatase , receptor , immunology , activator (genetics) , dentistry , biochemistry , enzyme
Objective Bacterial lipopolysaccharide ( LPS ) can induce inflammatory bone loss such as periodontal disease. The formation of osteoclasts depends on macrophage colony‐stimulating factor (M‐ CSF ) and receptor activator of nuclear factor kb ligand ( RANKL ). It has recently been reported that administration of an antibody of the M‐ CSF receptor c‐Fms completely blocked osteoclastogenesis and bone erosion induced by LPS in mouse calvaria. In this study, the effect of antibody against c‐Fms in the mouse periodontitis model by injection of LPS was investigated. Materials and Methods C57 BL 6/J mice were injected with LPS and anti‐c‐Fms antibody into the mesial gingiva of the first molar in the left mandible. Histological sections of periodontal tissue were stained for tartrate‐resistant acid phosphatase, and osteoclast numbers and ratio of alveolar bone resorption determined. Results The number of osteoclasts and ratio of alveolar bone resorption in mice administered both LPS and anti‐c‐Fms antibody was lower than those in mice administered LPS alone. The expression of RANKL receptor, RANK , was inhibited by the anti‐c‐Fms antibody in periodontal tissue. Conclusion M‐ CSF and/or its receptor are potential therapeutic targets for the treatment of bone resorption, caused by LPS , in periodontitis. Injection of an anti‐c‐Fms antibody might be useful for inhibition of pathological bone resorption in periodontitis.