Naringenin inhibits human osteoclastogenesis and osteoclastic bone resorption


Daniel Grenier, Groupe de Recherche en Écologie Buccale, Faculté de Médecine Dentaire, Université Laval, 2420 Rue de la Terrasse, Quebec City, Quebec G1V 0A6, Canada
Tel: +418 656 7341
Fax: +418 656 2861


Background and Objective:  Naringenin, a naturally occurring flavonoid, possesses a wide range of pharmacological properties. The purpose of this study was to investigate the effect of naringenin on human osteoclastogenesis and osteoclastic bone resorption.

Material and Methods:  Naringenin was tested in a human osteoclastogenesis model using primary osteoclast precursor cells activated by receptor activator of nuclear factor-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) for 6 days. Osteoclastogenesis was assessed by determining the number of tartrate-resistant acid phosphatase (TRAP)-stained multinuclear cells, while the secretion of factors involved in osteoclastogenesis was assessed using enzyme-linked immunosorbent assays. The effect of naringenin on bone resorption was investigated using an OsteoAssay human bone plate coupled with an immunoassay to evaluate the release of helical peptide 620–633 from the α1 chain of type I collagen.

Results:  Naringenin was non-toxic at the highest concentration used (50 μg/ml). Naringenin (10, 25 and 50 μg/ml) significantly inhibited osteoclastogenesis (by 29 ± 5, 57 ± 8 and 96 ± 1%, respectively). Naringenin also markedly inhibited the secretion of interleukin (IL)-1α (by 59%), IL-23 (by 87%) and monocyte chemoattractant protein-1 (by 58%). Lastly, naringenin (10, 25 and 50 μg/ml) significantly decreased the release of helical peptide 620–633, an indicator of bone resorption activity (by 44 ± 0.5, 73 ± 0.5 and 86 ± 1%, respectively).

Conclusions:  Naringenin can inhibit human osteoclastogenesis and osteoclastic bone resorption. It thus holds promise as a therapeutic or preventive agent for bone-related diseases such as periodontitis.