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01.12.2015 | Research article | Ausgabe 1/2015 Open Access

BMC Musculoskeletal Disorders 1/2015

The effects of zoledronate on the survival and function of human osteoblast-like cells

BMC Musculoskeletal Disorders > Ausgabe 1/2015
Kuo-Chin Huang, Chin-Chang Cheng, Po-Yao Chuang, Tien-Yu Yang
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​s12891-015-0818-5) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

Conceived and designed the experiments: KCH, CCC. Performed the experiments: KCH, CCC. Analyzed the data: PYC, TYY. Contributed reagents/materials/analysis tools: KCH, CCC, PYC, TYY. Contributed to the writing of the manuscript: KCH, CCC, PYC, TYY. All authors read and approved the final manuscript.



Prolonged bisphosphonate treatment might suppress bone remodeling to the extent that normal bone repair is impaired. While this adverse side effect is usually ascribed to the negative effects of bisphosphonates on osteoclast survival and function, these effects on osteoblasts are still unclear.


In the current study, we hypothesized that zoledronate (ZOL) at the μM level might present negative effects on osteoblast survival and function. In vitro analyses of proliferation, migration and differentiation were performed on human osteoblast-like cells.


Our results revealed that ZOL treatment dose- and time-dependently induced apoptosis of osteoblasts after concentrations had reached 10 μM (p < 0.001). The concentrations at which ZOL inhibited osteoblast migration by 50 % were between 10 and 15 μM. Moreover, there was a dose-dependent reduction in the extent of matrix mineralization, but without a concomitant inhibition of osteogenic differentiation in terms of secreted type I collagen and osteocalcin and of alkaline phosphatase activity per viable cell. Analyses of the expression of osteogenic genes confirmed that ZOL at the μM level had no effects on osteogenic differentiation of osteoblasts.


We concluded that ZOL at the μM level affected osteoblast survival and migration, but did not affect differentiation. The pathophysiological implications of ZOL at the μM level on skeletal disorders need to be investigated and clarified in the future researches.
Additional file 1: Figure S1. Zoledronate (ZOL) at the μM level presents a dose-dependently inhibitory effect on cellular proliferation of rat stromal cells (R7500). (EPS 825 kb)
Additional file 2: Figure S2. Zoledronate (ZOL) at the μM level presents a negative effect on matrix mineralization of rat stromal cells (R7500). (EPS 1961 kb)
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