Risedronate directly inhibits osteoclast differentiation and inflammatory bone loss
Risedronate, a nitrogen-containing bisphosphonate, is widely used in the clinical field for the treatment of osteoporosis. Risedronate is known to exert its effects through binding to hydroxyapatite in bone tissue, inhibiting osteoclastic activity, and inducing apoptosis of osteoclasts. The purpose of this study was to determine the effects of risedronate on osteoclast differentiation in vitro and on an inflammatory bone loss model in vivo. Risedronate inhibited osteoclast differentiation in co-culture of bone marrow cells (BMCs) and osteoblasts, and suppressed receptor activator of nuclear factor (NF)-kappaB ligand (RANKL)-mediated osteoclast differentiation from bone marrow-derived macrophages (BMMs) in a dose-dependent manner without toxicity. Risedronate significantly inhibited expression of c-Fos and nuclear factor of activated T cells (NFAT) c1 induced by RANKL. To examine the effect of risedronate on bone loss in vivo, we used a mouse model of lipopolysaccharide (LPS)-mediated bone loss. Micro-CT analysis of the femurs showed that LPS treatment caused bone loss. However, bone loss was significantly attenuated in mice administered with risedronate. Taken together, we conclude that risedronate exerts beneficial effects on osteoporosis by inhibiting osteoclast differentiation both directly and indirectly. In infectious conditions, the inhibitory effect of risedronate on bone erosion was excellent. Thus risedronate could be a treatment option for osteoporosis caused by inflammatory and infectious conditions.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2009 |
|---|---|
| Erschienen: |
2009 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:32 |
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| Enthalten in: |
Biological & pharmaceutical bulletin - 32(2009), 7 vom: 01. Juli, Seite 1193-8 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Kwak, Han Bok [VerfasserIn] |
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| Anmerkungen: |
Date Completed 08.10.2009 Date Revised 20.07.2019 published: Print Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM189707984 |
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| 100 | 1 | |a Kwak, Han Bok |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Risedronate directly inhibits osteoclast differentiation and inflammatory bone loss |
| 264 | 1 | |c 2009 | |
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| 500 | |a Date Completed 08.10.2009 | ||
| 500 | |a Date Revised 20.07.2019 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Risedronate, a nitrogen-containing bisphosphonate, is widely used in the clinical field for the treatment of osteoporosis. Risedronate is known to exert its effects through binding to hydroxyapatite in bone tissue, inhibiting osteoclastic activity, and inducing apoptosis of osteoclasts. The purpose of this study was to determine the effects of risedronate on osteoclast differentiation in vitro and on an inflammatory bone loss model in vivo. Risedronate inhibited osteoclast differentiation in co-culture of bone marrow cells (BMCs) and osteoblasts, and suppressed receptor activator of nuclear factor (NF)-kappaB ligand (RANKL)-mediated osteoclast differentiation from bone marrow-derived macrophages (BMMs) in a dose-dependent manner without toxicity. Risedronate significantly inhibited expression of c-Fos and nuclear factor of activated T cells (NFAT) c1 induced by RANKL. To examine the effect of risedronate on bone loss in vivo, we used a mouse model of lipopolysaccharide (LPS)-mediated bone loss. Micro-CT analysis of the femurs showed that LPS treatment caused bone loss. However, bone loss was significantly attenuated in mice administered with risedronate. Taken together, we conclude that risedronate exerts beneficial effects on osteoporosis by inhibiting osteoclast differentiation both directly and indirectly. In infectious conditions, the inhibitory effect of risedronate on bone erosion was excellent. Thus risedronate could be a treatment option for osteoporosis caused by inflammatory and infectious conditions | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 7 | |a Bone Density Conservation Agents |2 NLM | |
| 650 | 7 | |a Lipopolysaccharides |2 NLM | |
| 650 | 7 | |a NFATC Transcription Factors |2 NLM | |
| 650 | 7 | |a Nfatc1 protein, mouse |2 NLM | |
| 650 | 7 | |a Proto-Oncogene Proteins c-fos |2 NLM | |
| 650 | 7 | |a RANK Ligand |2 NLM | |
| 650 | 7 | |a p38 Mitogen-Activated Protein Kinases |2 NLM | |
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| 650 | 7 | |a Risedronic Acid |2 NLM | |
| 650 | 7 | |a KM2Z91756Z |2 NLM | |
| 650 | 7 | |a Etidronic Acid |2 NLM | |
| 650 | 7 | |a M2F465ROXU |2 NLM | |
| 700 | 1 | |a Kim, Jong Yun |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Kwang Jin |e verfasserin |4 aut | |
| 700 | 1 | |a Choi, Min-Kye |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Jeong-Joong |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Kwang Mee |e verfasserin |4 aut | |
| 700 | 1 | |a Shin, Yong-Il |e verfasserin |4 aut | |
| 700 | 1 | |a Lee, Myeung Su |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Hun Soo |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Jeung Woo |e verfasserin |4 aut | |
| 700 | 1 | |a Chun, Chul Hong |e verfasserin |4 aut | |
| 700 | 1 | |a Cho, Hae Joong |e verfasserin |4 aut | |
| 700 | 1 | |a Hong, Gi Youn |e verfasserin |4 aut | |
| 700 | 1 | |a Juhng, Seon Kwan |e verfasserin |4 aut | |
| 700 | 1 | |a Yoon, Kwon Ha |e verfasserin |4 aut | |
| 700 | 1 | |a Park, Byoung Hyun |e verfasserin |4 aut | |
| 700 | 1 | |a Bae, Ji Myung |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Joung-Kyue |e verfasserin |4 aut | |
| 700 | 1 | |a Oh, Jaemin |e verfasserin |4 aut | |
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