Comparative effects of risedronate, atorvastatin, estrogen and SERMs on bone mass and strength in ovariectomized rats

Uyar, Yıldız; Baytur, Yeşim Bülbül; İnceboz, Ümit; Demir, Bilge Çetinkaya; Gümüşer, Gül; Özbilgin, Kemal

doi:10.1016/j.maturitas.2009.03.018

Cited by 15 publications

(9 citation statements)

References 54 publications

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“…Some researchers demonstrated bone formation using statins in ovariectomized rats [14][15][16][17] . However, the ovariectomized rats were only used for the high-turnover osteoporosis model.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Osteogenic Effect of Local Administration of Fluvastatin using a Fluvastatin-gelatin Complex in Senile Osteoporosis Model Rat

Yasuda

Koji

Satô

et al. 2014

J. Hard Tissue Biology.

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Statins, inhibitors of 3-hydroxy-2-methyl-glutaryl coenzyme A reductase, were recently reported to promote the differentiation of osteoblasts produced by the stimulation of bone morphogenetic protein-2 (BMP-2). The aim of this study was to investigate the osteogenic effect of a local administration of fluvastatin in senile osteoporosis model rats using a fluvastatin-gelatin complex. The gelatin-hydrogel was put into cylindrical titanium tubes 1.5 mm in diameter and 2.2 mm high. It was then crosslinked by ultraviolet irradiation, after which it was lyophilized. Subsequently, the carriers were placed in the fluvastatin solution (300 μM) for one day to bind the alkaline gelatin and acidic statin electrostatically (fluvastatin-gelatin complex; statin group). A control group consisted of the carriers immersed in sterilized water. Specimens of both the statin group and the control group were implanted into the femur of 15-week-old male senile osteoporosis model rats (SHRSP). Radiographic analysis, histologic examination, and immunohistochemical staining (BMP-2 and Runx2) were then performed. At 14 and 21 days, the bone volumes of the newly formed bone in the statin group was significantly higher compared to those of the control group (P<0.05). Histological observation showed that a high level of new bone formation was present in the statin group compared to that of the control group during all time periods. At 7 days, positive immune reactions with BMP-2 and Runx2 were seen in the statin group. The local administration of the fluvastatin-gelatin complex facilitated bone formation in senile osteoporosis model rats.

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Section: Discussionmentioning

confidence: 99%

“…Some authors reported the osteogenic effects of the systemic administration of statins on osteoporosis using ovariectomized rats [14][15][16][17] .…”

Section: Introductionmentioning

confidence: 99%

Osteogenic Effect of Local Administration of Fluvastatin using a Fluvastatin-gelatin Complex in Senile Osteoporosis Model Rat

Yasuda

Koji

Satô

et al. 2014

J. Hard Tissue Biology.

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“…Estrogen (10 mg/kg) did not affect bone strength in the horizontal direction but significantly improved it in the vertical direction by 89.3% (Abdallah et al, 2014). In OVX rats, atorvastatin prevented the OVX-induced decreases in BMD and bone strength, improved bone hardness by about 43.3% restoring the original horizontal bone hardness, and repaired structure of both cortical and trabecular bone matrices in the head of the femur (Uyar et al, 2009). Orchidectomy decreased both BMD and load values of left femurs and increased serum levels of BALP, OPG, and CTX-1 compared to non-orchidectomized rats.…”

Section: Fig 3 Effects Of Treatments (For Eight Weeks) On Serum Levementioning

confidence: 92%

“…The OVX rats were randomly divided into five groups (n=8) treated daily for eight weeks by oral gavage as follows: OVX-untreated (saline), OVX+ E2 (17β-estradiol, 0.1 mg/kg (Huber et al, 2007)), OVX+AT (atorvastatin, 50 mg/kg (Uyar et al, 2009;Chang et al, 2011)), OVX+AT+LC (atorvastatin+ L-carnitine, 100 mg/kg (Moustafa and Boshra, 2011)), and OVX+AT+CQ (atorvastatin+CoQ10, 20 mg/kg (Chirapapaisan et al, 2012)). At the end of treatment, BMD and BMC were measured.…”

Section: Ovariectomy and Experimental Designmentioning

confidence: 99%

左卡尼汀(而非辅酶q10)提高阿托伐他汀在切除卵巢的老鼠的抗骨质疏松作用

Murad

2016

J. Zhejiang Univ. Sci. B

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Abstract:Objective: Statins' therapy in osteoporosis can aggravate muscle damage. This study was designed to assess which agent, L-carnitine or coenzyme Q10, could enhance the anti-osteoporotic effect of atorvastatin while antagonizing myopathy in ovariectomized rats. Methods: Forty-eight female Sprague Dawley rats were used; forty rats were ovariectomized while eight were sham-operated. Eight weeks post-ovariectomy, rats were divided into ovariectomized-untreated group and four ovariectomized-treated groups (n=8) which received by gavage (mg/(kg·d), for 8 weeks) 17β-estradiol (0.1), atorvastatin (50), atorvastatin (50)+L-carnitine (100), or atorvastatin (50)+coenzyme Q10 (20). At the end of therapy, bone mineral density (BMD), bone mineral content (BMC), and serum levels of bone metabolic markers (BMMs) and creatine kinase (CK) were measured. Femurs were used for studying the breaking strength and histopathological changes. Results: Treatment with atorvastatin+L-carnitine restored BMD, BMC, and bone strength to near normal levels. Estrogen therapy restored BMD and BMC to near normal levels, but failed to increase bone strength. Although atorvastatin and atorvastatin+coenzyme Q10 improved BMD, BMC, and bone strength, they failed to restore levels to normal. All treatments decreased BMMs and improved histopathological changes maximally with atorvastatin+L-carnitine which restored levels to near normal. Atorvastatin aggravated the ovariectomy-induced increase in CK level while estrogen, atorvastatin+L-carnitine, and atorvastatin+coenzyme Q10 decreased its level mainly with atorvastatin+L-carnitine which restored the level to near normal. Conclusions: Coadministration of L-carnitine, but not coenzyme Q10, enhances the anti-osteoporotic effect of atorvastatin while antagonizing myopathy in ovariectomized rats. This could be valuable in treatment of osteoporotic patients. However, further confirmatory studies are needed.

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“…It is thought that statins aVect both bone resorption and formation via several mechanisms [27][28][29][30][31][32][33], including (1) reduction in osteoclast diVerentiation and activation, (2) induction of osteoblast diVerentiation, (3) shunting of osteoprogenitor cells from the adipocytic to osteoblastic pathway, and (4) increased production of osteocalcin, a protein that factors in bone mineralization and calcium homeostasis. While animal studies have shown a strong correlation between statins, sustained bone mineral density, and improved fracture healing [34][35][36], human studies have been less clear. A meta-analysis of a half million patients by Hatzigeorgiou et al [37] found a 40% reduction in hip fractures and increased hip bone mineral density among statin users.…”

Section: Osteoporosismentioning

confidence: 99%

The pleiotropic effects of the hydroxy-methyl-glutaryl-CoA reductase inhibitors in rheumatologic disorders: a comprehensive review

2011

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The hydroxy-methyl-glutaryl-CoA reductase inhibitors (statins) are used extensively in the treatment for hyperlipidemia. They have also demonstrated a benefit in a variety of other disease processes, including a wide range of rheumatologic disorders. These secondary actions are known as pleiotropic effects. Our paper serves as a focused and updated discussion on the pleiotropic effects of statins in rheumatologic disorders and emphasizes the importance of randomized, placebo-controlled trials to further elucidate this interesting phenomenon.

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Comparative effects of risedronate, atorvastatin, estrogen and SERMs on bone mass and strength in ovariectomized rats

Cited by 15 publications

References 54 publications

Osteogenic Effect of Local Administration of Fluvastatin using a Fluvastatin-gelatin Complex in Senile Osteoporosis Model Rat

Osteogenic Effect of Local Administration of Fluvastatin using a Fluvastatin-gelatin Complex in Senile Osteoporosis Model Rat

左卡尼汀(而非辅酶q10)提高阿托伐他汀在切除卵巢的老鼠的抗骨质疏松作用

The pleiotropic effects of the hydroxy-methyl-glutaryl-CoA reductase inhibitors in rheumatologic disorders: a comprehensive review

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