Beijing Key Laboratory of Spine Diseases

Beijing, China

Beijing Key Laboratory of Spine Diseases

Beijing, China

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Li S.,Peking University | Li S.,Ansteel Group Hospital | Niu G.,Peking University | Niu G.,Beijing Key Laboratory of Spine Diseases | And 5 more authors.
Acta Mechanica Sinica/Lixue Xuebao | Year: 2017

Estrogen withdrawal in postmenopausal women increases bone loss and bone fragility in the vertebra. Bone loss with osteoporosis not only reduces bone mineral density (BMD), but actually alters bone quality, which can be comprehensively represented by bone post-yield behaviors. This study aimed to provide some information as to how osteoporosis induced by estrogen depletion could influence the evolution of post-yield microdamage accumulation and plastic deformation in vertebral bodies. This study also tried to reveal the part of the mechanisms of how estrogen deficiency-induced osteoporosis would increase the bone fracture risk. A rat bilateral ovariectomy (OVX) model was used to induce osteoporosis. Progressive cyclic compression loading was developed for vertebra testing to elucidate the post-yield behaviors. BMD, bone volume fraction, stiffness degradation, and plastic deformation evolution were compared among rats raised for 5 weeks (ovx5w and sham5w groups) and 35 weeks (ovx35w and sham35w groups) after sham surgery and OVX. The results showed that a higher bone loss in vertebral bodies corresponded to lower stiffness and higher plastic deformation. Thus, osteoporosis could increase the vertebral fracture risk probably through microdamage accumulation and plastic deforming degradation. © 2017 The Chinese Society of Theoretical and Applied Mechanics; Institute of Mechanics, Chinese Academy of Sciences and Springer-Verlag Berlin Heidelberg


Li S.,Peking University | Niu G.,Beijing Key Laboratory of Spine Diseases | Wu Y.,Peking University | Du G.,Peking University | And 5 more authors.
Osteoarthritis and Cartilage | Year: 2016

Objective: To explore the effect of vitamin D on turnover of articular cartilage with ovariectomy (OVX) induced OA, and to investigate transforming growth factor-β1 (TGF-β1) as a possible underlying mechanism mediated by 1α,25(OH)2D3.. Design: Sixty-six rats were randomly allocated into seven groups: sham plus control diet (SHAM+CTL), OVX+CTL diet, sham plus vitamin D-deficient (VDD) diet, OVX+VDD diet, and three groups of ovariectomized rats treated with different doses of 1α,25(OH)2D3. The cartilage erosion and the levels of serum 17β-estradiol, 1α,25(OH)2D3 and C-telopeptide of type II collagen (CTX-II) were measured. TGF-β1, type II Collagen (CII), matrix metalloproteinases (MMP)-9,-13 in articular cartilage were assessed by immunohistochemistry. TGF-β1 and CTX-II expression were measured in articular cartilage chondrocytes treated with/without tumor necrosis factor (TNF-α), 1α,25(OH)2D3, and TGF-β receptor inhibitor (SB505124) in vitro. Results: Cartilage erosion due to OVX was significantly reduced in a dose-dependent manner by 1α,25(OH)2D3 supplementation, and exacerbated by VDD. The expressions of TGF-β1 and CII in articular cartilage were suppressed by OVX and VDD, and rescued by 1α,25(OH)2D3 supplementation. The expression of MMP-9,-13 in articular cartilage increased with OVX and VDD, and decreased with 1α,25(OH)2D3 supplementation. In vitro experiments showed that 1α,25(OH)2D3 increased the TGF-β1 expression of TNF-α stimulated chondrocytes in a dose-dependent manner. 1α,25(OH)2D3 significantly counteracted the increased CTX-II release due to TNF-α stimulation, and this effect was significantly suppressed by SB505124. Conclusion: VDD aggravated cartilage erosion, and 1α,25(OH)2D3 supplementation showed protective effects in OVX-induced OA partly through the TGF-β1 pathway. © 2015 Osteoarthritis Research Society International.


PubMed | Peking University and Beijing Key Laboratory of Spine Diseases
Type: Journal Article | Journal: Osteoarthritis and cartilage | Year: 2016

To explore the effect of vitamin D on turnover of articular cartilage with ovariectomy (OVX) induced OA, and to investigate transforming growth factor-1 (TGF-1) as a possible underlying mechanism mediated by 1,25(OH)2D3.Sixty-six rats were randomly allocated into seven groups: sham plus control diet (SHAM+CTL), OVX+CTL diet, sham plus vitamin D-deficient (VDD) diet, OVX+VDD diet, and three groups of ovariectomized rats treated with different doses of 1,25(OH)2D3. The cartilage erosion and the levels of serum 17-estradiol, 1,25(OH)2D3 and C-telopeptide of type II collagen (CTX-II) were measured. TGF-1, type II Collagen (CII), matrix metalloproteinases (MMP)-9,-13 in articular cartilage were assessed by immunohistochemistry. TGF-1 and CTX-II expression were measured in articular cartilage chondrocytes treated with/without tumor necrosis factor (TNF-), 1,25(OH)2D3, and TGF- receptor inhibitor (SB505124) invitro.Cartilage erosion due to OVX was significantly reduced in a dose-dependent manner by 1,25(OH)2D3 supplementation, and exacerbated by VDD. The expressions of TGF-1 and CII in articular cartilage were suppressed by OVX and VDD, and rescued by 1,25(OH)2D3 supplementation. The expression of MMP-9,-13 in articular cartilage increased with OVX and VDD, and decreased with 1,25(OH)2D3 supplementation. Invitro experiments showed that 1,25(OH)2D3 increased the TGF-1 expression of TNF- stimulated chondrocytes in a dose-dependent manner. 1,25(OH)2D3 significantly counteracted the increased CTX-II release due to TNF- stimulation, and this effect was significantly suppressed by SB505124.VDD aggravated cartilage erosion, and 1,25(OH)2D3 supplementation showed protective effects in OVX-induced OA partly through the TGF-1 pathway.

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