Osteoporosis in experimental postmenopausal polyarthritis: the relative contributions of estrogen deficiency and inflammation.
Osteoporosis in experimental postmenopausal polyarthritis: the relative contributions of estrogen deficiency and inflammation.
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DOI：
10.1186/ar1753
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发表时间：
2005
影响因子：
4.9
通讯作者：
Carlsten H
中科院分区：
文献类型：
--
作者：
Jochems C;Islander U;Erlandsson M;Verdrengh M;Ohlsson C;Carlsten H
绝经后类风湿关节炎(RA)的全身性骨质疏松症是由雌激素缺乏和炎症性疾病引起的。这些因素中每一个的相对重要性都是未知的。本研究的目的是建立绝经后类风湿关节炎小鼠骨质疏松模型，并评价绝经和关节炎相关性骨质疏松症的相对重要性和机制。为了模拟绝经后类风湿性关节炎，DBA/1小鼠被切除卵巢，然后诱导II型胶原诱导的关节炎。处死小鼠后，收集爪子进行组织学检查，其中一只股骨测定骨密度(BMD)，血清分析骨吸收标记物(RatLaps；I型胶原交联物)、骨形成(骨钙素)和软骨破坏(软骨寡聚基质蛋白)，并评估抗原特异性和先天免疫反应性。去卵巢的小鼠表现出比假手术对照组更严重的关节炎。在实验结束时，关节炎对照组和非关节炎卵巢切除组小鼠的骨小梁丢失分别为26%和22%。去卵巢的关节炎小鼠的骨小梁密度下降了58%。有趣的是，关节炎患者的皮质骨密度降低，但不受激素水平的影响。此外，关节炎小鼠骨吸收和软骨破坏的标记物增加，而去卵巢小鼠的骨形成标记物增加。这项研究表明，内源性雌激素的丧失和炎症对实验性绝经后多发性关节炎的骨质疏松具有相加和同等的作用。骨重建和骨髓淋巴细胞表型的标记物表明，在该模型中，卵巢切除和关节炎引起的骨质疏松症的发生机制不同。
Generalized osteoporosis in postmenopausal rheumatoid arthritis (RA) is caused both by estrogen deficiency and by the inflammatory disease. The relative importance of each of these factors is unknown. The aim of this study was to establish a murine model of osteoporosis in postmenopausal RA, and to evaluate the relative importance and mechanisms of menopause and arthritis-related osteoporosis. To mimic postmenopausal RA, DBA/1 mice were ovariectomized, followed by the induction of type II collagen-induced arthritis. After the mice had been killed, paws were collected for histology, one femur for bone mineral density (BMD) and sera for analyses of markers of bone resorption (RatLaps; type I collagen cross-links, bone formation (osteocalcin) and cartilage destruction (cartilage oligomeric matrix protein), and for the evaluation of antigen-specific and innate immune responsiveness. Ovariectomized mice displayed more severe arthritis than sham-operated controls. At termination of the experiment, arthritic control mice and non-arthritic ovariectomized mice displayed trabecular bone losses of 26% and 22%, respectively. Ovariectomized mice with arthritis had as much as 58% decrease in trabecular BMD. Interestingly, cortical BMD was decreased by arthritis but was not affected by hormonal status. In addition, markers of bone resorption and cartilage destruction were increased in arthritic mice, whereas markers of bone formation were increased in ovariectomized mice. This study demonstrates that the loss of endogenous estrogen and inflammation contribute additively and equally to osteoporosis in experimental postmenopausal polyarthritis. Markers of bone remodeling and bone marrow lymphocyte phenotypes indicate different mechanisms for the development of osteoporosis caused by ovariectomy and arthritis in this model.
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影响因子：
4.1
作者：
Nishida, S;Tsurukami, H;Nakamura, T
通讯作者：
Nakamura, T
影响因子：
4.1
作者：
Yamasaki, D;Enokida, M;Teshima, R
通讯作者：
Teshima, R
影响因子：
2.1
作者：
OSTENSEN, M;AUNE, B;HUSBY, G
通讯作者：
HUSBY, G
DOI：
10.1073/pnas.251534698
发表时间：
2001-11-20
影响因子：
11.1
作者：
Roggia, C;Gao, YH;Pacifici, R
通讯作者：
Pacifici, R
影响因子：
20.3
作者：
Riggs, BL;Khosla, S;Melton, LJ
通讯作者：
Melton, LJ