金匮肾气丸联合葡萄糖酸钙对去势大鼠骨代谢的影响

目的观察金匮肾气丸联合葡萄糖酸钙对去卵巢大鼠骨代谢的影响,探究其防治骨质疏松(OP)的机制。方法将75只雌性大鼠随机分成假手术组,模型组,葡萄糖酸钙组,金匮肾气丸组,金匮肾气丸及葡萄糖酸钙联合用药组共5组,采用卵巢切除的方法制成OP动物模型,灌胃给药3个月后进行血清碱性磷酸酶(ALP)、骨钙素(OC)、白细胞介素-6(IL-6)等骨代谢指标的检测。结果金匮肾气丸联合葡萄糖酸钙治疗后,可明显降低去势大鼠升高的血清ALP、OC及IL-6水平,且效果优于单纯金匮肾气丸及葡萄糖酸钙。结论金匮肾气丸联合葡萄糖酸钙可显著改善骨代谢,抑制高骨转换过程,使骨形成与骨吸收趋于耦联,并使破骨细胞的分化增殖功能减弱,减少骨吸收,对OP具有较好的防治作用。     

雌激素和骨标志物与绝经后妇女骨质疏松的关系

目的探讨雌激素和骨标志物与绝经后妇女骨质疏松(OP)的关系。方法绝经后OP妇女71例为观察组,同期绝经后无OP妇女71例为对照组,行雌激素和骨标志物检测并分析其与绝经后妇女OP的相关性。结果观察组雌二醇、孕酮、骨密度值低于对照组(P<0.05)。观察组促卵泡成熟激素、促黄体生成激素、β-胶原降解产物、总骨Ⅰ型前胶原氨基酸延长链、骨钙素N端中分子高于对照组(P<0.05)。雌二醇、孕酮、骨密度值与OP呈明显负相关。促卵泡成熟激素、促黄体生成激素、β-胶原降解产物、总骨Ⅰ型前胶原氨基酸延长链、骨钙素N端中分子与OP呈明显正相关。结论雌激素和骨标志物与绝经后妇女OP的关系密切。监测雌激素和骨标志物可及早发现骨代谢异常,有助于防治绝经后妇女OP。     

骨质疏松骨折治疗的药物选择

骨质疏松(OP)患者受到轻微的外力就易发生骨质疏松性骨折(OPF).治疗OPF的同时须注重OP的治疗.近年来防治OP药物的研究已取得了长足的进展,针对OP的发病中骨吸收相对过度,而骨形成相对不足的特点,目前所采用的防治OP的药物主要有基础性用药如钙剂和维生素D、骨吸收抑制剂、骨形成促进剂,混合制剂及中药制剂五大类.     

基质金属蛋白酶-2 3 9在男性强直性脊柱炎中的表达及其与骨代谢的关系研究

强直性脊柱炎(ankvlosing spondylitis,AS)是一种病因不明的慢性全身性自身免疫性疾病.除关节及系统受累外,常合并骨质疏松症(OP),甚至在早期即可出现OP,AS继发OP的机制目前尚未完全阐明.基质金属蛋白酶类(MMPs)是骨吸收和骨重建的关键酶.本研究检测了 AS患者血清MMP-2、MMP-3、MMP-9的水平变化,分析了其与AS患者的骨代谢相关指标和骨密度(BMD)的相关关系,以探索AS及其继发OP的发病机制.     

新型钙离子通道TRPV5在骨质疏松症发病机制中的作用

TRPV5作为上皮Ca^2＋通道，主要在上皮组织中表达其独特的生理功能，与骨Ca^2＋代谢有着非常密切关系。近年发现TRPV5存在于人和鼠科破骨细胞（osteoclast，OC）吸收面微绒毛形成的刷状缘，与OC骨再吸收和在OC中Ca^2＋运输功能有密切关系。而OC的活性增强与骨质疏松（OP）有密切关系。因此，进一步研究TRPV5，对临床了解OP发病机制及其防治具有重要意义。     

活血补肾强骨固疏汤联合鹿瓜多肽注射液治疗老年骨质疏松患者90例

老年骨质疏松(OP)是一种以全身性骨量、骨密度损失及骨组织的微观结构退化为特征,并引起骨脆性增加、骨强度降低,骨折危险性增加的全身代谢性疾病,其直接病因是由于老年人内分泌功能的变化,促使骨吸收的激素增多,抑制骨吸收激素减少,加速了骨吸收,使老人发生严重的钙不足和负平衡[1].OP虽是一种自然老化,但通过药物治疗也可以延缓其进程,本文拟回顾分析采用中西医结合治疗老年OP患者的疗效,为其临床治疗提供依据.     

老年男性慢性阻塞性肺疾病患者骨代谢与骨密度的关系

目的　探讨老年男性慢性阻塞性肺疾病 (COPD)患者继发性骨代谢与骨密度 (BMD)变化的原因、临床特点及相互关系。方法　根据COPD肺功能诊断标准将 5 0例老年男性稳定期单纯COPD患者分为中度组和重度组 ,另设老年男性健康对照组 3 0例。检测并分析血气分析 ,BMD ,骨矿含量 (BMC) ,与骨吸收和骨形成有关的血、尿骨代谢生化指标的变化。结果　中、重度组患者的BMD和BMC较健康对照组明显降低 (P <0 .0 5或 0 .0 1) ,其中 ,重度组BMD、BMC的降低与氧分压降低明显相关 (r =0 .48～ 0 .5 3 ,P <0 .0 1)。骨吸收指标中尿钙 /肌酐比值明显升高 (P <0 .0 1) ;骨形成指标血清Ⅰ型前胶原羧基端前肽 ,碱性磷酸酶 ,骨钙素 ,2 5 (OH)D3 和雌二醇均明显升高 (P <0 .0 1或 0 .0 5 )。结论　根据WHO有关骨质疏松 (OP)诊断标准 ,多数老年男性COPD患者主要表现为骨量减低 ,很少发生OP ,这可能与机体代偿性对抗OP发生有关。其骨代谢特点与高转换Ⅰ型OP相似 ,与原发性老年男性Ⅱ型OP不同。治疗原发病 ,改善COPD患者缺氧状态可能是一种重要的防治方法。     

重视非酒精性脂肪性肝病并发的骨质疏松和肌少症

正骨骼和骨骼肌的解剖结构与生理功能有紧密关联。肌收缩是相连骨最大负重来源,而骨组织强度是由其负重决定的。肝脏、骨骼和骨骼肌所产生的细胞因子影响着彼此间代谢功能。非酒精性脂肪性肝病(NAFLD)与骨质疏松(OP)及肌少症(SP)之间存在着共同的发病机制。近来认为,它们相互间呈因果关联可促使临床结局恶化,应引起高度关注[1-2]。一、OP与SP的定义及其检测(一)OP OP为成骨细胞骨形成与破骨细胞骨吸收失衡,表现为骨密度和骨质量降低、骨微结构破坏、骨脆性增加及骨折风险增高。诊断金标准为双能量X线吸收(DXA)测定骨矿质密度(BMD),与同性别健康成人比较,BMD-2.5 SD诊断     

血管内皮生长因子与骨质疏松的关系

近年来血管内皮生长因子(vascular endothelial growth factor,VEGF)与骨质疏松的关系受到越来越多的关注,它不仅是一种重要的血管生长因子,更是一种骨生长因子,可以对骨代谢进行调节。一方面,VEGF能够偶联血管生成及骨生成,通过诱导新血管生成,血管侵入参与骨重建的过程;另一方面,也可以直接作用于成骨细胞及破骨细胞,作为骨代谢调节因子参与成骨细胞和破骨细胞的增生及分化,促进成骨及破骨作用。VEGF在骨质疏松中起着重要作用,也为骨质疏松的治疗提供了新的研究方向。本文就VEGF在骨质疏松中的最新研究进行综述。     

老年男性2型糖尿病合并骨质疏松症患者骨代谢生化指标分析

目的探讨老年男性2型糖尿病（T2DM）合并骨质疏松症（OP）患者血清骨形成与骨吸收生化指标随年龄变化及与OP的关系。方法根据是否合并OP,将185例老年男性T2DM患者分为OP组103例,非OP组82例。采用双能X线法检测骨密度,分别检测2组血清骨形成生化指标包括骨碱性磷酸酶（BAP）、骨钙素（OC）、Ⅰ型胶原氨基端前肽（PINP）,血清骨吸收生化指标Ⅰ型胶原C端肽（CTX）、空腹血糖（FPG）、空腹胰岛素（FINS）、糖化血红蛋白（HbA1c）、糖化血清白蛋白（GA）的浓度,并进行比较。结果 OP组的BMI及FINS、骨形成指标（BAP、OC、PINP）浓度低于非OP组,FPG、HbA1c、GA浓度及病程高于非OP组（P〈0.05）,骨吸收指标（CTX）浓度高于非OP组（P〉0.05）。OP组骨形成生化指标浓度低于骨量减少组（P〈0.05）,骨吸收指标浓度高于骨量减少组（P〉0.05）。OP组骨形成生化指标浓度与年龄呈负相关（P〈0.05）。结论老年男性T2DM合并OP的发生与骨形成能力不足有关,在治疗T2DM的同时,应重视早期预防和治疗OP。     

Osteoporosis in rheumatic diseases

Rheumatic diseases, characterized by chronic inflammation and damage to various organs and systems, include systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis and other connective tissue diseases. Bone is a target in many inflammatory rheumatic diseases. In recent years, the survival of patients with rheumatic diseases has increased markedly and the relationship between rheumatic diseases and osteoporosis (OP) has become more prominent. OP and related fragility fractures increase the morbidity and mortality of rheumatic disease. The cause of OP in rheumatic diseases is complex. The pathogenesis of OP in rheumatic diseases is multifactorial, including disease and treatment-related factors. Osteoimmunology, a crosstalk between inflammatory and bone cells, provides some insight into the pathogenesis of bone loss in systematic inflammatory diseases. The aim of this article is to review different risk factors in rheumatic diseases. Several factors play a role, such as chronic inflammation, immunological factors, traditional factors, metabolism and drug factors. Chronic inflammation is the most important risk factor and drug treatment is complex in patients with OP and rheumatic disease. Attention should be paid to bone loss in rheumatic disease. Optimal treatment of the underlying rheumatic disease is the first step towards prevention of OP and fractures. Apart from that, a healthy lifestyle is important as well as calcium and vitamin D supplementation. Bisphosphonates or denosumab might be necessary for patients with a low T score.     

Osteoporosis in scleroderma

OBJECTIVE: To review the literature describing the association of osteoporosis (OP) with scleroderma (SSc). METHODS: A Medline (PubMed) search identified all studies from 1966 to 2004 that investigated the association between OP and SSc. Search terms included "scleroderma," "systemic sclerosis," "osteoporosis, " "bone mineral density," "bone densitometry," and "prevalence." RESULTS: Eight case control studies and 1 retrospective study (comparing OP status to a reference standard) were identified. There is no clear association between bone mineral density (BMD) scores and scleroderma. Two of 4 studies have reported lower BMD scores in SSc, but appear not to have considered possible confounding risk factors. Earlier age of menopause has been reported in 2 of 3 studies, and thus, may be a confounder in some samples of women with SSc. Studies of bone metabolism markers have not provided any consistent explanatory mechanism for increased OP in SSc, and such markers may be unreliable in SSc as these are affected by the altered collagen turnover and fibrosis characteristic of SSc. CONCLUSIONS: It is unknown whether OP is truly increased in SSc or whether this association has been observed in some studies as a result of other confounding risk factors for OP. Clinical heterogeneity of SSc study samples and small sample sizes have contributed to the difficulty in obtaining valid estimates of the risk for the development of OP. There is no strong evidence in the literature for consistently lower BMD scores in SSc, or for altered biomarkers of bone resorption. Earlier menopause, corticosteroid use in some patients, and other factors secondary to SSc (such as malabsorption and inflammation), may be causal factors or may be confounders in studies of OP in SSc.     

Glucocorticoid-induced osteoporosis.

Endogenous cortisol excess and glucocorticoid (GC) treatment have a profound effect on bone metabolism, acting at many sites. The mechanism of GC action on bone turnover is complex and has not been elucidated completely. GCs increase bone resorption, inhibit bone formation and have an indirect action on bone by decreasing intestinal Ca2+ absorption, modifying vitamin D metabolism, and sustaining a marked hypercalciuria, with variable changes in plasma PTH levels; finally, GCs inhibit the gonadotropic and somatotropic axis. GC-induced osteoporosis is preventable, treatable and potentially reversible. The prevention and treatment of GC-induced osteoporosis include some general measures (as well as the use of the minimal effective dose of GC), Ca2+ and vitamin D supplementation and treatment with bone anabolic and antiresorptive agents. Recent trials suggest that bisphosphonates are an effective therapeutic tool in the treatment of GC-induced bone damage. Recent data on GC receptor-selective modulators indicate that these new molecules might induce only minimal bone loss while maintaining the typical anti-inflammatory properties of GC. Another new line of study for the prevention of GC-induced osteoporosis is the characterization of the individual's susceptibility to GC-induced bone damage.     

Serum concentrations of somatomedins and growth hormone in relation to bone metabolism in acromegaly and thyroid dysfunction

Many hormones are involved in the complex process of formation and resorption of bone. However, only somatomedin is found to directly stimulate cell replication and collagen synthesis in bone. This study was undertaken to examine a possible regulatory role of somatomedin in mediating the effects of growth hormone and thyroid hormones on bone metabolism. Bone metabolism and concentrations of somatomedins and growth hormones were studied in 17 acromegalic, 15 thyrotoxic and 14 hypothyroid patients, before and during treatment. During treatment of acromegalic and thyrotoxic patients parameters of bone turnover, both formation and resorption, decreased parallel to the decrease in concentration of somatomedin. During treatment of hypothyroid patients parameters of bone turnover increased. A positive correlation was found in acromegalic patients between changes in somatomedins and parameters of bone resorption (R = 0.82, P less than 0.01) as well as bone formation (R = 0.63, P less than 0.05) and in thyrotoxic patients between changes in somatomedin and bone resorption (R = 0.87, P less than 0.05). These data suggest that somatomedin may indeed play a role in the regulation of bone turnover. In addition, secondary effects on growth hormone concentrations were observed.     

Osteoporosis, body composition, and bone turnover in ankylosing spondylitis.

OBJECTIVE: To study the prevalence of osteoporosis (OP) and osteopenia in ankylosing spondylitis (AS) and to investigate the relationship between symptomatic and structural severity, the indices of bone turnover, and body composition. METHODS: Eighty patients with AS were enrolled prospectively: 52 men (65%) and 28 women, mean age 36.7 years +/- 11.5 (range 18-67); they were studied clinically, radiologically, and by dual energy x-ray absorptiometry. Sixty-three underwent biological assessment of bone turnover markers. RESULTS: OP and osteopenia as defined by the World Health Organization (T score < -2.5 SD and between -1 and -2.5 SD, respectively) were observed in 15 (18.7%) and 25 patients (31.2%) at the lumbar spine and in 11 (13.7%) and 33 patients (41.2%) at the femoral neck, respectively. Patients with OP had a lower body mass index (BMI) and fat mass percentage. There was a trend to a lower disease duration in patients with OP at the spine than in healthy subjects. Bone resorption markers (urinary D-pyridinoline or C-telopeptide concentrations) were increased in 34 patients (53.9%). Bone turnover markers were positively correlated with C-reactive protein concentration and Larsen radiological hip score; they were negatively correlated with Schober index and fat mass percentage. CONCLUSION: (1) OP is frequent in AS and can be observed in early stages of the disease. (2) Patients with AS are more susceptible to develop OP when they have low BMI, low fat mass percentage, and active and severe disease. OP was observed in parallel with increased bone resorption.     

血清微量元素变化对肝硬化骨代谢异常的影响及病理学改变

为探讨血清微量元素变化对肝硬化骨代谢异常的影响及病理学改变。采用原子吸收分光光度计等方法分别测定 32例肝硬化患者铜 (Cu)、锌 (Zn)、硒 (Se)、镉 (Cd)、铝 (Al)水平 ,并与 31例健康者对照。其中 17例患者及 12例健康者行骨组织学观察。结果表明 ,肝硬化组血清Zn、Se水平较对照组明显下降 (P <0 0 0 1,P <0 0 1) ,而血清Cd、Al水平明显升高 (P <0 0 0 1,P <0 0 0 1)。组织学发现 14例骨质疏松 (OP) ,OP发生率为 82 35 %。OP患者重度组血清Zn、Se水平较轻度组明显下降 (P <0 0 5 ,P <0 0 5 ) ,而血清Cd、Al水平显著升高 (P <0 0 1,P <0 0 1)。提示肝硬化患者血清Zn、Se、Cd、Al存在明显异常 ,在肝性骨病 (HBD)的形成过程中均起着不可忽视的作用。适当补充Zn、Se ,而减少Cd、Al摄入 ,对HBD的防治将产生有益作用     

机械振动对骨内细胞效应基础研究进展

机械振动为一种非侵入性的物理预防和治疗方法,能改善骨代谢状况和微观结构,抑制骨吸收,增强骨形成。骨细胞为感测机械应力载荷的细胞,既能探测骨加强、减弱以及修复微骨折的需要,也能探测骨小管内液体与循环激素变化。机械信号传导通过Wnt信号通路影响成骨细胞和破骨细胞RANKL信号,限制破骨细胞形成,促进成骨细胞分化。本文就机械振动对骨内细胞效应的研究进展进行综述。     

Entzündung und Knochenmetabolismus

A finely balanced relationship between bone resorption and bone formation is characteristic for a healthy bone metabolism. Osteoblasts are responsible for bone formation and osteoclasts for bone resorption. In general inflammatory and in particular chronic inflammatory processes influence osteoblast and osteoclast function directly or via indirect mechanisms. Bone metabolism can be influenced by the interaction of cytokines, hormones and growth factors with bone cells. A central factor involved in bone metabolism is the receptor activator of nuclear factor-κB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) system, which is influenced by different inflammatory processes. Usually, (chronic) inflammation results in increased bone loss. The molecular mechanisms and pathophysiological pathways of bone metabolism under the influence of inflammation are summarized in this review.     

Risk factors for osteoporosis in female patients with systemic lupus erythematosus

In the last years it has been recognized that patients with systemic lupus erythematosus (SLE) are at high risk of osteoporosis (OP) and fractures, both occurring through disease-specific (chronic arthritis, reduced physical activity, induction of cytokines promoting bone resorption, renal impairment, endocrine factors) and nondisease-specific mechanisms (sunshine avoidance with consequent vitamin D deficiency, glucocorticoids, immunosuppressants and chronic anticoagulants). Regarding anticoagulants, subcutaneous heparin is crucial against the risk of recurrent thromboembolism or pregnancy loss, specifically in patients with SLE and anti-phospholipid syndrome (APS). Thus heparin-induced OP represents one of the hazards of this treatment, first because heparin must be used long-term and secondly because pregnancy and lactation themselves may predispose to OP and fractures. Current data suggest the use of prophylaxis with calcium and vitamin D in all patients treated with heparin during pregnancy. Nevertheless glucocorticoid-induced OP (GIOP) is considered the most serious risk factor for OP and fractures in SLE patients. All guidelines recommend general measures and supplementation with calcium and vitamin D in all patients. However when considering premenopausal patients, there is no generally recommended treatment. Bisphosphonates, which are considered the first choice therapy for the prevention and treatment of GIOP, should be used 'cautiously' in these patients. Therefore the potential risks and lack of efficacy data on fracture risk reduction in premenopausal patients must be weighed against their proven efficacy in postmenopausal patients.     

Transforming growth factor-beta1 to the bone

TGF-beta1 is a ubiquitous growth factor that is implicated in the control of proliferation, migration, differentiation, and survival of many different cell types. It influences such diverse processes as embryogenesis, angiogenesis, inflammation, and wound healing. In skeletal tissue, TGF-beta1 plays a major role in development and maintenance, affecting both cartilage and bone metabolism, the latter being the subject of this review. Because it affects both cells of the osteoblast and osteoclast lineage, TGF-beta1 is one of the most important factors in the bone environment, helping to retain the balance between the dynamic processes of bone resorption and bone formation. Many seemingly contradictory reports have been published on the exact functioning of TGF-beta1 in the bone milieu. This review provides an overall picture of the bone-specific actions of TGF-beta1 and reconciles experimental discrepancies that have been reported for this multifunctional cytokine.