原发性骨疏松症致中老年人腰背疼痛的诊断和防治(附113例报告)

对原发性骨质疏松症引起中老年腰背疼痛113例。经保守治疗(9个月)86例,其疼痛减轻、骨量增加Ⅰ度者77.9％;手术治疗(13个月)27例,其疼痛减轻、骨量增加在Ⅰ度者85.2％。提示疗效良好(表1)。

鸡骨疏松症、肾炎与钙的相互关系

鸡骨疏松症、肾炎与钙的相互关系Ｋ．Ｇｅｊａｗｕａｔｓｕ著王婉兰摘译康奈尔大学女实验员，对某农场进行调查认为笼养蛋鸡发生骨疏松症有增加的趋向。而这种症状主要是由于饲料营养缺乏所致。若加强饲养管理是能够预防的。笼养致骨疏松症发生原因是鸡群开产提早。可能是...

不同配比和温度的国产骨水泥行经皮椎体成形术的临床研究

目的探讨用国产骨水泥行经皮椎体成形术的安全性和实用性,观察临床疗效。方法国产骨水泥(PMMA)预先常温和4℃冰箱贮藏调配时取出,常温下按粉剂(g):单体(ml):造影剂(ml)为2:1:1;3:2:1;1:1:1比例配制分组,共6组。自2002年6月-2003年8月采用国产PMMA行经皮椎体成形术(PVP)治疗疼痛性老年性骨质疏松性椎体压缩性骨折29例57椎,疼痛性椎体转移瘤2例6椎,共31例63椎。手术在C臂X线机透视下进行,经单或双侧椎弓根穿入骨穿针,国产PMMA按上述分组比例配制后注入伤病椎体内,同时分别测定各组的物料状态时期的时间及产热温度,观察患者在PMMA注入时的疼痛情况及术中、术后症状改善和功能恢复情况;腰背痛按Dennis分级评估。结果31例手术均顺利完成,无PMMA外漏压迫脊髓、神经根及肺栓塞等并发症的发生。术毕10％患者即觉疼痛消失,90％患者疼痛大部分缓解,于术后24-48小时全部患者完全缓解。腰背痛由术前P5改善为术后P1,跟踪拍X光线片显示术后的椎体高度无再丢失,局部转移瘤无复发。2例术后发现少量PMMA进入静脉中,未出现临床症状及并发症。结论国产骨水泥行经皮椎体成形术是安全可行的,常温下按粉剂(g):单体(ml):造影剂(ml)为3:2:1比例配制组成的物料状态时期最适宜行经皮椎体成形术,实用性强、临床疗效显著。

老年股骨粗隆间骨折半髋置换的初步探讨

目的：对于合并骨质疏松症的老年（〉75岁）患者,发生股骨粗隆间骨折,施行骨水泥型半髋置换术的初步探讨。方法：2009年10月-2012年10月,在宜宾市第一人民医院骨科住院,年龄〉75岁,并有骨质疏松症、发生股骨粗隆间骨折者,共23例。均施行单纯人工股骨头置换术（半髋———骨水泥型）,采用改良髋关节外侧切口。结果：共23例：男性9例,女性14例;年龄75-89岁,平均年龄82.5岁,均随访8月以上。15例于术后2周拄双拐步行;8例于术后3周拄双拐步行。未发现假体松动、断裂现象。结论：股骨粗隆间骨折大多采用DHS或髓内钉等手术方式。笔者发现,对于患者年龄较大且严重骨质疏松合并有多系统疾病的,治疗方法为人工股骨头置换,能达到早期进行功能锻炼、早期下地负重、术后并发症减少、减少痛苦的效果,值得在临床上推广应用。

骨科学(运动系疾病、矫形外科学)

9713677 肌肉疲劳和肌肉长度的相互作用及其对肌电图频率成分的影响/Doud JR//Electromyogr Clin Neurophysiol.-1995,35(6).-331～339 医科图9713678 坏死性筋膜炎的临床及微生物学物征/Brook I//J Clin Microbiol.-1995,33(9).-2382～2387 军医图9713679 以重组人γ干扰素长期治疗骨硬化症/Key L L//New Eng J Med.-1995,332(24).-1594～1599

Role of bisphosphonates in osteoporosis caused by adult growth hormone deficiency

In recent years,growth hormone and insulin-like growth factors have become key regulators of bone metabolism and remodeling,crucial for maintaining healthy bone mass throughout life.Studies have shown that adult growth hormone deficiency leads to alterations in bone remodeling,significantly affecting bone microarchitecture and increasing fracture risk.Although recombinant human growth hormone replacement therapy can mitigate these adverse effects,improving bone density,and reduce fracture risk,its effectiveness in treating osteoporosis,especially in adults with established growth hormone deficiency,seems limited.Bisphosphonates inhibit bone resorption by targeting farnesyl pyrophosphate synthase in osteoclasts,and clinical trials have confirmed their efficacy in improving osteoporosis.Therefore,for adult growth hormone deficiency patients with osteoporosis,the use of bisphosphonates alongside growth hormone replacement therapy is recommended.

Integrative analysis of bone-formation associated genes and immune cell infiltration in osteoporosis, and the prediction of active ingredients in targeted traditional Chinese medicine

Objective To explore the differential expression and mechanisms of bone formation-related genes in osteoporosis(OP)leveraging bioinformatics and machine learning methodologies;and to predict the active ingredients of targeted traditional Chinese medicine(TCM)herbs.Methods The Gene Expression Omnibus(GEO)and GeneCards databases were employed to conduct a comprehensive screening of genes and disease-associated loci pertinent to the pathogenesis of OP.The R package was utilized as the analytical tool for the identification of differentially expressed genes.Least absolute shrinkage and selection operator(LASSO)logis-tic regression analysis and support vector machine-recursive feature elimination(SVM-RFE)algorithm were employed in defining the genetic signature specific to OP.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses for the selected pivotal genes were conducted.The cell-type identification by estimating rela-tive subsets of RNA transcripts(CIBERSORT)algorithm was leveraged to examine the infiltra-tion patterns of immune cells;with Spearman’s rank correlation analysis utilized to assess the relationship between the expression levels of the genes and the presence of immune cells.Coremine Medical Database was used to screen out potential TCM herbs for the treatment of OP.Comparative Toxicogenomics Database(CTD)was employed for forecasting the TCM ac-tive ingredients targeting the key genes.AutoDock Vina 1.2.2 and GROMACS 2020 softwares were employed to conclude analysis results;facilitating the exploration of binding affinity and conformational dynamics between the TCM active ingredients and their biological targets.Results Ten genes were identified by intersecting the results from the GEO and GeneCards databases.Through the application of LASSO regression and SVM-RFE algorithm;four piv-otal genes were selected:coat protein(CP);kallikrein 3(KLK3);polymeraseγ(POLG);and transient receptor potential vanilloid 4(TRPV4).GO and KEGG pathway enrichment analy-ses revealed that these trait genes were predominantly engaged in the regulation of defense response activation;maintenance of cellular metal ion balance;and the production of chemokine ligand 5.These genes were notably associated with signaling pathways such as ferroptosis;porphyrin metabolism;and base excision repair.Immune infiltration analysis showed that key genes were highly correlated with immune cells.Macrophage M0;M1;M2;and resting dendritic cell were significantly different between groups;and there were signifi-cant differences between different groups(P<0.05).The interaction counts of resveratrol;curcumin;and quercetin with KLK3 were 7;3;and 2;respectively.It shows that the interac-tions of resveratrol;curcumin;and quercetin with KLK3 were substantial.Molecular docking and molecular dynamics simulations further confirmed the robust binding affinity of these bioactive compounds to the target genes.Conclusion Pivotal genes including CP;KLK3;POLG;and TRPV4;exhibited commendable significant prognostic value;and played a crucial role in the diagnostic assessment of OP.Resveratrol;curcumin;and quercetin;natural compounds found in TCM;showed promise in their potential to effectively modulate the bone-forming gene KLK3.This study provides a sci-entific basis for the interpretation of the pathogenesis of OP and the development of clinical drugs.

Unveiling osteoprotective potential of biologically active naringenin in rats with dexamethasone-induced osteoporosis

Objective To investigate the protective effects of naringenin(NRG)against dexamethasone(DEX)-induced osteoporosis(OP)in rats.Methods Molecular docking of NRG was done with AutoDock Vina 1.2.0 software.Forty-eight female Wistar rats were randomly divided into six groups(n=8 each):normal control(NC),DEX(7 mg/kg,i.m.),NRG-low(NRG-L;25 mg/kg,i.g.),NRG-medium(NRG-M;50 mg/kg,i.g.),NRG-high(NRG-H;100 mg/kg,i.g.),and alendronate(ALN;0.25 mg/d,i.g.)groups.OP was induced by administering DEX once a week for five weeks in all groups except NC group.Begining in the third week after the initial DEX administration,the rats in NRG-L,NRG-M,NRG-H,and ALN groups received the corresponding treatments daily for three weeks,while NC and DEX groups received no additional treatment.Serum samples were collected at the end of the experiment for biochemical,bone turnover,antioxidant,lipid profile,and inflammatory cytokine analyses.Femur bones underwent physical parameter testing and histopathological examination.Results The molecular docking results illustrated that NRG docked with calcitonin(CT),lowdensity lipoprotein(LDL),bone morphogenetic protein(BMP),vascular endothelial growth factor(VEGF)receptor,forkhead transcription factors,and osteoprogenitor cells showed good binding energy.In rats administered with 25,50,and 100 mg/kg NRG,there was a significant enhancement in serum biochemical indices,characterized by a reduction in tartrate-resistant acid phosphatase(TRAP),parathyroid hormone(PTH),and an elevation in osteocalcin(OC)and CT levels(P<0.05,P<0.01,and P<0.001,respectively).Despite no significant changes in thickness,weight,and length(P>0.05),there was a marked increase in bone mineral density(BMD)(P<0.01,P<0.001,and P<0.001,respectively).Antioxidant enzyme markers showed significant upregulation,with higher glutathione,superoxide dismutase,and catalase,and a concurrent decrease in malondialdehyde(MDA)(P<0.05,P<0.01,and P<0.001,respectively).The lipid profile also improved significantly,with lower cholesterol(CH),triglycerides(TG),and low-density lipoprotein(LDL)levels,and an increase in high-density lipoprotein(HDL)level(P<0.05,P<0.01,and P<0.001,respectively).Inflammatory cytokine levels were reduced,as evidenced by decreases in tumor necrosis factor(TNF),interleukin(IL)-6,and IL-1β(P<0.05,P<0.01,and P<0.001,respectively).Furthermore,histological alterations revealed obvious improvements,and the body weight of rats treated with NRG showed an increase compared with DEX group.Conclusion These findings imply that NRG exhibited a protective effect against DEX-induced OP in rats as it promotes the bone formation process by increasing the number of bone turnover markers including OC and CT,and restoring of antioxidant status,lipid metabolism,and inflammatory markers.

Dissecting Causal Relationships Between Plasma Metabolites and Osteoporosis:A Bidirectional Mendelian Randomization Study

Objective To investigate the causal relationships between plasma metabolites and osteoporosis via Mendelian randomization(MR) analysis.Methods Bidirectional MR was used to analyze pooled data from different genome-wide association studies(GWAS). The causal effect of plasma metabolites on osteoporosis was estimated using the inverse variance weighted method, intersections of statistically significant metabolites obtained from different sources of osteoporosis-related GWAS aggregated data was determined, and then sensitivity analysis was performed on these metabolites. Heterogeneity between single nucleotide polymorphisms was evaluated by Cochran's Q test. Horizontal pleiotropy was assessed through the application of the MR-Egger intercept method and the MRPRESSO method. The causal effect of osteoporosis on plasma metabolites was also evaluated using the inverse variance weighted method. Additionally, pathway analysis was conducted to identify potential metabolic pathways involved in the regulation of osteoporosis.Results Primary analysis and sensitivity analysis showed that 77 and 61 plasma metabolites had a causal relationship with osteoporosis from the GWAS data in the GCST90038656 and GCST90044600 datasets, respectively. Five common metabolites were identified via intersection. X-13684 levels and the glucose-to-maltose ratio were negatively associated with osteoporosis, whereas glycoursodeoxycholate levels and arachidoylcarnitine(C20) levels were positively associated with osteoporosis(all P < 0.05). The relationship between X-11299 levels and osteoporosis showed contradictory results(all P < 0.05). Pathway analysis indicated that glycine, serine, and threonine metabolism, valine, leucine, and isoleucine biosynthesis, galactose metabolism, arginine biosynthesis, and starch and sucrose metabolism pathways were participated in the development of osteoporosis.Conclusion We found a causal relationship between plasma metabolites and osteoporosis. These results offer novel perspectives with important implications for targeted metabolite-focused interventions in the management of osteoporosis.

Association of CA Repeat Polymorphism in Estrogen Receptor β Gene with Postmenopausal Osteoporosis in Chinese

Postmenopausal osteoporosis （PMO） is considered a polygenic disease. The estrogen receptor β （ESR2） gene is a candidate mediating the genetic influence on bone mass and the risk of osteoporosis. The aim of this study is to investigate the association of a cytosine-adenine （CA） repeat polymorphism in the fifth intron of the ESR2 gene with PMO in Chinese Han population. The CA repeat polymorphism was genotyped in a case-control study, involving 78 femoral neck PMO patients vs. 122 controls and 108 lumbar spine （L2-4） PMO patients vs. 92 controls. The （CA）n〈22 and （CA）n≥22 alleles were designated short （S） and long （L）, respectively. ESR2 genotype was categorically defined as SS （2 S alleles）, SL （having the mixed S and L alleles）, and LL （2 L alleles）. At both the femoral neck and the L2-4 region, LL genotype and L allele frequencies of the PMO group were significantly higher than those of the control group （P〈0.01）. The subjects with the SL, the LL, and the combined SL and LL genotype had a significant increased risk of PMO when compared with those with the SS genotype （P〈0.05）. After adjustments for age, years since menopause, menopausal age, and body mass index, logistic regression analysis showed that the subjects with the combined SL and LL genotype had increased risk of PMO when compared with those with the SS genotype both at the femoral neck （adjusted OR 4.923, 95% CI 1.986-12.203 , P=0.001） and the L2-4 （adjusted OR 2.267, 95% CI 1.121-4.598, P=0.023）. This extensive association study has identified the ESR2 CA repeat polymorphism to be independently associated with PMO at the femoral neck and the L2-4 in Chinese Han population. The data also suggested that the presence of the L allele may dominantly increase the risk of PMO at the two regions.

Non-alcoholic fatty liver disease connections with fat-free tissues: A focus on bone and skeletal muscle

The estimates of global incidence and prevalence of non-alcoholic fatty liver disease(NAFLD) are worrisome, due to the parallel burden of obesity and its metabolic complications. Indeed, excess adiposity and insulin resistance represent two of the major risk factors for NAFLD; interestingly, in the last years a growing body of evidence tended to support a novel mechanistic perspective, in which the liver is at the center of a complex interplay involving organs and systems, other than adipose tissue and glucose homeostasis. Bone and the skeletal muscle are fat- free tissues which appeared to be independently associated with NAFLD in several cross-sectional studies. The deterioration of bone mineral density and lean body mass, leading to osteoporosis and sarcopenia, respectively, are age-related processes. The prevalence of NAFLD also increases with age. Beyond physiological aging, the three conditions share some common underlying mechanisms, and their elucidations could be of paramount importance to design more effective treatment strategies for the management of NAFLD. In this review, we provide an overview on epidemiological data as well as on potential contributors to the connections of NAFLD with bone and skeletal muscle.

Osteoporosis in celiac disease and in endocrine and reproductive disorders

As the increase in lifespan brings to light diseases that were previously not clinically detectable,osteoporosis has become an issue of worldwide significance. The disease is marked by a loss of bone mass; the bones become less dense,fragile and more prone to fracturing. Because it is regulated by endocrine and environmental factors,osteoporosis presents a multifactorial etiopathogenesis,with the genetic component accounting for 70% of an individual variation in bone mass density (BMD),the principal determinant,with age,of fracture risk. Pathological conditions such as celiac disease (CD) exacerbate the process of bone loss,so that the occurrence of osteoporosis in celiac subjects is of particular note: indeed,the screening of osteoporosis patients for this disease is advisable,since it may be the only sign of undiagnosed CD. An increase in interleukin IL-1β,of the IL-1 system,in the relatives of celiac patients confirms the genetic predisposition to osteoporosis and its presence is evidence of an association between the two conditions. The direct effect on the bones of CD is secondary to poor absorption of calcium and vitamin D. In women osteoporosis is indirectly associated with early menopause and amenorrhea,and it may follow prolonged breast-feeding and frequent pregnancies,while in men it is associated with hypogonadism and GH deficit. These endocrine and non-endocrine factors exert their effects on bones by modulating the RANK/RANK-L/OPG system. An appropriate lifestyle from adolescence onwards,together with early diagnosis of and treatment for CD and primary and secondary endocrine pathologies are important for the prevention of damage to the bones.

Is osteoporosis a peculiar association with primary biliary cirrhosis?

AIM： （1） To compare the prevalence of osteoporosis （t-score ≤-2.5 SD） between stage IV PBC patients, and two groups of age- and sex-matched controls： one with hepatitis C virus （HCV）-related cirrhosis, and the other one consisting of a group of healthy subjects from the general population, （2） to identify the main risk factors for the development of bone loss. METHODS： Thirty-five stage IV PBC patients （mean age 52.5±10 years）, 49 females with HCV-related cirrhosis （mean age 52.9±5.8 years） and 33 healthy females （mean age 51.8±2.22 years） were enrolled in the study. Bone metabolism was evaluated by measuring serum calcium corrected for serum albumin （Ca corr.）, 25-hydroxy vitamin D （25-OH vit D）, parathyroid hormone, osteocaldn. Bone mineral density （BMD） was assessed at the lumbar spine by dual-photon X-ray absorptiometry. RESULTS： Osteoporosis was present in 5/35 PBC patients （14.2%） and in 7/49 HCV-related drrhotic patients （14.3%）, without any statistical difference between the two groups. Among healthy control subjects, none had osteoporosis. No difference was found between the three groups in serum parameters of bone metabolism. Univariate analysis showed that menopausal state and low BMI were significantly correlated with osteoporosis. Multivariate regression analysis showed that menopausal status, BMI〈23, and old age were independent variables significantly correlated with osteoporosis. CONCLUSION： PBC in itself has no negative influence on BMD. End-stage liver disease patients carry a disease-specific risk for osteoporosis, but have an effective risk of bone loss in relation to individual potential risk for each patient. A practical message should be taken into account, that is, every effort should be made to prevent osteoporosis when a patient has simple osteopenia, or if it is a woman in or near menopausal age.

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Low bone mineral density and the increased risk of fracture in gastrointestinal diseases have a multifactorial pathogenesis. Inflammatory bowel disease （IBD） has been associated with an increased risk of osteoporosis and osteopenia and epidemiologic studies have reported an increased prevalence of low bone mass in patients with IBD. Certainly, genetics play an important role, along with other factors such as systemic inflammation, malnutrition, hypogonadism, glucocorticoid therapy in IBD and other lifestyle factors. At a molecular level the proinflammatory cytokines that contribute to the intestinal immune response in IBD are known to enhance bone resorption. There are genes influencing osteoblast function and it is likely that LRP5 may be involved in the skeletal development. Also the identification of vitamin D receptors （VDRs） and some of its polymorphisms have led to consider the possible relationships between them and some autoimmune diseases and may be involved in the pathogenesis through the exertion of its immunomodulatory effects during inflammation. Trying to explain the physiopathology we have found that there is increasing evidence for the integration between systemic inflammation and bone loss likely mediated via receptor for activated nuclear factor kappa-B （RANK）, RANK-ligand, and osteoprotegerin, proteins that can affect both osteoclastogenesis and T-cell activation. Although glucocorticoids can reduce mucosal and systemic inflammation, they have intrinsic qualities that negatively impact on bone mass. It is still controversial if all IBD patients should be screened, especially in patients with preexisting risk factors for bone disease. Available methods to measure BMD include single energy x-ray absorptiometry, DXA, quantitative computed tomography （QCT）, radiographic absorptiometry, and ultrasound.DXA is the establish method to determine BMD, and routinely is measured in the hip and the lumbar spine. There are several treatments options that have proven their effectiveness, while new emergent therapies such as calcitonin and teriparatide among others remain to be assessed.

Effects of Zhuang Gu Zhi Tong Formula on Wnt/β-catenin Osteoporosis Pathway Antagonist SOST in Osteoporosis

Objective To observe the effects of Zhuang Gu Zhi Tong Formula (ZGZTF) on antagonist SOST in canonical Wnt/β-catenin signaling pathway in osteoporosis. Methods We analyzed the differential genes of patients with osteoporosis and normal subjects from the GEO database and then found SOST with specific expression. We analyzed SOST as an antagonist of the Wnt signaling pathway by the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Then we studied the effect of ZGZTF on SOST in Wnt signaling pathway. Osteoporosis model was induced by ovariectomy (OVX) in 8-week-old female Sprague–Dawley (SD) rats. After 12 weeks of treatment with ZGZTF by intragastric administration, the rats were put to death in batch. The changes of alkaline phosphatase (ALP), bone gla protein (BGP) and estradiol (E2) in serum were determined, and bone mineral density (BMD) and histomorphology of right femur were observed. Biomechanics of lumbar vertebra were measured, and the expression of SOST, Wnt3a,β-catenin, LRP5, Runx2, Osx and their mRNA involving the canonical Wnt/β-catenin signaling pathway were detected by Western blot, RT-PCR and Immunohistochemical analysis. All data were analyzed by SPSS 22.0. Results Twelve weeks of treatment with ZGZTF could significantly decrease the level of ALP and BGP in serum, increase the BMD of femurs, and improve the biomechanical capability of vertebral body in maximum loading and elastic modulus. Concerning histomorphology, we found ordered arrangement of trabeculae, slightly thinning of trabeculae and none obvious slight fractures in femurs after 12 weeks of treatment with ZGZTF. The expression of LRP5,β-catenin, Runx2 and Osx involved in the canonical Wnt/β-catenin signaling pathway was significantly up-regulated in the presence of ZGZTF,and the expression of SOST in this pathway was down-regulated. Conclusions These results suggest that ZGZTF may be antiosteoporosis by down-regulating SOST protein to promote Wnt/β-catenin signaling pathway.

The Effect of Acupuncture on Bone Mineral Density in Postmenopausal Women

According to the TCM theory that the kidney is in charge of the bone, the authors carried out a study on the effect of acupuncture on bone mineral density in 40 postmenopausal women with osteoporosis treated by the method of reinforcing the kidney to strengthen the bone, with satisfactory therapeutic results reported as follows.……

Prevalence of IgA-antiendomysial antibody in a patient cohort with idiopathic low bone mineral density

AIM:To investigate the frequency of serum IgA-antiendomysial antibody positivity in patients with low bone mineral density and to assess the risk group for screening of celiac disease. METHODS:One hundred and thirty-five patients (14 male,121 female) with idiopathic low bone mineral density were evaluated. The median age was 57.2 years (24-81). Antiendomysial antibody was determined by the immunofluorescence method using a commercial kit (INOVA Diagnostics Inc.,CA,USA),which employs a 5 μm thin cryostat section of monkey esophagus as a substrate. RESULTS:Of the 135 patients evaluated,13 were found to have positive IgA antiendomysial antibody test (9.6%) response. None of the patients had IgA deficiency. Endoscopic appearance and histological examination were normal in all of these patients. Seropositive patients had significantly lower age (48.9 ± 4.3 vs 59.2 ± 6.2,P < 0.05),higher ratio of male gender (61.5% vs 4.9%,P < 0.01) and pre-menopausal status (8.7% vs 1.3%,P < 0.01). Lumbar spine and femoral neck z-scores,but not t-scores were significantly lower in seropositive patients. Seropositive patients had lower serum 25 (OH) vitamin D,calcium and higher serum parathormone levels than seronegative patients. CONCLUSION:The screening of celiac disease in idiopathic osteoporosis should be restricted to patients without classical risk factors (younger,pre-menopausal,male gender) for osteoporosis. Bone mineral density measurements using z-scores should be considered for identifying risk groups for celiac disease.

Association Between Geranylgeranyl Pyrophosphate Synthase Gene Polymorphisms and Bone Phenotypes and Response to Alendronate Treatment in Chinese Osteoporotic Women

Objective To investigate the relationship between geranylgeranyl pyrophosphate synthase （GGPPS） gene polymorphisms and bone response to alendronate in Chinese osteoporotic women. Methods A total of 639 postmenopausal women with osteoporosis or osteopenia were included and randomly received treatment of low dose （70 mg per two weeks） or standard dose （70 mg weekly） of alendronate for one year. The six tag single nucleotide polymorphisms of GGPPS gene were identified. Bone mineral density （BMD）, serum cross-linked C-telopeptide of type I collagen （β-CTX）, and total alkaline phosphatase （ALP） were measured before and after treatment. GGPPS gene polymorphisms and the changes of BMD and bone turnover markers after treatment were analyzed. Results rs10925503 polymorphism of GGPPS gene was correlated to serumβ-CTX levels at baseline, and patients with TT genotype had significantly higher serum β-CTX level than those with TC or CC genotype （all P〈0.05）. No correlation was found between polymorphisms of GGPPS gene and serum total ALP levels, as well as BMD at baseline. After 12 months of treatment, lumbar spine and hip BMD increased and serum bone turnover markers decreased significantly （P〈0.01）, and without obvious differences between the low dose and standard dose groups （all P〉0.05）. However, GGPPS gene polymorphisms were uncorrelated to percentage changes of BMD, serum total ALP, and β-CTX levels （all P〉0.05）. Conclusion GGPPS gene polymorphisms are correlated to osteoclasts activity, but all tag single nucleotide polymorphisms of GGPPS gene have no influence on the skeletal response to alendronate treatment.