牙齿缺失与骨密度关系的研究

目的系统骨丢失与牙槽骨局部骨丢失致牙齿缺失之间的关系尚不清楚，通过检测健康藏族妇女的骨密度及其牙齿缺失状态，探讨其相关性。方法随机选择西藏拉萨40—79岁健康藏族妇女(无牙周疾病治疗史)135人，检查牙齿缺失状况确定缺牙原因。问卷调查排除系统病和服用影响骨密度和钙磷代谢药物史。同时用MetriScan TM(美国Alara公司提供)指骨骨密度仪进行骨密度测量，应用SPSS软件统计分析。结果随年龄增长，因牙周病而缺牙的人占同年龄人数的百分率逐渐升高，骨密度逐渐降低。结论骨质疏松症是牙周病的危险因子之一。     

Reduced bone density in women with fractures: Contribution of low peak bone density and rapid bone loss

Osteoporosis is regarded as a disease of the elderly because fractures occur late in life. Although excessive bone loss during aging is likely to contribute to the deficit in bone density, patients with fractures do not consistently have more rapid bone loss, greater bone resorption or lower bone formation (measured using biochemical or histomorphometric markers of bone turnover). The pathogenesis of the low bone density and bone fragility that characterize osteoporosis may begin during the first two decades of life. There are differences in the hormonal regulation of regional growth and mineral accrual, differences in the age of onset, rate and duration of linear growth and mineral accrual of the axial and appendicular skeleton, of cortical and trabecular bone, and of proximal and distal limb segments. Illnesses, risk or protective factors, and disorders of hormonal deficiency or excess may affect longitudinal growth, mineral accrual, or both, depending on the timing of exposure. Quantitatively larger and qualitatively different effects on bone density may result when exposure occurs during growth rather than during adulthood. The magnitude of these deficits and their location are likely to establish the relevance of regional age-related and sex hormone dependent bone loss. Thus, any unifying hypothesis concerning the epidemiology and pathogenesis of osteoporosis must consider the relative contributions of low peak bone density and bone loss to the deficit in bone density in adulthood. A great deal of research is needed to examine the physiology of longitudinal growth and mineral accrual as the pathogenesis of osteoporosis is at least partly explained by events occurring during the first 20 years of life.     

牙周附着丧失与骨密度关系的研究

目的探讨健康藏族成年妇女骨密度状态与牙周附着丧失的关系。方法随机选择35～69岁健康藏族成年妇女（无牙周疾病治疗史）141人，检查牙周组织状态，确定牙周附着丧失牙数及缺失牙数。问卷调查排除全身疾病和服用影响骨代谢药物史。并用MetriScan TM（美国Alara公司提供）指骨骨密度仪进行骨密度测量，采用单因素方差分析方法进行统计学分析。结果每一年龄段内，牙周附着丧失不同状态下妇女的骨密度在统计学上没有显著差异，但随着年龄增高，牙周附着丧失及缺失牙严重程度增加。结论骨密度减低是牙周附着丧失的危险因子。     

The oxidative metabolism of estradiol conditions postmenopausal bone density and bone loss.

Because lifelong exposure to estrogen is a strong determinant of bone mass, we asked whether metabolic conversion of estrogen to either inactive or active metabolites would reflect postmenopausal bone mineral density (BMD) and rate of bone loss. Biochemical markers of inactive estrogen metabolites, urinary 2-hydroxyestrogen (2OHE1) and 2-methoxyestrogen (2MeOE1), and active metabolites, urinary 16alpha-hydroxyestrone (16alphaOHE1), estradiol (E2), and estriol (E3), were determined in 71 untreated, healthy postmenopausal women (age, 47-59 years) followed prospectively for 1 year. Urinary 2MeOE1 was correlated negatively with baseline vertebral (anteroposterior [AP] projection, r = -0.23 andp < 0.05; lateral view, r = -0.27 and p < 0.05) and proximal femur bone density measured by dual-energy X-ray absorptiometry (DXA; total, r = -0.38 and p < 0.01; neck, r = -0.28 and p = 0.02; trochanter, r = -0.44 and p < 0.01). BMDs of women in the lowest quartile of urinary 2MeOE1 (< 15 ng/g) were significantly higher than those in the highest quartile at all skeletal sites (p < 0.05). Likewise, women in the lowest quartile of urinary 2OHE1/16alphaOHE1 ratio (< 1.6) did not experience bone loss after 1 year, in contrast to women in the higher quartiles. We propose that the rate of inactivation of estrogens through 2-hydroxylation may contribute to postmenopausal osteoporosis.     

Tooth loss and skeletal bone density in healthy postmenopausal women

Associations between dental status and skeletal bone density were investigated in a group of 329 healthy postmenopausal women with normal bone density. Bone mineral density (BMD) of the lumbar spine, femoral neck and distal radius were measured by dual-or single-photon absorptiometry. Number of teeth remaining were counted and presence of complete dentures noted by a nurse practitioner. Forty-eight women (15%) wore a complete maxillary and/or mandibular denture: 22 (7%) were completely edentulous and an additional 26 (8%) had one edentulous ridge. Among women without complete dentures (n=281), significant positive linear relationships were observed between number of teeth and BMD at the spine (p<0.05) and radius (p<0.01), controlling for years since menopause, pack-years of smoking, education and body mass index. BMD did not differ between the groups with and without dentures. However, women who acquired dentures after the age of 40 years had significantly lower mean spinal and radial BMD than women who acquired dentures at age 40 years or earlier (at the radius, 0.584±0.015 v 0.630±0.017 g/cm²,p<0.05; at the spine, 1.043±0.031 v 1.124±0.029 g/cm²,p=0.05). In linear regression analysis, significant independent correlations were found among all women (n=329) between number of teeth and age (partialr=–0.19,p<0.001), pack-years of cigarette use (partialr=–0.23,p<0.001) and years of education (partialr=+0.11,p<0.05). These associations between dental status and BMD support the hypothesis that systemic bone loss may contribute to tooth loss.     

CD38 is associated with premenopausal and postmenopausal bone mineral density and postmenopausal bone loss

One goal of osteoporosis research is to identify the genes and environmental factors that contribute to low bone mineral density (BMD) and fracture. Linkage analyses have identified quantitative trait loci (QTLs), however, the genes contributing to low BMD are largely unknown. We examined the potential association of an intronic polymorphism in CD38 with BMD and postmenopausal bone loss. CD38 resides in 4p15, where a QTL for BMD has been described. CD38−/− mice display an osteoporotic phenotype at 3 months, with normalization of BMD by 5 months. The CD38 polymorphism was identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis in 457 postmenopausal and 173 premenopausal Caucasian women whose spine and hip BMD was measured by dual energy X-ray absorptiometry (DXA). Influence of the CD38 polymorphism on bone loss was analyzed in 273 postmenopausal women over a follow-up of 2.94 ± 1.50 years. The CD38-PvuII polymorphism was significantly associated with premenopausal and postmenopausal (P = 0.001) lumbar spine BMD. Women homozygous for the G allele had >14% lower spinal BMD than women with GC/CC genotypes. An allele dose effect was observed at the spine in premenopausal (P = 0.002) and postmenopausal (P < 0.001) cohorts. The CD38-PvuII polymorphism was significantly associated with femoral neck BMD in pre- and postmenopausal women (P = 0.002 and P = 0.011, respectively). However, significance was lost following adjustment of hip BMD for covariates in the postmenopausal cohort (P = 0.081). The CD38-PvuII polymorphism was weakly associated with bone loss at the spine (P = 0.024), in postmenopausal women not taking hormone replacement therapy. We suggest that the CD38-PvuII polymorphism may influence the attainment and maintenance of peak BMD and postmenopausal bone loss.     

Association between TNFRSF1B polymorphisms and bone mineral density,bone loss and fracture

The TNFRSF1B gene, which encodes the p75 TNF receptor, is a strong functional and positional candidate gene for susceptibility to osteoporosis. In a previous study, we reported that polymorphic variation in the 3 untranslated region of TNFRSF1B was associated with femoral neck bone mineral density (BMD) in a population-based cohort of Scottish women. In order to further explore the role of TNFRSF1B as a candidate gene for osteoporosis, we have now studied the relationship between a promoter polymorphism in the TNFRSF1B gene and BMD, and determined whether this polymorphism interacts with other polymorphisms in TNFRSF1B to regulate bone mass, bone loss, and osteoporotic fracture. Analysis of individual polymorphisms showed weak associations between the G593A, T598G and T620C polymorphisms and femoral neck BMD (P=0.05–0.017). On haplotype analysis, the only significant association we observed was with FN BMD when haplotypes were grouped according to presence or absence of A593-T598-C620 alleles in the 3 UTR (0.897±0.005 versus 0.841±0.01; P<0.0001). These data show that allelic variation within the TNFRSF1B gene contributes to the genetic regulation of FN-BMD and show that it is the ATC haplotype in the 3UTR region of the gene, rather than other polymorphic variants, that seem to be responsible for the effects observed.The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint first author.     

Ultradistal and cortical forearm bone density in the assessment of postmenopausal bone loss and nonaxial fracture risk

Forearm bone mineral density (BMD) was measured by single-energy photon absorptiometry in 360 healthy females without known axial fractures, 202 of whom were postmenopausal. The three sites addressed included an ultradistal (U) region containing approximately 60% trabecular bone. The other sites, distal (D) and shaft (S), were progressively more cortical. Reproducibility was 1.7-1.9% CV. The earliest evidence of a significant correlation between BMD and years since menopause was seen in trabecular bone in subjects aged 45-55 years. Fractional decrease in BMD, relative to the premenopausal value, was significantly larger at U than at S for the decades 55-65 years and above. Fractional rates of bone loss at all sites were a maximum in the first postmenopausal decade, the rate at U being 0.035, approximately 1.5 times that at D or S. A total of 33 subjects reported 54 previous minimally traumatic nonaxial (MTNA) fractures. When BMD measurements of the entire study were divided into quintiles, the prevalence of MTNA fracture cases in the lowest quintile was eight times that of each of the upper three quintiles. Prevalence of fracture cases ranked by quintiles of BMD were not different for the three scan sites. Therefore, ultradistal measurements confer no advantages over distal or shaft BMD for discriminating past MTNA fracture cases but do show larger fractional rates of loss during the first postmenopausal decade.(ABSTRACT TRUNCATED AT 250 WORDS)     

乌鲁木齐地区人群放射吸收法测量指骨骨密度的研究

目的探讨通过放射吸收法(radiographic absorptiometry,RA),获得乌鲁木齐地区人群指骨正常骨峰值及骨质疏松的BMD参考值,为本地区骨质疏松的预防、诊断和治疗提供科学依据。方法本次受检者4828例均剔出骨代谢相关疾病及服用激素类药物史者,用美国Compu Med Osteo Gram-2000骨密度仪测定受检者非优势手的第2、3、4指中节指骨骨密度,按10岁一个年龄组男女各分7组。测试先用岛津XHD-150G 60 X线机对患者非优势手指进行摄片,使用相同摄影条件先后曝光两次。将数据通过美国柯达CR850系统以及Easywork影像工作站(mini PACS)对图像进行数字化处理、传输。最后采用美国Osteo Gram2000骨密度仪进行检测、分析(无片式诊断系统)。结果根据骨密度仪所提供的骨质疏松症诊断标准:本组4828例受检者中,提示骨质量减少(T值介于-1~-2.5之间)者1587例。其中男性548例,占34.5%(548/1587),女性1039例,占65.5%(1039/1587)。诊断骨质疏松症(T值低于-2.5)者1452例。其中,男性384例占26.4%(384/1452)。女性1068例,占73.6%(1068/1452)。本地区受检者骨质疏松患病率为30.0%。男女性骨质丢失率在40岁开始上升,并随着年龄的增长丢失率不断上升。女性44岁(平均44.2±2.6岁)以上开始绝经,绝经后骨量开始快速丢失,当绝经后16~20年时丢失率迅速加快,20年以后缓慢上升。男性骨量减少发生例数与女性有统计学差异(P0.01),女性骨质疏松发生例数与男性有统计学差异(P0.01)。乌鲁木齐地区女性绝经年龄与骨量丢失率成正比关系(r=0.9643,P0.01),绝经0~15年内骨量丢失率平稳上升,16~20年时骨量丢失明显加快,绝经21年以后骨量丢失率变缓,但仍处于上升趋势。结论通过运用放射吸收法对乌鲁木齐地区4828例受检者非优势手指骨骨密度的统计与分析,有效的反映了本地区人群骨矿含量及骨质疏松发病率,并与乌鲁木齐地区DXA与QCT的检测结果相似。但该检查技术辐射剂量低、扫描速度快、价格低廉,更适合基层医院用于临床诊断骨质疏松和预测骨折风险。     

Assessment of age and risk factors on bone density and bone turnover in healthy premenopausal women

The influence of age and risk factors on bone density and bone turnover was evaluated in 249 healthy premenopausal women. Risk factors were assessed by standardized questionnaires and included reproductive history and lifestyle factors (intake of calcium and vitamin D supplements, consumption of caffeine, smoking habits and physical activity). Bone mineral density (BMD) measurements were obtained in the distal forearm, the lumbar spine and the proximal femur. Bone turnover were assessed by plasma bone Gla proteins (pBGP) and fasting urinary hydroxyproline corrected for creatinine (fUHPr/Cr). Peak bone density seems to be achieved before the age of 30 years, whereafter we found no appreciable bone loss at any skeletal site. Accordingly, the levels of pBGP and fUHPr/Cr were increased before the age of 30, whereafter the values stabilized at a lower level. A dairy calcium intake above 660 mg/day significantly increased BMD in the spine and proximal femur by 3%–5%. Physical activity alone had no influence on BMD, but in combination with calcium intake an additive effect was observed. Women who had an active lifestyle (corresponding to at least 1 h of daily walking) and a dairy calcium intake above 660 mg/day had a 3%–7% increase in BMD compared with more sedentary women with a calcium intake below this limit. Vitamin D supplements, caffeine, smoking and reproductive history did not consistently influence BMD or bone turnover. Only pBGP was selectively reduced by smoking and current use of oral contraceptives, respectively. We conclude that there is no appreciable change in BMD before the menopause once skeletal maturity has been reached. Dietary calcium intake increases peak bone density and this positive effect can be potentiated by an active lifestyle. Other putative risk factors had no influence on premenopausal BMD.     

Ibandronate treatment reverses glucocorticoid-induced loss of bone mineral density and strength in minipigs

The Göttingen minipig is one of the few large animal models that show glucocorticoid (GC)-induced bone loss. We investigated whether GC-induced loss of bone mineral density (BMD) and bone strength in minipigs can be recovered by treatment with the bisphosphonate ibandronate (IBN).40 primiparous sows were allocated to 4 groups when they were 30 months old: GC treatment for 8 months (GC8), for 15 months (GC15), GC treatment for 15 months plus IBN treatment for months 8–15 (GC&;IBN), and a control group without GC treatment. Prednisolone was given at a daily oral dose of 1 mg/kg body weight for 8 weeks and thereafter 0.5 mg/kg body weight. IBN was administered intramuscularly and intermittently with an integral dose of 2.0 mg/kg body weight. BMD of the lumbar spine (L1–3) was assessed in vivo by Quantitative Computed Tomography (QCT) at months 0, 8, and 15. Blood and urine samples were obtained every 2–3 months. After sacrificing the animals lumbar vertebrae L4 were tested mechanically (Young's modulus and ultimate stress). Histomorphometry was performed on L2 and mineral content determined in ashed specimens of T12 and L4.In the GC&;IBN group, the GC associated losses in BMD of − 10.5% ± 1.9% (mean ± standard error of the mean, p < 0.001) during the first 8 months were more than recovered during the following 7 months of IBN treatment (+ 14.8% ± 1.2%, p < 0.0001). This increase was significantly larger (p < 0.0001) than the insignificant + 2.1% ± 1.2% change in group GC15. At month 15, the difference between groups GC&;IBN and GC15 was 22% (p < 0.01) for BMD, 48% (p < 0.05) for Young's modulus, and 31% (p < 0.14) for ultimate stress; bone-specific alkaline phosphatase showed trends to lower values (p < 0.2) while deoxypyridinoline was comparable.This minipig study demonstrates that GC-induced impairment of bone strength can be effectively and consistently treated by IBN. GC&;IBN associated alterations in BMD and bone turnover markers can be monitored in vivo using QCT of the spine and by biochemical analyses, reflecting the changes in bone strength.     

Assessment of bone mineral density in adults and children with Marfan syndrome

Recent studies indicate that decreased bone mineral density (BMD) occurs in the spine, femoral necks and greater trochanters of some adults and children with Marfan syndrome. Because there is uncertainty regarding the BMD status of patients with Marfan syndrome, we undertook an analysis of BMD in both adults and children with Marfan syndrome. Dual energy X-ray absorptiometry analysis was performed on a convenience sample of 51 patients (30 adults and 21 children) with diagnosed Marfan syndrome from 1993 to 2000. T-Scores (i.e. the number of standard deviations above or below the average normal peak bone density) were determined for comparison of adults. Mean±SD of individual BMD values were used for comparison of the data of children. Compared to standard values obtained from normal adult patients, adult males with Marfan syndrome demonstrated significantly reduced femoral neck BMD with an average T-score of -1.54 (P<0.001), diagnostic of osteopenia. Although osteopenia and osteoporosis were observed in several middle aged and pre- and postmenopausal women, the average T-score value for adult females and children were within normal limits. The etiology and full significance of decreased BMD in adult male patients with Marfan syndrome remain uncertain at the present time. Our results lead us to question the value of aggressive BMD evaluations by DXA in these patients, particularly prior to reaching mid-age. Further investigations will be required to shed insights into the natural history of BMD in adults and children with Marfan syndrome. Any application of bone mineral replacement therapy such as bisphosphonate, selective estrogen receptor modulators, hormone replacement therapy and vitamin D in these patients may be premature based on the existing evidence.     

Suppression of bone density loss and bone turnover in patients with hormone-sensitive prostate cancer and receiving zoledronic acid

OBJECTIVE: To report a randomized, placebo-controlled study of treatment with zoledronic acid every 3 months in patients with hormone-sensitive prostate cancer, both with and without bone metastases, to assess the effect on bone mineral density (BMD) and markers of bone turnover. PATIENTS AND METHODS: Eligible patients included those with prostate cancer and on androgen-deprivation therapy for <12 months. Patients received zoledronic acid 4 mg intravenously, or placebo, every 3 months for four treatments. BMD, urinary N-telopeptides of type I collagen (NTX), and serum bone alkaline phosphatase (BAP) were measured every 3 months. In all, 42 patients were randomized. RESULTS: After excluding BMD data from sites of known metastases, patients receiving zoledronic acid had a relative increase in BMD compared with those receiving placebo, of 4.2% and 7.1% at the femoral neck and lumbar spine, respectively. NTX and BAP decreased significantly in patients receiving zoledronic acid. NTX and BAP levels were significantly higher at baseline in patients with bone metastases than in those without. CONCLUSIONS: Treatment with zoledronic acid every 3 months preserved bone density and suppressed markers of bone turnover in patients with androgen-deprived prostate cancer, both with and without bone metastases.     

Prevention of loss of vertebral bone density in heart transplant patients.

Seventy-six patients (63 men, 13 women) have been followed up by vertebral bone density (VBD) studies from 3 to 36 months. VBD was measured by single-energy computerized tomographic scan. Before transplantation, VBD was found to be lower than in age-matched controls (less than 40 years of age [group 1], 96% of controls: 40 through 49 years of age [group 2], 77%; 50 to 60 years of age [group 3], 87%; more than 60 years of age [group 4], 76%). After transplantation, despite oral calcium supplements, VBD fell further in all but two patients (97%), which was almost certainly related to maintenance steroid and cyclosporine therapy, and was most marked in the older groups (group 2, 67% compared with age-matched controls at 6 months; group 3, 60%; group 4, 50%). Intensive therapy with synthetic salmon calcitonin (in 29 of 76 patients [38%]), testosterone (in 33 of 63 men [52%]), or estrogen (in 12 of 13 women [92%]) limited, but did not totally prevent, further loss in VBD; in patients who had shown an approximate 45% loss of VBD from pretransplantation levels, further loss was reduced to between 4% and 10%. Five patients increased bone density after calcitonin therapy. Despite significantly reduced VBD in several older patients, minor vertebral bone compression developed in only one patient. We recommend that all patients undergoing heart transplantation, particularly those over the age of 50 years, should be followed by VBD studies, and therapy should be administered to prevent VBD loss.     

异紫杉脂素治疗对去卵巢大鼠骨量流失和骨密度降低保护作用的机制研究

目的探索异紫杉脂素(isotaxiresinol,IXO)对去卵巢大鼠骨密度和骨量的影响,并探讨其作用机制。方法将大鼠随机分为以下各组:假手术组(Sham)、去卵巢大鼠组(OVX)、去卵巢大鼠+异紫杉脂素组(IXO)。其中IXO组大鼠给予异紫杉脂素100 mg/(kg·d)治疗12周。Micro-CT和HE切片观察骨组织变化。通过ELISA检查用于分析骨代谢指标,进行蛋白质印迹分析以评估PI3K、Akt和RUNX-2的蛋白表达。结果 12周时,OVX组大鼠骨密度和骨量较Sham组显著降低。而IXO能显著改善去卵巢大鼠的骨密度和股骨干骺端骨小梁微观结构。去卵巢大鼠在IXO给药治疗后可显著降低P1NP和β-CTX水平(P0.05);用IXO治疗可上调去卵巢大鼠的PI3K、Akt和RUNX-2蛋白表达。结论本研究提示异紫杉脂素可以通过激活PI3K/Akt信号通路对去卵巢大鼠骨量流失和骨密度降低起到保护作用。     

Progressive femoral cortical and cancellous bone density loss after uncemented tapered-design stem fixation

Background Aseptic implant loosening and periprosthetic bone loss are major problems after total hip arthroplasty (THA). We present an in vivo method of computed tomography (CT) assisted osteodensitometry after THA that differentiates between cortical and cancellous bone density (BD) and area around the femoral component.

Method Cortical and cancellous periprosthetic femoral BD (mg CaHA/mL), area (mm²) and contact area between the prothesis and cortical bone were determined prospectively in 31 patients 10 days, 1 year, and 6 years after uncemented THA (mean age at implantation: 55 years) using CT-osteodensitometry.

Results 6 years postoperatively, cancellous BD had decreased by as much as 41% and cortical BD by up to 27% at the metaphyseal portion of the femur; this decrease was progressive between the 1-year and 6-year examinations. Mild cortical hypertrophy was observed along the entire length of the diaphysis. No statistically significant changes in cortical BD were observed along the diaphysis of the stem.

Interpretation Periprosthetic CT-assisted osteodensitometry has the technical ability to discriminate between cortical and cancellous bone structures with respect to strain-adapted remodeling. Continuous loss of cortical and cancellous BD at the femoral metaphysis, a homeostatic cortical strain configuration, and mild cortical hypertrophy along the diaphysis suggest a diaphyseal fixation of the implanted stem. CT-assisted osteodensitometry has the potential to become an effective instrument for quality control in THA by means of in vivo determination of periprosthetic BD, which may be a causal factor in implant loosening after THA.     

2111例上海健康女性骨密度值测定与年龄相关骨丢失的研究

目的　建立上海市健康女性骨密度 (BMD)参考值数据库 ,为骨质疏松症的诊断及防治效果评估提供依据。方法　选取健康女性 2 111例 ,为上海市区的居民 ,汉族 ,年龄 2 0～ 84岁 ,分为13组。研究对象均详细填写健康调查表格 ,排除因继发性骨病或服用影响骨代谢药物 ,以及一些特殊职业者。用双能X线吸收仪 (HologicQDR - 2 0 0 0型 )测定所有对象的腰椎 (L1 - 4)、股骨颈 (Neck)、大转子 (Troch)、粗隆间 (Inter)及Ward’s三角区部位的BMD值。结果　峰值骨量 (PBM)出现的年龄段如下 :腰椎为 30～ 34岁 ,股骨近端为 2 0～ 2 4岁。此后 ,随年龄增长而BMD值下降 ,但在 4 0～ 4 4岁时BMD值均有较明显回升 (但低于各部位峰值 ) ,呈“沟壑状”。绝经后妇女在绝经后头 10年及 2 6～30年时有两个骨量快速丢失期 ,前者见于腰椎和股骨上端 ,年丢失率为 1 4 %～ 3 2 % ,后者仅见于股骨上端 ,年丢失率为 1 1%～ 1 4 %。腰椎部位BMD值在 75～ 79岁组略有回升。各部位骨量累积丢失率随年龄增长而增加。到 80岁时 ,各部位的骨量累积丢失为 2 8%～ 5 8% (比PBM)。骨质疏松症检出率在腰椎和Ward’s两部位最高 ,在 6 0～ 6 4岁组分别达 4 8%和 4 3% (以WHO诊断标准 ,T score<2 5SD)。 75岁以后 ,Ward’s部位检出率达 83%。结论     

Assessment of linkage and association of 13 genetic loci with bone mineral density

Bone mineral density (BMD), an important risk factor for osteoporosis, is a complex trait likely affected by multiple genes. The linkage and/or association of 13 polymorphic loci of seven candidate genes (estrogen receptor alpha [ERα] and beta [ERβ], calcium-sensing receptor, vitamin D receptor, collagen type 1α1, low-density lipoprotein [LDL] receptor-related protein 5 [LRPS], and transforming growth factor β1) were evaluated in 177 southern Chinese pedigrees of 674 subjects, with each pedigree identified through a proband having a BMD Z score of −1.28 or less at the hip or spine. A suggestive linkage was detected between the IVS1-351A/G polymorphism of ERα and spine BMD, and between the 1082G/A, 1730G/A, and D14S1026 polymorphisms of ERβ and BMD at both spine and hip. The quantitative transmission disequilibrium test (QTDT) detected total family association between 1730G/A of ERβ and BMD at spine and hip; between D14S1026 of ERβ and hip BMD; and between the 266A/G and 2220C/T polymorphisms of LRP5 and hip BMD. Similar total family associations were detected when only the females were analyzed. In addition, the IVS1-397T/C polymorphism of ERα was associated with spine BMD, and the 266A/G and 2220C/T polymorphisms of LRP5 were associated with femoral neck BMD in the females. A within-family association was detected with the IVS1-397T/C polymorphism of ERα, and the 266A/G and 2220C/T polymorphisms of LRP5 in the females. The effect of each polymorphism on BMD variance ranged from 1% to 4%. In conclusion, ERα, ERβ and LRP5 are important candidate genes determining BMD variation, especially in females.     

Obesity and postmenopausal bone loss: The influence of obesity on vertebral density and bone turnover in postmenopausal women

This study was undertaken to evaluate the effect of obesity on the postmenopausal bone mass. Bone mineral density, measured by dual photon absorptiometry of the lumbar spine, serum osteocalcin (OC), fasting urinary calcium to creatinine (Ca:Cr), serum estradiol (E2) dehydroepiandrosterone (DHA) and testosterone (T) were measured in 176 women aged 45–71 years. Women were divided into four groups according to their menopausal status and their weight: 49 perimenopausal, 28 obese perimenopausal, 49 obese postmenopausal. Within each population (perimenopausal and postmenopausal), mean age was the same, only weight was significantly different (p < 0.0001). For the two groups of postmenopausal women mean interval since menopause (YSM) was the same (5.8 ± 3 and 5.4 ± 5 yr). Comparison between groups revealed a significant effect of menopausal status and obesity on BMD and bone turnover. As compared to perimenopausal women, BMD was lower, OC and Ca: Cr higher only in nonobese-postmenopausal women. E2, T, DHA did not differ between the two groups of postmenopausal women. The results of this study suggest that even moderate obesity can play a protective role on postmenopausal bone loss.