Effects of neonatal estrogenization on rat bone development: A histomorphometric study

Summary The effects of a single dose of 500 μg of estradiol benzoate, administered on the first day of life, on rat bone development have been histomorphometrically studied at 15 days of age. Estrogenized animals presented decreased total tibial length (16.55±0.50 vs. 17.84±0.73 mm,P<0.05) and increased thickness of the cartilage growth plate (528.92±13.30 vs. 382.77±37.85 μm,P<0.01). This increase was mostly due to the presence of a wider (P<0.01) layer of hypertrophic cartilage in the estrogenized rats than in control ones. It might be related to the decreased number of chondroclasts (0.20±0.01 vs. 0.36±0.06 mm⁻¹,P<0.05) found in the resorption zone. Two metaphyseal zones have been considered. In the upper metaphyseal zone there was an increase in the surface density of the cartilaginous trabeculae (49.20±1.80 vs. 40.72±1.95 mm²/mm³,P<0.05), without changes in the volume density. It was related to the presence of thinner and more irregular trabeculae in the estrogenized animals. In the lower metaphyseal zone both the volume (0.19±0.01 vs. 0.14±0.01 mm³/mm³,P<0.01) and surface (34.83±3.01 vs. 26.52±2.46 mm²/mm³,P<0.05) densities of the osseous trabecular tissue were increased in estrogenized rats. No significant differences were found either in the number of osteocytes per area unit of osseous tissue or in the number of osteoclasts per unit length of trabecular osseous tissue.     

Cortical Bone Loss Following Gastric Bypass Surgery Is Not Primarily Endocortical

Roux-en Y gastric bypass (RYGB) surgery is an effective treatment for obesity; however, it may negatively impact skeletal health by increasing fracture risk. This increase may be the result not only of decreased bone mineral density but also of changes in bone microstructure, for example, increased cortical porosity. Increased tibial and radial cortical porosity of patients undergoing RYGB surgery has been observed as early as 6 months postoperatively; however, local microstructural changes and associated biological mechanisms driving this increase remain unclear. To provide insight, we studied the spatial distribution of cortical porosity in 42 women and men (aged 46 ± 12 years) after RYGB surgery. Distal tibias and radii were evaluated with high-resolution peripheral quantitative computed tomography (HR-pQCT) preoperatively and at 12 months postoperatively. Laminar analysis was used to determine cortical pore number and size within the endosteal, midcortical, and periosteal layers of the cortex. Paired t tests were used to compare baseline versus follow-up porosity parameters in each layer. Mixed models were used to compare longitudinal changes in laminar analysis outcomes between layers. We found that the midcortical (0.927 ± 0.607 mm⁻² to 1.069 ± 0.654 mm⁻², p = 0.004; 0.439 ± 0.293 mm⁻² to 0.509 ± 0.343 mm⁻², p = 0.03) and periosteal (0.642 ± 0.412 mm⁻² to 0.843 ± 0.452 mm⁻², p < 0.0001; 0.171 ± 0.101 mm⁻² to 0.230 ± 0.160 mm⁻², p = 0.003) layers underwent the greatest increases in porosity over the 12-month period at the distal tibia and radius, respectively. The endosteal layer, which had the greatest porosity at baseline, did not undergo significant porosity increase over the same period (1.234 ± 0.402 mm⁻² to 1.259 ± 0.413 mm⁻², p = 0.49; 0.584 ± 0.290 mm⁻² to 0.620 ± 0.299 mm⁻², p = 0.35) at the distal tibia and radius, respectively. An alternative baseline-mapping approach for endosteal boundary definition confirmed that cortical bone loss was not primarily endosteal. These findings indicate that increases in cortical porosity happen in regions distant from the endosteal surface, suggesting that the underlying mechanism driving the increase in cortical porosity is not merely endosteal trabecularization. © 2022 American Society for Bone and Mineral Research (ASBMR).     

Spinal cord injury causes more damage to bone mass, bone structure, biomechanical properties and bone metabolism than sciatic neurectomy in young rats

Introduction Although both spinal cord injury (SCI) and sciatic neurectomy (NX) can cause osteopaenia in young rats, the effects of these two injuries on cortical and cancellous bone may differ. The objective of this study was to compare the effects of SCI and NX on bone weight, bone material property, bone mass, bone geometry, trabecular microarchitecture, mechanical strength and bone turnover in young rats.Materials and methods Thirty six-week-old male Sprague-Dawley rats were randomised into three groups (10 per group): SCI, bilateral sciatic NX and untreated control (CON). All rats were killed on day 21. Bone mineral density (BMD) was studied using dual-energy X-ray absorptiometry (DXA). At death, the right proximal tibial metaphysis and the fourth lumbar vertebra were examined for bone structural geometric analysis by micro-computed tomography (CT) and then processed for histomorphometry to assess bone cell activity. Serum N-terminal telopeptide of type I collagen (NTX) and osteocalcin (OC) levels were analysed by enzyme-linked immunosorbent assay (ELISA). Biomechanical strength properties of the femur and humerus were measured by three-point bending, and the third lumbar vertebra and the proximal end of tibia were tested by compression.Results BMD in the sublesional areas of SCI rats was significantly lower than that of NX rats (proximal tibia, 0.176±0.018 g/cm² vs. 0.224±0.015 g/cm², P<0.001). Bone volume (BV/TV), trabecular number (Tb.N) and thickness (Tb.Th) in the tibial second spongiosa of SCI rats were significantly less than those in NX rats (BV/TV: 7.15±1.18% vs. 12.32±1.83%, P<0.001; Tb.N: 1.23±0.22 vs. 2.38±0.45, P<0.001; Tb.Th: 33.73±5.15 μm vs. 42.80±7.44 μm, P<0.01) and trabecular separation (Tb.Sp: 1,053.37±164.24 μm vs. 748.32±129.36 μm, P<0.01) was significantly greater than in NX rats. Furthermore, poorer trabecular connectivity was found in SCI rats than in NX rats (number of nodes, N.Nd/TV: 1.04±0.09 vs. 3.29±0.53; number of terminus, N.Tm/TV: 28.53±3.17 vs. 21.64±2.31, P<0.01). The bone formation rate of the tibial second spongiosa in SCI rats was significantly higher than in NX rats (2.06±0.13 vs. 1.53±0.09, P<0.001) and, also, the eroded surface in SCI rats was significantly higher than in NX rats (13.42±1.24 vs. 10.36±1.07, P<0.001). In addition, biomechanical tests showed that SCI rats had poorer biomechanical properties of the femur, proximal tibia and fourth lumbar vertebra than in NX rats. There were significantly higher levels of OC in SCI rats compared with NX rats (30.19±1.17 vs. 21.15±1.76, P<0.001). Also, serum NTX levels were significantly higher than in NX rats (51.60±2.61 vs. 33.85±1.93, P<0.001).Conclusion SCI caused more damage to bone mass, bone structure, biomechanical properties and bone metabolism than NX in young rats. This suggests that different mechanisms may underlie osteopaenia following SCI and NX.     

The effects of muscle-building exercise on bone mineral density of the radius,spine, and hip in young men

Summary We previously demonstrated that muscle-building exercise is associated with increases in serum Gla-protein, serum 1,25(OH)₂D, and urinary cyclic AMP. These studies were interpreted to mean that this form of exercise increases bone formation and modifies the vitamin D-endocrine system to provide more calcium for bone. The present investigation was carried out in normal young adult white men to determine the effects of exercise on bone mineral density at weight-bearing and nonweight-bearing sites. Twelve men who had regularly engaged in muscle-building exercises (use of weights, exercise machines, or both) for at least 1 year and 50 age-matched controls (aged 19–40 years) were studied. The body weights of the two groups were not different from each other (78±2 vs. 74±1 kg, NS). Bone mineral density (BMD) of the lumbar spine, trochanter, and femoral neck was measured by dual-photon absorptiometry, and BMD of the midradius was measured by single-photon absorptiometry. It was found that muscle-building exercise was associated with increased BMD at the lumbar spine (1.35±0.03 vs. 1.22±0.02 g/cm²,P<0.01), trochanter (0.99±0.04 vs. 0.86±0.02 g/cm²,P<0.01), and femoral neck (1.18 ±0.03 vs. 1.02±0.02 g/cm²,P<0.001) but not at the midradius (0.77±0.02 vs. 0.77±0.01 g/cm², NS). These studies provide additional evidence that muscle-building exercise is associated with increases in BMD at weight-bearing sites but not at nonweight-bearing sites.     

Cortical versus trabecular bone mass: Influence of activity on both bone components

Motivated by the controversy in the literature concerning the influence of activity on bone mass and on its cortical and trabecular components, a study was made using computed peripheral tomography (Stratec XCT 900) of the total, cortical, and trabecular bone mass of the dominant and nondominant upper extremities of 50 apparently normal subjects (average age 26±6 years). No differences were observed in the trabecular bone compartment, but the cortical compartment was greater (P<0.001) in the dominant extremity. There was also a significantly greater total bone mass in the dominant extremity which we attributed to greater cortical mass (P<0.025) given the highly significant correlation (r²=0.904, P=0.0001) between total and cortical bone mass and the less significant correlation between total and trabecular bone mass (r²=0.479, P=0.0001).     

Habitual dietary calcium intake and cortical bone loss in perimenopausal women: A longitudinal study

Summary During an 8-year follow-up study, the effect of habitual dietary calcium intake on cortical bone loss in 154 healthy perimenopausal women was examined. Dietary calcium intake, determined by the cross-check dietary history method, and cortical bone mineral content of the radius were measured annually. Habitual dietary calcium intake was calculated as the mean of the estimated daily dietary calcium intake during the follow-up period. The women were classified according to their habitual calcium intake: those with an intake below 800 mg/day (n=28), between 800 and 1350 mg/day (n=95), and above 1350 mg/day (n=31). The results show a continuous significant loss of cortical bone in all groups, amounting yearly to 1.3±0.25, 1.5±0.10, and 1.9±0.23% (mean±SE) for the groups with a low, medium, and high habitual calcium intake, respectively (P<0.01). The differences among the three groups did not reach statistical significance (P=0.11). Body mass index was found to be positively correlated with the negative changes in cortical bone mineral density (r=0.32,P<0.01), even after adjustments had been made for confounding factors. It is concluded that a habitual calcium intake exceeding 800 mg/day (the current Recommended Daily Allowance for adults) is ineffective in preventing cortical bone loss during early menopause. Body mass index is of major importance for the perimenopausal bone loss.     

A Histomorphometric Study of Cortical Bone of the Iliac Crest in Patients Treated with Glucocorticoids

The effects of glucocorticoids on cancellous bone remodeling and structure are well documented but there are no reported histomorphometric studies in human cortical bone in glucocorticoid-treated patients. We have performed a histomorphometric analysis of iliac crest cortical bone in 14 patients treated with glucocorticoids, 9 females and 5 males, aged 18 to 48 years (34.1 ± 7 years) (mean ± standard deviation [SD]). The underlying disease was cystic fibrosis in 8 patients; asthma 3; and nephrotic syndrome; Crohn disease and inflammatory pseudotumor of the liver in one patient each. Results were compared with an age-matched control group of 10 premenopausal women and 4 men aged 22 to 38 years (30.1 ± 4.8 years) who were not, howerver matched for underlying disease. Cortical bone indices were assessed by image analysis. Cortical width and area were similar in the two groups. However, cortical porosity, Haversian canal number, and density were higher in patients treated with glucocorticoids compared with controls (8.4 ± 8.9% vs. 5.1 ± 3.9%; P = 0.03) (45.9 ± 23.2 vs. 31.9 ± 24.4; P =0.003) (13.7 ± 9.4 vs. 6.7 ± 3.3/mm²; P = 0.00005). Haversian canal area did not differ significantly between groups. The mean wall width of the osteons, bone formation rate (μm²/μm/day) and mineral apposition rate (μm/day) were lower in treated patients compared to controls (48.8 ± 7.1 μm vs. 59.8 ± 12.9 μm; P = 0.01) (0.056 ± 0.040 vs. 0.095 ± 0.058; P = 0.05) and (0.59 ± 0.12 vs. 0.75 ± 0.11; P = 0.002). The proportion of canals with an eroded surface was lower in the treated compared with the control group, although this difference was not statistically significant. These results demonstrate that cortical porosity is increased in patients treated with long-term glucocorticoid therapy, due mainly to an increase in the number rather than size of Haversian canals. This may be because of increased bone resorption during the early stages of glucocorticoid therapy, in combination with long-term impairment of bone formation. Effects of the underlying disease on bone remodeling may also contributed to these changes and could not be excluded in the present study; since control subjects were not matched in terms of disease status.     

Trabecular and Cortical Microarchitecture in Postmenopausal HIV-Infected Women

Our objective was to assess the effects of HIV infection and antiretroviral therapy on trabecular and cortical microarchitecture in postmenopausal minority women. A subgroup of 106 (46 HIV-infected, 60 uninfected) postmenopausal Hispanic and African American women from an established cohort had areal bone mineral density (aBMD) measured by dual-energy X-ray absorptiometry and trabecular and cortical volumetric BMD (vBMD) and microarchitecture measured by high-resolution peripheral quantitative computed tomography (HRpQCT) at the radius and tibia. HIV-infected women were slightly younger (58 ± 1 vs. 61 ± 1 years, p = 0.08), and had lower body mass index (BMI; 28 ± 1 vs. 32 ± 1 kg/m², p < 0.01). BMI-adjusted aBMD Z scores were lower in HIV-infected women at the lumbar spine, total hip, and ultradistal radius. Serum N-telopeptide and C-telopeptide levels were also higher in HIV-infected women. Trabecular and cortical vBMD were similar at the radius, but cortical area (105.5 ± 2.4 vs. 120.6 ± 2.0 mm², p < 0.01) and thickness (956 ± 33 vs. 1,075 ± 28 μm, p < 0.01) at the tibia were approximately 11–12 % lower in HIV-infected women. Differences remained significant after adjusting for age, BMI, and race/ethnicity. In contrast, cortical porosity was similar in the two groups. Although HIV-infected postmenopausal women had lower aBMD at the spine, total hip, and ultradistal radius and higher levels of bone resorption markers, the only differences detected by HRpQCT were lower cortical thickness and area at the tibia.     

Bone Remodeling and Structure in Postmenopausal Women Treated with Long-Term, High-Dose Estrogen Therapy

Conventional hormone replacement therapy preserves bone mass predominantly by reducing bone turnover but does not exert significant anabolic skeletal effects. In contrast, high doses of estrogen have been shown to increase bone formation in animals and we have recently reported high bone mineral density values in women treated long-term with estradiol implant therapy. The aim of this study was to investigate the mechanisms by which high doses of estrogen may increase bone mass in postmenopausal women. Iliac crest biopsies were obtained from 12 women who had received long-term treatment with estradiol implants (at least 14 years), on demand, following hysterectomy and bilateral salpingo-oophorectomy. Indices of bone turnover, remodeling balance and cancellous bone structure were assessed by image analysis and compared with those of premenopausal women. Mean wall width was significantly higher in women treated with estradiol therapy than in premenopausal women (44.8 ± 4.8 vs 38.8 ± 2.8 mm; mean ± SD; p = 0.001) and eroded cavity area was significantly lower in the implant-treated women (3612 ± 956 vs 5418 ± 1404 mm²; p = 0.001). Bone formation rate at tissue level and activation frequency were lower in the women treated with implants, although the differences were not statistically significant. Indices of cancellous bone structure were generally similar between the two groups. These results provide the first direct evidence that high-dose estrogen therapy produces anabolic skeletal effects in postmenopausal women and indicate that these are achieved by stimulation of osteoblastic activity. Received: 18 August 1998 / Accepted: 9 December 1998     

Smoking is associated with impaired bone mass development in young adult men: A 5-year longitudinal study

It has previously been shown that smoking is associated with reduced bone mass and increased fracture risk, but no longitudinal studies have been published investigating altered smoking behavior at the time of bone mass acquisition. The aim of this study was to investigate the development of bone density and geometry according to alterations in smoking behavior in a 5‐year, longitudinal, population‐based study of 833 young men, age 18 to 20 years (baseline). Furthermore, we aimed to examine the cross‐sectional, associations between current smoking and parameters of trabecular microarchitecture of the radius and tibia, using high‐resolution peripheral quantitative computed tomography (HR‐pQCT), in young men aged 23 to 25 years (5‐year follow‐up). Men who had started to smoke since baseline had considerably smaller increases in areal bone mineral density (aBMD) at the total body (mean ± SD, 0.020 ± 0.047 mg/cm² versus 0.043 ± 0.040 mg/cm², p < 0.01) and lumbar spine (0.027 ± 0.062 mg/cm² versus 0.052 ± 0.065 mg/cm², p = 0.04), and substantially greater decreases in aBMD at the total hip (?0.055 ± 0.058 mg/cm² versus ?0.021 ± 0.062 mg/cm², p < 0.01) and femoral neck (?0.077 ± 0.059 mg/cm² versus ?0.042 ± 0.070 mg/cm², p < 0.01) than men who were nonsmokers at both the baseline and follow‐up visits. At the tibia, subjects who had started to smoke had a smaller increment of the cortical cross‐sectional area (CSA) than nonsmokers (8.1 ± 4.3 mm² versus 11.5 ± 8.9 mm², p = 0.03), and a larger decrement of trabecular volumetric BMD (vBMD) than nonsmokers (?13.9 ± 20.5 mg/mm³ versus ?4.1 ± 13.9 mg/mm³, p < 0.001). In the cross‐sectional analysis at follow‐up (23–25 years of age), smokers had significantly lower trabecular vBMD at the tibia (7.0%, p < 0.01) due to reduced trabecular thickness (8.9%, p < 0.001), as assessed using HR‐pQCT, than nonsmokers. In conclusion, this study is the first to report that men who start to smoke in young adulthood have poorer development of their aBMD at clinically important sites such as the spine and hip than nonsmokers, possibly due to augmented loss of trabecular density and impaired growth of cortical cross‐sectional area. © 2012 American Society for Bone and Mineral Research.     

Forearm bone mineral density in patients with rheumatoid arthritis

 The aims of the present study were to determine whether patients with rheumatoid arthritis (RA) show significantly lower forearm bone mineral density (BMD) than sex- and age-matched healthy controls, and to identify significant factors that are associated with their BMD loss. One hundred eighty-four patients with RA and 185 sex- and age-matched healthy controls were enrolled in the study: 71 men 37–68 years of age (RA, 31; controls, 40), 129 premenopausal women 30–48 years of age (RA, 67; controls, 62), and 169 postmenopausal women 48–69 years of age (RA, 86; controls, 83). The correlation of forearm BMD, measured by dual energy X-ray absorptiometry with anatomic grade in the wrist, functional class, duration of disease, steroid use, modified health assessment questionnaire (HAQ) score for the upper and lower extremities, levels of serum C-reactive protein and rheumatoid factor, erythrocyte sedimentation rate, and years since menopause (YSM) were examined by multiple regression analysis. In men with RA, no clinical factors were significantly correlated with forearm BMD, and the BMD did not differ significantly from that in controls (0.329 ± 0.060 [mean ± SD] vs. 0.351 ± 0.069 g/cm²). In premenopausal women with RA, the HAQ score for the upper extremities was positively correlated with forearm BMD (P < 0.05), but the BMD did not differ significantly from that in controls (0.298 ± 0.085 vs. 0.324 ± 0.088 g/cm²); in postmenopausal women with RA, YSM and anatomic grade in the wrist were negatively correlated with forearm BMD (P < 0.01 and P < 0.05), and the BMD was significantly lower than in controls (0.192 ± 0.063 vs. 0.223 ± 0.076 g/cm², P < 0.01). These findings suggest that forearm BMD loss in patients with RA may be accelerated in women after menopause, and that YSM and disuse of the wrist may be significant determinants of their forearm BMD loss. Received: February 18, 2002/ Accepted: May 23, 2002     

Androgen-Receptor Blockade Does Not Impair Bone Mineral Density in Adolescent Females

The effect of peripheral androgen hypersensitivity on bone mineral density (BMD) was investigated in a group of adolescent women with idiopathic hirsutism (n= 17; mean age 17.0 ± 1.7 years). The effect of long-term androgen-receptor blockade with flutamide (500 mg daily in two divided doses for 12 months) on BMD was assessed too. BMD was measured at lumbar spine (L2–L4) by a dual energy X-ray densitometer. Before flutamide treatment, patient BMD (1.14 ± 0.07 g/cm²) was not significantly different from that of the control group (1.16 ± 0.12 g/cm², n= 22), and was normal for age and sex (BMD 0.14 ± 0.69 SDS, P= NS vs. 0). After 12 months of treatment, absolute BMD in patients increased (1.18 ± 0.08 g/cm², P < 0.002), but SDS BMD did not change (0.21 ± 0.72, P= NS vs. baseline). Flutamide treatment determined a clinical, marked improvement of androgen hypersensitivity (Ferriman–Gallwey score: before 22.0 ± 6.2; 6 months: 13.2 ± 6.4, P < 0.003; 12 months; 7.6 ± 4.1, P < 0.001; acne score: before 3.8 ± 0.8; 3 months 0.8 ± 0.5, P < 0.001; later disappeared). The serum levels of 3α-androstenediol-glucoronide decreased (before: 8.6 ± 1.1 μg/liter; 12 months: 7.2 ± 1.0 μg/liter, P < 0.02), whereas the other endocrinological parameters did not change. No relationship was found between BMD and clinical or biochemical parameters of hyperandrogenism. We concluded that in adolescent women, peripheral hyperandrogenism is not associated with abnormal BMD; long-term treatment with flutamide, which blocks the androgen receptor, does not alter their BMD. Received: 19 February 96 / Accepted: 31 December 96     

Lower bone mineral density in children with type 1 diabetes is associated with poor glycemic control and higher serum ICAM-1 and urinary isoprostane levels

The purpose of the study was to investigate bone mineral density (BMD) in children with type 1 diabetes (DM1) and to establish the relationships between BMD, physical activity, glycemic control, and markers of systemic oxidative stress and inflammation. We studied 30 children with DM1, aged 4.7–18.6 years, and 30 healthy subjects, matched by sex, age, and body mass index (BMI). Mean duration of DM1 was 5.4 ± 3.4 years and mean glycosylated hemoglobin (HbA_1c) level over 12 months was 9.8 ± 1.5%. Lumbar and total bone mineral density (BMD, g/cm²) were measured by dual-energy X-ray absorptiometry (DXA). We calculated the apparent volumetric lumbar BMD (BMDvol, g/cm³) and total mineral content adjusted for age and height (BMCadj), and measured plasma intercellular adhesion molecule-1 (ICAM-1), high sensitivity C-reactive protein (hs-CRP), and urinary 8-iso-prostaglandin F_2a (F₂-IsoPs). Calcium (Ca) intake was assessed by questionnaire and physical activity by questionnaire and accelerometer (ActiGraph, count/h). Total BMCadj and lumbar BMDvol were significantly lower in children with DM1 than in controls (101.8 ± 7.7 vs. 107 ± 5.7%, P = 0.005; 0.32 ± 0.08 vs. 0.36 ± 0.09 g/cm³, P = 0.05, respectively). These differences were mostly caused by the differences in boys. Plasma ICAM-1 and hs-CRP levels were significantly higher in the DM1 group compared to the controls. Ca intake and urine F₂-IsoPs levels were similar between the groups. Diabetic boys were less active than controls (18231 ± 6613 vs. 24145 ± 7449 count/h, P = 0.04). In the DM1 group, lumbar BMDvol correlated inversely with urinary F₂-IsoPs (r = −0.5; P = 0.005) and plasma ICAM-1 levels (r = −0.4; P = 0.02), and also with HbA_1c levels after adjustment for age (r = −0.45; P < 0.05). Total BMCadj correlated inversely with HbA_1c levels (r = −0.4; P = 0.02). We conclude that children with DM1, particularly boys, have lower BMD. Poor glycemic control, elevated markers of oxidative stress, and inflammation are associated with lower BMD.     

钻取式柱状自体髂骨植骨术应用及供骨区术后并发症的临床分析

目的:探讨钻取式柱状自体髂骨植骨术的临床疗效及分析该植骨术对供骨区术后并发症的影响。方法 :自2014年3月至2016年10月,回顾性分析自体髂骨植骨患者68例,按照取骨方式不同,分为钻取式取骨(钻取组)和骨刀式取骨(骨刀组),每组34例。钻取组男24例,女10例;年龄23~53(40.06±5.60)岁;骨刀组男26例,女8例;年龄22~54(39.32±6.44)岁;观察并比较两组患者的取骨手术时间、术中供区出血量、术后供区伤口愈合时间及术后供区并发症等,并采用VAS评分对术后不同时期供区进行疼痛评价。结果:68例患者获得随访,时间12~24个月,钻取组平均16.9个月,骨刀组平均17.1个月。两组受区显示骨愈合结构,采用自体髂骨植骨术均见效果良好。两组手术操作时间差异无统计学意义(P0.05);两组术中供区出血量及术后供区伤口愈合时间差异均有统计学意义(P0.05);两组术后并发症(髂骨凹陷、麻木)差异有统计学意义(P0.05)。术后2周VAS评分两组差异无统计学意义(P0.05),术后6个月和1年钻取组VAS评分均比骨刀组低(1.85±0.61 vs 2.97±0.67,P=0.000;1.15±0.56 vs 2.41±0.61,P=0.000)。结论:术中无须大块特殊形状或较多皮质骨髂骨植骨时,用钻取式柱状自体髂骨植骨术操作简便、术后并发症少;能促进受区早期愈合,改善患者生活质量,较传统骨刀取骨优势明显。     

Influence of three different types of hypercalciuria on bone

 The relationship between bone mineral status and hypercalciuria is controversial. The effect on bone composition of different forms of hypercalciuria was studied in female rats made hypercalciuric by 7-week administration of oral furosemide (F, n=12), intraperitoneal 1,25-dihydroxy vitamin D (VD, n=11), or oral ammonium chloride (AC, n=12). Seven untreated rats served as controls (C). Hypercalciuria (mg/100 g per 24 h, mean ±SEM) of F (4.3±0.2), VD (4.1±0.4), and AC (3.9±0.3) groups was of similar intensity (C rats 1.3±0.1, P<0.01). Weight and length gains and serum CO₂, sodium, potassium, calcium, and phosphate were no different among the four groups. Bone was studied by dual-energy X-ray absorptiometry of left tibiae. AC rats had significantly less bone area (1.505±0.018 cm²) than VD and C (1.602±0.020 and 1.587±0.019 cm²). Bone mineral content was decreased in F (0.357±0.007 g) and AC (0.362±0.006 g) compared with VD (0.407±0.008 g) and C (0.389±0.009 g) groups. Bone mineral density was different between F (0.231±0.002 g/cm²) and VD and C rats (0.254±0.004 and 0.245±0.003 g/cm²), and also between AC (0.240±0.003 cm²) and VD rats. In these rat models, hypercalciuria of renal origin (F) and hypercalciuria caused by acid load (AC) adversely impaired bone mass. Received: 19 September 1997 / Revised: 28 July 1998 / Accepted: 29 July 1998     

Risedronate Preserves Bone Architecture in Early Postmenopausal Women In 1 Year as Measured by Three-Dimensional Microcomputed Tomography

Risedronate reduces the risk of vertebral fractures by up to 70% within the first year of treatment. Increases in bone mineral density or decreases in bone turnover markers explain only a portion of the anti-fracture effect, suggesting that other factors, such as changes in trabecular bone architecture, also play a role. Our objective was to determine the effects of risedronate on bone architecture by analyzing iliac crest bone biopsy specimens using three-dimensional microcomputed tomography (3-D µCT). Biopsy specimens were obtained at baseline and after 1 year of treatment from women enrolled in a double-blind, placebo-controlled study of risedronate 5 mg daily for the prevention of early postmenopausal bone loss. Trabecular architecture deteriorated in the placebo group (n = 12), as indicated by a 20.3% decrease in bone volume (25.1% vs. 20.0%, P = 0.034), a 13.5% decrease in trabecular number (1.649 vs. 1.426 mm^–1, P = 0.052), a 13.1% increase in trabecular separation (605 vs. 684 µm, P = 0.056), and an 86.2% increase in marrow star volume (3.251 vs. 6.053 mm³, P = 0.040) compared with baseline values. These changes in architectural parameters occurred in the presence of a concomitant decrease from baseline in lumbar spine bone mineral density (–3.3%, P = 0.002), as measured by dual energy x-ray absorptiometry. There was no statistically significant (P < 0.05) deterioration in the risedronate-treated group (n = 14) over the 1-year treatment period. Comparing the actual changes between the two groups, the placebo group experienced decreases in bone volume (placebo, –5.1%; risedronate, +3.5%; P = 0.011), trabecular thickness (placebo, –20 µm; risedronate, +23 µm; P = 0.032), and trabecular number (placebo, –0.223 mm^–1; risedronate, +0.099 mm^–1; P = 0.010), and increases in percent plate (placebo, +2.79%; risedronate, –3.23%; P = 0.018), trabecular separation (placebo, +79 µm; risedronate, –46 µm; P = 0.010) and marrow star volume (placebo, +2.80 mm³ ; risedronate, –2.08mm³; P = 0.036), compared with the risedronate group. These data demonstrate that trabecular architecture deteriorated significantly in this cohort of early postmenopausal women, and that this deterioration was prevented by risedronate. Although there is no direct link in this study between fracture and preservation of architecture, it is reasonable to infer that the preservation of bone architecture may play a role in risedronates anti-fracture efficacy.     

Morphometric and histological analysis of low-power laser influence on bone morphogenetic protein in bone defects repair

Bone morphogenetic proteins (BMPs) are secreted signaling molecules belonging to the transforming growth factor-β (TGF-β) superfamily. The objective of this study was to determine how gallium–aluminum–arsenium (GaAlAs) 650 nm laser influenced the action of BMPs on bone defects created in rat femurs. The sample consisted of 24 male albino Wistar rats. Group 1 was composed of rats with bone defects filled with bone-inducing substance, with the application of low-power laser. Group 2 contained rats with bone defects filled with a bone-inducing substance, without the application of low-power laser. Group 3 rats had bone defects not filled with a bone-inducing substance, with the application of low-power laser. Group 4 rats had bone defects and no treatment (control group). A bone defect was produced with drills. In groups 1 and 2 the defects were filled with a bone-inducing substance. The animals were treated with GaAlAs (50 mW) laser, energy density 4J/cm², for 80 ss on a 1 cm² area. Groups 2 and 4 were used as control. Bone samples were removed for histological procedures and morphometric analysis on the 7th, 14th and 21st days after surgery. Results obtained were subjected to statistical analysis. Rejection level for the null hypothesis was 0.05. Statistical differences were found in the comparison between group 1 (G1), G2, G3 and G4 [analysis of variance (ANOVA); P < 0.0134]. There was a statistically significant correlation between groups 1 and 4 (P < 0.01). The results of other correlations by Tukey’s post-hoc test were: group 1 vs group 3 (P = 0.341), group 1 vs group 2 (P = 0.862), group 2 vs group 4 (P = 0.061), group 2 vs group 3 (P = 0.744), and group 3 vs group 4 (P = 0.249). We concluded that the association of low-power laser with a bone-inducing substance produced better results than when low-power laser or BMPs were used alone.     

Effects of Long-Term Administration of Methotrexate on Bone Mineral Density in Rheumatoid Arthritis

Because previous studies of high-dose methotrexate usage have demonstrated an effect on bone formation and resorption, this study was done to determine whether long-term, low-dose use of methotrexate for the treatment of rheumatoid arthritis causes bone loss. Bone mineral density (BMD) of the lumbar spine and hip was measured in 10 Caucasian postmenopausal women who had never received methotrexate and 10 Caucasian postmenopausal women who had received the drug for 3 or more years. There were no significant differences in BMD at the lumbar spine (L2–L4) between patients who had used long-term methotrexate compared with patients never treated with methotrexate (1.08 ± 0.08 g/cm² versus 0.98 ± 0.14 g/cm², respectively; P= 0.08). Similarly, there were no significant differences in BMD at the femoral neck between methotrexate users and nonusers (0.81 ± 0.08 g/cm² versus 0.76 ± 0.15 g/cm², respectively; P= 0.42). These results suggest that long-term low-dose methotrexate treatment for rheumatoid arthritis is not associated with accelerated bone loss. Received: 16 October 1997 / Accepted: 9 July 1998     

不同声强低强度脉冲超声对SD大鼠骨髓间充质干细胞迁移的影响

目的探讨不同声强低强度脉冲超声(LIPUS)辐照对骨髓间充质干细胞(BMSCs)体外迁移的影响。方法将BMSCs分为空白对照组、30mW/cm~2组、60mW/cm~2组及90mW/cm~2组,对空白对照组仅行LIPUS假辐照操作,而对其余3组以相应声强进行辐照。以细胞划痕实验分析LIPUS对划痕愈合的促进作用,并通过MTT活性检测排除细胞增殖能力的干扰。采用transwell迁移实验评价各组BMSCs的迁移能力。通过FITC-鬼笔环肽染色检测F-肌动蛋白(Factin)表达结果 LIPUS辐照(空白对照组假辐照)后24h及48h,30mW/cm~2组、60mW/cm~2组、90mW/cm~2组及空白对照组间划痕面积差异均有统计学意义(F=26.559、106.110,P均0.001),且空白对照组划痕面积[辐照后24h:(0.93±0.26)mm~2,辐照后48h:(0.70±0.11)mm~2]最大,30mW/cm~2组[辐照后24h:(0.47±0.21)mm~2,辐照后48h:(0.19±0.10)mm~2]最小;而辐照后即刻各组间划痕面积差异无统计学意义(F=2.921,P=0.063)。LIPUS辐照(空白对照组假辐照)后即刻、24h及48h各组间吸光度差异均无统计学意义(F=1.616、0.720、1.408,P=0.196、0.544、0.378)。各组间穿过transwell小室上室的BMSCs细胞计数差异有统计学意义(F=43.145,P0.001),且30 mW/cm~2组细胞计数[(212.53±35.32)个]最大,空白对照组[(89.53±19.27)个]最小。F-actin染色显示,LIPUS辐照后BMSCs微丝增粗变长,数量增多。各组间相对荧光强度差异有统计学意义(F=64.350,P0.001),且30 mW/cm~2组相对荧光强度(125.43±17.43)最大,空白对照组(51.94±12.76)最小。结论 LIPUS可促进BMSCs体外迁移,声强为30mW/cm~2时促进效应最明显。     

Muscle mass deficits are associated with bone mineral density in men with idiopathic vertebral fracture

Introduction and hypothesis The causes of idiopathic vertebral fractures (IVF) in men are poorly understood. We hypothesised that in IVF, areal bone mineral density (aBMD) deficits would be associated with reduced muscle mass. Methods In this case-control study, 48 men (61.5 ± 12.1 years old) presenting with symptomatic IVF were compared with 48 healthy controls matched for age (±5 years) and stature (±5 cm). The aBMD and soft-tissue body composition were determined by dual energy X-ray absorptiometry (DXA). Muscle mass was defined as the ratio of appendicular lean mass to the square of height (ALMI). Sex hormones, IGF-I and its binding protein IGFBP-3 were measured by immunoassay. Results ALMI was significantly lower in IVF patients (8.27 ± 0.90 vs 8.65 ± 0.88 kg/m², t = 2.193, df = 47, P = 0.033 by paired sample t-test). Hierarchical regression analysis revealed that for IVF patients, ALMI explained the greatest proportion of variance in BMD at the lumbar spine, femoral neck and total hip (R ² _change = 16.4–22.7%, P = 0.012–0.002) and only IGFBP-3 explained variance in ALMI (R ² _change = 19.9%, P = 0.006). Conclusions In men with IVF, ALMI was reduced and associated with IGFBP-3. ALMI was identified as a novel factor that explained a greater proportion of variance in BMD than either fat mass or serum biochemistry. Electronic Supplementary Material The online version of this article (doi:) contains supplementary material, which is available to authorized users.