Objective: To establish serological biomarker models composed of bone turnover markers (BTMs), vitamin D (Vit D), and estradiol (E2) and to explore their auxiliary diagnostic value in girls with idiopathic central precocious puberty (ICPP).

Methods: Ninety-three girls with ICPP and 93 healthy girls were included in the ICPP group and the control group, respectively. The serum levels of total procollagen type 1 N-terminal propeptide (P1NP), N-terminal midfragment of osteocalcin (N-MID), β-C-terminal telopeptide of type 1 collagen (β-CTX), Vit D, E2, and other biochemical parameters were detected in all participants. Serological biomarker models for assistance with ICPP diagnosis were established by logistic regression analyses.

Results: Serum P1NP, β-CTX, Vit D, and E2 levels differed significantly between the two groups (p<0.05). Three models were established. Model 1 consisted of P1NP and β-CTX, and had an area under curve (AUC) of 0.764, sensitivity of 74.19%, and specificity of 72.04%. Model 2 consisted of P1NP, β-CTX, and Vit D, and had an AUC of 0.840, sensitivity of 83.87%, and specificity of 72.04%. Model 3 consisted of P1NP, β-CTX, Vit D, and E2, and had an AUC of 0.917, sensitivity of 82.80%, and specificity of 86.02%.

Conclusions: Serum P1NP, β-CTX, Vit D, and E2 levels may be effective indicators for auxiliary diagnosis of ICPP. Serological biomarker models composed of P1NP, β-CTX, Vit D, and E2 (models 1, 2, and 3) may have auxiliary diagnostic value for ICPP.

Keywords: P1NP; bone turnover marker; diagnostic model; idiopathic central precocious puberty; β-CTX.

Objective: Circulating osteoglycin may facilitate the crosstalk between bone and pancreas to empower adaptation of bone mass to whole body energy balance. We aimed to examine whether osteoglycin is associated with bone and metabolic parameters and if osteoglycin levels differ between patients with type 1 and 2 diabetes (T1D and T2D).

Design and methods: A cross-sectional study of 190 patients with diabetes mellitus and stable hemoglobin A1c (HbA1c) (97 T1D and 93 T2D) was conducted. S-osteoglycin was analyzed by ELISA. Unpaired t-tests were performed to test differences between patients with T1D and T2D and linear regression analyses were performed to investigate associations between osteoglycin, glycemic markers, bone turnover markers and characteristics.

Results: S-osteoglycin did not differ between patients with T1D and T2D (p=0.10). No associations were present between osteoglycin and age, gender, microvascular complications, HbA1c, or plasma glucose in T1D or T2D patients (p>0.05 for all). S-osteoglycin was not associated with levels of bone turnover markers (C-terminal cross-linked telopeptide of type-I collagen (CTX), P-procollagen type 1 amino terminal propeptide (P1NP), P-osteocalcin (OC), P-sclerostin, S-osteoprotegerin (OPG) or S-Receptor Activator of Nuclear factor Kappa beta Ligand (RANKL)) in neither T1D or T2D patients (p>0.05 for all).

Conclusion: Osteoglycin levels were similar in T1D and T2D patients. Osteoglycin did not correlate with glucose, HbA1c or any other biochemical marker of bone turnover. Thus, we did not find evidence supporting the existence of an osteoglycin-bone-pancreas axis.

Clinical trial registration: ClinicalTrials.gov, identifier NCT01870557.

Keywords: bone; bone turnover; diabetes mellitus; hyperglycemia; osteoglycin.

Background: Osteoporosis is an asymptomatic bone disorder leading to altered bone microarchitecture, mineralization and strength. Musa paradisiaca has been reported to have antioxidant and anti-inflammatory effects in various diseases. Its impact on postmenopausal osteoporosis has not been investigated yet.

Purpose: The intention of the current study was to evaluate the bone regeneration and osteoprotective potential of extract and fraction of M. paradisiaca flower in ovariectomized (Ovx) Sprague Dawley (SD) rats, a model of post-menopausal bone loss. The study also aims to identify osteogenic compounds from active fraction.

Methods: Ethanolic extract (MFE) and butanolic fraction (MFE-Bu) from flower of M. paradisiaca were prepared and their efficacy was tested in rat femur osteotomy model at different doses. Effective dose from both extract (250 mg/kg) and fraction (50 mg/kg) were taken for study in osteopenic bone loss model. PTH was taken as reference standard (20 µg/kg/twice a week). Bones were harvested at autopsy for dynamic and static histomorphometry. Serum was collected for ELISA. Pure compounds were isolated from butanolic fraction (MFE-Bu), and were assessed for their osteogenic effect.

Results: MFE and MFE-Bu were observed for their potential in bone healing and prevention of bone loss. Both MFE and MFE-Bu promoted new bone regeneration at injury site as assessed by microCT and calcein dye labeling studies. These also led to restoration of bone microarchitecture deteriorated as a result of osteopenia and improved bone biomechanical properties. Extract as well as the fraction exhibited dual bone anabolic and anti-resorptive properties where they elevated serum procollagen type I N-terminal propeptide (P1NP), a bone formation marker and suppressed serum C-telopeptide of type I collagen (CTX-1), a bone resorption marker. As many as four osteogenic compounds were isolated from MFE-Bu. Oleracein-E was found to be the most potent osteogenic agent based on osteoblast differentiation, mineralization assays, qPCR and protein expression studies.

Conclusion: Our studies demonstrates that ethanolic extract from the flower of M. paradisiaca and its butanolic fraction exhibit dual osteogenic and anti-resorptive potential, and have an advantage over PTH which though promotes bone formation but is also bone catabolic in nature.

Keywords: Bone formation; Bone microarchitecture; Bone resorption; Musa paradisiaca; Osteoporosis.

Psoriasis is a chronic inflammatory disease of the skin and joints. More recent data emphasize an association with dysregulated glucose and fatty acid metabolism, obesity, elevated blood pressure and cardiac disease, summarized as metabolic syndrome. TNF-α and IL-17, central players in the pathogenesis of psoriasis, are known to impair bone formation. Therefore, the relation between psoriasis and bone metabolism parameters was investigated. Two serum markers of either bone formation-N-terminal propeptide of type I procollagen (P1NP) or bone resorption-C-terminal telopeptide of type I collagen (CTX-I)-were analyzed in a cohort of patients with psoriasis vulgaris. In patients with psoriasis, P1NP serum levels were reduced compared to gender-, age-, and body mass index-matched healthy controls. CTX-I levels were indistinguishable between patients with psoriasis and controls. Consistently, induction of psoriasis-like skin inflammation in mice decreases bone volume and activity of osteoblasts. Moreover, efficient anti-psoriatic treatment improved psoriasis severity, but did not reverse decreased P1NP level suggesting that independent of efficient skin treatment psoriasis did affect bone metabolism and might favor the development of osteoporosis. Taken together, evidence is provided that bone metabolism might be affected by psoriatic inflammation, which may have consequences for future patient counseling and disease monitoring.

Keywords: bone metabolism; chronic inflammatory diseases; osteoporosis; psoriasis; skin.

Objective: To observe the changes in the related indicators of bone formation and bone resorption in severely burned rats. Methods: The experimental research method was adopted. Thirty female Sprague-Dawley rats aged 6 to 8 weeks were divided into sham injury group, 12% total body surface area (TBSA) full-thickness burn group, and 24%TBSA full-thickness burn group according to the random number table, with 10 rats in each group. The rats were treated on the back correspondingly, after which, the burned rats were rehydrated by intraperitoneal injection according to the Parkland formula, and the wound was coated with 20 g/L iodophor until wound healing. On post injury day (PID) 28, the tibia tissue of rats in each group was collected. The new bone tissue and the number of osteoclasts were observed after staining with Masson and tartrate-resistant acid phosphatase, respectively. The abdominal aortic blood of rats in each group was harvested for serum preparation. The bone metabolism indexes of serum calcium ion and phosphorus ion concentration were determined by the methyl thymol blue colorimetric method and phosphomolybdic acid method, respectively. The serum levels of bone formation marker of aminoterminal propeptide of type 1 procollagen (P1NP) and bone resorption marker of beta-carboxy-terminated peptide of type Ⅰ collagen (β-CTX) were determined by enzyme-linked immunosorbent assay. The first lumbar spine tissue of rats in each group was collected, and the mRNA expression levels of osteoprotegerin, receptor activator of nuclear factor-κB ligand (RANKL), tumor necrosis factor receptor-associated factor 6 (TRAF-6), nuclear factor of activated T cell 1 (NFATC1), c-Fos, and c-Src were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction. Data were statistically analyzed with one-way analysis of variance, Bonferroni method, Welch test, Games-Howell test, Kruskal-Wallis test, Mann-Whitney U test, and Bonferroni correction. Results: On PID 28, compared with that in sham injury group, the formation of new bone tissue in the tibia tissue of rats in the two burn groups was decreased, and the larger the burn area, the more obvious the decrease. The numbers of osteoclasts in the tibia tissue of rats in the two burn groups were similar, both significantly more than the number in sham injury group. On PID 28, the serum calcium ion concentration and serum level of β-CTX of rats in the three groups were similar (P>0.05). The serum phosphorus ion concentration of rats in 24%TBSA full-thickness burn group was significantly higher than that in 12%TBSA full-thickness burn group (P<0.05), and the serum phosphorus ion concentrations in the two burn groups were significantly higher than the concentration in sham injury group (P<0.01). The serum level of P1NP of rats in 24%TBSA full-thickness burn group was significantly lower than that in sham injury group (P<0.01). On PID 28, the mRNA expression levels of osteoprotegerin in the first lumbar spine tissue of rats in sham injury group, 12%TBSA full-thickness burn group, and 24%TBSA full-thickness burn group were 1.01±0.20, 1.71±0.83, and 2.24±0.51, respectively, and that in 24%TBSA full-thickness burn group was significantly higher than that in sham injury group (P<0.01). The mRNA expression level of RANKL in the first lumbar spine tissue of rats in 24%TBSA full-thickness burn group was 1.31±0.17, which was significantly higher than 1.00±0.14 in sham injury group and 0.97±0.10 in 12%TBSA full-thickness burn group (P<0.01). The mRNA expression levels of TRAF-6, NFATC1 (Z=3.141, 3.782), and c-Src in the first lumbar tissue of rats in 12%TBSA full-thickness burn group and 24%TBSA full-thickness burn group and the mRNA expression level of c-Fos in the first lumbar tissue of rats in 12%TBSA full-thickness burn group were significantly higher than those in sham injury group (P<0.05 or P<0.01). The mRNA expression levels of c-Fos and c-Src in the first lumbar spine tissue of rats in 12%TBSA full-thickness burn group were significantly higher than those in 24%TBSA full-thickness burn group (P<0.01). Conclusions: Severe burns can cause a decrease in the generation of new bone tissue, an increase in the number of osteoclasts and the serum phosphorus ion concentration, and a decrease in the serum level of P1NP in rats. The level of osteoprotegerin, RANKL, TRAF-6, NFATC1, c-Fos, and c-Src in bone tissue showed an increasing trend while the level of NFATC1, c-Fos, and c-Src showed a decreasing trend with the increase of burn area.

目的： 研究严重烧伤大鼠骨形成及骨吸收相关指标的变化。 方法： 采用实验研究方法。将30只6~8周龄SD雌性大鼠按随机数字表法分为假伤组、12%体表总面积（TBSA）Ⅲ度烧伤组、24%TBSAⅢ度烧伤组，每组10只。于各组大鼠背部进行相应处理，之后仅烧伤大鼠按Parkland公式经腹腔注射补液，创面外涂20 g/L碘伏，直至创面愈合。伤后28 d，取各组大鼠胫骨组织，分别行Masson、抗酒石酸酸性磷酸酶染色，观察新生骨组织、破骨细胞数量；取各组大鼠腹主动脉血制备血清，分别采用甲基百里酚蓝比色法、磷钼酸法测定骨代谢指标血清钙离子、磷离子浓度，采用酶联免疫吸附测定法检测血清中骨形成标志物Ⅰ型前胶原氨基端前肽（P1NP）和骨吸收标志物β-Ⅰ型胶原羧基端肽（β-CTX）水平；取各组大鼠第1腰椎组织，采用实时荧光定量反转录PCR法检测护骨因子、核因子κB受体激活蛋白配体（RANKL）、肿瘤坏死因子受体相关因子6（TRAF-6）、活化T细胞核因子1（NFATC1）、c-Fos、c-Src的mRNA表达水平。数据处理采用单因素方差分析、Bonferroni法、Welch检验、Games-Howell检验、Kruskal-Wallis检验、Mann-Whitney U检验及Bonferroni校正。 结果： 伤后28 d，与假伤组比较，2个烧伤组大鼠胫骨组织中新生骨组织生成均减少，烧伤面积越大减少越明显；2个烧伤组大鼠胫骨组织中破骨细胞数量相近，均较假伤组明显增多。伤后28 d，3组大鼠血清钙离子浓度、血清中β-CTX水平相近（P>0.05）；24%TBSAⅢ度烧伤组大鼠血清磷离子浓度明显高于12%TBSAⅢ度烧伤组（P<0.05），且2个烧伤组大鼠血清磷离子浓度均显著高于假伤组（P<0.01）；24%TBSAⅢ度烧伤组大鼠血清中P1NP水平明显低于假伤组（P<0.01）。伤后28 d，假伤组、12%TBSAⅢ度烧伤组、24%TBSAⅢ度烧伤组大鼠第1腰椎组织中护骨因子mRNA表达水平分别为1.01±0.20、1.71±0.83、2.24±0.51，其中24%TBSAⅢ度烧伤组明显高于假伤组（P<0.01）；24%TBSAⅢ度烧伤组大鼠第1腰椎组织中RANKL mRNA表达水平为1.31±0.17，明显高于假伤组的1.00±0.14与12%TBSAⅢ度烧伤组的0.97±0.10（P<0.01）；12%TBSAⅢ度烧伤组、24%TBSAⅢ度烧伤组大鼠第1腰椎组织中TRAF-6、NFATC1（Z=3.141、3.782）、c-Src mRNA表达水平及12%TBSAⅢ度烧伤组大鼠第1腰椎组织中c-Fos mRNA表达水平均明显高于假伤组（P<0.05或P<0.01）；12%TBSAⅢ度烧伤组大鼠第1腰椎组织中c-Fos、c-Src mRNA表达水平均明显高于24%TBSAⅢ度烧伤组（P<0.01）。 结论： 严重烧伤可引起大鼠新生骨组织生成减少及破骨细胞数量增多，血清磷离子浓度升高与血清中P1NP水平下降，骨组织中护骨因子、RANKL、TRAF-6、NFATC1、c-Fos、c-Src呈升高趋势，且NFATC1、c-Fos、c-Src随烧伤总面积增加呈下降趋势。.

Background: Compared with a natural process, surgically induced menopausal women have a higher bone loss rate. This study aims to evaluate early treatment with estradiol valerate on bone turnover markers after surgically induced menopause.

Methods: This prospective study included 41 pre and perimenopausal women who underwent hysterectomy with oophorectomy for benign gynecologic conditions. Two weeks after the operation, all participants were assessed for menopausal hormone therapy (MHT) indications. Estrogen therapy was prescribed for those who had indications and accepted treatment (hormone treatment group). The others who had no MHT indication were allocated to the no-treatment group. Serum CTX and P1NP levels at preoperative and 12 weeks postoperative were measured and set as the primary outcome. Within the same group, serum CTX and P1NP before and after surgical menopause were analyzed using Wilcoxon signed-rank test. ANCOVA was used to compare serum CTX and P1NP at 12 weeks after surgical menopause between the two groups. Spearman's rank correlation coefficient analysis analyzed the correlation between age and baseline bone turnover markers. A p-value of < 0.05 was considered statistically significant.

Results: At 12 weeks after surgery, there were no significant differences in serum CTX and P1NP levels in the hormone treatment group compared to baseline. In contrast, serum CTX and P1NP levels were significantly elevated among women who did not receive hormone treatment (p-value < 0.001 and 0.002, respectively). Serum CTX and P1NP at 12 weeks were significantly different between the two groups (p-value < 0.001 and 0.004, respectively).

Conclusion: Early estrogen administration with oral estradiol valerate could significantly suppress the high bone remodeling in surgically induced menopausal women. Trial registration Thai Clinical Trial Registry identification number TCTR20190808004, retrospective registered since 2019-08-08. http://www.thaiclinicaltrials.org/show/TCTR20190808004 .

Keywords: Bone turnover markers; Estradiol valerate; Serum CTX; Serum P1NP; Surgical menopause.

Background: Markers of bone metabolism (MBM) play an important role in fracture evaluation, and changes have been associated with increased fracture risk. The purpose of the present study was to describe changes in MBM in premenopausal women with distal radial fractures.

Methods: Premenopausal women with distal radial fractures (n = 34) and without fractures (controls) (n = 39) were recruited. Serum MBM in patients with distal radial fractures were obtained at the time of the initial presentation, 6 weeks, and 3, 6, and 12 months. MBM included 25(OH) vitamin D, PTH, osteocalcin, P1NP, BSAP, CTX, sclerostin, DKK1, periostin, and TRAP5b. Areal bone mineral density (aBMD) was assessed with dual x-ray absorptiometry, and the bone material strength index (BMSi) was assessed with microindentation.

Results: Most MBM reached peak levels at 6 weeks after the injury, including osteocalcin (+17.7%), sclerostin (+23.5%), and DKK1 (12.6%). Sclerostin was lower (-27.4%) and DKK1 was higher (+22.2%) at 1 year after the fracture. CTX declined below baseline levels at 6 and 12 months, whereas TRAP5b, BSAP, and periostin did not significantly change. At 12 months, sclerostin was lower (p = 0.003) and DKK1 was higher (p = 0.03) in the distal radial fracture group than in the control group. Greater fracture severity was associated with greater increases in P1NP and BSAP. aBMD and BMSi were not associated with fracture.

Conclusions: Distal radial fractures caused increases in several MBM, which typically peaked at 6 weeks after injury and gradually decreased over 6 months. Sclerostin and DKK1 remained below and above baseline at 1 year, respectively. Increasing fracture severity resulted in larger changes in MBM. aBMD and BMSi did not discriminate between patients with distal radial fractures and controls. Continued efforts to identify markers of skeletal fragility in young women are warranted to mitigate future fracture risk.

Level of evidence: Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence.

Ginsenosides are active compounds that are beneficial to bone metabolism and have anti-osteoporosis properties. However, very few clinical investigations have investigated the effect of ginseng extract (GE) on bone metabolism. This study aims to determine the effect of GE on improving bone metabolism and arthritis symptoms in postmenopausal women with osteopenia. A 12-week randomized, double-blind, placebo-controlled clinical trial was conducted. A total of 90 subjects were randomly divided into a placebo group, GE 1 g group, and GE 3 g group for 12 weeks based on the random 1:1:1 assignment to these three groups. The primary outcome is represented by bone metabolism indices consisting of serum osteocalcin (OC), urine deoxypyridinoline (DPD), and DPD/OC measurements. Secondary outcomes were serum CTX, NTX, Ca, P, BsALP, P1NP, OC/CTX ratio, and WOMAC index. The GE 3 g group had a significantly increased serum OC concentration. Similarly, the GE 3 g group showed a significant decrease in the DPD/OC ratio, representing bone resorption and bone formation. Moreover, among all the groups, the GE 3 g group demonstrated appreciable improvements in the WOMAC index scores. In women with osteopenia, intake of 3 g of GE per day over 12 weeks notably improved the knee arthritis symptoms with improvements in the OC concentration and ratios of bone formation indices like DPD/OC.

Keywords: WOMAC; arthritis symptoms; bone metabolism; ginseng extract; osteopenia.

Objective: The risk factors for the most common adverse reactions of two types of antiosteoporosis drugs in the first treatment of postmenopausal osteoporosis were analyzed to investigate the relationship between the occurrence of adverse reactions and different bone transition states and vitamin D levels.

Methods: A total of 381 postmenopausal women who were diagnosed with osteoporosis in the Osteoporosis Clinic of Ningxia Medical University General Hospital from January 2017 to June 2020 were enrolled. A telephone follow-up survey was conducted on the mentioned subjects. According to the survey results, the mentioned subjects were selected according to their first use of antiosteoporosis drugs. They were divided into zoledronic acid and teriparatide acetate groups. The subjects in the two groups were divided into two groups according to the presence or absence of adverse reactions after medication and according to vitamin D level and P1NP level, and the correlation between the two factors and the occurrence of adverse reactions was analyzed.

Results: Among the 307 patients treated with zoledronic acid for antiosteoporosis, 99 patients developed acute phase adverse reactions (APR+), accounting for 32.2% of the total subjects. 56.7 percent of the subjects had vitamin D deficiency. The 25(OH)D level of the APR + subjects was 16.75 ± 9.20 ng/mL, significantly lower than that of the APR- patients (23.68 ± 10.67 ng/mL). Serological P1NP level in APR+ patients was 73.95 ± 34.50 ng/ml, significantly higher than that of APR- patients with 55.80 ± 36.91 ng/ml. Musculoskeletal symptoms were observed in 14 of the 74 subjects treated with teriparatide acetate, accounting for 18.9% of the total subjects. The 25(OH)D level was deficient in 59.5% of the subjects. The 25(OH)D level of the subjects with musculoskeletal symptoms was 15.96 ± 8.17 ng/ml, while that of the subjects without musculoskeletal symptoms was 20.86 ± 8.52 ng/ml, which showed no statistical significance. The reason was considered to be related to the small sample size included in the study. The P1NP level of subjects with musculoskeletal symptoms was 96.85 ± 58.52 ng/ml, significantly higher than the P1NP level of subjects without musculoskeletal symptoms (55.28 ± 27.87 ng/ml).

Conclusions: The 25(OH)D level in vivo was negatively correlated with the acute phase adverse reactions after the first infusion of zoledronic acid. When the rate of bone formation is increased and osteoblasts are active, the risk of acute phase adverse reactions is increased with the use of zoledronic acid as antiosteoporosis therapy. There was no significant correlation between 25(OH)D levels and musculoskeletal symptoms after teriparatide acetate treatment of osteoporosis. When the rate of bone formation is increased and osteoblasts are active, the risk of adverse reactions to musculoskeletal symptoms is increased with antiosteoporosis treatment with teriparatide acetate.

Both vitamin D and insulin-like growth factor 1 (IGF-1) play essential roles in bone metabolism and may interact during prepubertal bone accrual. We investigated the association of low serum 25-hydroxyvitamin D (25(OH)D) (<20 ng/mL) with the circulating bone turnover markers, when compared to their interaction with IGF-1.

Subjects and methods: Serum 25(OH)D, IGF-I, P1NP (N-terminal propeptide of type I procollagen), and CTX-1 (C-terminal telopeptide of type I collagen) were measured, and the bone turnover index (BTI) was calculated in 128 healthy children, aged 9-11 years.

Results: Mean 25(OH)D concentration was 21.9 ± 4.9 ng/mL, but in 30.5% of participants it was <20 ng/mL (<50 nmol/L). We observed a trend for higher P1NP (p < 0.05) and IGF-1 (p = 0.08), towards lower 25(OH)D in tertiles. Levels of P1NP in the lowest 25(OH)D tertile (<20 ng/mL) were the highest, while CTX and BTI remained unchanged. Additionally, 25(OH)D negatively correlated with IGF-1, while the correlation with P1NP was not significant. A strong positive correlation of IGF-1 with P1NP and BTI but weak with CTX was observed. Low 25(OH)D (<20 ng/mL) explained 15% of the IGF-1 variance and 6% of the P1NP variance.

Conclusions: Low levels of 25(OH)D do not unfavorably alter bone turnover. It seems that serum 25(OH)D level may not be an adequate predictor of bone turnover in children.

Keywords: 25-hydoxyvitamin D; bone mineral accrual; bone turnover markers; insulin-like growth factor 1.

Methylsulfonylmethane (MSM) is a naturally occurring anti-inflammatory compound that effectively treats multiple degenerative diseases such as osteoarthritis and acute pancreatitis. Our previous studies have demonstrated the ability of MSM to differentiate stem cells from human exfoliated deciduous (SHED) teeth into osteoblast-like cells. This study examined the systemic effect of MSM in 36-week-old aging C57BL/6 female mice in vivo by injecting MSM for 13 weeks. Serum analyses showed an increase in expression levels of bone formation markers [osteocalcin (OCN) and procollagen type 1 intact N-terminal propeptide (P1NP)] and a reduction in bone resorption markers [tartrate-resistant acid phosphatase (TRAP) and C-terminal telopeptide of type I collag (CTX-I)] in MSM-injected animals. Micro-computed tomographic images demonstrated an increase in trabecular bone density in mandibles. The trabecular bone density tended to be higher in the femur, although the increase was not significantly different between the MSM- and phosphate-buffered saline (PBS)-injected mice. In mandibles, an increase in bone density with a corresponding decrease in the marrow cavity was observed in the MSM-injected mice. Furthermore, immunohistochemical analyses of the mandibles for the osteoblast-specific marker - OCN, and the mesenchymal stem cell-specific marker - CD105 showed a significant increase and decrease in OCN and CD105 positive cells, respectively. Areas of bone loss were observed in the inter-radicular region of mandibles in control mice. However, this loss was considerably decreased due to stimulation of bone formation in response to MSM injection. In conclusion, our study has demonstrated the ability of MSM to induce osteoblast formation and function in vivo, resulting in increased bone formation in the mandible. Hence, the application of MSM and stem cells of interest may be the right combination in alveolar bone regeneration under periodontal or other related diseases that demonstrate bone loss.

Keywords: aging mice; bone formation; methylsulfonylmethane; osteoblasts; osteoclasts.

Zoledronic acid (ZOL) is a therapy inhibiting bone resorption. In this study, generic ZOL (Yigu®) showed its clinical efficacy consistency with original ZOL (Aclasta®) in Chinese postmenopausal women with osteoporosis. This study provides a practical basis for the application of Yigu® in Chinese population.

Introduction: Yigu® has been approved its bioequivalence to Aclasta®. However, the clinical efficacy and safety of Yigu® have not been evaluated yet. Here, we compared the effectiveness and safety between Yigu® and Aclasta® in Chinese postmenopausal women with osteoporosis and assessed the efficacy of intravenous infusion of ZOL.

Methods: This was a randomized open-label, active-controlled study in postmenopausal women with osteoporosis of 14 clinical centers in China. Postmenopausal women with osteoporosis were recruited and randomized to receive a single infusion of 5 mg Yigu® or Aclasta®. The primary endpoint was the percentage change in bone mineral density (BMD) at lumbar spine after 12 months of treatment and was assessed for equivalence. The secondary endpoint was the percentage change in BMD at proximal femur after 12 months. Additional secondary endpoints were percentage changes in BMD at the above sites after 6 months of treatment and changes in bone turnover biomarkers during ZOL treatment. Safety was also evaluated and compared between two groups.

Results: A total of 458 postmenopausal women with osteoporosis were enrolled (n = 227, Yigu®; n = 231, Aclasta®). The mean percentage change in the BMD had no statistical difference at the lumbar spine (5.32% vs 5.18%), total hip (2.72% vs 2.83%), and femoral neck (2.37% vs 2.81%) between Yigu® and Aclasta® groups after 12 months of treatment. The mean difference of BMD change at the lumbar spine after 12 months between two groups was 0.15% (95% CI: - 0.71 to 1.00, equivalence margin: - 1.5%, 1.5%), demonstrating the treatments were equivalent. Meanwhile, the decreases in the P1NP and β-CTX showed no difference between two groups after 14 days and 6 and 12 months of treatment. As regards the whole sample, BMD significantly increased after 12 months of treatment. Also, serum C-terminal telopeptide of type 1 collagen (β-CTX) and procollagen 1 N-terminal peptide (P1NP) significantly decreased at each visit period. The overall adverse events were comparable and quite well between two groups.

Conclusion: Intravenous infusion of zoledronic acid achieved the potent anti-resorptive effects which led to significant increase in BMD of Chinese postmenopausal women with osteoporosis. Yigu® was equivalent to Aclasta® with respect to efficacy and safety.

Keywords: BMD; P1NP; Postmenopausal osteoporosis; Zoledronic acid; β-CTX.

Background: Excessive vitamin A (VA) can cause bone resorption and impair growth. Government-mandated VA supplementation (VAS) and adequate intake through dietary fortification and liver consumption led to excessive VA in South African children.

Objectives: We evaluated the relationship of VAS and underlying hypervitaminosis A assessed by retinol isotope dilution (RID) with measures of growth and bone turnover in this cohort.

Methods: Primary outcomes in these children (n = 94, 36-60 mo) were anthropometric measurements [height-for-age (HAZ), weight-for-age (WAZ), and weight-for-height (WHZ) Z-scores]; serum bone turnover markers [C-terminal telopeptide of type I collagen (CTX) and N-terminal propeptide of type I procollagen (P1NP)]; and inflammation defined as C-reactive protein (CRP ≥ 5 mg/L) and/or α1-acid glycoprotein (AGP ≥1 g/L). VA status was previously measured by RID-estimated total body VA stores (TBSs) and total liver VA reserves (TLRs), and serum retinol and carotenoid concentrations, before and 4 wk after children were administered 200,000 IU VAS. Serum 25-hydroxyvitamin D3 was measured by ultra-performance LC. (Registered at Clinicaltrials.gov NCT02915731).

Results: In this largely hypervitaminotic A cohort, HAZ, WAZ, and WHZ were negatively associated with increasing TLRs, where TLRs predicted 6-10% of the variation before VAS (P < 0.05), increasing to 14-19% 4 wk after VAS (P < 0.01). Bone resorption decreased after VAS (P < 0.0001) while formation was unaffected. Neither CTX nor P1NP were correlated with TLRs at either time. Serum carotenoids were low. One child at each timepoint was vitamin D deficient (<50 nmol/L). CRP and AGP were not associated with growth measurements.

Conclusions: Excessive TLRs due to dietary vitamin A intake and supplementation is associated with lower anthropometric measures and bone resorption decreased after supplementation. Vitamin A supplementation programs should monitor VA status with biomarkers sensitive to TLRs to avoid causing negative consequences in children with hypervitaminosis A.The Clinical Trial Registry number is NCT02915731: https://clinicaltrials.gov/ct2/show/NCT02915731.

Keywords: bone health; serum carotenoids; stable isotope; vitamin a; vitamin d.

Purpose: To investigate the differences of several serum markers among population with different bone mass and to explore the utility of new potential biomarker for the diagnosing and screening for postmenopausal osteoporosis (PMOP).

Materials and methods: A total of 1055 postmenopausal women were screened and gathered data on BMD screening, biological samples, and questionnaire information. A liquid chip assay was used to measure serum IL-6, IGF-1, BMP-2, VEGF, leptin and FGF23. The predictive value of the indicator panels was assessed using the area under the receiver-operator characteristic curve (AUC). Statistical analyses were conducted by using SAS 9.4 and R software 4.1.1. Figures were created in GraphPad Prism 8.0.

Results: When compared against the normal group, in addition to the vitamin D, the PMOP group showed a significant increase in median values for other indicators (P < 0.05), especially in P1NP and β-CTX. Among the six cytokines representing different osteoporosis mechanisms, currently, we found that only IGF-1 and leptin showed significant differences between the groups. Also, the liquid chip assay results showed that IGF-1 and leptin, as newer cytokines in osteoporosis, not only have significant differences between groups, but also have a strong correlation with each other (P < 0.05). Then, we reported the accuracy of different indicator combinations by using AUC and, moreover, we demonstrated that IGF-1 with leptin did significantly provide incremental value to the AUC of conventional indexes, it markedly improved diagnostic efficacy, displaying an IDI of 9.45% (P = 0.000).

Conclusion: IFG-1 and leptin seem to be key biomarker associated with PMOP. The high prevalence of PMOP makes these cytokines might bear the potential of becoming a very useful screening test also for clinical follow-up of patients.

Keywords: biomarkers; cytokine; diagnose; menopause.

Increased interleukin-6 (IL-6) has been observed in the bone tissue of fibrous dysplasia of bone/McCune-Albright syndrome (FD/MAS) and is possibly involved in the increased bone destruction and bone pain characterizing this disease. The TOCIDYS trial was a randomized, placebo-controlled, 1 year, cross-over, proof-of-concept trial, conducted in patients not responding to bisphosphonates, using monthly intra-venous tocilizumab (a monoclonal antibody to the IL-6 receptor) at 8 mg/kg or a matching placebo for 6 months. Over the following 6 months, they received tocilizumab if they first had placebo, and vice-versa. We measured change in serum CTX after 6 months of treatment, compared with baseline (primary endpoint). Other endpoints were the change in bone pain, change in P1NP, bone alkaline phosphatase, osteocalcin and ICTP, and variation of quality of life. The analysis relied on ANOVA, with sequence of treatment, period and treatment as factors and accounting for a potential carry-over effect. We have randomized 8 patients with FD/MAS in each sequence who all completed the first 6 months treatment period. During the second 6 months period, 3 patients stopped therapy, so the efficacy analysis set included 13 patients. We observed no significant change in serum CTX and other biochemical markers of bone turnover between the tocilizumab and placebo groups. There was no significant change in the level of bone pain on tocilizumab, although 3 patients had a sharp decrease in pain while on active drug, with progressive relapse on placebo for 2 of them, but with some degree of improvement in a few patients while on placebo. The SF-36 quality of life scale was not significantly changed. We conclude that tocilizumab does not decrease bone turnover in FD/MAS when administered in patients who fail to respond to bisphosphonates. Tocilizumab does not reduce bone pain in most patients, but a substantial effect in a subset cannot be ruled out in this trial powered for markers but not for pain.

Keywords: Fibrous dysplasia of bone; Interleukin-6; McCune-Albright syndrome; Tocilizumab.

Objective: While serum bone turnover markers (BTMs) and bone mineral density (BMD) have been confirmed as useable risk assessment tools for postmenopausal osteoporosis, the associations between BTMs and BMD changes are still ambiguous. The aim of this study was to explore the underlying associations between BTMs and BMD changes in postmenopausal women.

Methods: Between January 2015 and October 2020, 135 postmenopausal women were retrospectively enrolled. They were divided into two groups according to lumbar spine (LS) 1-4 BMD change (1 y T-score minus baseline T-score, Group 1 [n = 36] < 0 and Group 2 [n = 99] ≥ 0). The changes of BTMs (N-terminal middle segment osteocalcin [N-MID], propeptide of type I procollagen [P1NP], and β-C-terminal telopeptide of type I collagen [β-CTX]) and their associations with LS 1-4 BMD change were analyzed. The biochemical indices and clinical parameters related with LS 1-4 BMD change were also evaluated.

Results: The 1 year N-MID, P1NP, β-CTX and Phosphorus in Group 2 were lower than those in Group 1 (P < 0.05), their changes within 1 year were significantly negatively correlated with LS 1-4 BMD change (R2 = -0.200, P < 0.001; R2 = -0.230, P < 0.001; R2 = -0.186, P < 0.001; R2 = -0.044, P = 0.015; respectively). Except for the Phosphorus change (area under the curve [AUC] = 0.623), the changes of N-MID, P1NP, and β-CTX and their 1 year levels had similar AUC to diagnose the short-term LS 1-4 BMD change (AUC > 0.7 for all, with the AUC of 1 y P1NP being the largest at 0.803). Binary logistic regression analysis showed that the physical activity and drug intervention were the determinant factors for the LS 1-4 BMD change (odds ratio = 6.856, 95% confidence interval: 2.058-22.839, P = 0.002; odds ratio = 5.114, 95% confidence interval: 1.551-16.864, P = 0.007; respectively).

Conclusions: Declining N-MID, P1NP, β-CTX, and Phosphorus are associated with the short-term increase of LS 1-4 BMD within 1 year. Physical activity and drug intervention are factors significantly influencing the change of LS 1-4 BMD in postmenopausal women.

Purpose: Cementless tibial components migrate initially until osseointegration and preserve periprosthetic bone. Cemented tibial components are fixed from surgery but loose periprosthetic bone. Little is known about bone formation and resorption biomarkers in relation to component fixation and bone mineral density (BMD) changes of cementless and cemented total knee arthroplasty. We hypothesize a similar migration of cemented and cementless tibial components between 1- and 2-year follow-up indicating a stable long-term fixation.

Methods: In a prospective patient-blinded randomized study, we compared cementless (n = 27) and cemented (n = 26) tibial components with radiostereometry measured migration (MTPM = Maximum Total Point Motion: point of component that migrates the most) and changes in BMD and biochemical bone turnover markers (BTMs) until 24 months after surgery.

Results: The mean MTPM between 12 and 24 months were similar between groups with - 0.06 mm (95% CI - 0.23; 0.11) in the cementless group compared to 0.02 mm (95% CI - 0.07; 0.11) in the cemented group. However, there was a higher proportion of cementless components (16/25) than cemented components (7/24) with continuous migration (MTPM > 0.2 mm) (p = 0.02). In the medial and anterior region below the tibial components, the BMD increased by mean 1.8% and 7.4% for cementless components and decreased by mean 8.6% and 4.2% for cemented components until 24-month follow-up. In both groups, BTMs initially showed increased bone resorption (CTx) and bone formation (P1NP) followed by normalization to pre-operative levels at 6 months post-surgery.

Conclusion: More cementless components than cemented components showed continues migration which suggest a higher risk of early revision. Bone turnover increased post-surgery in both groups, but did not explain the difference in change in periprosthetic BMD.

Level of evidence: I.

Keywords: Bone mineral density; Bone turnover markers; Knee arthroplasty; Radiostereometry analysis.

Cold temperature activates the sympathetic nervous system (SNS) to induce bone loss by altering bone remodeling. Brown adipose tissue (BAT) is influenced by the SNS in cold environments. Many studies have confirmed a positive relationship between BAT volume and bone mass, but the influence and mechanism of BAT on bone in vivo and in vitro is still unknown. Two-month-old C57/BL6j male mice were exposed to cold temperature (4°C) to induce BAT generation. BAT volume, bone remodeling and microstructure were assessed after 1 day, 14 days and 28 days of cold exposure. CTX-1, P1NP and IL-6 levels were detected in the serum by ELISA. To determine the effect of BAT on osteoclasts and osteoblasts in vitro, brown adipocyte conditional medium (BAT CM) was collected and added to the differentiation medium of bone marrow-derived macrophages (BMMs) and bone marrow mesenchymal stem cells (BMSCs). Micro-CT results showed that the bone volume fraction (BV/TV, %) significantly decreased after 14 days of exposure to cold temperature but recovered after 28 days. Double labeling and TRAP staining in vivo showed that bone remodeling was altered during cold exposure. BAT volume enlarged after 14 days of cold stimulation, and IL-6 increased. BAT CM promoted BMSC mineralization by increasing osteocalcin (Ocn), RUNX family transcription factor 2 (Runx2) and alkaline phosphatase (Alp) expression, while bone absorption was inhibited by BAT CM. In conclusion, restoration of bone volume after cold exposure may be attributed to enlarged BAT. BAT has a beneficial effect on bone mass by facilitating osteogenesis and suppressing osteoclastogenesis.

Keywords: bone remodeling; cold exposure; interleukin-6; osteoblast; osteoclast.

Objective: The aim of this study was to investigate whether the modified Atkins diet (MAD), a variant of the ketogenic diet, has an impact on bone- and calcium (Ca) metabolism.

Methods: Two groups of adult patients with pharmacoresistant epilepsy were investigated. One, the diet group (n = 53), was treated with MAD for 12 weeks, whereas the other, the reference group (n = 28), stayed on their habitual diet in the same period. All measurements were performed before and after the 12 weeks in both groups. We assessed bone health by measuring parathyroid hormone (PTH), Ca, 25-OH vitamin D (25-OH vit D), 1,25-OH vitamin D (1,25-OH vit D), phosphate, alkaline phosphatase (ALP), and the bone turnover markers procollagen type 1 N-terminal propeptide (P1NP) and C-terminal telopeptide collagen type 1 (CTX-1). In addition, we examined the changes of sex hormones (estradiol, testosterone, luteinizing hormone, follicle-stimulating hormone), sex hormone-binding globulin, and leptin.

Results: After 12 weeks of MAD, we found a significant reduction in PTH, Ca, CTX-1, P1NP, 1,25-OH vit D, and leptin. There was a significant increase in 25-OH vit D. These changes were most pronounced among patients <37 years old, and in those patients with the highest body mass index (≥25.8 kg/m²), whereas sex and type of antiseizure medication had no impact on the results. For the reference group, the changes were nonsignificant for all the analyses. In addition, the changes in sex hormones were nonsignificant.

Significance: Twelve weeks of MAD treatment leads to significant changes in bone and Ca metabolism, with a possible negative effect on bone health as a result. A reduced level of leptin may be a triggering mechanism. The changes could be important for patients on MAD, and especially relevant for those patients who receive treatment with MAD at an early age before peak bone mass is reached.

Keywords: antiseizure medications; bone health; ketogenic diet; leptin; sex hormones.

Introduction: Recent studies in postmenopausal women have found associations of follicle-stimulating hormone (FSH) levels with both glucose metabolism and bone turnover. The objective of the study was to investigate whether FSH may contribute to suppressed bone turnover markers (BTMs) in postmenopausal women with type 2 diabetes (T2D).

Materials and methods: 888 postmenopausal women with T2D, 352 nondiabetes (prediabetes plus normoglycemia) were included from the METAL study. HbA1c, sex hormones, 25-hydroxy vitamin D (25(OH)D), serum procollagen type I N-terminal propeptide (P1NP), and β-C-terminal telopeptide (β-CTX) were measured.

Results: P1NP and β-CTX decreased in postmenopausal T2D women compared with nondiabetes controls (both p < 0.001). The major factors responsible for the changes in P1NP were HbA1c (β = - 0.050, p < 0.001), 25(OH)D (β = - 0.003, p = 0.006), FSH (β = 0.001, p = 0.044) and metformin (β = - 0.109, p < 0.001), for β-CTX were HbA1c (β = - 0.049, p < 0.001), body mass index (BMI) (β = - 0.011, p = 0.005), 25(OH)D (β = - 0.003, p = 0.003), FSH (β = 0.002, p = 0.022) and metformin (β = - 0.091, p = 0.001) in postmenopausal T2D women based on multivariate regression analysis. With the increase in HbA1c, FSH decreased significantly (p for trend < 0.001). Mediation analysis demonstrated that FSH partly mediated the suppression of LnP1NP and Lnβ-CTX by HbA1c (β = - 0.009 and - 0.010, respectively), and Lnβ-CTX by BMI (β = - 0.015) when multiple confounders were considered (all p < 0.05).

Conclusion: HbA1c was the crucial determinant contributing to the suppression of BTMs. FSH might play a novel mediation role in BTM suppression due to HbA1c or BMI.

Keywords: Bone turnover markers; Follicle stimulating hormone; HbA1c; Postmenopausal women; Type 2 diabetes.

Serum P1NP, one of the important biomarkers for bone turnover, is commonly used for the prediction of bone fracture and the prognosis of osteoporosis after therapy. We developed a P1NP chemiluminescence assay and evaluated changes in bone metabolism markers in lung transplant patients. The screened 2 P1NP antibodies with constructed antigens and α-1 chain antigens expressed by the Corynebacterium glutamate expression system were applied into assay development. The assay performance was evaluated to examine the reliability. A normal Q-Q plot was used to establish male reference interval. Changes of bone metabolism markers before and after lung transplantation in 19 patients were evaluated. The linear factor R of P1NP reagent was greater than 0.99. The limit of detection was 3.32 ng/ml. The precision of the three batches of P1NP reagents was lower than 8%. Method comparison with Roche P1NP reagent showed that the correlation coefficient R ² was 0.91. In the monitoring of bone mass in a short time, bone metabolism markers can better indicate the change of bone mass, while the traditional bone mineral density detection is lagging behind the bone metabolism markers. P1NP and β-CrossLap to bone mass change in patients after lung transplantation, and P1NP and β-CrossLap are very good clinical markers for bone mass monitoring.

Backgrounds: The incidences of osteoporosis, fracture, and vascular calcification increase concordantly with the progression of chronic kidney disease (CKD). CKD-mineral bone disease (CKD-MBD) induced by hyperphosphatemia is a major pathophysiologic mechanism. The effects of phosphate binders on bone turnover biomarkers and bone mineral density (BMD) in hemodialysis patients are still inconclusive. Our aim is to demonstrate the effects of these phosphate binders on different aspects of CKD-MBD.

Methods: We conducted a prospective cohort of 65 hemodialysis patients to investigate the effect of 12-month monotherapy of phosphate binders composing calcium-based phosphate binders (CPB) or non-calcium-based phosphate binders (NCPB), including sevelamer and lanthanum, on bone turnover biomarkers and BMD changes. The performance of bone turnover biomarkers to predict low BMD was attentively determined.

Results: When compared with CPB, NCPB use was associated with higher levels of bone turnover biomarkers. NCPB was also associated with lower BMD at lumbar and distal radius. Total procollagen type 1 N-terminal propeptide (P1NP), bone-specific alkaline phosphatase (BALP), and tartrate-resistant acid phosphatase 5b (TRAP5b) provided the best performance for diagnosing low BMD in hemodialysis patients.

Conclusions: Switching from CPB to NCPB might increase bone biomarkers and prevent the development of adynamic bone disease. On the contrary, NCPB should be cautiously used in hemodialysis patients who already had low BMD. P1NP, BALP, and TRAP5b could be used to guide the appropriate management, including anti-resorptive and anabolic medications, and predict low BMD in hemodialysis patients treated with phosphate binders. This article is protected by copyright. All rights reserved.

Keywords: bone biomarkers; bone mineral density; chronic kidney disease; hemodialysis; phosphate binders.

The association between selective serotonin reuptake inhibitor (SSRI) treatment and lower bone mineral density (BMD) remains controversial, and further research is required. This study aimed to compare the BMD, levels of bone formation and bone metabolism markers in medicated premenopausal Singaporean women with major depressive disorder (MDD) and matched healthy controls. We examined 45 women with MDD who received SSRI treatment (mean age: 37.64 ± 7) and 45 healthy controls (mean age: 38.1 ± 9.2). BMD at the lumbar spine, total hip and femoral neck were measured using dual-energy X-ray absorptiometry. We also measured bone formation markers, procollagen type 1 N-terminal propeptide (P1NP) and bone metabolism markers, osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa-Β ligand (RANKL). There were no significant differences in the mean BMD in the lumbar spine (healthy controls: 1.04 ± 0.173 vs. MDD patients: 1.024 ± 0.145, p = 0.617, left hip (healthy controls: 0.823 ± 0.117 vs. MDD patients: 0.861 ± 0.146, p = 0.181) and right hip (healthy controls: 0.843 ± 0.117 vs. MDD patients: 0.85 ± 0.135, p = 0.784) between healthy controls and medicated patients with MDD. There were no significant differences in median P1NP (healthy controls: 35.9 vs. MDD patients: 37.3, p = 0.635), OPG (healthy controls: 2.6 vs. MDD patients: 2.7, p = 0.545), RANKL (healthy controls: 23.4 vs. MDD patients: 2178.93, p = 0.279) and RANKL/OPG ratio (healthy controls: 4.1 vs. MDD patients: 741.4, p = 0.279) between healthy controls and medicated patients with MDD. Chronic SSRI treatment might not be associated with low BMD in premenopausal Singaporean women who suffered from MDD. This finding may help female patients with MDD make an informed decision when considering the risks and benefits of SSRI treatment.

Keywords: bone mineral density; major depressive disorder; premenopause; selective serotonin reuptake inhibitor (SSRI); women.

Background: Chemerin has been suggested to be a risk factor for osteoporosis; however, its relationship with osteoporotic fracture is poorly understood. Herein, we intend to explore the association between serum chemerin and osteoporotic fracture.

Methods: A total of 111 elderly women patients diagnosed with osteoporotic fracture were selected as the observation group, and 40 healthy subjects were enrolled as controls. Dual-energy X-ray absorptiometry, enzyme-linked immunosorbent assay, electrochemiluminescence immunoassay, and biochemical analysis were separately performed to determine body bone mineral density (BMD), chemerin levels, bone turnover markers, and other parameters. Pearson's correlation analysis was conducted to examine a relationship between chemerin and laboratory parameters. Moreover, the levels of chemokine-like receptor 1 (CMKLR), C-C motif chemokine receptor-like 2 (CCRL2), collagen type I alpha (COLA1), and runt-related transcription factor-2 (RUNX2) were confirmed by quantitative polymerase chain reaction, and the effect of chemerin on osteogenic differentiation of hFOB1.19 cells was indicated by tartrate-resistant acid phosphatase and alkaline phosphatase double staining.

Results: A higher level of chemerin was generally detected in patients with osteoporotic fracture compared with those without (P<0.05). Compared with controls, lower BMD levels and higher β-CTx and P1NP levels were detected in patients with osteoporotic fracture (all P<0.05). Interestingly, chemerin level was negatively correlated to BMD, but positively related to P1NP and β-CTx. Risk of osteoporotic fracture was 2.75-fold higher in subjects with each standard deviation increment of chemerin. Compared with controls, there were no significant differences in CMKLR1 and CCRL2 mRNA after incubation with osteogenic differentiation medium (all P>0.05), whereas there was a remarkable decrease of COLA1 and RUNX2 after incubation with chemerin for nine days (all P<0.05). Furthermore, prolonged incubation with chemerin enhanced osteoclast differentiation and maturation, consequently contributing to an increased risk of fracture.

Conclusion: Chemerin is a strong and independent risk factor for osteoporosis-related fracture among elderly Chinese women.

Keywords: chemerin; elderly women; osteoporotic fracture; risk factor.