The bone turnover marker (BTM) measurement in osteoporosis treatment includes evaluation of bone metabolism status or evaluation of bone loss risk level, determination of fracture risk, and evaluation of drug treatment. Currently, by using the BTM, it has become possible to evaluate and select an effective treatment for osteoporosis. The BTM has become widely used as a clinical test item in actual clinical practice. Patients' low adherence to osteoporosis medication regimens increases the risk of vulnerable fractures and affects the cost effectiveness of therapeutics. A joint working group has been established, with International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) and International Osteoporosis Foundation (IOF) in a central role. The joint policy document of the joint working group is intended to increase the international application of BTM in clinical medicine, and to eliminate blood type I procollagen-N-propeptide (P1NP) and type I collagen cross-linked C-telopeptide (CTX) in observational research and intervention studies, in order to eliminate the inherent uncertainty of these measurements in clinical use. Current osteoporotic drug treatment has been proven to prevent bone fractures, but poor adherence to dosage regimens is an ongoing problem in clinical practice; various attempts have been made to improve adherence. Low adherence to an osteoporosis medication regimen increases the risk of fracture, and affects cost effectiveness. The BTM is an effective indicator in monitoring reactivity to osteoporosis drug therapy, and can be used to individually evaluate guidelines for treatment continuity and medication. In addition, providing BTM information to patients has reportedly improved their adherence to therapeutics, thereby potentially improving both the outcome and cost-effectiveness of osteoporosis drug therapy.

"The guideline for prevention and treatment of osteoporosis 2011" shows methods and precautions for evaluations of therapeutic effects of drugs for osteoporosis, in terms of bone mineral measurements, bone turnover markers, and vertebral deformities and fractures. Bone mineral measurements are effective, but responsible for just some part of the observed reduction in the risk of vertebral fracture. Bone turnover markers enable early and easy evaluations for the effectiveness of drugs, such as bone-resorption inhibitors or bone-formation accelerators. In particular, TRACP-5b and P1NP are user-friendly, because of small daily and day-to-day variations, as well as large amount of changes with therapy. SQ methods are well designed for X-ray evaluations of vertebral deformities and fractures with high convenience and reproducibility, good for not only epidemiological study, but daily practice.

Bone is a dynamic tissue that is in a constant state of remodeling. Bone turnover markers (BTMs), procollagen type I N-terminal propeptide (P1NP) and C-terminal telopeptides of type I collagen (CTX), provide sensitive measures of bone formation and resorption, respectively. This study used ultra-high-resolution metabolomics (HRM) to determine plasma metabolic pathways and targeted metabolites related to the markers of bone resorption and formation in adults. This cross-sectional clinical study included 34 adults (19 females, mean 27.8 years), without reported illnesses, recruited from a US metropolitan area. Serum BTM levels were quantified by an ELISA. Plasma HRM utilized dual-column liquid chromatography and mass spectrometry to identify metabolites and metabolic pathways associated with BTMs. Metabolites significantly associated with P1NP (p < 0.05) were significantly enriched in pathways linked to the TCA cycle, pyruvate metabolism, and metabolism of B vitamins important for energy production (e.g., niacin, thiamin). Other nutrition-related metabolic pathways associated with P1NP were amino acid (proline, arginine, glutamate) and vitamin C metabolism, which are important for collagen formation. Metabolites associated with CTX levels (p < 0.05) were enriched within lipid and fatty acid beta-oxidation metabolic pathways, as well as fat-soluble micronutrient pathways including, vitamin D metabolism, vitamin E metabolism, and bile acid biosynthesis. P1NP and CTX were significantly related to microbiome-related metabolites (p < 0.05). Macronutrient-related pathways including lipid, carbohydrate, and amino acid metabolism, as well as several gut microbiome-derived metabolites were significantly related to BTMs. Future research should compare metabolism BTMs relationships reported here to aging and clinical populations to inform targeted therapeutic interventions.

Keywords: bone; metabolism; microbiome; nutrition; osteoblast; osteoclast.

To evaluate the effects of two fall-prevention and anti-osteoporotic protocols in elderly patients with osteopenia (OPA).

Methods: The present randomized controlled study included patients with OPA (n =123). The age of these patients was ≥80 years old, with the mean age of 83.54 ± 2.99 years, and the male-to-female ratio was 2.97:1.00. Fall-prevention guidance was given to all patients. Patients in the experiment group (n = 62) orally received 600 mg/d of calcium carbonate, 0.5 μg/d of alfacalcidol, and 70 mg/week of alendronate, while patients in the control group (n = 61) orally received 600 mg/d of calcium carbonate and 0.5 μg/d of alfacalcidol for 18 months. The grip strength, gait speed, bone turnover markers, serum calcium, serum phosphorus, parathyroid hormone (PTH), and bone mineral density were measured, and the Timed Up and Go (TUG) test and the chair rising test (CRT) were performed. Falls, fragility fractures, medication compliance, and side effects of the drugs were recorded.

Results: The serum levels of bone turnover markers (type I procollagen amino-terminal peptide [P1NP], type I collagen carboxyl terminal peptide [β-CTx], and osteocalcin [OC]) decreased, while the bone mineral density of the lumbar spine and bilateral femoral neck increased after treatment in the experiment group (P < 0.05, P < 0.01). The rate of change in bone mineral density of the bilateral femoral neck was higher in the experiment group than the control group (3.43% vs 0.03%, P < 0.05; 2.86% vs -0.02%, P < 0.01). After treatment, the proportion of patients with increased hip T scores in the experiment group (66.1%, 41/62) was significantly higher than the proportion (35.0%, 21/60) in the control group (P = 0.001). The incidence of fall decreased in both groups after treatment compared to that before treatment (54.8% vs 33.9% and 54.1% vs 36.7%, respectively; P < 0.05). The incidence of fragility fractures was lower in the experiment group than the control group (8.1% vs 20.0%, P = 0.057). During the intervention period, the incidence of fragility fractures in patients who did not fall (3.8%, 3/79) was significantly lower than that in patients who fell (32.6%, 14/43) (P = 0.000). The risk of fragility fractures was significantly lower in patients who did not fall compared to patients who fell (relative risk: 0.117, 95% confidence interval: 0.035-0.384).

Conclusion: The combination of alendronate sodium with alfacalcidol and calcium can significantly improve the bone mineral density of the lumbar spine and femoral neck. For older patients with OPA, subjectively paying attention to avoiding falls can significantly reduce the risk of fragility fractures.

Keywords: Fall; Fragility fracture; Older; Osteopenia; Sodium alendronate.

Peripheral quantitative computed tomography scans of the distal and midshaft radius were performed in 514 European men aged 40-79 years at baseline and a median of 4.3 years later. Age-related changes in volumetric bone mineral density (vBMD) and bone geometry were greater in men with higher biochemical markers of bone turnover at baseline.

This study aimed to determine prospective change in bone density and geometry at the radius in men and examine the influence of bone turnover markers and sex hormones on that change.

Men aged 40-79 years were recruited from population registers in Manchester (UK) and Leuven (Belgium). At baseline, markers of bone formation (P1NP and osteocalcin) and resorption (β-cTX and ICTP) were assessed. Total and bioavailable testosterone and oestradiol were also measured. Peripheral quantitative computed tomography (pQCT) was used to scan the radius at distal and midshaft sites at the baseline assessment and a median of 4.3 years later.

Five hundred fourteen men, mean (SD) age of 59.6 (10.5) years, contributed to the data. At the midshaft site, there was a significant decrease in mean cortical vBMD (-0.04 %/year), bone mineral content (BMC) (-0.1 %/year) and cortical thickness (-0.4 %/year), while total and medullary area increased (+0.5 and +2.4 %/year respectively). At the distal radius, total vBMD declined (-0.5 %/year) and radial area increased (+0.6 %/year). Greater plasma concentrations of bone resorption and formation markers were associated with greater decline in BMC and cortical area at the midshaft and total vBMD at the distal site. Increased bone resorption was linked with an increase in total and medullary area and decrease in cortical thickness at the midshaft. Sex hormone levels were unrelated to change in pQCT parameters.

Age-related changes in vBMD and bone geometry are greater in men with higher biochemical markers of bone turnover at baseline. Sex hormones have little influence on change in pQCT parameters.

Long-term effects of breastfeeding on maternal bone are not fully understood. Excessive maternal bone loss stimulated by serotonin signaling during lactation may increase bone fragility later in life. We hypothesized inhibiting non-neuronal serotonin activity by feeding a small molecule inhibitor of the rate-limiting enzyme in serotonin synthesis (tryptophan hydroxylase 1; TPH1) would preserve maternal bone post-weaning without affecting neonatal bone. Small molecule TPH1 inhibitor LP778902 (~100 mg/kg) or control chow was fed to C57BL/6 dams throughout pregnancy and lactation and blood collected on days 1 and 21 of lactation. Dams returned to a common diet post-weaning, and were aged to 3 months or 9 months post-weaning. Pups were euthanized at weaning. The effect of TPH1 inhibition on dam and pup femoral bone was determined by micro-computed tomography. Peripartum dietary supplementation with LP778902 decreased maternal serum serotonin concentrations (P=0.0007) and reduced bone turnover, indicated by serum P1NP (P=0.01) and CTX (P=0.02) concentrations, on day 21 of lactation. Repressed bone turnover from TPH1 inhibition was not associated with structural changes in maternal femur at either 3 or 9 months post-weaning. By contrast, neonates exposed to peripartum LP778902 demonstrated differences in trabecular and cortical femoral bone compared to pups from control dams, with fewer (P=0.02) and thinner (P=0.001) trabeculae as well as increased trabecular spacing (P=0.04). Additionally, cortical porosity was increased (P=0.007) and cortical TMD was decreased (P=0.005) in pups of LP778902 dams. Small molecule TPH1 inhibitors should be carefully considered in pregnant and lactating women, given potential risks to neonatal bone development.

In general, markers of bone formation and markers of bone resorption are changing synergistically, so the monitoring of any osteoclastic and any osteoblastic marker should reflect the rate of bone transformation. The aim of the study is to monitor the bone metabolism markers in postmenopausal women with osteoporosis and osteopenia along with the variations caused by the effects of bisphosphonate therapy. The study involved 55 women of average age of 57.95 years, with osteopenia or osteoporosis. The patients with osteoporosis were treated with bisphosphonates (75 mg once a week); the laboratory tests were performed before the treatment and 6 months later. Patients with osteopenia were evaluated at the first assessment and 6 months later. The tests included bone densitometry, dual-energy X-ray absorptiometry, osteocalcin, alkaline phosphatase, collagen 1 N-terminal pro-peptide (P1NP), and beta C telopeptide of type I collagen (CTX). The mean T-score was -2.80 ± 0.63 before therapy and -2.64 ± 0.45 6 months later (p < 0.001). Women with osteoporosis had elevated levels of osteocalcin and P1NP at the first assessment, whereas the alkaline phosphatase level did not change with the treatment. After the introduction of antiresorptive therapy, the levels of osteocalcin and P1NP significantly decreased (p < 0.001). In the group with osteopenia, the biochemical markers activity were increased in both assessments. In patients with osteoporosis, Beta-CTX was increased in the first evaluation, and decreased after treatment (p = 0.001). The results indicate that the assessment of biochemical markers of bone metabolism show excellent results in the assessment of prognosis, monitoring the course and the response to various treatment regimens of osteoporosis and evince strong correlation with standard densitometry and dual-energy X-ray absorptiometry procedures. P1NP and CTX show better diagnostic applicability compared with osteocalcin and alkaline phosphatase. The analysis of the activity of biochemical markers may obtain early information on the therapeutic response, before definitive assessment by bone density measurements.

Adequate protein intake during development is critical to ensure optimal bone gain and to attain a higher peak bone mass later. Using a mild protein restriction model in Balb/C mice consuming 6% of their total energy intake as soy protein (LP-SOY)-for which we observed a significantly lower femoral cortical thickness, bone volume, trabecular number, and thickness reduction-we evaluated the effects of monosodium glutamate (MSG) supplementation at different concentrations (0.5, 1, 5, 10, and 20 g/kg of diet) on bone characteristics in LP-SOY-fed mice. After 6 and 12 weeks, LP-SOY-fed mice had lower BMD and reduced body weight related to lower lean mass, which was associated with a reduced IGF-1 level. The negative effect of the LP-SOY diet on BMD correlated with impaired bone formation. MSG supplementation, at 5, 10, and 20 g/kg of diet, and PTH injection, used as a positive control, were able to improve BMD and to increase osteoblast activity markers (P1NP and osteocalcin), as well as glutamine plasma concentration. An analysis of bone microarchitecture found that cortical bone was less sensitive to protein restriction than trabecular bone, and that MSG ingestion was able to preserve bone quality through an increase of collagen synthesis, although it did not allow normal bone growth. Our study reinforces the view that glutamate can act as a functional amino acid for bone physiology and support clinical investigation of glutamate supplementation in adults characterized by poor bone status, notably as a result of insufficient protein intake. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

Biochemical markers of bone turnover are higher in young adult men than in middle-aged men or young adult women. Nonetheless, little is known about the determinants and clinical significance hereof. The present study examined determinants of serum bone turnover markers in men around peak bone mass age, and explored whether bone turnover at this age predicts subsequent changes in bone mass. We used cross-sectional and longitudinal data from 973 and 428 healthy men, respectively, aged 25 to 45 years at baseline, including baseline procollagen type I amino-terminal propeptide (P1NP), osteocalcin, and C-terminal telopeptide of type I collagen (CTX) from fasting serum samples, baseline questionnaire-assessed physical activity levels, and baseline and follow-up dual-energy X-ray absorptiometry-derived areal bone mineral density (aBMD) and body composition. Mean follow-up time was 12.4 ± 0.4 years. At baseline, all bone turnover markers were inversely associated with total body fat mass (β ≤ -0.20, p < 0.001), and positively with physical activity during sports activities (β ≥ 0.09, p ≤ 0.003), and, albeit not independently from fat mass, total body lean mass (β ≥ 0.20, p ≤ 0.003). Mean annual aBMD changes in the longitudinal cohort were -0.19% ± 0.24% at the total body, -0.14% ± 0.42% at the spine, -0.49% ± 0.47% at the femoral neck, and -0.25% ± 0.37% at the total hip (all p < 0.001). Higher bone turnover markers at baseline were associated with larger decreases in aBMD at all measurement sites (β ≤ -0.08, p ≤ 0.081 for P1NP; β ≤ -0.16, p ≤ 0.002 for osteocalcin; and β ≤ -0.21, p < 0.001 for CTX). In conclusion, our findings show that sports activities and body composition, primarily fat mass, are the main identified determinants of bone turnover in men around peak bone mass age. Further, bone turnover at this age is an important determinant of subsequent changes in bone mass, with higher levels of bone turnover markers being associated with greater decreases in aBMD. © 2017 American Society for Bone and Mineral Research.

The Matrilin3 gene (MATN3) encodes an extracellular matrix protein, which modulates chondrocyte differentiation. The aim of this study was to test for association of MATN3 polymorphisms with bone mineral density (BMD), fracture, vertebral fracture, bone turnover or 25-hydroxyvitamin D [25(OH)D] in postmenopausal women. A community-based population of 1488 postmenopausal women was randomly selected in Beijing. The history of fracture and vertebral fracture was obtained via questionnaire and vertebral X-ray respectively. BMD of lumbar spine (2-4), femoral neck and total hip were measured by dual energy X-ray absorptiometry. Serum N-terminal procollagen of type 1 collagen (P1NP), β-isomerized type I collagen C-telopeptide breakdown products (β-CTX) and 25(OH)D were quantified. Binary logistic regression revealed that Haplotype-4 was significantly associated with vertebral fracture risk in both additive model (p=0.023, OR=1.521) and dominant model (p=0.028, OR=1.623). The significance remained after 10,000 permutation tests to correct multiple testing (p=0.042). Re-selected age matched vertebral fracture case-control groups revealed similar associations in additive model (p=0.014, OR=1.927, 95%CI=1.142-3.253) and in dominant model (p=0.011, OR=2.231, 95%CI=1.200-4.148). However, no significant association was found between MATN3 polymorphisms and serum β-CTX, P1NP, 25(OH)D levels, or BMD. In linear regression, Haplotype-2 approached marginal significance in association with femoral neck BMD T-score (p=0.050), but this would account for only 0.2% of BMD variation in our sample. This study suggests that Haplotype-4 of MATN3 is associated with vertebral fracture risk independent of BMD in Chinese postmenopausal women. Efforts should be made to replicate our finding in other, similar and ethnically diverse, populations.

Objectives: This study aimed to evaluate the effects of royal jelly (RJ) supplementation on bone metabolism in postmenopausal women.

Methods: This was a randomized, double-blind, placebo-controlled clinical trial. Seventy-two healthy postmenopausal women aged 45-60 years within 5 years after menopause were randomized into two groups: women in the RJ group (n = 36) received capsules containing dried RJ (equivalent to 3000 mg of fresh RJ); and women in the placebo group (n = 36) received placebo daily for 6 months. Bone mineral density (BMD) of the lumbar spine (L2-L4) and left proximal femur, hip structural analysis (HSA) of the left hip, and bone turnover markers were measured.

Results: Although women in the placebo group experienced a significant loss of BMD and deterioration in HSA parameters of the femur, no significant differences were found in these parameters in women in the RJ group. The levels of total procollagen type 1 N-terminal propeptide (P1NP) and tartrate-resistant acid phosphatase decreased significantly in the placebo group; however, the total P1NP level, a marker of bone formation, was not significantly different in the RJ group at postintervention compared with baseline.

Conclusion: RJ consumption may ameliorate decreases in femoral BMD and strength in postmenopausal women.

Keywords: Bone mineral density; hip structural analysis; menopause; osteoporosis; royal jelly.

Type 1 diabetes mellitus (T1DM) is associated with low bone mass and a higher risk for fractures. Dickkopf-1 (Dkk1), which inhibits Wnt signaling, osteoblast function, and bone formation, has been found to be increased in the serum of patients with T1DM. Here, we investigated the functional role of Dkk1 in T1DM-induced bone loss in mice. T1DM was induced in 10-week-old male mice with Dkk1-deficiency in late osteoblasts/osteocytes (Dkk1^f/f;Dmp1-Cre, cKO) and littermate control mice by 5 subsequent injections of streptozotocin (40 mg/kg). Age-matched, non-diabetic control groups received citrate buffer instead. At week 12, calvarial defects were created in subgroups of each cohort. After a total of 16 weeks, weight, fat, the femoral bone phenotype and the area of the bone defect were analyzed using µCT and dynamic histomorphometry. During the experiment, diabetic WT and cKO mice did not gain body weight compared to control mice. Further they lost their perigonadal and subcutaneous fat pads. Diabetic mice had highly elevated serum glucose levels and impaired glucose tolerance, regardless of their Dkk1 levels. T1DM led to a 36% decrease in trabecular bone volume in Cre- negative control animals, whereas Dkk1 cKO mice only lost 16%. Of note, Dkk1 cKO mice were completely protected from T1DM-induced cortical bone loss. T1DM suppressed the bone formation rate, the number of osteoblasts at trabecular bone, serum levels of P1NP and bone defect healing in both, Dkk1-deficient and sufficient, mice. This may be explained by increased serum sclerostin levels in both genotypes and the strict dependence on bone formation for bone defect healing. In contrast, the number of osteoclasts and TRACP 5b serum levels only increased in diabetic control mice, but not in Dkk1 cKO mice. In summary, Dkk1 derived from osteogenic cells does not influence the development of T1DM but plays a crucial role in T1DM-induced bone loss in male mice by regulating osteoclast numbers.

Patients with anorexia nervosa (AN) have low serum IGF-I levels that may contribute to a lower bone mineral mass. We investigated the effects of a fermented, protein-fortified, dairy product on serum IGF-I levels in patients with AN during an in-hospital refeeding program.

In this multicenter, randomized, double-blind, placebo-controlled, clinical trial conducted at 3 university hospitals and 3 private clinics in France and Switzerland, 62 women recently admitted with confirmed AN and with a baseline low serum IGF-I level were randomized to 2 daily isocaloric fresh cheese pots containing either 15 g/150 g or 3 g/150 g (controls) of protein for 4 weeks. The primary outcome was the change in IGF-I levels.

In the primary intention-to-treat analysis, mean serum IGF-I levels increased during the intervention phase from 22.9 ± 1.5 to 28.6 ± 1.3 nmol/L (means ± SEM) (+20.2%) in the intervention group and from 20.2 ± 1.2 to 25.7 ± 1.5 nmol/L (+16.8%) in controls. In a preplanned analysis of covariance with repeated measures, the between-group difference was close to statistical significance (P = 0.071). In a post-hoc mixed-regression model analysis, the difference was statistically significant (4.9 nmol/l increase; P = 0.003), as was the change of the ratio IGF-I/IGF-BP3 (P=0.004). There was no between-group difference in biochemical markers of bone turnover (osteocalcin, P1NP, CTX) or in serum parathyroid hormone level. Serum calcium levels slightly increased during the intervention phase in the higher protein group (P = 0.02). IGF-BP2 decreased significantly more in the intervention group during the follow up period at week 4 after supplements cessation (P = 0.019).

Intake of a fermented, protein-fortified, isocaloric dairy product during 4 weeks may slightly increase serum IGF-I levels in women with AN, without significant changes in bone turnover markers.

NCT01823822 (www.clinicaltrials.gov).

Oosthuyse, T, Bosch, AN, Kariem, N, and Millen, AME. Mountain bike racing stimulates osteogenic bone signaling and ingesting carbohydrate-protein compared with carbohydrate-only prevents acute recovery bone resorption dominance. J Strength Cond Res XX(X): 000-000, 2020-Mountain biking, unlike road cycling, includes vibrational accelerations but whether it stimulates osteogenic signaling remains unknown. Furthermore, exercise nutrition influences bone turnover, and the effect of ingesting protein during multiday racing was investigated. We measured plasma bone turnover markers, C-terminal telopeptide of type1-collagen (β-CTX) and N-terminal propeptides of type1-procollagen (P1NP), and osteocyte mechanosensory signaling factor, sclerostin (SOST), corrected for plasma volume change, before (pre-day 1) and 20-60 minutes after (post-day 3) a multiday mountain bike race in 18 male cyclists randomly assigned to ingest carbohydrate-only (CHO-only) or carbohydrate-with-casein protein hydrolysate (CHO-PRO) during racing. Fourteen cyclists (n = 7 per group) completed the race, and data were analyzed with p < 0.05 accepted as significant. Plasma SOST decreased similarly in both groups (mean ± SD, CHO-only: 877 ± 451 to 628 ± 473 pg·ml-1, p = 0.004; CHO-PRO: 888 ± 411 to 650 ± 443 pg·ml-1, p = 0.003), suggesting that osteocytes sense mountain biking as mechanical loading. However, the bone formation marker, P1NP, remained unchanged in both groups, whereas the bone resorption marker, β-CTX, increased in CHO-only (0.19 ± 0.034 to 0.31 ± 0.074 ng·ml-1, p = 0.0036) but remained unchanged in CHO-PRO (0.25 ± 0.079 to 0.26 ± 0.074 ng·ml-1, p = 0.95). Mountain bike racing does stimulate osteogenic bone signaling but bone formation is not increased acutely after multiday mountain biking; investigation for a delayed effect is warranted. The acute recovery increase in bone resorption with CHO-only is prevented by ingesting CHO-PRO during racing.

Context: Dimethandrolone undecanoate (DMAU) is being developed as a male contraceptive. Daily oral administration of DMAU, a potent androgen that is not aromatized, markedly suppresses serum testosterone (T) and estradiol (E2) in healthy men. E2 deficiency can increase bone resorption in men.

Objective: Assess changes in bone turnover markers with DMAU administration in a 28-day study.

Design: Randomized, double-blind, placebo-controlled study.

Setting: Two academic medical centers.

Participants: Healthy men, 18-50 years old (n=81).

Intervention: Men received 0, 100, 200 or 400 mg of oral DMAU for 28 days. Serum C-terminal telopeptide of type I collagen (CTX; bone resorption marker) and procollagen type I amino-terminal propeptide (P1NP; bone formation marker) were measured on days 1 and 28.

Main outcome measures: Changes in bone turnover markers and serum hormones over the treatment period.

Results: On day 28, median serum T and E2 were markedly suppressed in all treatment groups versus placebo (p<0.0001 for both). Change (%) in serum P1NP significantly differed across treatment groups (p=0.007): serum P1NP significantly increased in the 200 mg (5%, IQR -7 to 27%) and 400 mg (22%, IQR -1 to 40%) groups relative to placebo (-8%, IQR -20 to 0%). Change (%) in serum CTX did not differ between groups (p=0.09).

Conclusions: DMAU administration for 28 days to healthy men leads to marked suppression of serum T and E2, yet increases P1NP, a serum marker of bone formation. Longer-term studies of the potent androgen DMAU are warranted to determine its impact on bone health in men.

Keywords: Androgen; Bone formation marker.

UNASSIGNED

Retrospective cohort study.

UNASSIGNED

To assess bone mineral density (BMD) and bone metabolism ≥27 years after surgery in female patients who underwent spinal fusion for adolescent idiopathic scoliosis (AIS) during adolescence and to determine their associations with physical performance.

UNASSIGNED

There are no studies investigating postsurgical BMD in middle-aged AIS patients.

UNASSIGNED

This study included 23 patients who provided informed consent among 229 female patients with AIS who underwent spinal fusion from 1968 until 1988. Average age at the time of observation was 48.8 years. BMD was measured at the left femoral neck, and the levels of two bone metabolism markers-procollagen type 1 N-terminal propeptide (P1NP) and tartrate-resistant acid phosphatase 5b (TRACP-5b)-were measured from blood samples. Physical performance was measured using grip strength, sit-ups, sit-and-reach, side step, and standing long jump.

UNASSIGNED

Mean BMD was 0.784 g/cm2. According to the World Health Organization diagnostic criteria, one subject (4.3%) had osteoporosis, whereas nine subjects (39.1%) had osteopenia. In patients with osteoporosis or osteopenia, P1NP and TRACP-5b levels were high, and BMD loss was because of high metabolic turnover. All calculated standard scores for physical performance were lower in the study cohort than in healthy individuals. There was a positive correlation between BMD and the standard score for grip strength, whereas there were weak positive correlations between BMD and the standard scores for side step and standing long jump.

UNASSIGNED

In female AIS patients who underwent spinal fusion in adolescence, 4.3% and 39.1% had osteoporosis and osteopenia, respectively, ≥27 years after surgery. Exercise performance of these patients was poor compared with the national standards. In these patients, increased physical activity should be encouraged to prevent BMD loss in middle age.

OBJECTIVE

Teriparatide (TPD) is a skeletal anabolic agent used in patients with severe post-menopausal osteoporosis (PMO) and steroid-induced osteoporosis who are at hish risk of fracture. Predictors of therapeutic response to teriparatide in real-life setting are not well characterised. We investigated potential factors associated with teriparatide response in post-menopausal women with established osteoporosis.

METHODS

We carried out a retrospective survey of 48 women, aged 73.2 [7.5] years with severe osteoporosis and prevalent fractures treated with TPD according to the NICE criteria. BMD was measured at baseline, 6-12 and 18-24 months at the lumbar spine (LS), total hip (TH) and femoral neck (FN). Bone turnover markers, serum 25 (OH)vitamin D were determined at 3-12 and 12-24 months.

RESULTS

BMD increased at 6-12 months (% change mean [SEM] 6.5 [1.1] p = 0.004) and 18-24 months (8.45 % [1.2] p<0.001) at the LS. A significant increase in BMD was observed at FN (3.1 [1.3] % p = 0.02). Changes in BMD at the TH was higher in patients younger than 73 years compared to older women (% change in BMD 4.13 [1.64] % v/s -1.7 [1.1] p = 0.007). Baseline 25 (OH) vitamin D correlated with change in P1NP at 3-12 months (r = 0.45 p = 0.049).

CONCLUSIONS

TPD-induced changes in BMD at the TH appears may be dependent on age. Vitamin D status may influence the early anabolic effect to TPD. Our data suggest that these factors may be important considerations when initiating and optimising treatment with TPD, although further larger studies are needed to confirm these findings.

Teriparatide is an anabolic therapy used to treat patients with osteoporosis and is only approved for 2 years of treatment. This is the first study to look at two common osteoporosis drugs in maintaining its beneficial effects: denosumab and zoledronic acid. Denosumab treatment was associated with the greatest increase in bone mineral density (BMD) at the femoral neck and lumbar spine, an amount that was statistically greater than no treatment and zoledronic acid treatment.

BACKGROUND

Teriparatide, a hallmark treatment for osteoporosis, has been shown to increase BMD and bone turnover. This can be measured using BMD scans, N-terminal propeptide of type-1 collagen (P1NP) for bone formation and C-terminal telopeptide (CTX) for bone resorption. This study examines the effects of the two most common antiresorptive drugs prescribed following 2 years of teriparatide treatment: zoledronic acid and denosumab. The purpose of this study is to quantify the beneficial effects of teriparatide and compare the ability of each antiresorptive drug to maintain the effects.

METHODS

Ninety-four patients with prior fragility fractures were identified from a bone health clinic associated with a level I trauma center. All of the study participants completed 2 years of treatment with teriparatide between 2008 and 2013 followed by 2 years of treatment with zoledronic acid, denosumab, or no treatment. After excluding patients with insufficient laboratory data, 64 patients remained for analysis in this retrospective cohort study. Bone mineral density was measured in the lumbar spine and femoral neck.

RESULTS

Following completion of teriparatide, patients who were started on denosumab showed the largest increase in bone mineral density after 2 years of treatment: lumbar spine 4.94% ± 8.2%, femoral neck 5.68% ± 6.7%.

CONCLUSIONS

Patients who elected to discontinue osteoporosis treatment experienced a significant decline in the change in BMD compared to the change on teriparatide putting them at higher risk for recurrence of fragility fractures. Patients on denosumab following teriparatide had the largest increase in BMD.

Introduction: The thyroid parafollicular hormone calcitonin (CT) shows particularly high blood levels in early childhood, a period of high bone turnover, which decrease with increasing age. Data about the physiological role of CT during infancy, childhood, and adolescence are contradictory or lacking.

Objective: We hypothesize that CT demonstrates age-related correlations with parameters of bone growth and turnover as well as with parameters of calcium homeostasis.

Methods: 5,410 measurements of anthropometric data and venous blood samples were collected from 2,636 participants of the LIFE Child study, aged 2 months-18 years. Univariate correlations and multiple regression analysis were performed between serum CT and anthropometric indicators (height standard deviation scores [SDS] and BMI-SDS), markers of calcium (Ca) homeostasis (Ca, parathyroid hormone, 25-OH vitamin D, and phosphate [P]), bone formation (procollagen type 1 N-terminal propeptide [P1NP], osteocalcin), and bone resorption (β-CrossLaps).

Results: CT was significantly associated with Ca (β = 0.26, p < 0.05) and P1NP/100 (β = 0.005, p < 0.05) in children aged 2 months-1.1 years. These relations were independent of age and sex and could not be confirmed in children aged 1.1-8 years. Independent of age, sex, puberty, P, and height SDS CT showed a significant positive relation to Ca (β = 0.26; p < 0.001) in children aged 8-18 years.

Conclusions: Our findings suggest a unique association between CT and Ca in periods of rapid bone growth and point to a possible involvement of CT in promoting bone formation during the first year of life.

Keywords: Bone metabolism; Calcitonin; Calcium homeostasis; Growth.