The diurnal rhythm of bone remodeling suggests nocturnal dietary intervention to be most effective. This study investigated the effect of bedtime ingestion of a calcium-fortified, milk-derived protein matrix (MBPM) or maltodextrin (CON) on acute (0-4 h) blood and 24-h urinary change in biomarkers of bone remodeling in postmenopausal women with osteopenia. In CON, participants received 804 ± 52 mg calcium, 8.2 ± 3.2 µg vitamin D and 1.3 ± 0.2 g/kg BM protein per day. MBPM increased calcium intake to 1679 ± 196 mg, vitamin D to 9.2 ± 3.1 µg and protein to 1.6 ± 0.2 g/kg BM. Serum C-terminal cross-linked telopeptide of type I collagen (CTX) and procollagen type 1 amino-terminal propeptide (P1NP), and urinary N-telopeptide cross-links of type I collagen (NTX), pyridinoline (PYD) and deoxypyridinoline (DPD) was measured. Analyzed by AUC and compared to CON, a -32% lower CTX (p = 0.011, d = 0.83) and 24% (p = 0.52, d = 0.2) increase in P1NP was observed for MBPM. Mean total 24 h NTX excreted in MBPM was -10% (p = 0.035) lower than CON. Urinary PYD and DPD were unaffected by treatment. This study demonstrates the acute effects of bedtime ingestion of a calcium-fortified, milk-based protein matrix on bone remodeling.

The aim of the present study was to analyze the effects of methylprednisolone pulse therapy (MPPT) courses on bone metabolism in patients with Graves' ophthalmopathy (GO). A retrospective analysis of 45 patients with moderate-to-severe active GO who received 1 or 2 courses of MPPT was performed. Of these, 16 patients underwent 2 courses of treatment. Bone metabolic markers and the density of the lumbar spine (L1-4), femoral neck and total hip were measured using a dual-energy X-ray bone density instrument, and the differences in bone metabolism prior to and after treatment were determined for each group and compared. The results indicated that serum I collagen N-terminal peptide (P1NP) and serum β-collagen crosslinked C-terminal peptide (CTX) were markedly decreased after the first pulse of treatment. In those patients who received a second course of MPPT, CTX levels were significantly decreased, but P1NP was not significantly different from the baseline value. CTX and P1NP levels remained unchanged between the first and second course of MPPT; similarly, there were no changes from baseline in 25(OH) vitamin D3 and bone mineral density after the first and second course of MPPT. However, the level of 25(OH) vitamin D3 was significantly elevated after the second course compared with the first course. In conclusion, the side effects of MPPT on bone metabolism were marginal and a second course of MPPT did not worsen bone metabolism. These MPPT regimens may therefore be considered to be a safe and effective treatment option for patients with moderate-to-severe active GO.

There are limited studies regarding bone health among people living with HIV (PLHIV) in Asia. We compared bone mineral density (BMD), serum 25-hydroxyvitamin D (25(OH)D) status and bone turnover markers (serum procollagen type1 N-terminal propeptide (P1NP), osteocalcin (OC) and C-terminal cross-linking telopeptide of type1 collagen) among 302 antiretroviral therapy (ART) naive PLHIV compared to 269 HIV-uninfected controls from Thailand. People aged ≥30 years, with and without HIV infection (free of diabetes, hypertension, and active opportunistic infection) were enrolled. BMD at the lumbar spine, total hip, and femoral neck were measured using Hologic DXA at baseline and at 5 years. We analyzed BMD, serum 25(OH)D levels, and bone turnover markers at the patients' baseline visit. PLHIV were 1.5 years younger and had lower BMI. PLHIV had higher mean serum 25(OH)D level and similar BMD to the controls. Interestingly, PLHIV had significantly lower bone formation (serum P1NP and OC), particularly those with low CD4 count. Only a few participants had low bone mass. ARV naïve middle-aged PLHIV did not have lower BMD or lower vitamin D levels compared to the controls. However, PLHIV had lower bone formation markers, particularly those with low CD4 count. This finding supports the benefit of early ART.

BACKGROUND

The aim of the study was to explore the association between the vitamin D pathway gene variations and the bone biomarkers response to calcium and low dose calcitriol supplementation in postmenopausal Chinese women.

METHODS

A total of 110 healthy postmenopausal Chinese women (61.51 ± 6.93 years) were enrolled. The participants were supplemented with calcium (600 mg/d) and calcitriol (0.25 μg/d), for 1 year. Four biomarkers, serum levels of beta C-terminal cross-linked telopeptides of type I collagen (β-CTX), amino-terminal propeptide of type I collagen (P1NP), parathyroid hormone (PTH) and 25-hydroxyvitamin D [25(OH)D] were measured at baseline and 12-month follow-up. Multivariate regression models were established to explore the statistical association between the change rate of the four biomarkers and 15 key genes within the vitamin D metabolic pathway.

RESULTS

This exclusion process left 98 participants for analysis. Serum levels of P1NP, β-CTX and PTH were significantly decreased at the 12-month follow-up (all p < 0.05). Serum 25(OH)D level had no significant change (p>> 0.05). No association was found between the vitamin D pathway gene polymorphisms and bone biomarkers response to calcium and low dose calcitriol supplementation.

CONCLUSIONS

Genetic background of postmenopausal Chinese women might not influence supplemental response of the biomarkers to calcium and low dose calcitriol.

Pre-exposure prophylaxis (PrEP) with tenofovir disoproxil fumarate-emtricitabine (TDF-FTC) reduces bone mineral density in HIV-uninfected men who have sex with men (MSM). We hypothesized that PrEP with TDF-FTC would increase bone turnover markers (BTMs) at week 24 and that vitamin D supplementation from weeks 24 to 48 would blunt this increase. Participants were from a cohort of 398 MSM and transgender women who received daily TDF-FTC for PrEP. At week 24, a prospective intervention group initiated vitamin D3 4,000 IU daily. Concurrent controls were selected from the cohort who took ≤400 IU/day of vitamin D3 matched by age, race, and body mass index. The primary endpoint was the change in procollagen-I N-terminal propeptide (P1NP) from weeks 24 to 48. Paired t-tests were used to compare changes in BTMs between intervention and controls. Among 48 intervention-control pairs, median age was 33 years. At baseline, 68.9% of the intervention group and 77.3% of controls were vitamin D sufficient (≥20 ng/mL, p = .94). P1NP, C-telopeptide, parathyroid hormone (PTH), and 25-OH vitamin D3 did not increase significantly at week 24. P1NP fell by a mean ± SD of -27.6 ± 49.9 pg/mL from weeks 24 to 48 with vitamin D and -2.5 ± 40.2 pg/mL in controls (p = .01). There were no significant between-group differences in the weeks 24-48 change in C-telopeptide, PTH, or 25-OH vitamin D3. Vitamin D3 supplementation with 4,000 IU/day resulted in a significant reduction in the BTM P1NP compared with controls, suggesting that this intervention has potential to improve bone health during PrEP.

BACKGROUND

Recent studies showed association between hyperaldosteronism and low bone density among patients with primary aldosteronism (PA) due to secondary hyperparathyroidism. Our objective is to assess bone turnover markers (BTM) and bone mineral density (BMD) of PA patients compared to essential hypertension.

METHODS

This was an open-label, prospective, case-controlled study, conducted over 12 months. Fifty-two consecutive patients referred for secondary hypertension were screened. Eighteen patients with confirmed PA (diagnosis based on the Endocrine Society clinical guideline) and seventeen matched controls with essential hypertension were recruited. BTM (CTX and P1NP), BMD, intact parathyroid hormone (iPTH), and bone profile were assessed at baseline and three months following treatment among the PA patients. Calcium intake was assessed using a validated questionnaire. Primary outcomes were the changes of bone markers and BMD following treatment of PA, and their relation to other parameters.

RESULTS

PA patients had significantly lower serum calcium and higher iPTH despite comparable vitamin D levels with control group. Both BTM were significantly higher among the PA group. BMD of lumbar spine, neck of femur and distal radius did not differ between groups. Three months following treatment, there were significant: 1) reduction in BTM; 2) improvement in the lumbar spine BMD; 3) reduction in iPTH level; and 4) increment of serum 25-OH vitamin D level.

CONCLUSIONS

Our findings support that bone loss and potential fracture risk among PA patients are likely a result of aldosterone-mediated secondary hyperparathyroidism. Patients with early PA may already exhibit increased bone turnover despite no significant changes in BMD.

BACKGROUND

Clinical and radiographic examinations detect delayed or nonunion only after the event has occurred. Biochemical markers of bone turnover (BTMs) are promising laboratory tools that offer an early insight into the likelihood of delayed union. We hypothesized that BTMs display temporal variations following fractures and the behavior of BTMs differ between normal and delayed union of fractures.

METHODS

This was a prospective study of patients with closed fracture of tibia treated with intramedullary, interlocking nailing. BTM assays (NTX, BSAP, P1NP and osteocalcin) and clinical and radiographic assessments were obtained preoperatively and postoperatively at 8,12, 24, 36 and 72 weeks. Temporal trend of elevation of serum levels of BTMs post-fracture was the primary assessment criterion and radiographic and clinical assessment of fracture union were the secondary assessment criteria.

RESULTS

The average time for fracture union was 15.24 weeks (range 15-19 weeks). The values of both bone formation and resorption markers peaked at the eighth week following the fracture. Resorption markers returned to baseline by 36 weeks. Among the formation markers, BSAP levels showed the smallest increase and returned to baseline earlier (36 weeks) than P1NP and osteocalcin (72 weeks). P1NP showed the most dramatic change, increasing to 2.5 times the mean baseline level at 8 weeks in normal union of fractures. The levels of bone formation markers (BSAP, OC, PINP) were significantly lower in patients with delayed union. There was no significant difference in the levels of the resorption marker (NTX) between normal and delayed union patients.

CONCLUSIONS

Serial monitoring of biochemical markers of bone turnover can be used as an adjunct to clinical and radiological observations to predict delayed union LEVEL OF EVIDENCE: Level 2 (prospective observational study).

Objective: To characterize relationships between quantitative computed tomography bone mineral density measurements and other qualitative and quantitative imaging measures, as well as clinical metrics, in patients with autosomal dominant osteopetrosis type 2 (ADO2).

Materials and methods: Clinical and radiologic parameters of 9 adults and 3 children with autosomal dominant osteopetrosis type 2 were assessed including lumbar spine quantitative computed tomography (QCT), radiographic skeletal survey (skull base thickening; Erlenmeyer flask deformity; endobone pattern; and spine density pattern (endplate sclerosis, "anvil" appearance, or diffuse sclerosis)), dual-energy x-ray absorptiometry (DXA), tibial peripheral quantitative computed tomography (pQCT) volumetric bone mineral density (vBMD), bone turnover markers, and bone marrow failure or visual impairment.

Results: The skeletal parameter most divergent from normal was lumbar spine QCT Z-score (+ 3.6 to + 38.7). Lumbar QCT Z-score correlated positively with pQCT tibial diaphysis vBMD (Pearson correlation r = 0.73, p = 0.02) and pQCT tibial metaphysis vBMD (r = 0.87, p < 0.01). A trend towards positive lumbar QCT Z-score correlation with serum P1NP/CTX ratio (r = 0.54, p = 0.10) and lumbar DXA Z-score (r = 0.55, p = 0.10) were observed. Bone marrow failure and vision impairment occurred in those with most severe quantitative and qualitative measures, while those with less severe radiographic features had the lowest QCT Z-scores.

Conclusion: Lumbar spine QCT provided the most extreme skeletal assessment in ADO2, which correlated positively with other radiologic and clinical markers of disease severity. Given the quantification of trabecular bone and greater variation from normal with wider range of values, lumbar QCT Z-scores may be useful to determine or detect impact of future treatments.

Keywords: ADO2; Osteoclast; Osteopetrosis; Quantitative computed tomography.

Context: Premenopausal women with idiopathic osteoporosis (IOP) have abnormal skeletal microarchitecture and variable tissue-level bone formation rate (BFR).

Objectives: Compare 6 months (M) of teriparatide versus placebo on areal bone mineral density (aBMD) by dual-energy x-ray absorptiometry (DXA), bone turnover markers (BTMs) and BFR at 3M by quadruple-labeled transiliac biopsy. Characterize 12M and 24M effects of teriparatide on aBMD and whether BTMs and BFR predict response.

Design: 6M phase 2 randomized controlled trial (RCT) followed by open extension.

Setting: Tertiary referral centers.

Patients: Premenopausal women with IOP.

Interventions: A total of 41 women were randomized to either teriparatide 20 mcg (n = 28) or placebo (n = 13). After 6M, those on placebo switched to teriparatide for 24M; those on teriparatide continued for 18M.

Main outcome measures: 6M RCT: Between-group differences in lumbar spine (LS) aBMD (percent change from baseline), 3M BFR, and hypercalcemia. Open-label extension: Within-group change in LS aBMD over 12M and 24M. Secondary outcomes included aBMD change at other sites and relationship between BTMs, BFR, and changes in aBMD.

Findings: Over 6M, LS aBMD increased by 5.5% (95% CI: 3.83, 7.19) in teriparatide and 1.5% (95% CI: -0.73, 3.83) in placebo (P = 0.007). There were increases in 3M BTMs, and BFR (cancellous and endocortical BFR: between-groups P = 0.004). Over 24M, teriparatide increased LS aBMD by 13.2% (95% CI: 10.3, 16.2), total hip by 5.2% (95% CI: 3.7, 6.7) and femoral neck by 5.0% (95% CI: 3.2, 6.7; all P ≤ 0.001). Serum N-terminal propeptides of procollagen type 1 (P1NP) and 3M endocortical BFR were moderately associated with LS aBMD response. Teriparatide was well-tolerated.

Conclusions: Teriparatide increased BFR and formation markers and was associated with marked aBMD improvements in most premenopausal women (82%) with IOP.

Keywords: bone biopsy; bone turnover markers; premenopausal osteoporosis; teriparatide.

Prolonged glucocorticoid (GC) administration causes secondary osteoporosis (GIOP) and non-traumatic osteonecrosis. LLP2A-Ale is a novel bone-seeking compound that recruits mesenchymal stem cells to the bone surface, stimulates bone formation, and increases bone mass. The purpose of this study was to determine if treatment with LLP2A-Ale alone or in combination with parathyroid hormone (PTH) could prevent or treat GIOP in a mouse model. Four-month-old male Swiss-Webster mice were randomized to a prevention study with placebo, GC (day 1-28), and GC + LLP2A-Ale (IV, day 1) or a treatment study with placebo, GC (days 1-56), GC + LLP2A-Ale (IV, day 28), GC + PTH, and GC + LLP2A-Ale + PTH (days 28-56). Mice were killed on day 28 (prevention study) or on day 56 (treatment study). The study endpoints included bone mass, bone strength, serum markers of bone turnover (P1NP and CTX-I) and angiogenesis (VEGF-A), surface-based bone turnover, and blood vessel density. LLP2A-Ale prevented GC-induced bone loss and increased mechanical strength in the vertebral body (days 28 and 56) and femur (day 56). LLP2A-Ale, PTH, and LLP2A-Ale + PTH treatment significantly increased the mineralizing surface, bone formation rate, mineral apposition rate, double-labeled surface, and serum P1NP level on day 56. LLP2A-Ale and PTH treatment increased femoral blood vessel density and LLP2A-Ale increased serum VEGF-A on day 28. Therefore, LLP2A-Ale monotherapy could be a potential option to both prevent and treat GC-induced osteoporosis and bone fragility.

Various markers of bone turnover are already under clinical use in Japan, and mostly for clinical investigation in some countries. Standard values including ranges and variations are summarized in the previous edition of the guideline. The information of additional new markers adapted by government is summarized including clinical features in the new edition 2012. Among the new markers, the methods for measurement for TRACP-5b and ucOC are developed in Japan. As P1NP and TRACP-5b levels are not affected by meals, biological variations are smaller compared with other markers. ucOC is unique because it is to evaluate vitamin K insufficiency for bone. New bone markers adapted in the Japanese guideline 2012 will facilitate clinicians to utilize of metabolic markers of bone for osteoporosis treatment.

Highly sensitive and multiplexed in vitro detection of osteoporosis-related biochemical markers were carried out based on the membrane-based microwave-mediated electrochemical immunoassay (MMeEIA), where we can dramatically reduce the sample preparation time by shortening the incubation time of conjugation to obtain sensitive detection based on three dimensional conjugation of antibodies with target antigens in nylon membrane disk. C-terminal cross-linked telopeptide of type I collagen (CTx), Osteocalcin (OC), parathyroid hormone (PTH), and N-terminal propeptide of type I collagen (P1NP), which can be utilized to monitor the progress of osteoporosis, were quantified using their corresponding antibody immobilized in membranes. Coefficient of variations in this intra- and inter-assays were within 8.0% for all markers. When compared with data obtained from clinically used standard equipment (Roche modular E170), their coefficients of determination, R² values, are mostly more than 0.9. They show that the results obtained from MMeEIA are in good agreement with that from the conventional clinical instruments.

The measurement of biochemical markers for bone metabolism is officially approved in clinical practice for osteoporosis in Japan for the purpose of assessment of bone metabolism and thus for rational selection of anti-osteoporotic drug and the early determination of its effect. In 2011 version of guideline for protection and treatment for osteoporosis and 2012 version of guideline for bone metabolic marker, the novel marker, such as P1NP, which responds precisely to newly-approved PTH (1-34) with bone-formation stimulating effect was focused. Furthermore, the effect of renal dysfunction on the markers which were secreted into urine was also emphasized because of the apparent increases in their serum levels independent of bone metabolic state.

Osteoporosis is a disease with low bone mass and disorganization of the internal microarchitecture of bone tissue. Determination of biochemical markers allows for early diagnosis of changes in bone tissue metabolism. The search for a marker whose biological function could be directly connected with bone metabolism, clearly indicating a connection between its concentration and risk fracture as well as response to treatment, continues. Currently measurement of collagen-derived markers of bone resorption is used in the majority of cases. They are, first of all, telopeptides of collagen type 1 localized on the amino end-N-terminal telopeptide of type 1 collagen (NTX), as well as on the carboxy end-C-telopeptide of type 1 collagen (CTX) of collagen molecule. Among markers of bone synthesis, special attention is paid to the procollagen type 1 carboxy-terminal propeptide (POCP) and procollagen type 1 amino-terminal propeptide (P1NP). Simultaneous application of bone synthesis and resorption markers allows for a full imaging of the bone remodeling process and application of biochemical markers in the diagnosis and therapy of osteoporosis.

OBJECTIVE

Osteoporosis is a major public health problem that reduces bone strength and increases fracture risk. Teriparatide is an established and the only currently available anabolic therapy for the treatment of postmenopausal osteoporosis (PMO) with a recommended daily dose of 20 μg given subcutaneously. However, there are limited data regarding the long-term effect of once-weekly teriparatide therapy on bone mineral density (BMD), bone turnover markers (BTMs), and anabolic bone window.

METHODS

In this prospective observational study, 26 patients with PMO were treated with weekly teriparatide therapy (60 μg) for 2 years. BMD was measured at baseline, 12 months, and 24 months. The bone formation marker type 1 collagen C-terminal propeptide (P1NP) and the bone resorption marker C-terminal telopeptide of type 1 collagen (CTx) were measured at baseline; 6 weeks; and 6, 12, 18, and 24 months.

RESULTS

BMDs at the lumbar spine increased by 3.1% and 10.8% after 1 and 2 years of weekly teriparatide therapy, respectively. The T-score increased significantly at the lumbar spine compared to baseline after 2 years of therapy (P = .015). Serum P1NP levels increased significantly at 6 months (P = .024), peaked at 1 year, and remained above the baseline even after 2 years. Serum CTx levels decreased significantly at 6 months (P = .025) and remained below baseline after 2 years of teriparatide therapy.

CONCLUSIONS

Weekly teriparatide therapy (60 μg) appears to be as effective as daily teriparatide for the treatment of PMO by extending the anabolic bone window.

BACKGROUND

AE = adverse event; BMD = bone mineral density; BTM = bone turnover marker; CTx = C-terminal telopeptide of type 1 collagen; DXA = dual-energy X-ray absorptiometry; iPTH = intact parathyroid hormone; P1NP = type 1 collagen C-terminal propeptide; PMO = postmenopausal osteoporosis.

UNASSIGNED

Controversial experimental and clinical evidences have raised questions regarding the role of B12 and insulin-like growth factor 1 (IGF-1) on osteoblast function and bone health. In this study, we aimed to determine if the serum levels of B12, IGF-1 and procollagen type 1 N-terminal propeptide (P1NP) are associated with different degrees of bone mineral density (BMD).

UNASSIGNED

A total of 287 subjects (190 women and 97 men; mean age 53 years) volunteered for evaluation of BMD and serum levels of B12, IGF-1 and P1NP; BMD at lumbar spine and proximal femur was evaluated by means of dual-energy X-ray absorption (DEXA) and expressed as T-score; serum concentrations of vitamin B12 and IGF1 were measured with a chemiluminescent immunoassay on Access II Beckman Coulter and DiaSorin Liaison XL analyzers, respectively; P1NP was assessed in 61 women and 35 men with reduced T-score on Roche Modular platform.

UNASSIGNED

A total of 101 subjects (66 women and 35 men) had a reduced BMD (T-score < -1) or osteoporosis with a T-score < -2.5, while 186 (124 women and 62 men) had a normal BMD. No significant difference in the B12 levels was observed between the subjects with reduced BMD (mean 265.15 pg/mL, 95% CI: 236 - 294.25) and those with normal BMD (mean 243.91, 95% CI: 225.78 - 262.03) (P = 0.1990); lower levels of IGF-1 were observed in the group with reduced BMD (mean 138.7 pg/mL, 95% CI: 126.75 - 150.83) than in that with normal BMD (mean 167.34, 95% CI: 136.49 - 198.18) (P< 0.001); serum levels of P1NP were significantly lower in 22 subjects younger than 50 years (mean 44.8 ng/mL, 95% CI: 36.4 - 53.1) vs. 74 subjects>> 50 years old (mean 53.3, 95% CI: 34.3 - 72.3) (P < 0.001), and in women (mean 45.3, 95% CI: 37.6 - 52.9) vs. men (mean 62, 95% CI: 23 - 101) (P < 0.001).

UNASSIGNED

We found no significant association between B12 levels and BMD, but significant associations of lower levels of IGF1 with reduced BMD and lower levels of P1NP with younger age and female sex were found; additional studies to further investigate the association of serum levels of B12, growth factors and biochemical turnover markers with human bone health are needed.

OBJECTIVE

Hyperkyphosis, accentuated curvature of the thoracic spine, is often attributed to osteoporosis, yet its underlying pathophysiology is not well understood. Bone turnover markers (BTM) reflect the dynamic process of bone formation and resorption. This study examined the association between serum BTM levels and kyphosis in community-dwelling older adults.

METHODS

Between 2003 and 2006, 760 men and women in the Rancho Bernardo Study age 60 and older had blood drawn and kyphosis measured. Fasting serum was assayed for N-telopeptide (NTX) and procollagen type 1 n-terminal propeptide (P1NP), markers of bone resorption and formation, respectively. Participants requiring two or more 1.7 cm blocks under their head to achieve a neutral supine position were classified as having accentuated kyphosis. Analyses were stratified by sex and use of estrogen therapy (ET). Odds of accentuated kyphosis were calculated for each standard deviation increase in log-transformed BTM.

RESULTS

Mean age was 75 years. Overall, 51% of 341 non-ET using women, 41% of 111 ET-using women, and 75% of 308 men had accentuated kyphosis. In adjusted models, higher P1NP and NTX were associated with decreased odds of accentuated kyphosis in non-ET using women (P1NP: OR = 0.78 [95% CI, 0.58-0.92]; NTX: OR = 0.68 [95% CI, 0.54-0.86]), but not in men or ET-using women (p>> 0.05).

CONCLUSIONS

The selective association of higher bone turnover with reduced odds of accentuated kyphosis in non-ET using women suggests that elevated BTM were associated with a lower likelihood of hyperkyphosis only in the low estrogen/high BTM environment characteristic of postmenopausal women who are not using ET.

The Maternal Vitamin D Osteoporosis (MAVIDOS) trial reported higher total body bone mineral content in winter-born infants of mothers receiving vitamin D supplementation [1000 IU/day cholecalciferol] compared with placebo from 14 weeks gestation until delivery. This sub-study aimed to determine whether antenatal vitamin D supplementation altered postnatal bone formation in response to mechanical stimulation. Thirty-one children born to MAVIDOS participants randomised to either placebo (n=19) or cholecalciferol (n=12) were recruited at age 4-5 years. Children received whole body vibration (WBV) for 10 minutes on 5 consecutive days. Fasting blood samples for bone homeostasis, 25 hydroxyvitamin D (25OHD), parathyroid hormone (PTH), and bone turnover markers (Pro-collagen Type 1 N-terminal propeptide, P1NP; Cross-linked C-telopeptide of Type I Collagen, CTX) were collected pre-WBV and on day 8 (D8). Mean changes (D) in P1NP (ng/ml) between baseline and D8 in the vitamin-D intervention and placebo groups were 40.6 and -92.6 respectively and mean changes (Δ) in CTX (ng/ml) were 0.034 (intervention) and -0.084 (placebo) respectively. Between-group DP1NP difference was 133.2ng/ml [95% CI 0.4, 266.0; p=0.049] and ΔCTX 0.05ng/ml (95% CI -0.159, 0.26ng/mL; p=0.62). Antenatal vitamin-D supplementation resulted in increased P1NP in response to WBV, suggesting early life vitamin D supplementation increases the anabolic response of bone to mechanical loading in children.

OBJECTIVE

Recombinant parathyroid hormone (rPTH) increases bone mineral density (BMD). However, certain other potential effects of rPTH remain to be studied. The aim of this study is to identify whether bone turnover markers, relevant biochemical parameters or total body fat and muscle composition affect the response to rPTH and to establish if these parameters in particular change during treatment.

METHODS

One hundred seventy-two participants were treated with rPTH, and 128 subjects who fully complied with the therapy and completed their investigations including biochemical bone markers and total body composition at baseline, 6 months and 1 year of the treatment were divided into responder and non-responder groups. A total body dual-energy X-ray absorptiometry (DXA) scanner was used to assess the body muscle, fat and bone composition.

RESULTS

rPTH significantly increased BMD spine at 1 year (p = 0.000). Twenty-four-hour urinary calcium was significantly increased at 6 months in the responder group (p = 0.00). There was a trend to an increase in the fat and muscle mass (p = 0.52 and 0.45, respectively), and it was not negatively affected by rPTH. Bone turnover markers (P1NP and OC) did not show statistically significant difference over time between responders and non-responders (p = 0.74 and p = 0.19, respectively).

CONCLUSIONS

Hypercalciuria which is a frequent feature in osteoporotic population may predict non-responders at 6 months of rPTH, and it may help to optimise individual patient's treatment. Unlike endogenous PTH in pathological conditions, rPTH is anabolic to bone and has no detrimental effects on the body fat and muscle composition.

OBJECTIVE

Monthly regimen of minodronate for osteoporosis more than two years has not been reported yet. The aim of this study is to elucidate the effect of monthly minodronate (M-MIN) on bone mineral density (BMD) and serum pentosidine (Pen) during 27 months.

METHODS

The study consisted of 52 newly treated patients (73.3 ± 8.8 years) (new group) and 47 patients (75.9 ± 9.5 years) who were switched from either alendronate or risedronate (switch group). Monthly minodronate (50 mg/every 4 weeks) was administered for 27 months. Lumbar, femoral neck, and total hip BMDs and serum pentosidine were monitored at baseline and after 9, 18, and 27 months of treatment.

RESULTS

In the new condition, lumbar, neck, and total hip BMDs increased significantly by 9.07%, 3.15%, and 3.06%, respectively. Only the lumbar BMD significantly increased in the switch condition. Serum Pen increased in both groups in a time-dependent manner. In the group switch, multivariate logistic regression analysis revealed that the initial change in serum intact procollagen type I N-terminal propeptide (P1NP) at 9 months was an independent predictor of changes in neck and total hip BMDs at 27 months (OR = 1.039, 95% CI 1.003-1.077, p = 0.032 for neck and OR = 1.055, 95% CI 1.009-1.104, p = 0.020 for total hip).

CONCLUSIONS

Monthly minodronate treatment increased BMDs in newly treated patients over 27 months. Serum Pen increased with M-MIN therapy, possibly indicating prolonged bone turnover. The initial 9-month changes in serum P1NP predicted the 27-month changes in hip BMDs when M-MIN replaced alendronate or risedronate.