21Jun 2017
MPubmed

This narrative review considers the key challenges facing healthcare professionals and policymakers responsible for providing care to populations in relation to bone health. These challenges broadly fall into four distinct themes: (1) case finding and management of individuals at high risk of fracture, (2) public awareness of osteoporosis and fragility fractures, (3) reimbursement and health system policy and (4) epidemiology of fracture in the developing world. In the developing world, robust epidemiological estimates of fracture incidence are required to inform policy development. As the aging of the baby boomer generation is upon us, this review provides a comprehensive analysis of how bone health can be improved worldwide for all.

Osteoporos Int. 2017 May;28(5):1507-1529. doi: 10.1007/s00198-016-3894-y.

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Harvey NC, McCloskey EV, Mitchell PJ, Dawson-Hughes B, Pierroz DD, Reginster JY, Rizzoli R, Cooper C, Kanis JA.

21Jun 2017
MPubmed

A case series of six women with postmenopausal osteoporosis who had received continuous denosumab for 7 years and were then given a single infusion of zoledronate (5 mg) is reported. During denosumab treatment, bone mineral density (BMD) in the spine increased 18.5% (P = 0.006), and total hip BMD by 6.9% (P = 0.03). Post-zoledronate BMDs were measured 18-23 months after treatment, and there were significant declines at each site (P spine = 0.043, P hip = 0.005). Spine BMD remained significantly above the pre-denosumab baseline (+9.3%, P = 0.003), but hip BMD was not significantly different from baseline (-2.9%). At the time of post-zoledronate BMD measurements, serum PINP levels were between 39 and 60 μg/L (mean 52 μg/L), suggesting that the zoledronate treatment had not adequately inhibited bone turnover. It is concluded that this regimen of zoledronate administration is not adequate to preserve the BMD gains that result from long-term denosumab treatment.

Calcif Tissue Int. 2017 May 13. doi: 10.1007/s00223-017-0288-x.

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Reid IR, Horne AM, Mihov B, Gamble GD

21Jun 2017
MPubmed

Type 1 and type 2 diabetes are generally accepted to be associated with increased bone fracture risk. However, the pathophysiological mechanisms of diabetic bone disease are poorly understood, and whether the associated increased skeletal fragility is a comorbidity or a complication of diabetes remains under debate. Although there is some indication of a direct deleterious effect of microangiopathy on bone, the evidence is open to question, and whether diabetic osteopathy can be classified as a chronic, microvascular complication of diabetes remains uncertain. Here, we review the current knowledge of potential contributory factors to diabetic bone disease, particularly the association between diabetic microangiopathy and bone mineral density, bone structure, and bone turnover. Additionally, we discuss and propose a pathophysiological model of the effects of diabetic microvascular disease on bone, and examine the progression of bone disease alongside the evolution of diabetes.

Lancet Diabetes Endocrinol. 2017 May 22. pii: S2213-8587(17)30134-1. doi: 10.1016/S2213-8587(17)30134-1.

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Shanbhogue VV, Hansen S, Frost M, Brixen K, Hermann AP

21Jun 2017
MPubmed

If oversuppression of bone turnover explained the association between bisphosphonate use and atypical subtrochanteric femur fractures (AFF), this could be reversed with anabolic treatment such as teriparatide. They conducted a prospective, open-label study in patients previously treated with bisphosphonates who sustained AFF, examining the response to 24-month treatment with teriparatide on bone mineral density (BMD), trabecular bone score (TBS), bone turnover markers (BTM), and fracture healing as well as quantitative histomorphometry. Treatment with teriparatide resulted in increases in BTM and lumbar spine BMD, as has been reported for patients without AFF. There was no significant effect of teriparatide on hip BMD, mineralizing surface to bone surface (MS/BS), or TBS and no consistent effect on fracture healing. In the context of a patient who has experienced an AFF after receiving bisphosphonate treatment, therapy with teriparatide for 24 months would be expected to increase BMD and BTM (and probably reduce the risk of fractures resulting from osteoporosis) but should not be relied on to aid in healing of the AFF.

J Bone Miner Res. 2017 May;32(5):1027-1033. doi: 10.1002/jbmr.3081. Epub 2017 Feb 7.

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Watts NB, Aggers D, McCarthy EF, Savage T, Martinez S, Patterson R, Carrithers E, Miller PD.

21Jun 2017
MPubmed

The relative efficacy and harms of balloon kyphoplasty (BK) for treating vertebral compression fractures (VCF) are uncertain. The clinical importance of the greater improvements with BK versus NSM is unclear, may be due to placebo effect, and may not counterbalance short-term AE risks. Outcomes appeared similar between BK and other surgical interventions.Well-conducted randomized trials comparing BK with sham would help resolve remaining ncertainty about the relative benefits and harms of BK.

J Bone Miner Res. 2017 May 17. doi: 10.1002/jbmr.3170. [Epub ahead of print]

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Rodriguez AJ, Fink HA, Mirigian L, Guañabens N, Eastell R, Akesson K, Bauer DC, Ebeling PR

 

25May 2017
MPubmed

This study has as objectives: To estimate the preferences of osteoporotic patients for medication attributes, and analyse data from seven European countries.

In total, 1124 patients completed the experiment, with a sample of between 98 and 257 patients per country. They found statistically significant differences in patients’ preferences for anti-osteoporosis medications between countries, especially for the mode of administration. Our findings emphasized that international treatment recommendations should allow for local adaptation, and that understanding individual preferences is important if we want to improve the quality of clinical care for patients with osteoporosis.

Rheumatology (Oxford). 2017 Apr 6. doi: 10.1093/rheumatology/kex071

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Hiligsmann M, Dellaert BG, Dirksen CD, Watson V, Bours S, Goemaere S, Reginster JY, Roux C, McGowan B, Silke C, Whelan B, Diez-Perez A), Torres E, Papadakis G, Rizzoli R, Cooper C,Pearson G, Boonen A

25May 2017
MPubmed

Bone has recently emerged as a pleiotropic endocrine organ that secretes at least two hormones, FGF23 and osteocalcin, which regulate kidney function and glucose homeostasis, respectively. These findings have raised the question of whether other bone-derived hormones exist and what their potential functions are. Here we identify, through molecular and genetic analyses in mice, lipocalin 2 (LCN2) as an osteoblast-enriched, secreted protein. Loss- and gain-of-function experiments in mice demonstrate that osteoblast-derived LCN2 maintains glucose homeostasis by inducing insulin secretion and improves glucose tolerance and insulin sensitivity. In addition, osteoblast-derived LCN2 inhibits food intake. LCN2 crosses the blood-brain barrier, binds to the melanocortin 4 receptor (MC4R) in the paraventricular and ventromedial neurons of the hypothalamus and activates an MC4R-dependent anorexigenic (appetite-suppressing) pathway. These results identify LCN2 as a bone-derived hormone with metabolic regulatory effects, which suppresses appetite in a MC4R-dependent manner, and show that the control of appetite is an endocrine function of bone.

Nature. 2017 Mar 16;543(7645):385-390. doi: 10.1038/nature21697. Epub 2017 Mar 8.

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Mosialou I, Shikhel S, Liu JM, Maurizi A, Luo N, He Z, Huang Y, Zong H, Friedman RA, Barasch J, Lanzano P, Deng L, Leibel RL, Rubin M, Nicholas T, Chung W, Zeltser LM, Williams KW, Pessin JE, Kousteni S.

25May 2017
MPubmed

Periostin is an extracellular matrix protein, and in bone is expressed most highly in the periosteum. It increases bone formation through osteoblast differentiation, cell adhesion, Wnt signalling and collagen cross-linking. We hypothesised that serum periostin would be high at times of life when cortical modeling is active, in early adulthood and in older age, and that it would correlate with cortical bone measures, bone turnover and hormones that regulate cortical modeling. We conducted a cross-sectional observational study of 166 healthy men and women at three skeletal stages; the end of longitudinal growth (16-18years), peak bone mass (30-32years) and older age (over 70years). We measured serum periostin with a new ELISA optimised for human serum and plasma which recognises all known splice variants (Biomedica). We measured the distal radius and distal tibia with HR-pQCT, and measured serum PINP, CTX, sclerostin, PTH, IGF-1, estradiol and testosterone. Periostin was higher at age 16-18 than age 30-32 (1253 vs 842pmol/l, p<0.001), but not different between age 30-32 and over age 70. Periostin was inversely correlated with tibia cortical thickness and density (R -0.229, -0.233, both p=0.003). It was positively correlated with PINP (R 0.529, p<0.001), CTX (R 0.427, p<0.001) and IGF-1 (R 0.440, p<0.001). When assessed within each age group these correlations were only significant at age 16-18, except for PINP which was also significant over age 70. We conclude that periostin may have a role in IGF-1 driven cortical modeling and consolidation in young adults, but it may not be an important mediator in older adults.

Bone. 2017 Jun;99:8-13. doi: 10.1016/j.bone.2017.03.041. Epub 2017 Mar 16.

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Walsh JS, Gossiel F, Scott JR, Paggiosi MA, Eastell R.