Prevalence of hypovitaminosis D in Japanese pregnant women in winter

Prevalence of hypovitaminosis D in Japanese pregnant women in winter

Abstracts / Bone 44 (2009) S121–S130 366 Prevalence of hypovitaminosis D in Japanese pregnant women in winter A. Suzukia, M. Shibataa, T. Sekiyab, S...

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Abstracts / Bone 44 (2009) S121–S130

366 Prevalence of hypovitaminosis D in Japanese pregnant women in winter A. Suzukia, M. Shibataa, T. Sekiyab, S. Sekiguchia, S. Asanoa, Y. Udagawab, M. Itoha a Dept. of Endocrinology, Fujita Health University, Toyoake, Aichi, Japan b Dept. of Obstetrics, Fujita Health University, Toyoake, Aichi, Japan Serum 25-hydroxyvitamin D (25-OHD) concentrations are thought to accurately reflect vitamin D stores, and vitamin D deficiency causes secondary hyperparathyroidism, which can lead to osteomalacia, irreversible bone loss and increased risk of fracture. In addition, recent studies suggest that hypovitaminosis D in mother could influence neuromuscular diseases of their children in the future. We have recently reported that seasonal changes of 25-OHD concentrations in normal Japanese population (Ono et al., J Bone Miner Metab 23:147–151, 2005), and the existence of hypovitaminosis D especially in winter even in sunny area in Japan. The aim of the present study is to investigate the prevalence of hypovitaminosis D in Japanese pregnant women in winter. All of the participants were the residents of Tokai area in Japan (N35.3, E137.0). Serum concentration of 25-OHD in 20 pregnant women after 30th weeks of their gestation was determined by direct radioimmunoassay. Mean 25-OHD levels were 13.5 ng/ml. Eighteen subjects out of 20 women showed hypovitaminosis D, which was defined as serum 25-OHD concentration was equal to or less than 20 ng/ml. Mean serum intact parathyroid hormone (iPTH), serum bone-specific alkaline phosphatase (BAP) and serum type I collagen N-terminal telopeptide (NTx) were 34.5 pg/ml, 24.4U/l, 14.0 nmolBCE/l, respectively. Serum 25-OHD levels were not associated with either iPTH, BAP, NTx, corrected calcium or phosphate concentrations in these subjects. There were four patients with hyperetention during pregnancy, and two mothers had babies with intrauterine growth retardation and one had her baby with major malformation. However, serum concentration of 25-OHD in these subjects were not lower than those in other subjects. In conclusion, our results suggest the high prevalence of hypovitaminosis D in Japanese pregnant women in winter without major effect on calcium-phosphate metabolism.

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density are reduced because PTH increases intracortical porosity. (iv) HypoP patients have normal cortical area and thickness. We propose that endocortical resorption contributes minimally to cortical thinning while cortical density is increased due to reduced intracortical porosity. Trabecular thickness will be increased while numbers are reduced due to reduced age related perforation (which can increase trabecular numbers). We assessed morphology using HR-pQCT in 5 patients with untreated PHPT, median age 58 years (range 30–73); 5 patients with surgically treated PHTP, median age 55 years (range 34–58) and 3 patients with post-surgical HypoP, median age 53 years (range 45–54). Morphology is expressed as z scores (number of standardised deviations from the sex-and age-specific mean). Results for treated and untreated PHPT were combined. Tibial cortical area (mean z score 0.97 ± SEM 0.72 vs-0.36 ± SEM 0.22; p = 0.03) and cortical thickness (mean z score 0.91 ± SEM 0.64 vs − 0.29 ± SEM 0.20; p = 0.03) was increased in HypoP but decreased in PHPT patients (refer to Fig. 1). Tibial trabecular parameters were normal in HypoP but were reduced in PHPT patients (refer to Fig. 1). Similar data were found in the radius (not shown). While inferences are constrained by the small sample sizes in this pilot study, the data is suggestive that PTH excess is deleterious to both cortical and trabecular bone.

Fig. 1. Tibial bone parameters.

(1) Seeman E et al. Journal of Clinical Investigation 1982; 69(6): 1302–1309. (2) Zebaze R et al. Abstract 1101 ASBMR 2008.

doi:10.1016/j.bone.2009.01.280 doi:10.1016/j.bone.2009.01.281

367 Effect of parathyroid hormone deficiency and excess on cortical and trabecular micro-architecture T.D.T. Vu, A. Ghasem-Zadeh, X. Wang, Z. Roger, E. Seeman Austin Health Endocrinology Department, Melbourne University, West Heidelberg, VIC, Australia Patients with secondary hypoparathyroidism (HypoP) have increased bone mineral density (BMD) while patients with primary hyperparathyroidism (PHTP) have reduced BMD at cortical sites but normal or high BMD at trabecular sites. These observations suggest that parathyroid hormone (PTH) excess produces cortical thinning by endocortical resorption but is anabolic at trabecular sites (Seeman E et al. Journal of Clinical Investigation 1982; 69(6): 1302–1309). Recent work suggests that age-related intracortical remodelling produces coalescent cavities trabecularizing the cortex leading to cortical thinning from ‘within' rather than by endocortical resorption (Zebaze R et al. Abstract 1101 ASBMR 2008). We hypothesize that (i) trabecular number and thickness is reduced, not increased in PHTP. (ii) Cortical remnants outside the endocortical surface are ‘seen’ as trabeculae and factitiously elevate trabecular number and thickness. (iii) Cortical area, thickness and

368 Polyethylene particles activate pro-osteoclastogenic signalling pathways in human primary osteoblasts and osteocytes K.J. Welldona, C. Holdingc, D.R. Haynesc, D.W. Howieb, D.M. Findlaya,d, G.J. Atkinsa,d a Bone Cell Biology Group/Discipline of Orthopaedics and Trauma, The University of Adelaide, Adelaide, SA, Australia b Discipline of Orthopaedics and Trauma, The University of Adelaide, Adelaide, SA, Australia c Discipline of Pathology, The University of Adelaide, Adelaide, SA, Australia d Hanson Institute, Adelaide, SA, Australia The reaction of orthopaedic periprosthetic tissues to polyethylene (PE) wear particles is thought to account for much of the osteolysis associated with aseptic loosening and implant failure. While cells of the monocyte/macrophage lineage are implicated, evidence suggests that osteoblastic cells may also be affected by PE. In this study we developed a novel and robust in vitro cell culture system that replicates the 3-dimensional (3D) environment of the osteoblast, while juxtaposing the cells and PE particles. We report that normal human bone-derived cells (NHBC), shown previously to represent human primary osteoblasts, undergo differentiation in