04Dic 2014
wiley-logo

Journal of Bone and Mineral Research, Vol. 29, No. 12, December 2014, pp 2537–2544. doi: 10.1002/jbmr.2309.

The studies found that diffuse matrix damage regions in living cortical bone undergo a direct microstructural and mechanically effective repair. The direct repair of these submicron-size cracks in living bone occurs without activating the bone remodeling that are needed to remove larger, typical linear microcrack from bone. The mechanisms responsible for the direct repair of small crack damage in bone are currently under investigation, but given their position in the bone and extensive infiltration throughout the bone matrix, it seems likely that osteocytes play a central role in this direct repair process.

Autor: Seref-Ferlengez Z, Basta-Pljakic J, Kennedy OD, Philemon CJ, Schaffler MB.
04Dic 2014
wiley-logo

J Bone Miner Res. 2014 Dec;29(12):2529-33. doi: 10.1002/jbmr.2387.

Accordingly, this Perspective provides evidence that the “undetermined significance” portion of the MGUS acronym may be best replaced in favor of the term “monoclonal gammopathy of skeletal significance” (MGSS) in order to more accurately reflect the enhanced skeletal risks inherent in this condition.

Autor: Drake MT.
04Dic 2014
wiley-logo

J Bone Miner Res. 2014 Dec;29(12):2545-51. doi: 10.1002/jbmr.2283

Percentage change from baseline in TH and FN BMD at months 12 and 24 was greater (p < 0.05) in ZOL-treated patients compared with placebo in most subgroups. Treatment-by-subgroup interactions (p <  0.05) indicated that a greater effect on BMD was observed for TH BMD at month 12 in females, in patients in the lower tertile body mass index at baseline (≤22.6 kg/m2), and in patients with baseline FN BMD T-score of ≤ –2.5; for FN BMD in patients who received ZOL for >6 weeks post-surgery; and for TH and FN BMD in patients with a history of one or more prior fractures. All interactions were limited to the first 12 months after treatment with none observed for the 24-month comparisons.

Autor: M.JS,OrwigDL,LylesKW,N.L,BoonenS,AdachiJD,RecknorC,Colón-E.CS,M.P,Bucci-RC,SuG,JohnsonR,PieperCF
04Nov 2014
Springer

Calcif Tissue Int. 2014 Dec;95(6):477-94. doi: 10.1007/s00223-014-9923-y

We have conducted a systematic review of all the various aspects of Gaucher disease, focusing on different skeletal manifestations, pathophysiology of bone alterations, clinical symptoms, and current diagnostic and therapeutic approaches.

Autor: 1. Marcucci G, Zimran A, Bembi B, Kanis J, Reginster JY, Rizzoli R, Cooper C, Brandi ML.
05Oct 2014
wiley-logo

J Bone Miner Res. 2014 Nov;29(11):2357-68. doi: 10.1002/jbmr.2267.

As in humans, FD lesions in mice developed only in the postnatal life; a defined spatial and temporal pattern characterized the onset and progression of lesions across the skeleton. In individual bones, lesions developed through a sequence of three distinct histopathological stages: a primary modeling phase defined by endosteal/medullary excess bone formation and normal resorption; a secondary phase, with excess, inappropriate remodeling; and a tertiary fibrous dysplastic phase, which reproduced a full-blown replica of the human bone pathology in mice of age ≥1 year. Gsα mutations are sufficient to cause FD, and are per se compatible with germline transmission and normal embryonic development in mice. Our novel murine lines constitute the first model of FD.

Autor: Saggio,Remoli,Spica,Cersosimo,Sacchetti,Robey,Holmbeck,Cumano,Boyde,Bianco,Riminucci
05Oct 2014
wiley-logo

J Bone Miner Res. 2014 Nov;29(11):2307-22. doi: 10.1002/jbmr.2373.

Review studies of bone regeneration in genetically modified mouse models, during aging, following environmental exposure, and in the setting of disease that provide insights regarding the role of multipotent cells and their regulation during fracture repair. Complementary animal models and ongoing scientific discoveries define an increasing number of molecular and cellular targets to reduce the morbidity and complications associated with fracture repair. Last, some new and exciting areas of stem cell research such as the contribution of mitochondria function, limb regeneration signaling, and microRNA (miRNA) posttranscriptional regulation are all likely to further contribute to our understanding of fracture repair as an active branch of regenerative medicine.

Autor: Hadjiargyrou M, J O’Keefe RJ.
05Oct 2014
bone logo

Bone 67; 246–256. doi: 10.1016/j.bone.2014.07.014. Epub 2014 Jul 15

Studies using dual-energy X-ray absorptiometry and quantitative computed tomography for longitudinal assessment of changes at the hip have consistently shown increases in areal and volumetric bone mineral density, cortical thickness, and finite element-estimated hip strength in patients treated with teriparatide. Finally, in clinical fracture-outcome trials, treatment with teriparatide has been shown to reduce the risk of nonvertebral fracture, a composite endpoint that includes hip fracture. Taken together, this body of evidence suggests that teriparatide positively affects the hip in patients with osteoporosis.

Autor: Eriksen EF, Keaveny TM, Gallagher ER, Krege JH.
05Sep 2014
wiley-logo

J Bone Miner Res. 2014 Oct;29(10):2131-40. doi: 10.1002/jbmr.2293

In this invited perspective, we highlight the magnitude of the problem across biomedical fields and address the relevance of these concerns to the field of bone and mineral metabolism. We also suggest how our specialty journals, our scientific organizations, and our community of bone and mineral researchers can help to overcome this troubling trend.

Autor: Manolagas SC1, Kronenberg HM.
05Sep 2014
wiley-logo

J Bone Miner Res. 2014 Oct;29(10):2224-9. doi: 10.1002/jbmr.2248.

In conclusion, our study shows that lung cancer screening participants have a substantial vertebral fracture burden. Fractures are more common in current smokers, who also have lower bone density. We could not confirm that COPD is independently associated with vertebral fractures.

Autor: Jong WU1,Jong PA,Vliegenthart R,Isgum I,Lammers JW,Oudkerk M,van der Aalst C,Koning HJ,M.Hoesein FA
05Sep 2014
bone logo

Bone. 2014 Sep 28;69C:139-147. doi: 10.1016/j.bone.2014.09.016. [Epub ahead of print]

This study examined the role of NPP1 in osteocytes, osteoclasts and cortical bone, using a mouse model lacking NPP1 (Enpp1−/−) he cortical bone from Enpp1−/− mice was thinner and less porous, with a larger marrow space. Scanning electron microscopy (SEM) revealed a decrease in the size and number of blood vessel channels in the cortical bone as well as a 40% reduction in the mean plan area of osteocyte lacunae. We noted that the number of viable osteocytes isolated from the long bones of Enpp1−/− mice was decreased ≤50%. In contrast, osteoclast formation and resorptive activity were unaffected by NPP1 deletion. μCT and histological analysis of Enpp1−/− mice also revealed calcification of the joints and vertebrae as well as soft tissues including the whisker follicles, ear pinna and trachea. This calcification worsened as the animals aged. Together, these data highlight the key role of NPP1 in regulating calcification of both soft and skeletal tissues

Autor: Mark O.R.Hajjawi,V.E.MacRae,C. Huesa, A. Boyde, J. L. Millán,Timothy R. Arnett, Isabel R. Orriss