Bone
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The epidemiology and trends in wrist fracture admissions to public and private acute hospitals in New South Wales (NSW), Australia, between July 1993 and June 2003 were examined using routinely collected hospital separations statistics. During the study period, the number of hospital separations for wrist fractures increased by 71% in men, an average yearly increase of 6.5%, and by 43% in women, an average yearly increase of 3.9%. ⋯ This decrease was more pronounced in males and was accompanied by a rise in the proportion of wrist fractures resulting from high energy mechanisms such as transport, violence and machinery-related incidents. The difference in hospitalised wrist fracture rates between men and women could not be explained solely on the basis of the role played by osteoporosis, indicating the need for more research to improve our understanding of the underlying factors of this type of fracture in older people.
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Large bony defects and non-unions are still a complication in trauma and orthopedic surgery. Treatment strategies include the use of autogenous materials (iliac crest), allogenic bone, bone substitutes, and currently stimulation with growth factors such as BMP-2, BMP-7 or the growth factors containing platelet-rich plasma (PRP). Another source of bone graft material might be the cuttings produced during intramedullary reaming. ⋯ BMP-4 was not measurable in any sample. The bony reaming debris is a rich source of growth factors with a content comparable to that from iliac crest. The irrigation fluid from the reaming also contains growth factors.
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Bone disorders with increased osteoclastic bone resorption are frequently associated with bone pain and inhibitors of osteoclasts reduce bone pain. Osteoclasts degrade bone minerals by secreting protons through the vacuolar H+-ATPase, creating acidic microenvironments. Because acidosis is a well-known cause of pain, we reasoned that osteoclasts cause pain through proton secretion. ⋯ Moreover, F-11 cells transfected with the transient receptor potential channel vanilloid subfamily member 1 (TRPV1) showed increased acid-induced nuclear c-Fos expression compared with parental F-11 cells. Finally, bafilomycin A1, an inhibitor of the vacuolar H+-ATPase, reversed the hyperalgesia and down-regulated ASIC1a mRNA expression in the DRGs. These results led us to propose that osteoclasts play a part in CFA-induced inflammatory pain through an activation of the acid-sensing receptors including ASICs and TRPV1 by creating acidosis.