Radiology of Osteoporosis by Stephan Grampp

By Stephan Grampp

This moment variation of ''Radiology of Osteoporosis'' has been absolutely up to date so one can symbolize the present state of the art. It presents a complete evaluation of osteoporosis, the pathologic stipulations that supply upward thrust to osteoporosis, and the issues which are often encountered. a set of adverse situations regarding pitfalls is gifted, with suggestions to their resolution. The ebook could be useful to all with an curiosity in osteoporosis.

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1997) and osteoclastic bone resorption (Oursler et al. 1991). Recently, Eghbali-Fatourechi et al. (2003) demonstrated that in early postmenopausal women, upregulation of RANKL on bone marrow cells is an important determinant of increased bone resorption as a consequence of low estrogen levels. Women with (type 1) osteoporosis appear to have an enhanced responsiveness of bone resorption in the presence of estrogen deficiency (Riggs et al. 2003). Estrogen insufficiency thus results in unrestrained bone resorption and an overall increase in bone turnover, with enhanced calcium mobilization from bone as a consequence.

Studies using quantitative backscattered electron imaging demonstrated that in osteoporotic women the relative calcium content of bone is significantly lower than that of healthy individuals (Roschger et al. 2001). 1 Genetics of Osteoporosis Several pieces of evidence strongly suggest that genetic factors are major determinants of peak bone mass. Bone mineral density is more highly correlated in monozygotic than in dizygotic twins (Pocock et al. 1987). Moreover, family studies noted a significant correlation of bone mass in mother–daughter pairs (Matkovic et al.

In 1994 Morrison et al. demonstrated that bone density is also associated with the frequency of a certain vitamin D receptor allele. Since then the association between bone mineral density and vitamin D receptor polymorphisms has been studied extensively, albeit with disputed results (for review see Cooper 1999). Interestingly, vitamin D receptor polymorphisms appear to influence bone mineral density not only in primary but also in secondary osteoporosis such as in patients with ankylosing spondylitis (Obermayer-Pietsch et al.

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