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BMC Cancer 2008
Does increased local bone resorption secondary to breast and prostate cancer result in increased cartilage degradation?Abstract: The study included 132 breast and prostate cancer patient, where presence of bone metastases was graded according to the Soloway score. Total bone resorption (CTXItotal) and cartilage degradation (CTXII) were determined.Breast and prostate cancer patients with bone metastases revealed significant increased levels of CTXItotal at Soloway scores 1 and higher compared to patients without bone metastases (p < 0.001). CTXII was statistically elevated at score 3 and 4 (p < 0.01). CTXII/CTXItotal significantly decreased at score 3 and 4 (p < 0.001). Levels of CTXItotal, CTXII and CTXII/CTXItotal changed +900%, +130%, and -90%, respectively at Soloway score 4 compared to score 0. The in vitro experiments revealed that osteoclasts released CTXI fragments but not CTXII from bone specimens. The same was observed for cathepsin K.Data suggest that an uncoupling between bone resorption and cartilage degradation occurs in breast and lung cancer patient.Bone metastases are common in breast and prostate cancer patients causing an abnormal high bone remodeling at these sites of metastasis destroying the bone structure. Bone metastases occur in more than 50% of these patients with advanced disease [1,2]. The pathology of bone metastasis is characterized by a vicious cycle where the equilibrium between the bone resorbing cells "osteoclasts" and the bone forming cells "osteoblasts" is unbalanced causing highly elevated activity and number of cells [2].Bone and cartilage degradation can be measured in serum and urine samples by biochemical markers such as bone resorption by CTXI [3] and cartilage degradation by CTXII [4]. These markers have been used extensively for the evaluation of these parameters in basic, pre-clinical and clinical studies [5].Anti-resorptive drugs have been shown to cause a decrease in both cartilage degradation and bone resorption both in postmenopausal women and Paget's disease patients [6-8] indicating a coupling between the two processes. Type II collagen has be
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