@entity1566 ( @entity1566 ) has been associated with a marked @entity79 , especially short-term after injury. The absence of mechanical load, mediated by osteocyte mechanosensory function, seems to be a causative factor related to @entity604 in this condition. However, the pathogenesis and clinical management of this process remain unclear. Therefore, the aim of the study was to analyze the effect of recent @entity1566 on the Wnt pathway antagonists, sclerostin and @entity5741 ( @entity5741 ), and their relationship with bone turnover and @entity79 ( @entity79 ) evolution. Forty-two @entity1 (aged 35        14yrs) with a recent (<6months) complete @entity1566 were prospectively included. Sclerostin and @entity5741 , bone turnover markers (bone formation: PINP, bone ALP; resorption: sCTx) and @entity79 (lumbar spine, proximal femur, total body and lower extremities [DXA]) were assessed at baseline and at 6 and 12 months. The results were compared with a healthy control group. 22/42 @entity1 completed the 12-month follow-up. At baseline, @entity1566 @entity1 showed a marked increase in bone markers (PINP and sCTx), remaining significantly increased at up to 6 months of follow-up. Additionally, they presented significantly increased @entity5741 values throughout the study, whereas sclerostin values did not significantly change. @entity79 markedly decreased at the proximal femur (-20.2        5.4%, p   <   0.01), total body (-5.7        2.2%, p   =   0.02) and lower extremities (-13.1        4.5%, p   =   0.01) at 12 months. Consequently, 59% of @entity1 developed densitometric @entity170 at 12 months. @entity1 with higher @entity5741 values (>58   pmol/L) at baseline showed higher sublesional @entity79 loss. In conclusion, this study shows that short-term after @entity1566 there is a marked @entity79 and @entity604 , the latter associated with an increase in @entity5741 serum levels. The persistence of increased levels of this Wnt antagonist throughout the study and their relationship with the magnitude of @entity604 suggests a contributory role of this mediator in this process.

Effect of recent XXXX on wnt signaling antagonists (sclerostin and @entity5741 ) and their relationship with @entity604 . A 12-month prospective study.

@entity1 :: ('9606', 'Species') :: ['Patients', 'patients'] @entity604 :: ('MESH:D016301', 'Disease') :: ['bone loss'] @entity170 :: ('MESH:D010024', 'Disease') :: ['osteoporosis'] @entity79 :: ('MESH:D001847', 'Disease') :: ['increase in bone loss and bone remodeling', 'increase in bone turnover', 'bone mineral density', 'BMD'] @entity5741 :: ('22943', 'Gene') :: ['Dkk-1', 'Dickkopf'] @entity1566 :: ('MESH:D013119', 'Disease') :: ['Spinal cord injury', 'SCI']
@entity1566 :: (MESH:D013119,Disease) :: ['spinal cord injury']
