11 research outputs found

    Increased serum OPG in atrophic nonunion shaft fractures

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    Background Bone repair alteration is hypothesized for nonunion fracture pathogenesis. Since it is involved in osteoclast regulation, the RANK/RANKL/OPG system (receptor activator of nuclear factor kB/its ligand/osteoprotegerin) may play a role. Materials and methods Serum OPG, free RANKL, bone alkaline phosphatase (BAP), osteocalcin (OC), and urinary deoxypyridinoline (DPD) were determined in 16 male patients (20\u201339 years) with long bone atrophic nonunion fractures. Serum markers were also measured in 18 agematched male controls who healed from the same type of fractures within six months, and in 14 age-matched male controls who were healing from the same fractures one month after injury. One-way ANOVA and Bonferroni\u2019s test were used for statistical analysis. Results Only OPG was significantly higher (0.56 sd 0.11 ng/ml) in the patients compared to healed (0.26 sd 0.04 ng/ml; P\0.001) and healing (0.29 sd 0.09 ng/ml; P\0.001) controls. The patients\u2019 DPD levels were normal. No correlations were found between bone markers and the characteristics of the subjects in all groups. Conclusions A normal steady state of bone metabolism seems to be present in patients with atrophic nonunion fractures, despite the high serum OPG. The reason for the inability of the patients\u2019 OPG to inhibit osteoclastic activity is unknown. Osteoblast activity also appears normal, so another cellular source of OPG can be hypothesized
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