Increased serum OPG in atrophic nonunion shaft fractures |
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Authors: | Daniele Marchelli Luca P Piodi Costantino Corradini Luca Parravicini Cesare Verdoia Fabio M Ulivieri |
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Institution: | 1. U.O. Medicina Nucleare, Centro per la Diagnosi e la Terapia delle Osteoporosi, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Via F. Sforza 35, 20122, Milan, Italy 2. U.O. Gastroenterologia 2, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Via F. Sforza 35, 20122, Milan, Italy 3. Clinica Ortopedica e Traumatologica, Centro Studi e Ricerche in Traumatologia dello Sport, Università degli Studi di Milano c/o I Divisione, Istituto Ortopedico G. Pini, Piazza A. Ferrari 1, 20122, Milan, Italy
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Abstract: | 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 (20–39 years) with long bone atrophic nonunion fractures. Serum markers were also measured in 18 age-matched
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’s 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’ 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’ 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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Keywords: | Bone turnover markers Nonunion Osteoprotegerin Shaft fractures |
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