Increased sclerostin associated with stress fracture of the third metacarpal bone in the Thoroughbred Racehorse

29 Jan 2018

Abstract Objectives: The exact aetiopathogenesis of microdamage induced long bone fractures remains unknown. These fractures are likely the result of inadequate bone remodeling in response to damage. This study aims to identifiesy an association of osteocyte apoptosis, the presence of osteocytic osteolysis and any alterations in sclerostin expression with fracture of the third metacarpal bone of (Mc-III) thoroughbred (TB) racehorses. Methods: 30 Mc-III bones were obtained; 10 from bones fractured during racing, 10 from the contralateral limb and 10 from control horses. Each Mc- III bone was divided into fracture site, condyle, condylar groove and sagittal ridge. Microcracks and diffuse microdamage were quantified. Apoptotic osteocytes were measured using TUNEL staining. Cathepsin K, matrix metalloproteinase -13 (MMP-13), HtrA1 and sclerostin expression was analysed. of apoptotic cells between contralateral limb and unraced control, however, there were significantly less apoptotic cells in fractured samples (p<0.02). Immunohistochemistry showed that in the deep zones of the fractured samples sclerostin expression was significantly higher (p<0.03) of the total number of osteocytes. No increase in cathepsin K, MMP-13 or HtrA1 was present.