Horse riding is a popular competitive sport and leisure pursuit worldwide. Previous research has highlighted the unpredictable and independent nature of horses and high injury risk inherent in travelling at speeds of up to 65kph, 3-metres above the ground on an animal weighing between 450–500kg. In Ireland, jockeys register with the Turf Club as either professional or amateur with the remaining riders participating as unregistered. The aim of this study is to determine the national incidence of acute spinal cord injury (ASCI) and vertebral body injury (VBI) in horse riding in the Republic of Ireland, and to compare and contrast injury characteristics in registered and unregistered riders over an 11-year period (1995–2005). Chart review and structured telephone interview was performed in all cases to determine mechanism of injury, discipline, protective equipment, immediate management and whether the rider considered the injury could be prevented. American Spinal Injuries Association (ASIA) impairment score was used to classify outcome. Data for injuries sustained in competitive racing, for both registered and unregistered riders, was correlated with Irish Turf Club race records to ensure accuracy.
Aseptic loosening is the single most important long-term complication of total joint arthroplasty. Wear debris induced inflammation stimulates osteoclastic resorption of bone. Cellular mechanisms involved in osteoblast viability in PWD induced inflammation is poorly understood. Wear induced inflammation increases osteoblast necrosis and susceptibility to death by apoptosis. PMMA cement has a detrimental effect on osteoblast resistance to apoptosis, and that this is via an receptor mediated pathway. Osteoblast cell cultures (Human and MG63) were grown with and without PMMA cement and assessed for apoptosis and necrosis. TNF-α or Fas antibody simulated inflammation. Viability and apoptosis with PI exclusion, flow cytometry and western blotting assessed response. Cement induced osteoblast necrosis up to 1 hour. This effect was negated after 24 hours. Culture of osteob1asts on cement had no direct effect on spontaneous apoptosis but susceptibility to inflammation was increased. Polymerised cement has no direct effect on osteoblast cell death. Effects are mediated by inhibiting expression of anti-apoptotic protein (Bcl-2), and increasing susceptibility to inflammatory. Osteoblast resistance to death may represent a novel and important factor in aseptic loosening. The role of gene therapy is explored.