Abstract
Aseptic loosening has become the single most important long-term complication of total joint replacements. The pathophysiology of this loosening is multifactorial in origin ranging from mechanical wear, poor surgical technique, thermal damage and the inflammatory response to particulate wear debris. Cytokines are released in response to macrophage activation by particulate wear debris (PWD), the resultant inflammatory cascade stimulates osteoclastic resorption of bone. The failure of remodelling and repair mechanisms may be as a result of Osteonecrosis from cement (PMMA).
Hypothesis: That PMMA increases Osteoblast susceptibility to necrosis and apoptosis following inflammatory challenge.
Materials and Methods: Osteoblast cell cultures were grown on PMMA cement plates and assessed for apoptosis and necrosis by PI exclusion staining, morphological changes on light and electron microscopy and flow cytometry.
Results: PMMA induced osteonecrosis is highest at 1 hour (34.45) in comparison to control levels (4.55). There is no significant change in Apoptosis at 24 hours. Culture of the Osteoblasts on cement and delayed stimulation with TNF-α causes increased Apoptosis and Necrosis.
Conclusion: PMMA cement causes Osteoblast necrosis in the early stages of polymerisation, after 24 hours there is little increase in apoptosis/necrosis. However Osteoblasts that grow in contact with cement are more susceptible to apoptosis and necrosis following TNFα challenge. This may prove to be an important step in the pathogenesis of Aseptic loosening.
The abstracts were prepared by Mr Ray Moran. Correspondence should be addressed to him at the Irish Orthopaedic Association, Secretariat, c/o Cappagh Orthopaedic Hospital, Finglas, Dublin
