The medial malleolus, once believed to be the primary stabilizer of the ankle, has been the topic of conflicting clinical and biomechanical data for many decades. Despite the relevant surgical anatomy being understood for almost 40 years, the optimal treatment of medial malleolar fractures remains unclear, whether the injury occurs in isolation or as part of an unstable bi- or trimalleolar fracture configuration. Traditional teaching recommends open reduction and fixation of medial malleolar fractures that are part of an unstable injury. However, there is recent evidence to suggest that nonoperative management of well-reduced fractures may result in equivalent outcomes, but without the morbidity associated with surgery. This review gives an update on the relevant anatomy and classification systems for medial malleolar fractures and an overview of the current literature regarding their management, including surgical approaches and the choice of implants. Cite this article: Abstract
Pathological assessment of periprosthetic tissues is important, not only for diagnosis, but also for understanding the pathobiology of implant failure. The host response to wear particle deposition in periprosthetic tissues is characterised by cell and tissue injury, and a reparative and inflammatory response in which there is an innate and adaptive immune response to the material components of implant wear. Physical and chemical characteristics of implant wear influence the nature of the response in periprosthetic tissues and account for the development of particular complications that lead to implant failure, such as osteolysis which leads to aseptic loosening, and soft-tissue necrosis/inflammation, which can result in pseudotumour formation. The innate response involves phagocytosis of implant-derived wear particles by macrophages; this is determined by pattern recognition receptors and results in expression of cytokines, chemokines and growth factors promoting inflammation and osteoclastogenesis; phagocytosed particles can also be cytotoxic and cause cell and tissue necrosis. The adaptive immune response to wear debris is characterised by the presence of lymphoid cells and most likely occurs as a result of a cell-mediated hypersensitivity reaction to cell and tissue components altered by interaction with the material components of particulate wear, particularly metal ions released from cobalt-chrome wear particles. Cite this article: Professor N. A. Athanasou. The pathobiology and pathology of aseptic implant failure.
