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Potential Mechanisms of PTA: Cell Death

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Abstract

Post-traumatic osteoarthritis is the development of secondary osteoarthritis after severe traumatic joint injury, especially one that involves an intra-articular fracture. The initial acute injury causes structural damage to the matrix of articular cartilage, which is accompanied by cellular responses ranging from the upregulation of matrix degradative and synthetic pathways, activation, release of oxidants and inflammatory cytokines, and cell death. In the chronic phase, residual alterations in joint biomechanics such as instability secondary to chronic joint laxity (following ligament rupture) or abnormality in articular surface geometry (such as malreduction associated with intra-articular fractures) compound the initial injury and can lead to ongoing matrix degradation with concomitant cell death. This chapter contrasts the various types of cell death that have been documented after mechanical injury, reviews the potential mechanisms and pathways leading to post-traumatic cell death, discusses possibilities for therapy to prevent cell death as a means of reducing ongoing degeneration, and suggests directions for future research that are necessary to advance our understanding of cellular death and the relevant therapeutic implications.

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Correspondence to Shawn P. Grogan Ph.D. or Darryl D. D’Lima M.D., Ph.D. .

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Grogan, S.P., Lotz, M.K., D’Lima, D.D. (2015). Potential Mechanisms of PTA: Cell Death. In: Olson, MD, S., Guilak, PhD, F. (eds) Post-Traumatic Arthritis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-7606-2_15

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