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|Title:||A hypothesis matrix for studying biomechanical factors associated with the initiation and progression of posttraumatic osteoarthritis|
|Source:||Thambyah, A. (2005). A hypothesis matrix for studying biomechanical factors associated with the initiation and progression of posttraumatic osteoarthritis. Medical Hypotheses 64 (6) : 1157-1161. ScholarBank@NUS Repository. https://doi.org/10.1016/j.mehy.2004.12.004|
|Abstract:||In this paper the current theories on how osteoarthritis (OA) may be initiated and progressed is described. This is done in relation to the biomechanical events that would predispose the joint to the degenerative process, as well as further progression of the process within an 'OA' cycle. The relationship between the types of loading to the type of joint damage that occurs is discussed. Subsequently the influence on the rate at which OA progresses from the trauma, is presented within a hypotheses matrix. For the type of tissue damage, four phases are distinguished, phase I: superficial cells or matrix only, phase II: deeper chondral region, phase III: the tidemark or calcified region, and phase IV: subchondral bone region. The biomechanical event (A) is stipulated as having a possibility of six outcomes. (A3) is the direct damage to the calcified cartilage near the tidemark that leads most rapidly into the cycle for OA to develop and progress. Another three outcomes (A1, A2 and A4) involve damage to regions other than the calcified cartilage near the tidemark. These three outcomes involve the cells or matrix, chondral or subchondral regions. It is hypothesised that damage involved in one of these three outcomes results in all likelihood to a new level of joint deficiency or vulnerability. This new predisposition could lead to A3 type outcome and directly into the OA progression cycle or result in more A1, A2 or A4 type outcomes which remains out of the OA cycle. The biomechanical events are therefore used to predict the risk of mechanically driven OA and the rapidity in which it progresses in relation to joint loading. © 2004 Elsevier Ltd. All rights reserved.|
|Source Title:||Medical Hypotheses|
|Appears in Collections:||Staff Publications|
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