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Journal Article

Citation

Nguyen BM. Med. Hypotheses 2013; 80(6): 806-809.

Affiliation

Darebin Community Health Service, Department of Podiatry, 125 Blake Street, East Reservoir, Victoria 3073, Australia. Electronic address: bnguyen@vahs.org.au.

Copyright

(Copyright © 2013, Elsevier Publishing)

DOI

10.1016/j.mehy.2013.03.016

PMID

23566656

Abstract

Knee malalignment and associated pathological abnormal forces transmitted through the knee is thought to provoke joint protective mechanism in reflex arthrogenous muscle inhibition (AMI) and the start of the idiopathic knee osteoarthritis process. The current prevailing hypothesis is AMI initiates quadriceps muscle weakness, cause aberrant loading of the knee joint and focal cartilage destruction. This paper investigates for evidence in the literature if this conceptual framework is consistent with the clinical evidence, and if there is an alternative explanation to AMI hypothesis for the pathogenesis of idiopathic knee osteoarthritis. One crucial question yet to be answered by the AMI hypothesis is; where are the initial aggravating factors of reflex AMI emanate from? AMI hypothesis relies on joint damage and changes in joint homeostasis to provoke a reflex arthrogenous response which can be found later in the development of knee OA. Myofascial trigger point (MTrP) hypothesis only relies on muscle tightness, pain and weakness to detect early pathological neuromuscular changes including knee instability and falls in the elderly. AMI is implicated in the knee OA pathological process but much later on when there are changes in joint homeostasis and joint cartilage damage have occurred. Falls in the elderly is a result of early pathological neuromuscular changes. The MTrP hypothesis is more sensitive and advanced in the early detection of neuromuscular impairment and pathological changes, allowing early intervention, prevention of falls in the elderly and idiopathic knee osteoarthritis.


Language: en

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