Table of Contents
Pain Research and Treatment
Volume 2011, Article ID 647967, 13 pages
Review Article

Repeated Muscle Injury as a Presumptive Trigger for Chronic Masticatory Muscle Pain

1Department of Neural and Pain Sciences, University of Maryland, 650 West Baltimore Street, Baltimore, MD 21201, USA
2Graduate Program in Life Sciences, University of Maryland, 650 West Baltimore Street, Baltimore, MD 21201, USA
3Department of Orthopaedics, University of Maryland, 20 Penn Street, Baltimore, MD 21201, USA

Received 31 January 2011; Accepted 14 April 2011

Academic Editor: Cyril Rivat

Copyright © 2011 Dean Dessem and Richard M. Lovering. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


skeletal muscles sustain a significant loss of maximal contractile force after injury, but terminally damaged fibers can eventually be replaced by the growth of new muscle (regeneration), with full restoration of contractile force over time. After a second injury, limb muscles exhibit a smaller reduction in maximal force and reduced inflammation compared with that after the initial injury (i.e., repeated bout effect). In contrast, masticatory muscles exhibit diminished regeneration and persistent fibrosis, after a single injury; following a second injury, plasma extravasation is greater than after a single injury and maximal force is decreased more than after the initial injury. Thus, masticatory muscles do not exhibit a repeated bout effect and are instead increasingly damaged by repeated injury. We propose that the impaired ability of masticatory muscles to regenerate contributes to chronic muscle pain by leading to an accumulation of tissue damage, fibrosis, and a persistent elevation and prolonged membrane translocation of nociceptive channels such as P2X3 as well as enhanced expression of neuropeptides including CGRP within primary afferent neurons. These transformations prime primary afferent neurons for enhanced responsiveness upon subsequent injury thus triggering and/or exacerbating chronic muscle pain.