Effect of Experimentally Induced Muscle Pain on Standardized Jaw Opening
Objective: The influence of pain on jaw dynamics is unclear. The Pain Adaptation Model (PAM) proposes that increased antagonist and decreased agonist muscle activity reduces jaw displacement and velocity to protect against further pain. Our aim was to determine the effect of pain on replication of jaw movements and muscle activity. Methods: Fourteen asymptomatic subjects participated in an ethics-approved within-subject design. Experimental pain was induced in right masseter muscle with hypertonic saline (4.5%; 0.2 ml bolus then tonic infusion 6-9 ml/hr for 16 mins). Pain intensity was maintained between 40-60 mm on 100-mm visual analogue scale. During no pain (baseline) and pain conditions, subjects performed standardized jaw opening by tracking a computer-controlled target. A jaw tracking system (JAWS3D, Switzerland) recorded jaw movements from the mid-incisor point. Electromyographic (EMG) activity was recorded from inferior head of lateral pterygoid muscle (location verified by computer tomography) with fine-wire electrodes, and from temporalis, masseter and submandibular muscles with surface electrodes. EMG root-mean-square values were calculated for each 0.5 millimeter increment of mandibular movement. Results: In pain trials, 72% of subjects could perform jaw opening similar to baseline trials (P<0.05) during goal-directed tasks. However, 28% of subjects showed significantly decreased displacement and velocity of movement (P<0.05). With pain, 60% of antagonist muscles significantly increased EMG activity and 14% agonist muscle significantly decreased as in PAM. Nevertheless 68% of agonist muscles showed an increase in EMG activity which was not consistent with PAM. Conclusion: Most subjects were able to perform standardized jaw opening in the presence of pain which may be related to increased agonist and antagonist muscle activity. However, there was some evidence suggesting that pain could decrease jaw velocity and displacement indicative of a protective mechanism. Acknowledgments: Supported by the Australian NHMRC and Australian Dental Research Foundation, Inc.
Division: Australian/New Zealand Division Meeting
Meeting:2005 Australian/New Zealand Division Meeting (Queenstown, New Zealand) Location: Queenstown, New Zealand
Year: 2005 Final Presentation ID:72 Abstract Category|Abstract Category(s):Scientific Groups
Authors
Sae-lee, Daraporn
( University of Sydney, Westmead, N/A, Australia
)
Whittle, Terry
( University of Sydney, Westmead, N/A, Australia
)
Wanigaratne, Kamal
( University of Sydney, Westmead, N/A, Australia
)
Peck, Chris C.
( University of Sydney, Westmead, N/A, Australia
)
Murray, Greg M.
( University of Sydney, Westmead, N/A, Australia
)