Weakness in Mouse Masticatory Muscles by Repetitive Contractions with Forced Lengthening

The etiology of myofascial tenderness and pain of masticatory muscles in humans is difficult to understand. Parafunctional oral habits such as tooth grinding or vigorous chewing are thought to be factors. The objective of this study was to determine if masticatory muscles are susceptible to weakness...

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Veröffentlicht in:Journal of dental research 1995-02, Vol.74 (2), p.642-648
Hauptverfasser: Hutchins, M.O., Skjonsby, H.S., Brazeau, G.A., Parikh, U.K., Jenkins, R.M.
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container_end_page 648
container_issue 2
container_start_page 642
container_title Journal of dental research
container_volume 74
creator Hutchins, M.O.
Skjonsby, H.S.
Brazeau, G.A.
Parikh, U.K.
Jenkins, R.M.
description The etiology of myofascial tenderness and pain of masticatory muscles in humans is difficult to understand. Parafunctional oral habits such as tooth grinding or vigorous chewing are thought to be factors. The objective of this study was to determine if masticatory muscles are susceptible to weakness and injury induced by repetitive, dynamic, forced-lengthening contractions. Results would support the hypothesis that contraction-induced injuries could occur in hyperactive masticatory muscles of humans in response to parafunctional oral habits. Mice were anesthetized and randomly assigned to three groups: non-treated controls, treated by repetitive passive jaw opening, or treated by repetitive isometric tetanic contractions with lengthening by jaw opening. In each treatment group, masticatory muscle injury was evaluated by contractile tension, plasma creatine kinase, and muscle glycogen. Contractile tension was determined at different stimulation frequencies and was significantly decreased 5 min, 4 h, and 72 h after repetitive contraction/lengthening. Plasma creatine kinase was significantly elevated at 4 but not at 72 h post-treatment in mice subjected to repetitive contraction/lengthening. Masticatory muscle glycogen was not significantly different in any groups at 4 or 72 h post-treatment. These results indicate that contraction injuries can be induced in masticatory muscle of mice by forced lengthening contractions which simulate eccentric contractions.
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Parafunctional oral habits such as tooth grinding or vigorous chewing are thought to be factors. The objective of this study was to determine if masticatory muscles are susceptible to weakness and injury induced by repetitive, dynamic, forced-lengthening contractions. Results would support the hypothesis that contraction-induced injuries could occur in hyperactive masticatory muscles of humans in response to parafunctional oral habits. Mice were anesthetized and randomly assigned to three groups: non-treated controls, treated by repetitive passive jaw opening, or treated by repetitive isometric tetanic contractions with lengthening by jaw opening. In each treatment group, masticatory muscle injury was evaluated by contractile tension, plasma creatine kinase, and muscle glycogen. Contractile tension was determined at different stimulation frequencies and was significantly decreased 5 min, 4 h, and 72 h after repetitive contraction/lengthening. Plasma creatine kinase was significantly elevated at 4 but not at 72 h post-treatment in mice subjected to repetitive contraction/lengthening. Masticatory muscle glycogen was not significantly different in any groups at 4 or 72 h post-treatment. 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Parafunctional oral habits such as tooth grinding or vigorous chewing are thought to be factors. The objective of this study was to determine if masticatory muscles are susceptible to weakness and injury induced by repetitive, dynamic, forced-lengthening contractions. Results would support the hypothesis that contraction-induced injuries could occur in hyperactive masticatory muscles of humans in response to parafunctional oral habits. Mice were anesthetized and randomly assigned to three groups: non-treated controls, treated by repetitive passive jaw opening, or treated by repetitive isometric tetanic contractions with lengthening by jaw opening. In each treatment group, masticatory muscle injury was evaluated by contractile tension, plasma creatine kinase, and muscle glycogen. Contractile tension was determined at different stimulation frequencies and was significantly decreased 5 min, 4 h, and 72 h after repetitive contraction/lengthening. Plasma creatine kinase was significantly elevated at 4 but not at 72 h post-treatment in mice subjected to repetitive contraction/lengthening. Masticatory muscle glycogen was not significantly different in any groups at 4 or 72 h post-treatment. 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Parafunctional oral habits such as tooth grinding or vigorous chewing are thought to be factors. The objective of this study was to determine if masticatory muscles are susceptible to weakness and injury induced by repetitive, dynamic, forced-lengthening contractions. Results would support the hypothesis that contraction-induced injuries could occur in hyperactive masticatory muscles of humans in response to parafunctional oral habits. Mice were anesthetized and randomly assigned to three groups: non-treated controls, treated by repetitive passive jaw opening, or treated by repetitive isometric tetanic contractions with lengthening by jaw opening. In each treatment group, masticatory muscle injury was evaluated by contractile tension, plasma creatine kinase, and muscle glycogen. Contractile tension was determined at different stimulation frequencies and was significantly decreased 5 min, 4 h, and 72 h after repetitive contraction/lengthening. 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subjects Analysis of Variance
Animals
Creatine Kinase - blood
Cumulative Trauma Disorders - complications
Dentistry
Female
Glycogen - metabolism
Masticatory Muscles - metabolism
Masticatory Muscles - physiopathology
Mice
Mice, Inbred Strains
Muscle Contraction - physiology
Muscle Fatigue - physiology
Temporomandibular Joint Dysfunction Syndrome - etiology
title Weakness in Mouse Masticatory Muscles by Repetitive Contractions with Forced Lengthening
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