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| Quintessence Publishing: Journals: JOP |
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Journal of Orofacial Pain
Edited by Barry J. Sessle, BDS, MDS, BSc, PhD, FRSC
Official Journal of the American Academy of Orofacial Pain,
and the European, Australian, Asian, and Ibero-Latin Academies of Craniomandibular Disorders
ISSN 1064-6655
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Publication:
Spring 2003
Volume
17 , Issue
2
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Pain Intensity, Illness Duration, and Protein Catabolism in Temporomandibular Disorder Patients with Chronic Muscle Pain
Neil R. McGregor, BDS, MDSc, PhD, Mariann Zerbes, PhD, Suzanne H. Niblett, BSc, R. Hugh Dunstan, PhD, Timothy K. Roberts, PhD, Henry L. Butt, PhD, Iven J. Klineberg, BSc, MDS, PhD
Pages: 112–124 PMID: 12836499 |
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Aims: To investigate whether the duration of chronic pain in temporomandibular
disorder (TMD) patients is associated with a net
depletion of amino acids, and a distinct process from pain intensity.
Methods: Twenty-nine patients defined by the research diagnostic
criteria/TMD as having Type 1a muscle pain (TMD1A
group), and 34 age- and sex-matched control subjects, were
assessed for variation in urinary organic and amino acid excretion
by gas chromatography-mass spectrometry. Results: The TMD1A
patients’ mean pain intensity, assessed on a visual analog scale
(VAS), was 5.4 (95% confidence limits: 4.5 to 6.3), TMD1A illness
duration was 5.0 ± 1.2 (SD) years, number of body areas
with pain/subject was 6.3 ± 2.4 (range 0 to 10), and symptom
prevalence from the Symptom Check List-90-Revised (SCL-90-R)
was 25.5 ± 11.3 symptoms/subject, which was higher than the
controls (5.2 ± 5.0 symptoms/subject, P .001). TMD1A patient
illness duration was positively correlated with symptom prevalence
and body pain distribution, and all were independent of pain
intensity. The TMD1A patients had: (1) an increased
tyrosine:leucine ratio; and (2) reduced leucine concentrations
(both P .001), which suggests deregulated catabolism. Pain
intensity was associated with: (1) changes in the multivariate urinary
metabolite excretion patterns (P .001); (2) reduced leucine
concentrations (P .001); and (3) increases in total urinary
metabolites (P .04), and in 2 unidentified molecules, UM28 (P
.001) and CFSUM1 (P .002). TMD1A illness duration was
associated with lower (1) urinary metabolite concentrations and
(2) succinic acid and combined glutamine + glutamic acid levels,
suggesting a progressive depletion of metabolite reserves.
Conclusion: In TMD1A patients, total amino acid excretion was
positively correlated with pain intensity and negatively correlated
with illness duration, which indicated that illness duration was
associated with a different set of metabolic anomalies compared
with those identified for pain intensity.
J OROFAC PAIN 2003;17:112–124.
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