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Unlabelled: There is good evidence that poor sleep quality increases risk of painful temporomandibular disorder (TMD). However, little is known about the course of sleep quality in the months preceding TMD onset, and whether the relationship is mediated by heightened sensitivity to pain. The Pittsburgh Sleep Quality Index was administered at enrollment into the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) prospective cohort study. Thereafter the Sleep Quality Numeric Rating Scale was administered every 3 months to 2,453 participants. Sensitivity to experimental pressure pain and pinprick pain stimuli was measured at baseline and repeated during follow-up of incident TMD cases (n = 220) and matched TMD-free controls (n = 193). Subjective sleep quality deteriorated progressively, but only in those who subsequently developed TMD. A Cox proportional hazards model showed that risk of TMD was greater among participants whose sleep quality worsened during follow-up (adjusted hazard ratio = 1.73, 95% confidence limits = 1.29, 2.32). This association was independent of baseline measures of sleep quality, psychological stress, somatic awareness, comorbid conditions, nonpain facial symptoms, and demographic characteristics. Poor baseline sleep quality was not significantly associated with baseline pain sensitivity or with subsequent change in pain sensitivity. Furthermore the relationship between sleep quality and TMD incidence was not mediated via baseline pain sensitivity or change in pain sensitivity.Perspective: Subjective sleep quality deteriorates progressively before the onset of painful TMD, but sensitivity to experimental pain does not mediate this relationship. Furthermore, the relationship is independent of potential confounders such as psychological stress, somatic awareness, comorbid conditions, nonpain facial symptoms, and various demographic factors. [ABSTRACT FROM AUTHOR]

Abstract: Persistent stressors associated with sociodemographic disadvantage exert a physiologic toll, labeled “allostatic load,” that contributes to disparities in some health conditions. We investigated the contribution of allostatic load to pain prevalence in U.S. adults. Interviews with 14,184 adults in the 1999–2004 National Health and Nutrition Examination Survey asked about severe headache, pain that lasted >24 hours, and widespread pain. Ten biomarkers of allostatic load were quantified from blood (glycated hemoglobin), serum (C-reactive protein, homocysteine, cholesterol, triglycerides), urine (creatinine, albumin), and physical measurements (body mass index, systolic and diastolic blood pressure). Log-binomial regression models estimated prevalence ratios (PRs) and 95% confidence intervals (95% CIs). Prevalence ranged from 3.4% for widespread pain to 26.9% for pain >24 hours. After adjustment for demographic characteristics, low income was associated with greater prevalence of pain >24 hours (PR = 1.65, 95% CI = 1.49, 1.83), severe headache (PR = 2.05, 95% CI = 1.68, 2.50), and widespread pain (PR = 3.67, 95% CI = 2.56, 5.27). Racial/ethnic minorities had lower prevalence of all 3 pain conditions than non-Hispanic whites. While greater allostatic load was associated with elevated prevalence of pain, allostatic load did not meaningfully attenuate PRs associated with income or race/ethnicity. We conclude that greater pain prevalence among low-income groups is not explained by greater allostatic load. Perspective: In U.S. adults, pain occurs more frequently in lower-income groups, although the relationship is not attributable to their experience of greater allostatic load. While allostatic load contributes to population variation in pain, other etiologic mechanisms contributing to pain are needed to account for income disparities in pain. [Copyright &y& Elsevier]