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Subjective Sleep Quality Deteriorates Before Development of Painful Temporomandibular Disorder.

ABSTRACT: 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.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.

SUBMITTER: Sanders AE

PROVIDER: S-EPMC4885773 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Subjective Sleep Quality Deteriorates Before Development of Painful Temporomandibular Disorder.

Sanders Anne E AE Akinkugbe Aderonke A AA Bair Eric E Fillingim Roger B RB Greenspan Joel D JD Ohrbach Richard R Dubner Ronald R Maixner William W Slade Gary D GD

The journal of pain 20160221 6

<h4>Unlabelled</h4>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 Numeri ...[more]

PMID: 26902644

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Project description:In 2006, the OPPERA project (Orofacial Pain: Prospective Evaluation and Risk Assessment) set out to identify risk factors for development of painful temporomandibular disorder (TMD). A decade later, this review summarizes its key findings. At 4 US study sites, OPPERA recruited and examined 3,258 community-based TMD-free adults assessing genetic and phenotypic measures of biological, psychosocial, clinical, and health status characteristics. During follow-up, 4% of participants per annum developed clinically verified TMD, although that was a "symptom iceberg" when compared with the 19% annual rate of facial pain symptoms. The most influential predictors of clinical TMD were simple checklists of comorbid health conditions and nonpainful orofacial symptoms. Self-reports of jaw parafunction were markedly stronger predictors than corresponding examiner assessments. The strongest psychosocial predictor was frequency of somatic symptoms, although not somatic reactivity. Pressure pain thresholds measured at cranial sites only weakly predicted incident TMD yet were strongly associated with chronic TMD, cross-sectionally, in OPPERA's separate case-control study. The puzzle was resolved in OPPERA's nested case-control study where repeated measures of pressure pain thresholds revealed fluctuation that coincided with TMD's onset, persistence, and recovery but did not predict its incidence. The nested case-control study likewise furnished novel evidence that deteriorating sleep quality predicted TMD incidence. Three hundred genes were investigated, implicating 6 single-nucleotide polymorphisms (SNPs) as risk factors for chronic TMD, while another 6 SNPs were associated with intermediate phenotypes for TMD. One study identified a serotonergic pathway in which multiple SNPs influenced risk of chronic TMD. Two other studies investigating gene-environment interactions found that effects of stress on pain were modified by variation in the gene encoding catechol O-methyltransferase. Lessons learned from OPPERA have verified some implicated risk factors for TMD and refuted others, redirecting our thinking. Now it is time to apply those lessons to studies investigating treatment and prevention of TMD.

Project description:Temporomandibular disorder (TMD) is a musculoskeletal condition characterized by pain and reduced function in the temporomandibular joint and/or associated masticatory musculature. Prevalence in the United States is 5% and twice as high among women as men. We conducted a discovery genome-wide association study (GWAS) of TMD in 10,153 participants (769 cases, 9,384 controls) of the US Hispanic Community Health Study/Study of Latinos (HCHS/SOL). The most promising single-nucleotide polymorphisms (SNPs) were tested in meta-analysis of 4 independent cohorts. One replication cohort was from the United States, and the others were from Germany, Finland, and Brazil, totaling 1,911 TMD cases and 6,903 controls. A locus near the sarcoglycan alpha ( SGCA), rs4794106, was suggestive in the discovery analysis ( P = 2.6 × 106) and replicated (i.e., 1-tailed P = 0.016) in the Brazilian cohort. In the discovery cohort, sex-stratified analysis identified 2 additional genome-wide significant loci in females. One lying upstream of the relaxin/insulin-like family peptide receptor 2 ( RXP2) (chromosome 13, rs60249166, odds ratio [OR] = 0.65, P = 3.6 × 10-8) was replicated among females in the meta-analysis (1-tailed P = 0.052). The other (chromosome 17, rs1531554, OR = 0.68, P = 2.9 × 10-8) was replicated among females (1-tailed P = 0.002), as well as replicated in meta-analysis of both sexes (1-tailed P = 0.021). A novel locus at genome-wide level of significance (rs73460075, OR = 0.56, P = 3.8 × 10-8) in the intron of the dystrophin gene DMD (X chromosome), and a suggestive locus on chromosome 7 (rs73271865, P = 2.9 × 10-7) upstream of the Sp4 Transcription Factor ( SP4) gene were identified in the discovery cohort, but neither of these was replicated. The SGCA gene encodes SGCA, which is involved in the cellular structure of muscle fibers and, along with DMD, forms part of the dystrophin-glycoprotein complex. Functional annotation suggested that several of these variants reside in loci that regulate processes relevant to TMD pathobiologic processes.

Project description:To evaluate the effect of photobiomodulation therapy (PBMT) on painful temporomandibular disorders (TMD) patients in a randomized, double-blinded, placebo-controlled manner. Participants were divided into a masseter myalgia group (n = 88) and a temporomandibular joint (TMJ) arthralgia group (n = 87) according to the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD). Both groups randomly received PBMT or placebo treatment once a day for 7 consecutive days, one session. The PBMT was applied with a gallium-aluminum-arsenide (GaAlAs) laser (wavelength = 810 nm) at pre-determined points in the masseter muscle (6 J/cm2, 3 regions, 60 s) or TMJ region (6 J/cm2, 5 points, 30 s) according to their most painful site. Pain intensity was rated on a 0-10 numerical rating scale (NRS) and pressure pain thresholds (PPT) and mechanical sensitivity mapping were recorded before and after the treatment on day 1 and day 7. Jaw function was assessed by pain free jaw opening, maximum unassisted jaw opening, maximum assisted jaw opening, maximum protrusion and right and left excursion. Data were analyzed with a mixed model analysis of variance (ANOVA). Pain intensity in arthralgia patients decreased over time (P < 0.001) for both types of interventions, however, PBMT caused greater reduction in pain scores than placebo (P = 0.014). For myalgia patients, pain intensity decreased over time (P < 0.001) but without difference between interventions (P = 0.074). PPTs increased in both myalgia (P < 0.001) and TMJ arthralgia patients over time (P < 0.001) but without difference between interventions (P ≥ 0.614). Overall, PBMT was associated with marginally better improvements in range of motion compared to placebo in both myalgia and arthralgia patients. Pain intensity, sensory function and jaw movements improve after both PBMT and placebo treatments in myalgia and arthralgia patients indicating a substantial non-specific effect of PBMT.

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Subjective Sleep Quality Deteriorates Before Development of Painful Temporomandibular Disorder.

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Subjective Sleep Quality Deteriorates Before Development of Painful Temporomandibular Disorder.

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