Dataset Information

Pressure pain thresholds fluctuate with, but do not usefully predict, the clinical course of painful temporomandibular disorder.

ABSTRACT: Central sensitization elicits pain hypersensitivity and is thought to be causally implicated in painful temporomandibular disorder (TMD). This causal inference is based on cross-sectional evidence that people with TMD have greater sensitivity than controls to noxious stimuli. We tested this inference in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) prospective cohort study of 3258 adults with no lifetime history of TMD when enrolled (visit 1). During 5 years of follow-up, 1 group labeled "persistent TMD cases" (n=72) developed first-onset TMD by visit 2 that persisted ? 6 months until visit 3. Another group labeled "transient TMD cases" (n=75) developed first-onset TMD at visit 2, which resolved by visit 3. Randomly sampled "controls" (n=126) remained TMD-free throughout all 3 visits. At each visit, pressure pain thresholds (PPTs) were measured by algometry at 10 cranial and bodily sites. In persistent TMD case patients, mean PPTs reduced 43 kPa (P<.0001) between visits 1 and 2 and thereafter did not change significantly. In transient TMD case patients, mean PPTs reduced 41 kPa (P<.001) between visits 1 and 2, and then increased 20 kPa (P<.001) by visit 3. These patterns were similar after excluding cranial sites symptomatic for TMD. Importantly, visit 1 PPTs had no clinically useful prognostic value in predicting first-onset TMD (odds ratio [OR]=1.07, P=.15). Among first-onset case patients, visit 2 PPTs were modest predictors of persistent TMD (OR=1.36, P=.002). In this longitudinal study, PPTs reduced when TMD developed then rebounded when TMD resolved. However, premorbid PPTs poorly predicted TMD incidence, countering the hypothesis that PPTs signify mechanisms causing first-onset TMD.

SUBMITTER: Slade GD

PROVIDER: S-EPMC4197095 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature

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Pressure pain thresholds fluctuate with, but do not usefully predict, the clinical course of painful temporomandibular disorder.

Slade Gary D GD Sanders Anne E AE Ohrbach Richard R Fillingim Roger B RB Dubner Ron R Gracely Richard H RH Bair Eric E Maixner William W Greenspan Joel D JD

Pain 20140815 10

Central sensitization elicits pain hypersensitivity and is thought to be causally implicated in painful temporomandibular disorder (TMD). This causal inference is based on cross-sectional evidence that people with TMD have greater sensitivity than controls to noxious stimuli. We tested this inference in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) prospective cohort study of 3258 adults with no lifetime history of TMD when enrolled (visit 1). During 5 years of follow-u ...[more]

PMID: 25130428

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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:This study evaluates contributions of jaw injury and experimental pain sensitivity to risk of developing painful temporomandibular disorder (TMD). Data were from the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) nested case-control study of incident painful TMD. Injury and subsequent onset of painful TMD were monitored prospectively for ≤5 y in a community-based sample of 409 US adults who did not have TMD when enrolled. At baseline, thermal-pressure and pinprick pain sensitivity, as potential effect modifiers, were measured using quantitative sensory testing. During follow-up, jaw injury from any of 9 types of potentially traumatic events was determined using quarterly (3-monthly) health update questionnaires. Study examiners classified incident painful TMD, yielding 233 incident cases and 176 matched controls. Logistic regression models, estimated incidence odds ratios (IORs), and 95% confidence limits (CLs) were used for the association between injury and subsequent onset of painful TMD. During follow-up, 38.2% of incident cases and 13.1% of controls reported 1 or more injuries that were 4 times as likely to be intrinsic (i.e., sustained mouth opening or yawning) as extrinsic (e.g., dental visits, whiplash). Injuries due to extrinsic events (IOR = 7.6; 95% CL, 1.6-36.2), sustained opening (IOR = 5.4; 95% CL, 2.4-12.2), and yawning (IOR = 3.4; 95% CL, 1.6-7.3) were associated with increased TMD incidence. Both a single injury (IOR = 6.0; 95% CL, 2.9-12.4) and multiple injuries (IOR = 9.4; 95% CL, 3.4,25.6) predicted greater incidence of painful TMD than events perceived as noninjurious (IOR = 1.9; 95% CL, 1.1-3.4). Injury-associated risk of painful TMD was elevated in people with high sensitivity to heat pain (IOR = 7.4; 95% CL, 3.1-18.0) compared to people with low sensitivity to heat pain (IOR = 3.9; 95% CL, 1.7-8.4). Jaw injury was strongly associated with elevated painful TMD risk, and the risk was amplified in subjects who had enhanced sensitivity to heat pain at enrollment. Commonly occurring but seemingly innocuous events, such as yawning injury, should not be overlooked when judging prognostic importance of jaw injury.

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:Background:Patients with chronic orofacial pain due to temporomandibular disorders (TMD) display alterations in somatosensory processing at the jaw, such as amplified perception of tactile stimuli, but the underlying mechanisms remain unclear. This study investigated one possible explanation, namely hypervigilance, and tested if TMD patients with unilateral pain showed increased attending to somatosensory input at the painful side of the jaw. Methods:TMD patients with chronic unilateral orofacial pain (n = 20) and matched healthy volunteers (n = 20) performed a temporal order judgment (TOJ) task indicated which one of two tactile stimuli, presented on each side of the jaw, they had perceived first. TOJ methodology allows examining spatial bias in somatosensory processing speed. Furthermore, after each block of trials, the participants rated the perceived intensity of tactile stimuli separately for both sides of the jaw. Finally, questionnaires assessing pain catastrophizing, fear-avoidance beliefs, and pain vigilance, were completed. Results:TMD patients tended to perceive tactile stimuli at the painful jaw side as occurring earlier in time than stimuli at the non-painful side but this effect did not reach conventional levels of significance (p = .07). In the control group, tactile stimuli were perceived as occurring simultaneously. Secondary analyses indicated that the magnitude of spatial bias in the TMD group is positively associated with the extent of fear-avoidance beliefs. Overall, intensity ratings of tactile stimuli were significantly higher in the TMD group than in the control group, but there was no significant difference between the painful and non-painful jaw side in the TMD patients. Discussion:The hypothesis that TMD patients with chronic unilateral orofacial pain preferentially attend to somatosensory information at the painful side of the jaw was not statistically supported, although lack of power could not be ruled out as a reason for this. The findings are discussed within recent theories of pain-related attention.

Dataset Information

Pressure pain thresholds fluctuate with, but do not usefully predict, the clinical course of painful temporomandibular disorder.

Publications

Pressure pain thresholds fluctuate with, but do not usefully predict, the clinical course of painful temporomandibular disorder.

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