Potential Psychosocial Risk Factors for Chronic TMD: Descriptive Data and Empirically Identified Domains from the OPPERA Case-Control Study

University of Florida, College of Dentistry, and North Florida/South Georgia Veterans Health System, Gainesville, Florida 32610-3628, USA.
The journal of pain: official journal of the American Pain Society (Impact Factor: 4.01). 11/2011; 12(11 Suppl):T46-60. DOI: 10.1016/j.jpain.2011.08.007
Source: PubMed


Case-control studies have consistently associated psychosocial factors with chronic pain in general, and with temporomandibular disorders (TMD) specifically. Moreover, a handful of prospective studies suggest that preexisting psychosocial characteristics represent risk factors for new onset TMD. The current study presents psychosocial findings from the baseline case-control study of the Orofacial Pain Prospective Evaluation and Risk Assessment (OPPERA) cooperative agreement. For this study, 1,633 TMD-free controls and 185 TMD cases completed a battery of psychosocial instruments assessing general psychosocial adjustment and personality, affective distress, psychosocial stress, somatic awareness, and pain coping and catastrophizing. In bivariate and demographically adjusted analyses, odds of TMD were associated with higher levels of psychosocial symptoms, affective distress, somatic awareness, and pain catastrophizing. Among controls, significant gender and ethnic group differences in psychosocial measures were observed, consistent with previous findings. Principal component analysis was undertaken to identify latent constructs revealing 4 components: stress and negative affectivity, global psychosocial symptoms, passive pain coping, and active pain coping. These findings provide further evidence of associations between psychosocial factors and TMD. Future prospective analyses in the OPPERA cohort will determine if the premorbid presence of these psychosocial factors predicts increased risk for developing new onset TMD. PERSPECTIVE: This article reports baseline psychosocial findings from the OPPERA Study, a large prospective cohort study designed to discover causal determinants of TMD pain. Findings indicate significant differences between TMD cases and TMD-free controls across multiple psychosocial constructs, and future analyses will determine whether these psychosocial factors increase risk for new onset TMD.

Download full-text


Available from: Joel Greenspan,
  • Source
    • "Thus, the second null hypothesis has to be rejected—that the sympathetic signal is not contributory to the regulation of potential comorbid factors involved in condylar subchondral bone loss. Although the relationship between TMD and dysphoria— including depression, anxiety, tension, and stress—has been suggested by several clinical reports (Slade et al. 2007; Fillingim et al. 2011; Calixtre et al. 2014), the pathogenic mechanism underlying such a relationship remains obscure. Epidemiologic studies have implicated that psychological stresses such as depression and anxiety are responsible for reduction in BMD of the lumbar spine and proximal femur and increased incidence of osteoporosis (Kahl et al. 2005; Erez et al. 2012). "
    K Jiao · L Niu · X Xu · Y Liu · X Li · F R Tay · M Wang ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Degenerative changes of condylar subchondral bone occur frequently in temporomandibular disorders. Although psychologic stresses and occlusal abnormalities have been implicated in temporomandibular disorder, it is not known if these risks represent synergistic comorbid factors that are involved in condylar subchondral bone degradation that is regulated by the sympathetic nervous system. In the present study, chronic immobilization stress (CIS), chemical sympathectomy, and unilateral anterior crossbite (UAC) were sequentially applied in a murine model. Norepinephrine contents in the subjects' serum and condylar subchondral bone were detected by ELISA; bone and cartilage remodeling parameters and related gene expression in the subchondral bone were examined. Subchondral bone loss and increased subchondral bone norepinephrine level were observed in the CIS and UAC groups. These groups exhibited decreased bone mineral density, volume fraction, and bone formation rate; decreased expressions of osterix, collagen I, and osteocalcin; but increased trabecular separation, osteoclast number and surface, and RANKL expression. Combined CIS + UAC produced more severe subchondral bone loss, higher bone norepinephrine level, and decreased chondrocyte density and cartilage thickness when compared to CIS or UAC alone. Sympathectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine level in all experimental subgroups when compared to the vehicle-treated counterparts. Norepinephrine also decreased mRNA expression of osterix, collagen I, and osteocalcin by mesenchymal stem cells at 7 and 14 d of stimulation and increased the expression of RANKL and RANKL/OPG ratio by mesenchymal stem cells at 2 h. In conclusion, CIS and UAC synergistically promote condylar subchondral bone loss and cartilage degradation; such processes are partially regulated by norepinephrine within subchondral bone. © International & American Associations for Dental Research 2015.
    Journal of dental research 03/2015; 94(6). DOI:10.1177/0022034515577677 · 4.14 Impact Factor
  • Source
    • "The overarching goal of the MAPP Research Network is to provide findings useful for designing future clinical trials and ultimately to improve clinical management for UCPPS patients. Importantly, the design and goals of the MAPP Network are complementary to other large phenotyping efforts for non-urologic pain conditions being conducted, such as the OPPERA study [32]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Urologic chronic pelvic pain syndrome (UCPPS) may be defined to include interstitial cystitis/bladder pain syndrome (IC/BPS) and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). The hallmark symptom of UCPPS is chronic pain in the pelvis, urogenital floor, or external genitalia often accompanied by lower urinary tract symptoms. Despite numerous past basic and clinical research studies there is no broadly identifiable organ-specific pathology or understanding of etiology or risk factors for UCPPS, and diagnosis relies primarily on patient reported symptoms. In addition, there are no generally effective therapies. Recent findings have, however, revealed associations between UCPPS and “centralized” chronic pain disorders, suggesting UCPPS may represent a local manifestation of more widespread pathology in some patients. Here, we describe a new and novel effort initiated by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the U.S. National Institutes of Health (NIH) to address the many long standing questions regarding UCPPS, the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network. The MAPP Network approaches UCPPS in a systemic manner, in which the interplay between the genitourinary system and other physiological systems is emphasized. The network’s study design expands beyond previous research, which has primarily focused on urologic organs and tissues, to utilize integrated approaches to define patient phenotypes, identify clinically-relevant subgroups, and better understand treated natural history and pathophysiology. Thus, the MAPP Network provides an unprecedented, multi-layered characterization of UCPPS. Knowledge gained is expected to provide important insights into underlying pathophysiology, a foundation for better segmenting patients for future clinical trials, and ultimately translation into improved clinical management. In addition, the MAPP Network’s integrated multi-disciplinary research approach may serve as a model for studies of urologic and non-urologic disorders that have proven refractory to past basic and clinical study. Trial registration ClinicalTrials.gov identifier: NCT01098279 “Chronic Pelvic Pain Study of Individuals with Diagnoses or Symptoms of Interstitial Cystitis and/or Chronic Prostatitis (MAPP-EP)”.
    BMC Urology 08/2014; 14(1):57. DOI:10.1186/1471-2490-14-57 · 1.41 Impact Factor
  • Source
    • "All of these studies reported sleep quality as being one dimension represented by one global PSQI score. Some of these studies reported only a global PSQI score and defined poor sleep quality as the global PSQI score being larger than 5 [35,38,39]. However, Yatani et al. [2] used the median cutoff of a global PSQI score ≥ 10 to divide “good” and “poor sleepers”. "
    [Show abstract] [Hide abstract]
    ABSTRACT: This study assessed the dimensional structure of sleep quality with the Pittsburgh Sleep Quality Index (PSQI) and investigated its psychometric properties in cases with temporomandibular disorders (TMD). A convenience sample of 609 TMD cases (age: 37.1 + 13.1 yrs, 18-67 yrs, 85% female) of the multi-center Validation Project meeting Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) and with sufficient PSQI data were included in this study. To investigate PSQI scores' dimensionality, exploratory factor analysis was used. Factors were identified using the Scree plot. To investigate internal consistency, Cronbach's alpha was calculated. Analyses were separately performed for TMD cases with (N = 496) and TMD cases without a pain-related diagnosis (N = 113). The mean PSQI score for all TMD cases was 7.1 + 4.0 units, range: 0-19. The exploratory factor analysis identified one factor for cases with at least one pain-related TMD diagnosis as well as one factor for cases with a pain-free TMD diagnosis that explained 41% of the variance in cases with pain-related TMD and 37% in cases with pain-free TMD. Internal consistency for PSQI scores was alpha of 0.75 in cases with pain-related TMD, alpha of 0.66 in cases with pain-free TMD and alpha = 0.75 for all TMD cases. Sleep quality in TMD patients is a unidimensional construct and can therefore be represented by one summary score; a finding that is in line with previous reports in TMD patients.
    Health and Quality of Life Outcomes 01/2014; 12(1):10. DOI:10.1186/1477-7525-12-10 · 2.12 Impact Factor
Show more