Temporomandibular joint disorders (TMD) are a prevalent and costly public health challenge, affecting a large number of otherwise generally healthy adults. Yet they remain poorly understood. Peripheral and central alterations in pain processing systems contribute to the large individual differences seen in the severity and persistence of pain in TMD. This complexity and heterogeneity mandates a comprehensive, multidimensional approach that systematically determines causal and mechanistic linkages to clinical pain. Pain-related catastrophizing (CAT) and sleep continuity disturbance (SCD) are two modifiable risk factors for TMD and other idiopathic pain conditions that influence the pronociceptive mechanisms underlying pain amplification and clinical pain. The proposed study examines whether reducing these risk factors alters pain modulatory systems and pain-evoked inflammatory activity in patients with (TMD). Women meeting RDC criteria for TMD and study entry criteria will be randomized to receive cognitive therapy for catastrophizing, behavioral therapy for sleep continuity disturbance, or TMD disease education. In addition to a comprehensive clinical assessment, polysomnographic measures of sleep and laboratory measures of pain sensitivity and modulatory systems, inflammatory activity, autonomic activity, and adrenocortical function will be completed before after randomization. Reductions in CAT and SCD are expected to reduce pain-evoked inflammatory activity and improve pain modulation, which are expected to precede reductions in clinical TMD pain. With the inclusion of PSG and diaries, our methods allow us to examine potential interplay between CAT and SCD. Specifically, we will examine whether reductions in CAT and SCD to reduce arousal during sleep and whether these effects are mediated by treatment-specific reductions in pre-sleep arousal. Because both sleep disturbance and catastrophizing are modifiable risk factors, our findings promise to promote the development of new treatments and prophylactic approaches for this chronic illness that affects millions of Americans in the prime of their adult lives.

Public Health Relevance

Although poorly understood, the pathophysiology of temporomandibular joint disorders (TMD) includes amplification of pain that may be exacerbated by insomnia and pain-related catastrophizing. The proposed study will examine whether reducing sleep disturbance or reducing pain catastrophizing in patients with TMD changes biological processes involved in pain amplification in TMD.

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Research Project (R01)
Project #
5R01DE019731-05
Application #
8898049
Study Section
Special Emphasis Panel (ZRG1-CFS-M (80))
Program Officer
Riddle, Melissa
Project Start
2011-08-22
Project End
2016-07-31
Budget Start
2015-08-01
Budget End
2016-07-31
Support Year
5
Fiscal Year
2015
Total Cost
$697,353
Indirect Cost
$252,583
Name
Johns Hopkins University
Department
Psychiatry
Type
Schools of Medicine
DUNS #
001910777
City
Baltimore
State
MD
Country
United States
Zip Code
21205
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Finan, Patrick H; Smith, Michael T (2013) The comorbidity of insomnia, chronic pain, and depression: dopamine as a putative mechanism. Sleep Med Rev 17:173-83