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.
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.
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