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Temporomandibular disorders (TMD) are idiopathic orofacial pain conditions. Inflammation—particularly elevated circulating levels of interleukin-6 (IL-6)—is associated with pain symptoms. Prior work in healthy samples has shown that trait positive affect (PA) is associated with lower IL-6, but that poor sleep attenuates PA and elevates IL-6. Although poor sleep has been associated with increased IL-6 in chronic pain, the effects of trait PA on IL-6 and potential moderation by sleep are not known. We thus investigated the effect of PA on circulating IL-6 and moderation of that effect by sleep, in 118 women with TMD and at least subclinical insomnia. Participants completed the insomnia severity index at baseline and subsequently completed a 14-day daily diary assessing sleep continuity, PA and negative affect. Sleep continuity was objectively assessed with wrist actigraphy over the same period. Both diary and actigraphy data were aggregated by computing person means. IL-6 was measured via blood samples obtained at 5 intervals prior to (i.e., resting), during and following an evoked pain testing session involving painful mechanical, heat and cold stimuli. PA did not predict resting or pain-evoked IL-6. However, multiple measures of sleep interacted with PA in the prediction of resting IL-6. Specifically, diary total sleep time (TST; b = -0.002, p = .003) and insomnia severity (b = .02, p = .03) moderated the effect of PA on resting IL-6, such that higher PA predicted lower resting IL-6 only when insomnia severity was lower or TST was higher. Remaining measures of sleep continuity were not significant moderators. Lower self-reported TST and higher insomnia severity eroded the salutary effects of PA on resting IL-6, underscoring sleep as a key intervention target in TMD. Modulation of positive affect's effect on IL-6 could be a pathway through which poor sleep impacts TMD-related outcomes. 3R01DE019731-05S1.
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