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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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© 2021 Published by Elsevier Inc.