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Clinical Pain-related Outcomes and Inflammatory Cytokine Response to Pain Following Insomnia Improvement in Adults With Knee Osteoarthritis.

ABSTRACT: OBJECTIVES:Clinical insomnia is known to affect pain, but mechanisms are unclear. Insomnia can dysregulate inflammatory pathway, and inflammation plays a mediating role in pain. It is unclear whether insomnia-related alterations in inflammation can be modified with insomnia improvement, and if such alterations parallel improvement in pain. The current study objective was to provide proof of concept for the role of insomnia in inflammation and pain by testing whether improving insomnia would reduce pain and related physical function, and, concurrently, modulate inflammatory responses. MATERIALS AND METHODS:Thirty adults with osteoarthritis knee pain and insomnia (Insomnia Severity Index >10) provided baseline measures of osteoarthritis and laboratory pain, and serial blood samples for inflammatory biomarkers, interleukin 6, and tumor necrosis factor ?, before and after pain testing. To manipulate insomnia, participants were randomly assigned to a 6-week cognitive-behavioral therapy for insomnia (n=16); or wait-list control (n=14). At 8-weeks (time 2), all measures were repeated. To directly test insomnia improvement effects, participants were grouped by insomnia status at time 2 after confirming baseline equivalency on all outcomes. RESULTS:Compared with those maintaining insomnia at time 2 (Insomnia Severity Index ?8; n=18), those whose insomnia improved at time 2 (n=12) had significantly improved physical functioning, decline in knee pain during transfer activities, and attenuated increase in interleukin 6 and less decrease in tumor necrosis factor ? across the pain testing session. DISCUSSION:These findings suggest further exploration of inflammatory pathways linking clinical insomnia, and its improvement, to chronic pain.

SUBMITTER: Heffner KL

PROVIDER: S-EPMC6219931 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Project description:BackgroundInflammatory mediators in the synovial fluid (SF) play critical roles in the initiation and development of pain in knee osteoarthritis (KOA). However, data for inflammatory marker expression are conflicting, and the role of SF inflammatory mediators in neuropathic pain is not clear. Therefore, the aim of this study was to identify SF inflammatory mediators associated with nociceptive and neuropathic pain in KOA.MethodsLevels of IL-1?, IL-6, TNF-?, macrophage colony-stimulating factor, MMP-3, MMP-13, metalloproteinase with thrombospondin motifs 5, calcitonin gene-related peptide, neuropeptide Y, substance P and bradykinin were measured using enzyme-linked immunosorbent assays in 86 patients. Nociceptive pain was assessed using the numeric rating scale (NRS), visual analog scale (VAS) and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain score. Neuropathic pain was determined using the PainDETECT questionnaire. Moreover, knee function was evaluated by the WOMAC score and range of motion (ROM) assessments. Radiological grade was defined using the Kellgren-Lawrence (K-L) grading scale.ResultsPain scores measured using different methods correlated highly with each other. A worse K-L grade and knee function were associated with worse pain. Expression of IL-1? and IL-6 was increased in the early stage compared with the late stage. The NRS score correlated positively with age, K-L grade, and the WOMAC score and negatively with ROM and TNF-? expression. The VAS correlated positively with age, K-L grade, and the WOMAC score but negatively with ROM and levels of IL-1?, IL-6 and TNF-?. The WOMAC pain score did not correlate with any of the inflammatory mediators measured; it correlated only with ROM. The PainDETECT score correlated only with the WOMAC score. Expression of other inflammatory mediators did not correlate with any of the pain scores.ConclusionsIL-1?, IL-6 and TNF-? play critical roles in pain in the early stage of KOA and correlate with pain. The catabolic enzymes and neuropeptides measured do not correlate with nociceptive and neuropathic pain. New biomarkers related to pain in the late stage need to be further investigated.

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Clinical Pain-related Outcomes and Inflammatory Cytokine Response to Pain Following Insomnia Improvement in Adults With Knee Osteoarthritis.

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