Working toward mechanistic pain phenotyping in osteoarthritis

Crow, Joshua A.; Fillingim, Roger B.

doi:10.1016/j.joca.2021.11.018

Cited by 4 publications

(4 citation statements)

References 15 publications

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“…These groups differed significantly across multiple measures of psychological functioning, clinical and experimental pain sensitivity, and pain-related interference and disability. In a recent editorial, Crow et al 6 noted limitations in mechanistic understanding of MEP and chronic pain, in-general, due to the complexity of interactions between the variables above, among others. Many previous studies, including the current study, are limited by the absence of premovement pain ratings.…”

Section: Introductionmentioning

confidence: 99%

“…Several reviews address current understanding of MEP, 12,20,30 being described as "pain during walking," 23 "pain that is brought on or aggravated by movement and or stimulation," 30 or more descriptively as "pain triggered or exacerbated by active or passive movement and clearly differentiated from background, ongoing, spontaneous pain." 1,6 The definition was most recently expanded to "pain that is acutely provoked and experienced in response to active or passive movement of the involved tissues," such as naturally occurring or experimentally standardized active range of motion, muscle contraction, or any form of physical or daily activity. 12 Earlier studies of MEP primarily involved postsurgical pain.…”

Section: Introductionmentioning

confidence: 99%

“…In fact, research of individuals with OA suggests that different mechanisms mediate MEP vs spontaneous pain. 6 Scholars posit a need to expand outcomes to include MEP, 2,6,30 and elucidating characteristics of MEP is critical to understanding the pathogenesis, diagnostic and prognostic values, and specific treatment targets of MEP.…”

Section: Introductionmentioning

confidence: 99%

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A domain-oriented approach to characterizing movement-evoked pain

Crow,

Joseph,

Miao

et al. 2024

PR9

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Introduction: Movement-evoked pain (MEP) impacts a substantial proportion of US adults living with chronic pain. Evidence suggests that MEP is influenced by numerous biopsychosocial factors and mediated by mechanisms differing from those of spontaneous pain. However, both characteristic and mechanistic knowledge of MEP remain limited, hindering effective diagnosis and treatment. Objectives: We asked (1) can chronic pain, functional, psychosocial, and behavioral measures be grouped into descriptive domains that characterize MEP? and (2) what relationships exist between biopsychosocial factors across multiple domains of MEP? Methods: We formed 6 characteristic domains from 46 MEP-related variables in a secondary analysis of data from 178 individuals (aged 45–85 years) with knee pain. Ratings of pain during 3 functional activities (ie, Balance, Walking, Chair Stand) were used as primary MEP variables. Pearson correlations were calculated to show linear relationships between all individual domain variables. Relationships between variables were further investigated through weighted correlation network analysis. Results: We observed a unique combination of pain characteristics associated with MEP apart from general pain. Notably, minutes doing physical activity were inversely associated with multiple variables within 4 of the 6 domains. Weighted correlation network analysis largely supported our classification of MEP domains. Additional interdomain relationships were observed, with the strongest existing between MEP, Mechanical Pain, and Multiple Pain Characteristics and Symptoms. Additional relationships were observed both within and between other domains of the network. Conclusion: Our analyses bolster fundamental understanding of MEP by identifying relevant mechanistic domains and elucidating biopsychosocial and interdomain relationships.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A domain-oriented approach to characterizing movement-evoked pain

Crow,

Joseph,

Miao

et al. 2024

PR9

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“…The common drugs for OA pain management were NASIDs, acetaminophen, and opioid analgesics. Based on the side effects of drugs and the not wellunderstanding pathogenesis, the current strategy for OA pain relief is not satisfied by patients [3]. Thus, research on the mechanisms of OA pain offers critical new insights for the development of pain treatment.…”

Section: Introductionmentioning

confidence: 99%

GSK-3β inhibition alleviates arthritis pain via reducing spinal mitochondrial reactive oxygen species level and inflammation

Yang

Sun

Zhen³

et al. 2023

PLoS ONE

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Pain is the main symptom of osteoarthritis, which severely reduces the patients’ quality of life. Stimulated neuroinflammation and elevated mitochondrial oxidative stress are associated arthritis pain. In the present study, arthritis model was established by intra-articular injection of complete Freund’s adjuvant (CFA) on mice. Knee swelling, pain hypersensitivity and motor disability were observed in CFA-induced mice. In spinal cord, neuroinflammation was triggered and presented as severe infiltration of inflammatory cells and up-regulated expressions of glial fibrillary acidic protein (GFAP), nuclear factor-kappaB (NF-κB), PYD domains-containing protein 3 (NLRP3), cysteinyl aspartate specific proteinase (caspase-1) and interleukin-1 beta (IL-1β). Mitochondrial function was disrupted and characterized as elevated expressions of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), dihydroorotate dehydrogenase (DHODH) and cytochrome C (Cyto C), and reduced expressions of Bcl-2 and Mn-superoxide dismutase (Mn-SOD) activity. Meanwhile, as a potential target for pain management, glycogen synthase kinase-3 beta (GSK-3β) activity was up-regulated in CFA induced mice. To explore potential therapeutic options for arthritis pain, GSK-3β inhibitor TDZD-8 was intraperitoneally injected for three days on CFA mice. Animal behavioral tests found that TDZD-8 treatment elevated mechanical pain sensitivity, suppressed spontaneous pain and recovered motor coordination. Morphological and protein expression analysis indicated that TDZD-8 treatment decreased spinal inflammation score and inflammatory related protein levels, recovered mitochondrial related protein levels, and increased Mn-SOD activity. In summary, TDZD-8 treatment inhibits GSK-3β activity, reduces mitochondrial mediated oxidative stress, suppresses spinal inflammasome response, and alleviates arthritis pain.

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