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Mechanisms for Joint Pain in Rheumatoid Arthritis (RA): from Cytokines to Central Sensitization

Abstract

Purpose of Review

Pain in rheumatoid arthritis (RA) may be due to different etiologies, ranging from peripheral inflammation to dysregulation of central nervous system (CNS) processing. This review evaluates relevant literature published on RA pain mechanisms in recent years.

Recent Findings

Despite successes of disease-modifying antirheumatic drugs (DMARDs), pain persists for many RA patients. Studies involving patient-reported outcomes, quantitative sensory testing, and neuroimaging indicate that, in addition to joint inflammation, abnormalities in CNS pain processing may contribute to pain. Some DMARDs (e.g., janus kinus inhibitors) may work via multiple pathways to decrease pain. Adjunctive treatments (e.g., antidepressants, antiepileptics) may also be useful in managing pain in RA patients with well-controlled disease.

Summary

Both peripheral and central mechanisms play key roles in the expression of pain in RA. To effectively manage pain, physicians need accurate assessment tools to identify the pathways involved in each patient so that treatments may be appropriately targeted.

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References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

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Correspondence to Yvonne C. Lee.

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Conflict of Interest

Yvonne Lee reports grants from the National Institutes of Health (grant no. R01AR064850) during the conduct of the study and grants from Pfizer, and is an unpaid member of an advisory board for Lilly. Angela Zhang declares no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Bone and Joint Pain

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Zhang, A., Lee, Y.C. Mechanisms for Joint Pain in Rheumatoid Arthritis (RA): from Cytokines to Central Sensitization. Curr Osteoporos Rep 16, 603–610 (2018). https://doi.org/10.1007/s11914-018-0473-5

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Keywords

  • Pain
  • Rheumatoid arthritis
  • Disease activity
  • Inflammation