Pain and affective distress in arthritis: relationship to immunity and inflammation

ABSTRACT

Introduction: Most arthritides are associated with pain and psychological distress (clinically significant depression and anxiety). Pain and depression are mutually exacerbating; both may continue even when joint involvement appears well controlled.

Area covered: There is strong evidence that arthritis-related stress impacts the central nervous system and, together with peripheral inflammatory changes, can cause central sensitization that can lead to chronic pain and worsening of affective distress. Cytokines and chemokines participate both in joint inflammation and in central sensitization. We review evidence of these relationships in five arthritides, namely rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, gout, and in osteoarthritis of the hips and knees. Central sensitization in these conditions results in long-lasting pain and psychological distress.

Expert commentary: Chronic pain and depression are important but often neglected in the clinical assessment and treatment of arthritis. The potential role of biologic cytokines and Janus kinase inhibitors in dealing with these symptoms needs further study.

KEYWORDS:

• Arthritis
• pain
• distress
• inflammation
• depression
• cytokine
• chemokine
• central sensitization
• biologics

Article Highlights

• Pain is a cardinal feature of arthritis and may be partly due to CNS sensitization.

• Depression is very common in arthritis and may precede its onset.

• Pain and depression interact bidirectionally in the CNS.

• Cytokines and chemokines contribute in the CNS to pain, depression, and their interaction.

• This interaction is not exclusive to chronic, immunologically induced arthritis but has also been documented in gout, and degenerative joint disease.

• There is some evidence that biologic agents may have a direct beneficial effect on pain and depression.

• FM is common in most forms of arthritis and contributes to both pain and depression in these diseases.

• CNS sensitization may lead to prolonged adverse effects on pain and mood that may not improve in concert with successful treatment of the joint disease.

• The role of CNS sensitization must be considered in the clinical assessment and treatment of arthritis.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This article was not funded.