Pain in Rheumatoid Arthritis: Models and Mechanisms

Abstract

Pain is one of the most challenging symptoms for patients with rheumatoid arthritis (RA). RA-related pain is frequently considered to be solely a consequence of inflammation in the joints; however, recent studies show that multiple mechanisms are involved. Indeed, RA pain may start even before the disease manifests, and frequently does not correlate with the degree of inflammation or pharmacological management. In this aspect, animal studies have the potential to provide new insights into the pathology that initiate and maintain pain in RA. The focus of this review is to describe the most commonly used animal models for studies of RA pathology, which have also been utilized in pain research, and to summarize findings providing potential clues to the mechanisms involved in the regulation of RA-induced pain.

KEYWORDS:

• cytokines
• glia cells
• inflammation
• nerve injury markers
• neuropeptides
• pain
• prostaglandins
• rheumatoid arthritis
• TLR4

Financial & competing interests disclosure

The authors wish to acknowledge that this work is supported by Swedish Research Council, Swedish Foundation for Strategic Research, Ragnar Söderberg Foundation, William K Bowes Foundation, Knut and Alice Wallenberg Foundation, Karolinska Institutet Foundations and Konung Gustaf V’s Jubilee Foundation. The authors have no other 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 apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The authors wish to acknowledge that this work is supported by Swedish Research Council, Swedish Foundation for Strategic Research, Ragnar Söderberg Foundation, William K Bowes Foundation, Knut and Alice Wallenberg Foundation, Karolinska Institutet Foundations and Konung Gustaf V’s Jubilee Foundation. The authors have no other 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 apart from those disclosed. No writing assistance was utilized in the production of this manuscript.