Not All Pain in Rheumatic Disease is Inflammatory Save

The term nociplastic pain refers to pain arising from altered central nervous system processing, without evidence of tissue or nerve damage. Fibromyalgia is the prototype of this condition. 

In a session at the Global Rheumatology Summit, Dr. Daniel Clauw, an expert on the topic, explained that fibromyalgia can occur in isolation in a “top-down” fashion, or can be secondary to inflammatory autoimmune diseases in a “bottom-up” fashion. He also emphasized that nociplastic pain often coexists with neuropathic or nociceptive pain in the patients we see regularly.

In a subsequent session, EULAR president-elect Dr. Laure Gossec explained that patients with chronic pain disorders, particularly women, tend to have worse outcomes in pain management and disease control. Contributing factors include cognitive bias among treating physicians, who may fail to recognize nociplastic pain, attribute symptoms to anxiety or emotional factors, or underestimate their severity.

Further evidence of the impact of nociplastic pain across the spectrum of rheumatic diseases was presented at ACR 2026. Abstract 1337 examined nociplastic pain features in a cohort of 83 adults with axial spondyloarthritis (axSpA) using the Fibromyalgia Survey Questionnaire (FSQ) and quantitative sensory testing (QST). Nociplastic features appeared in 32.5% of participants and correlated strongly with lower pressure pain thresholds and higher disease activity (ASDAS-CRP). Similarly, abstract 1354 reported a single-center, cross-sectional study from India that assessed fibromyalgia in 151 adults with SpA using the 2016 ACR criteria. Fourteen patients (9.3%) had fibromyalgia. They were more often female and had significantly worse disease activity (BASDAI, ASDAS-CRP), functioning (BASFI), and quality of life (ASQoL).

In abstract 2823, authors used data from the CPIRA cohort of 283 patients with established, active rheumatoid arthritis and clustered them into four phenotypes based on symptoms and inflammation. Patients in cluster 3 had a high symptom burden with only modest inflammation, scored higher on pain interference, pain catastrophizing, and depression than the other clusters, and responded least to treatment changes.

Lastly, abstract 2824 used data from the FORWARD databank to evaluate inflammatory (type 1) versus nociplastic (type 2) features, based on patient-reported outcomes, in adults with SLE (301 followed longitudinally for a median of about 4 years). Depression and opioid use increased across the nociplastic gradient, reaching 49% for both in the Mixed group (type 1 and type 2 features). Nociplastic and mixed states were chronic, with about 37% of patients remaining persistently above the nociplastic threshold.

In conclusion, nociplastic features are common, more frequent in women, and linked to higher disease activity scores, greater depression, more opioid use, and poorer treatment response. When symptom-driven scores are mistaken for active inflammation, patients risk unnecessary treatment escalation. Routine screening with validated tools, along with attention to the coexistence of different pain mechanisms, can help us treat the right pain with the right therapy.