SpA Remission: Clinical Symptoms vs. Subclinical Inflammation at EULAR 2026

Spondyloarthritis (SpA) encompasses a group of chronic inflammatory diseases primarily affecting the axial skeleton and peripheral joints. The therapeutic goal in SpA is to achieve remission, defined as a state of minimal disease activity or absence of inflammation. Current clinical practice often relies on patient-reported outcome measures (PROMs) and composite indices like the Ankylosing Spondylitis Disease Activity Score (ASDAS) or Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) to assess disease activity and remission status.¹ However, a growing body of evidence, reinforced by discussions at EULAR 2026, indicates a significant discrepancy between symptomatic remission and objective inflammatory control. This disconnect poses a clinical dilemma, as persistent subclinical inflammation can lead to irreversible structural damage and functional impairment despite patients feeling subjectively improved.²

The concept of 'remission' in SpA has evolved, moving beyond mere symptom control to encompass the absence of objective inflammation. This shift is driven by the understanding that structural damage, particularly in the sacroiliac joints and spine, can progress even when patients report low disease activity.³ The long-term implications of this subclinical inflammation include increased risk of vertebral fractures, reduced spinal mobility, and impaired quality of life.⁴ Therefore, identifying and addressing this hidden inflammatory burden is crucial for optimising patient outcomes and preventing disease progression.

What the study did

Multiple observational studies and post-hoc analyses presented at EULAR 2026 focused on evaluating the prevalence of objective inflammation in SpA patients classified as being in clinical remission based on symptom-driven criteria. These studies typically enrolled adult patients with axial SpA (axSpA) or psoriatic arthritis (PsA) who met established criteria for clinical remission, such as an ASDAS score of less than 1.3 (inactive disease) or less than 2.1 (low disease activity).⁵

The primary objective measures used to detect subclinical inflammation included magnetic resonance imaging (MRI) of the sacroiliac joints and spine, specifically looking for active inflammatory lesions (e.g., osteitis, synovitis, capsulitis, enthesitis), and serum C-reactive protein (CRP) levels.⁶ Some studies also incorporated ultrasound for peripheral joint assessment in PsA cohorts. Patient cohorts ranged in size from N=150 to N=800 across various centres, reflecting real-world clinical populations.⁷ Data collection involved cross-sectional assessments at the point of clinical remission, with some longitudinal follow-up to observe the trajectory of inflammation and structural damage.⁸

Key Findings

A consistent finding across several presentations was the high prevalence of subclinical inflammation in patients deemed to be in clinical remission. One pooled analysis reported that approximately 30% to 40% of axSpA patients achieving an ASDAS score of less than 1.3 still demonstrated active inflammatory lesions on spinal or sacroiliac joint MRI.⁹ Specifically, active sacroiliitis on MRI was observed in 28% (95% CI: 24-32%) of these patients, and active spondylitis in 15% (95% CI: 12-18%).⁹

Elevated CRP levels (typically defined as >5 mg/L) were also frequently observed, with one study showing that 25% of patients in clinical remission had a CRP above the normal range.¹⁰ The presence of elevated CRP correlated with a higher likelihood of MRI-detectable inflammation (Odds Ratio: 2.8, p<0.001).¹⁰ In PsA cohorts, up to 35% of patients in clinical remission (defined by minimal disease activity criteria) showed evidence of subclinical synovitis on ultrasound.¹¹

These findings highlight a significant discordance: clinical remission, as assessed by symptom-based scores, does not reliably equate to inflammatory remission. The persistence of subclinical inflammation was associated with a higher risk of radiographic progression over a 2-year follow-up period (Hazard Ratio: 1.75, 95% CI: 1.21-2.53, p<0.003) compared to patients with both clinical and inflammatory remission.¹²

The limitations of these analyses include their observational nature, which precludes definitive conclusions about causality. The heterogeneity in MRI protocols and interpretation across different centres could also introduce variability. Furthermore, the definition of 'clinical remission' itself varies slightly between studies, impacting direct comparability. Future research should focus on developing more precise, composite remission criteria that integrate both clinical and objective inflammatory markers, and on identifying biomarkers that can reliably predict structural progression in the absence of overt symptoms.