PO:32:189 | Salivary gland alterations in systemic sclerosis: a comprehensive ultrasound study and autoantibody correlation

Bixio Riccardo¹, Francesca Pistillo¹, Luca Idolazzi¹, Francesca Nava¹, Beatrice Gabrielli¹, Emanuela Perrucchini², Ombretta Viapiana¹, Maurizio Rossini¹. | ¹Rheumatology Unit, University of Verona VERONA Italy; ²WellAgeing DESENZANO DEL GARDA Italy.

Background. Salivary gland involvement in systemic sclerosis (SSc) is often underrecognized, despite the potential clinical burden of sicca syndrome in affected patients. This study investigates the association between autoantibody profiles and salivary gland (SG) ultrasonographic findings in individuals with SSc.

Materials and Methods. In this monocentric cross-sectional study, patients with SSc, classified according to the 2013 ACR/EULAR criteria, underwent clinical evaluation, immunoblot testing, and SG ultrasonography. Imaging assessments included grey-scale (GS) scoring based on the OMERACT scoring system; power Doppler ultrasound (PDUS), graded as 0 (normal) or 1 (pathological) for each SG; and shear wave elastography (SWE), with stiffness values measured in meters per second (m/s). Patients were stratified by autoantibody profile into the following groups: anti-centromere antibody (ACA) only, anti-topoisomerase I antibody (ATA) only, anti-Sjögren syndrome type A antibody (SSA) with or without additional antibodies, and other autoantibody positivity. Sicca syndrome was defined clinically as objective and/or subjective evidence of ocular (xerophthalmia) and/or oral (xerostomia) dryness, in the absence of Sjögren’s syndrome (SS) based on the 2016 ACR/EULAR criteria or other identifiable causes.

Results. A total of 123 patients with SSc were included (median age 61 years [IQR 55–71], 89.4% female), distributed as follows: ACA+ 32.5%, ATA+ 26.0%, SSA+ 16.3%, and other autoantibody profiles 25.2%. Patients in the SSA+ group showed significantly higher GS scores compared to other groups (p < 0.001), indicating more severe salivary gland involvement. No significant differences were observed in PDUS scores (p = 0.872) or in SWE measurements (parotid glands: p = 0.422; minor salivary glands: p = 0.873), as reported in Table 1. Regarding GS alterations, the SSA+ group had the highest proportions of Grade 2 (36.8%) and Grade 3 (15.8%) lesions, while the ATA+ group had the highest proportion of Grade 0 lesions (75.0%), with a significant difference in the distribution across groups (p = 0.001). Overall, the prevalence of sicca syndrome was high (74.8%), with no significant difference between groups (p = 0.256). Notably, 5 patients (25%) in the SSA+ group met the classification criteria for SS.

Conclusions. This study demonstrates a strong association between anti-SSA antibodies and severe salivary gland involvement in SSc, suggesting a potential direct tissue-damaging effect. Anti-SSA positivity was linked to Sjögren-like ultrasound changes regardless of other autoantibodies, while the prevalence of sicca symptoms remained high and consistent across groups—pointing to additional SSc-specific determinants of sicca syndrome that may not be fully captured by ultrasound assessment.