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Introduction Intestinal disease is the main driver of GI related morbidity in Systemic Sclerosis (SSc), with approximately 15% of patients progressing to severe forms requiring nutritional support [10.1093/rheumatology/key350]. Loss of physiological motility is postulated to be the main pathologic culprit of lower GI involvement in SSc, but standardized tools for quantifying GI dysmotility are lacking. Building on the growing experience employing magnetic resonance enterography (MRE) for the assessment of small bowel function in inflammatory bowel diseases (IBD), we implemented a new quantitative imaging assessment of the small bowel for phenotyping of intestinal disease in SSc.Material and Methods SSc patients with severe GI burden, defined by UCLA GIT2.0 total score >1 and ScleroID lower GI >7 (upper quartile of score distribution*) were invited to participate to the study. MREs were performed following oral administration of 1 L of 2% mannitol solution to distend and provoke gut contractility. A CE marked tool, GI-Quant, was used to generate motility heatmaps and enable analysis of contractility; values >200 motility units (mu), considered normal based on IBD standards [10.1007/s00330-012-2514-2] were validated in local Healthy Control cohort. Single-slice segments exceeding the lower limit of normal were quantified and visualised, the others were classified as hypomotile ( figure 1A). Summary scores were then extracted from 2D small bowel ROI. Mean/median global scores and percent below lower limit of normal (200 mu) were analysed by Wilcoxon rank-sum test (R version 4.5.1).Results 12 patients with severe reported GI burden (8 lcSSc) were enrolled in this pilot study. Motility scores were significantly different between patients and HC [median (IQR) GIQuant score 214.00 (173.25-258.50) vs 303.00 (296.00-314.25) respectively, (p= 0.018)] ( figure 1B). LcSSc patients had worse overall motility than dcSSc with same patient reported burden [181.50 (154.00–258.5)], vs [248.50 (228.50–271.7)]. Distribution of GIQuant was bimodal in SSc and driven by a variable amount of hypomotile small bowel [median (IQR) 89.02% (72.51%–95.06%) vs 97.81% (97.10%–98.39%), p=0.046] (figure 1C). All patients (5/12- 41.7%) with extensive segmental hypomotility had lcSSc.Conclusions This pilot study provides the first evidence that gut dysmotility in SSc is variable despite high patient reported GI burden and it is driven by small bowel segments severely hypomotile rather than a generalised dysmotility. A larger cohort is currently enrolling to extend these findings and identify clinical and demographic features linked with segmental loss of motility of the small bowel in SSc.*S.Colak, ...., F.Del Galdo, RMD Open, 2025 (in press, corresponding abstract https://doi.org/10.1016/j.ard.2025.05.879)Abstract OC.49 Figure 1