Time‐dependent histopathological remodelling of the appendix in patients with ulcerative colitis

AIMS: To characterize the endoscopic features of periappendiceal lesions and histopathological features of appendiceal lesions in patients with conventional ulcerative colitis (UC), particularly in relation to disease duration, and compare these findings to those observed in patients with primary sclerosing cholangitis-associated UC (PSC-UC) to clarify differences in appendiceal involvement and underlying pathophysiology. METHODS AND RESULTS: This retrospective, two-centre study included 158 UC patients and 7 PSC-UC patients undergoing total colectomy involving the appendix between 2011 and 2025. Twenty-five non-UC patients served as controls. Pathologists blindly evaluated appendiceal sections for active inflammation, fibrous obliteration (FO) and crypt architectural distortion. Among patients with UC, 92% of the appendices exhibited active inflammation or FO, frequently accompanied by chronic architectural distortion and mucosal destruction, whereas no controls showed active inflammation. Appendiceal lesions in patients with UC demonstrated time-dependent changes: active inflammation was predominant (64%) within 5 years of disease onset, whereas complete FO was most frequent (75%) after 20 years. In cases with preoperative periappendiceal red patch, histological continuity from distal FO to proximal active inflammation was confirmed within the same appendix. Conversely, despite extensive colonic inflammation, no PSC-UC cases exhibited active appendiceal inflammation, and most appendices remained histologically intact. CONCLUSIONS: Appendiceal lesions in patients with conventional UC show a time-dependent transition from active inflammation to long-term fibrous obliteration. These findings suggest that appendiceal inflammation may be more relevant in the early phase of disease, with possible implications for appendectomy-based therapeutic strategies. The absence of appendiceal inflammation in patients with PSC-UC further supports a pathophysiological difference from conventional UC.