Colitis-Associated Dysplasia in Inflammatory Bowel Diseases: From Pathogenesis to Treatment

Patients with inflammatory bowel diseases (IBDs), including ulcerative colitis and Crohn's disease with colonic involvement, are at increased risk of colorectal cancer as a result of chronic intestinal inflammation. Colitis-associated dysplasia represents the principal premalignant lesion in this setting and constitutes the critical link between sustained inflammation and colorectal carcinogenesis. IBD-associated dysplasia develops due to the inflamed mucosal field and follows a distinct, inflammation-driven pathway characterized by field cancerization, multifocality, and early genetic and epigenetic alterations.

This review explores the potential cellular and molecular mechanisms that contribute to colitis-associated dysplasia. These mechanisms include chromosomal instability, oncogenic mutations, epigenetic remodeling, metabolic reprogramming, and immune dysregulation. Particular emphasis is placed on the histological assessment and diagnostic classification of dysplasia in IBD, encompassing both conventional and nonconventional dysplastic subtypes and the associated diagnostic challenges. In addition, contemporary strategies for dysplasia detection are discussed, highlighting advances in endoscopic techniques and emerging imaging modalities that aim to improve lesion recognition. Current evidence guiding the management of dysplastic lesions is also reviewed, with focus on endoscopic resection techniques, surgical indications, and individualized post-resection surveillance strategies.

Colitis-associated dysplasia is a biologically distinct and clinically heterogeneous precursor to colorectal cancer in IBD. Optimal management requires an integrated, multidisciplinary approach combining expert histopathological evaluation, advanced endoscopic detection, and individualized therapeutic decision-making. Continued advances in diagnostic strategies may further improve risk stratification and outcomes for patients with IBD.