J Pathol Transl Med.  2021 Mar;55(2):83-93. 10.4132/jptm.2021.02.17.

Non-conventional dysplastic subtypes in inflammatory bowel disease: a review of their diagnostic characteristics and potential clinical implications

• Choi WT

• KMID: 2513893
• DOI: http://doi.org/10.4132/jptm.2021.02.17

Abstract

The early detection and grading of dysplasia is the current standard of care to minimize mortality from colorectal cancer (CRC) in patients with inflammatory bowel disease. With the development of advanced endoscopic resection techniques, colectomy is now reserved for patients with invisible/flat dysplasia (either high-grade [HGD] or multifocal low-grade dysplasia) or endoscopically unresectable lesions. Although most pathologists are familiar with the morphologic criteria of conventional (intestinal type) dysplasia, the most well-recognized form of dysplasia, an increasing number of diagnostic material has led to the recognition of several different morphologic patterns of epithelial dysplasia. The term “non-conventional” dysplasia has been coined to describe these changes, but to date, the recognition and full appreciation of these novel forms of dysplasia by practicing pathologists is uneven. The recognition of these non-conventional subtypes is becoming increasingly important, as some of them appear to have a higher risk of developing HGD or CRC than conventional dysplasia or sporadic adenomas. This review describes the morphologic characteristics of all seven non-conventional subtypes that have been reported to date as well as our current understanding of their clinicopathologic and molecular features that distinguish them from conventional dysplasia or sporadic adenomas.

Keyword

Colorectal neoplasm; Dysplasia; Inflammatory bowel disease; Non-conventional

Figure

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  Fig. 1. Algorithms for management of endoscopically visible/polypoid dysplasia (A) versus invisible/flat dysplasia (B) in inflammatory bowel disease patients undergoing surveillance colonoscopies.

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  Fig. 2. Conventional dysplasia. (A) Invisible/flat low-grade dysplasia shows a tubular architecture lined by crowded, pencillate, hyperchromatic nuclei involving both crypts and surface epithelial cells. While goblet cells are reduced, they are easily identified. (B) Invisible/flat highgrade dysplasia shows severe cytologic and architectural atypia.

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  Fig. 3. Hypermucinous and crypt cell dysplasias. (A) Hypermucinous dysplasia demonstrates a tubulovillous lesion with mild nuclear atypia and prominent mucinous differentiation. (B) Superficial fragments of hypermucinous dysplasia show prominent mucinous cells with minimal to no nuclear atypia. (C, D) Crypt cell dysplasia is characterized by mostly round-to-oval or slightly elongated, hyperchromatic nuclei with mild nuclear enlargement and crowding limited to the crypt base without surface involvement. Increased mitoses are present (D).

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  Fig. 4. Dysplasia with increased Paneth cell differentiation and goblet cell deficient dysplasia. (A, B) Dysplasia with increased Paneth cell differentiation shows increased Paneth cell differentiation involving multiple dysplastic crypts. (C, D) Goblet cell deficient dysplasia is defined by a complete or near-complete absence of goblet cells, leading to intensely bright eosinophilic cytoplasm. Eosinophilic luminal secretion is often seen in goblet cell deficient dysplasia (C).

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  Fig. 5. Three subtypes of serrated dysplasia. (A) Sessile serrated lesion (SSL)–like dysplasia demonstrates a dilated L-shaped crypt at the interface with muscularis mucosa. (B) Traditional serrated adenoma (TSA)–like dysplasia shows villiform projections lined by elongated nuclei with intensely eosinophilic cytoplasm and ectopic crypts. (C) Serrated dysplasia not otherwise specified (NOS) shows a complex serrated architecture without definite features of SSL-like dysplasia or TSA-like dysplasia. (D) Another case of serrated dysplasia NOS mimics a hyperplastic polyp, but it shows full-thickness dysplasia with papillary or pseudopapillary changes on the surface epithelium.

Reference

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