[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Gastrointestinal tract](https://durgical.com/en/general-pathology/areas/gi/) › Crohn disease

# Crohn disease

- Lesion

Crohn disease can inflame any part of the gut, in separate patches and through the whole wall, causing narrowings, fistulas and abscesses.

Updated Nov 12, 2026

## Key points

- Skip lesions: sharply separated diseased segments with normal bowel between them.
- Earliest lesion: aphthous ulcer; then long serpentine ulcers, cobblestone mucosa and deep knife-like fissures.
- Transmural inflammation: thick rubbery wall, strictures (string sign), creeping fat over the serosa.
- Non-caseating granulomas in any layer, nodes or outside the gut (about a third of cases).
- Fistulas to bowel, bladder, vagina or skin; perianal disease.
- Terminal ileal disease: B12 and bile-salt malabsorption (gallstones, oxalate kidney stones).

## What it is

Crohn disease can involve any part of the gastrointestinal tract, most often the terminal ileum, ileocaecal valve and caecum. About two in five patients have small-bowel disease only, about a third have both small bowel and colon, and the rest have colonic disease alone. The inflammation is patchy (skip lesions) and transmural, which explains its typical complications: strictures, fissures, fistulas and abscesses. Non-caseating granulomas are a hallmark but are found in only about a third of cases.

## Structure

- Gross: segmental thick wall with narrow lumen, linear ulcers, cobblestoning, creeping fat.
- Micro: neutrophils attack crypts (cryptitis, crypt abscesses); abrupt transition from ulcer to normal mucosa.
- Chronic injury: crypt distortion and branching, pseudopyloric metaplasia, Paneth cell metaplasia in the left colon, mucosal atrophy.
- Transmural lymphoid aggregates and submucosal fibrosis with muscle hypertrophy.
- Non-caseating granulomas, even in uninvolved segments.

## Step by step

- Barrier loss and microbial sensing defects start inflammation at lymphoid-rich sites such as the terminal ileum.
- Aphthous ulcers form over lymphoid follicles.
- Ulcers coalesce into long linear ulcers separated by swollen mucosa (cobblestones).
- Inflammation crosses the whole wall; fissures deepen into fistulas or abscesses.
- Repeated healing lays down fibrosis and muscle hypertrophy: strictures and obstruction.

## Clinical notes

- Intermittent diarrhoea, abdominal pain and fever; about one in five begins acutely and mimics appendicitis.
- Extra-intestinal disease: uveitis, migratory polyarthritis, sacroiliitis and ankylosing spondylitis, erythema nodosum, clubbing, primary sclerosing cholangitis (less often than in ulcerative colitis).
- Anti-Saccharomyces cerevisiae antibodies (ASCA) favour Crohn disease.
- Disease often recurs at the anastomosis after resection; smoking worsens it.

## Memory aid

Crohn: Cobblestones, Creeping fat, Clefts (fissures) and Continuity broken by skip lesions; granulomas in a third.

## Test yourself

Think of the answer, then tap the question to see it.

## Which part of the gut is most often involved in Crohn disease?

The terminal ileum, ileocaecal valve and caecum.

## Why do fistulas form in Crohn disease but rarely in ulcerative colitis?

Crohn inflammation is transmural, so fissures can tunnel through the entire wall into neighbouring organs or skin.

## What proportion of Crohn cases show granulomas?

About a third; their absence does not exclude the diagnosis.

## What is creeping fat?

Mesenteric fat that wraps over the serosal surface of the bowel in transmural Crohn disease.

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## Connections

## Related 7

- [Inflammatory bowel disease: pathogenesis](https://durgical.com/en/general-pathology/inflammatory-bowel-disease-pathogenesis/)
- [Ulcerative colitis vs Crohn disease](https://durgical.com/en/general-pathology/ulcerative-colitis-vs-crohn-disease/)
- [Colitis-associated neoplasia: dysplasia in long-standing IBD](https://durgical.com/en/general-pathology/colitis-associated-neoplasia-dysplasia-in-long-standing-ibd/)
- [Intestinal obstruction](https://durgical.com/en/general-pathology/intestinal-obstruction/)
- [Granulomatous inflammation: caseating vs non-caseating, the causes to know](https://durgical.com/en/general-pathology/granulomatous-inflammation-caseating-vs-non-caseating-the-causes-to-know/)
- [Fibrosis in organs: TGF-β and the myofibroblast](https://durgical.com/en/general-pathology/fibrosis-in-organs-tgf-and-the-myofibroblast/)
- [Chronic inflammation: causes, cells and features](https://durgical.com/en/general-pathology/chronic-inflammation-causes-cells-and-features/)

## Related conditions 6

- [Crohn disease](https://durgical.com/en/conditions/crohn-disease/)
- [Small bowel obstruction](https://durgical.com/en/conditions/small-bowel-obstruction/)
- [Anorectal abscess and fistula](https://durgical.com/en/conditions/anorectal-abscess-and-fistula/)
- [Megaloblastic anaemia (B12 or folate deficiency)](https://durgical.com/en/conditions/megaloblastic-anaemia/)
- [Iron deficiency anaemia](https://durgical.com/en/conditions/iron-deficiency-anaemia/)
- [Primary sclerosing cholangitis](https://durgical.com/en/conditions/primary-sclerosing-cholangitis/)

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Crohn Disease](https://www.ncbi.nlm.nih.gov/books/NBK436021/) (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/crohn-disease/
