The document provides a comprehensive overview of inflammatory bowel disease (IBD) histopathology, detailing incidence rates, diagnostic requirements, and key histological findings for both Crohn's disease (CD) and ulcerative colitis (UC). It emphasizes the differences in therapy for UC and CD, the importance of differentiation in diagnosis, and identifies dysplasia as a critical marker for colorectal cancer risk associated with IBD. The document also discusses the influence of disease stage on diagnostics and highlights specific microscopic features relevant to each type of IBD.

1. Inflammatory Bowel Disease (IBD)
Histopathology
Ferenc Pinter MD, PharmD, PhD
Surgical and Pathological Department
National Cancer Institute
Budapest, Hungary

3. Incidence
ECCO-EpiCom
2010 & 2011:
Crohns: 37%
UC: 53%
IBD unclassified: 10%
Eastern Europe:
11,3 / 100 000

4. Ulcerative Colitis Crohn’s Disease
Age-Specific Incidence of IBD *
Incidence in both CD and UC have 2 peaks
( in 3 rd and 6 th decades ).
10
0
2
4
6
8
0 20 40 60 80
10
0
2
4
6
8
0 20 40 60 80
Age (yrs) Age (yrs)

5. Etiology + Pathogenesis

6. Etiology: Smoking

7. Surgical therapy: UC vs. CD

8. Requirements for Dx
 ≥5 sites x ≥2 biopsies
• rectum  terminal ileum
• colonoscopy + ileoscopy
 2-3 tissue levels (step sections) x ≥5 serial sections
 Clinical information
• endoscopic findings
• age
• duration
• treatment
• comorbidities
• travel history

9. Macroscopy - Localisation
CDUC
Whole GI tractEspecially colonLocation
Skip lesionsDiffuseDistribution
Often involvedNo (except backwash ileitis)Ileum
RightLeftLeftRightColon
Typically sparedInvolved in >90%Rectum

10. Macroscopy – Mucosa & wall demage
CDUC
Aphtous,
confluent deep
SuperficialUlcers
+Mucosal atrophy
+Inflammatory polyps
+Cobblestone pattern
+ (except fulmimant colitis)Deep fissures
+ (except fulmimant colitis)Fistulae
NormalWall thickness
+Fat wrapping
+Strictures

11. Microscopy - Inflammation
CDUC
FocalDiffuse (proximally )
Acute/chronic
inflammation
Transmural
Transmucosal
(sometimes in submucosa)
Localisation
Transmural
Frequent in mucosa,
submucosa
Lymphoid aggregates
+ (except ruptured crypts)Granulomas
+ (except fulmimant colitis)Serositis
+Crypt abcesses

12. Microscopy – Mucosal architecture/epithelial abnormality
CDUC
FocalDiffuseCrypt architectural irregularity
FocalDiffuseCrypt epithelial polymorphs
+Mucin depletion
+Paneth cell metaplasia
+Neuronal hyperplasia
+Muscular hypertrophy
+Pyloric gland metaplasia

13. Microscopy – UC stages
 Early stage disease:
• focal/diffuse basal plasmacytosis
 Longstanding disease:
• crypt architectural irregularity
• lamina propria cellularity 
• continous  discontinous !!!
 Quiescent disease:
• crypt architectural irregularity
• crypt density 
• neutrophils 
• basal plasmacytosis 
Relapse

14. CD diagnosis
 Granulomas (not related to crypt injury)
 Focal chronic inflammation
 Focal crypt irregularity

15. CMV reactivation – Predictive value
Immunsupressive
therapy
CMV reactivation
UC: 10-57% CD: 0-30%Steroid-refr > steroid-resp
25-30% 0-10%
HE – sensitivity: 10-87% IHC – sensitivity: 93%

16. CRC
Risk factors:
IBD  Risk of
malignancy
• Young age
• Long disease duration
• Extensive large bowel involvement
• Primary sclerosing cholangitis
• Polypoid mucosal lesions
• Family history of CRC
p53 IHC+:
Dysplasia: 33-67%
CRC: 83-95%
Regenerating epithel:
occasional

17. Summary
 UC/CD  different therapy  differentiation is important
 Differentiation: - granuloma formation: +/-
- inflammation: focal/diffuse
- wall structure change: focal/diffuse
 Diagnostics is impacted by IBD stage (early/chronic/quiscent)
 Dysplasia is the most reliable marker of CRC risk.
This should be evaluated in areas with chronic inflammation and
confirmation by an independent expert GI pathologist is
recommended.