Overview

• Prevalence: 1 case per 500 population

• Incidence: ∼ 6 cases per 100,000 population per year [1]

• Sex: ♂ = ♀

• Typical age of onset: bimodal distribution with one peak at 15–35 years and another one at 55–70 years [2][3]

• Populations with higher prevalence [4]

  • Individuals of Northern European descent

  • Individuals of Ashkenazi Jewish descent

Immune dysregulation and dysbiosis, which promotes chronic inflammation, the ultimate cause of which is not fully understood.

• Familial aggregation

• Genetic predisposition (e.g., mutation of the NOD2 gene, HLA-B27 association)

• Tobacco smoke

Nicotine consumption is the only (known) controllable risk factor for CD. Therefore, smoking cessation is especially important in patients with CD.

Inflammation

Inflammation is most likely caused by immune dysregulation.

• Dysregulation of IL-23-Th17 signaling → unrestrained Th17 cell function → inflammation → local tissue damage (edema, erosions/ulcers, necrosis) → obstruction, fibrotic scarring, stricture, and strangulation of the bowel [5]

• Mutations in the nucleotide oligomerization binding domain 2 (NOD2) protein are likely involved in the development of CD.

Abscess and fistula formation

• Intestinal aphthous ulcers → transmural fissures and inflammation of the intestinal walls → adherence of other organs or the skin → penetration of tissue → microperforation and abscess formation → macroperforation into these structures → fistula formation