Describe the epidemiology.
Prevalence: 1 case per 500 population
Incidence: ∼ 6 cases per 100,000 population per year 
Sex: ♂ = ♀
Typical age of onset: bimodal distribution with one peak at 15–35 years and another one at 55–70 years 
Populations with higher prevalence 
Individuals of Northern European descent
Individuals of Ashkenazi Jewish descent
What is the cause?
Immune dysregulation and dysbiosis, which promotes chronic inflammation, the ultimate cause of which is not fully understood.
List risk factors.
Genetic predisposition (e.g., mutation of the NOD2 gene, HLA-B27 association)
Nicotine consumption is the only (known) controllable risk factor for CD. Therefore, smoking cessation is especially important in patients with CD.
Describe the pathophysiology.
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 
Mutations in the nucleotide oligomerization binding domain 2 (NOD2) protein are likely involved in the development of CD.
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