There is a genetic association with Crohn's disease, primarily with variations of the NOD2gene and its protein, which senses bacterial cell walls. Siblings of affected individuals are at higher risk.^[11] Males and females are equally affected. Smokers are two times more likely to develop Crohn's disease than nonsmokers.^[12] Crohn's disease affects between 400,000 and 600,000 people in North America.^[13] Prevalence estimates for Northern Europe have ranged from 27–48 per 100,000.^[14] Crohn's disease tends to present initially in the teens and twenties, with another peak incidence in the fifties to seventies, although the disease can occur at any age.^[1][15] There is no known pharmaceutical or surgical cure for Crohn's disease. Treatment options are restricted to controlling symptoms, maintaining remission, and preventing relapse. The disease was named after gastroenterologist Burrill Bernard Crohn, who, in 1932, together with two other colleagues at Mount Sinai Hospital in New York, described a series of patients with inflammation of the terminal ileum, the area most commonly affected by the illness.^[16]

The diagnosis of Crohn's disease can sometimes be challenging,^[19] and a number of tests are often required to assist the physician in making the diagnosis.^[15] Even with a full battery of tests, it may not be possible to diagnose Crohn's with complete certainty; a colonoscopy is approximately 70% effective in diagnosing the disease, with further tests being less effective. Disease in the small bowel is particularly difficult to diagnose, as a traditional colonoscopy allows access to only the colon and lower portions of the small intestines; introduction of the capsule endoscopy^[88] aids in endoscopic diagnosis. Multinucleated giant cells, a common finding in the lesions of Crohn's disease, are less common in the lesions of lichen nitidus.^[89]