New knowledge continues to impact on the patho-genesis and treatment of the chronic inflammatory intestinal disorder described by Dr Burrill Bernard Crohn in the early 1930s.1 However, for over a century prior to this report physicians knew of the existence of a non-tuberculous ileitis. Characterized by transmural, chronic mucosal inflammation involving any portion of the gastrointestinal tract from the lips to the perineum, Crohn's disease frequently involves the small intestine, especially the terminal ileum. Diarrhea, abdominal pain, malnutrition and growth delay are common features of disease that involves the small intestine. Rectal bleeding and extraintestinal manifestations are more commonly associated with colonic involvement. Although the clinical features of the disease are similar in adults and children, complications of chronic inflammation are most frequently seen in adults who by nature of their age, have had inflammation for a longer period of time. Growth retardation and delays in sexual maturation are issues faced primarily by children with Crohn's disease.

The diagnosis of Crohn's disease remains a clinical-pathological diagnosis. Despite the availability of new serological tests, radiological and pathological features are needed to establish a diagnosis. Granulomata or chronic inflammation involving the small and large intestine will enable an experienced pathologist to establish the diagnosis with some certainty. However, if only colonic involvement is present, one may have difficulty distinguishing Crohn's colitis from ulcerative colitis. The distribution of the inflammation, such as rectal sparing or predominantly right-sided disease, may favor Crohn's over ulcerative colitis.

Inflammatory bowel disease (IBD) is thought to result from inappropriate and ongoing activation of the mucosal immune system driven by the presence of normal luminal flora.2 Despite many advances, the relationship between the environment and the immunogenetics of the host remains unclear. Crohn's disease and ulcerative colitis are collectively referred to as inflammatory bowel diseases, and they are thought to be distinct entities with significant overlap in pathogenesis, clinical presentation and therapeutic management. Understanding the potential mechanism of mucosal immune dysregulation and developing effective therapies in children will not only improve our management of Crohn's disease, but may also prevent the complications of chronic inflammation seen in adults with Crohn's disease. This new knowledge will ultimately improve the life quality of all patients with Crohn's disease.

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