In 1932, Crohn, Ginzburg and Oppenheimer accurately described, from resected specimens, the homogeneous picture of a sub-acute or chronic necrotising, cicatrising and fistulating inflammation involving the terminal ileum alone. Since then, this structure has been blurred by a model that presents Crohn’s disease as a heterogeneous family of inflammatory intestinal phenotypes. Burrill Crohn refused to accept any complex concept as compatible with his pristine description and, while contemporary physicians did not listen, recent findings from genetic association studies are in favour of his position. Nowadays, the causation of Crohn’s disease is still unidentified, but evidence of a complex interplay of genetic, environmental, immunological and psychosomatic factors as contributors to pathogenesis is accumulating.¹ However, without a causative agent, a diagnostic gold standard for Crohn’s disease is lacking. This necessitates an intricate and laborious work-up of features of intestinal inflammation. These are characteristic, but not specific enough to be free from pitfalls and non-conformities.

There are many hypotheses regarding the pathomechanism of Crohn’s disease. The disease results in a chronic transmural inflammatory response, which progresses over a varying period of time, leading to architectural alterations of the bowel wall. This is regardless of whether Crohn’s disease is driven and maintained by a dysregulation of the innate immune response, primary defects in the intestinal mucosal barrier, loss of tolerance to resident microbial flora, defects in T-cell programmed cell death, impairments of regulatory T-cell activation and function, an imbalance of pro- and anti-inflammatory cytokines or a combination of all of these factors. Some evidence suggests that the younger the patient at onset of disease, the more aggressive the course. Fibrostenosis results from the thickening of the muscularis propria and the deposition of collagen. Fistula formation results from degradation of the extracellular matrix. Consequently, intestinal surgery is inevitable in up to 70% of patients, and may precipitate secondary functional intestinal disorders. Instead of posing a cure, surgery aims to remedy complications derived from the inexorable inflammatory process, as Crohn’s disease recurs within weeks to months of ileal resection and ileocolonic anastomosis in the neoterminal ileum. The evolution of these new lesions mimics the natural history of the disease at its onset.