Disease behaviour in Crohn’s disease is dynamic and not stable over time In their landmark paper of 1932, Crohn, Ginzburg, and Oppenheimer1 described “a disease of the terminal ileum, affecting mainly young adults and characterised by a subacute or chronic necrotising and cicratrising inflammation. The ulceration of the mucosa is accompanied by a disproportionate connective tissue reaction . . . which frequently leads to stenosis of the lumen of the intestine, associated with the formation of multiple fistulas”. In the intervening years however, the term Crohn’s disease has been introduced, and now covers a heterogeneous range of clinical presentations, including the classical phenotype of regional ileitis. A number of attempts have been made to subclassify patients with Crohn’s disease into subgroups with similar stable phenotypic characteristics. These attempts have been catalysed first by attempts to individualise therapy, and most recently by progress in understanding the molecular genetics of Crohn’s disease, and the need to relate genotype to disease phenotype. Indeed, it is increasingly clear that assigning disease phenotype may be difficult, but critical in determining the successful outcome of genetic association and linkage studies. The experience of the Toronto group is particularly instructive in this respect, demonstrating that the erroneous assignation of phenotype may lead to a 40% loss of power in linkage studies.2 The Vienna classification of the working party of the World Congress of Gastroenterology proposed a subclassification of Crohn’s disease according to three overriding phenotypic characteristics, implicated in detailed studies of populations in Europe and North America—age, location of disease, and disease behaviour.3 It is the subclassification of disease behaviour into inflammatory (non-stricturing non-penetrating), stricturing …