One hypothesis is that creeping fat exerts a break-like effect on inammation in CD [27]. If that were the case, then mucosal and mural mesenchymal disease mani­festations would be expected to decrease, wherever mesenteric disease increased. The reverse is the case and mesenteric, mucosal and mural disease manifestations all increase in tandem in Crohn’s disease. This and other observations have meant the concept of protecting against inammation, or exerting a break-like effect on inammation, has been largely superseded by the hypothesis that the mesentery exerts a net pathobiological effect in Crohn’s disease [1, 19]. Examination of resec­tion specimens demonstrates a mesenteric transition zone where creeping fat com­mences, and gradually worsens (Fig. 7.2). Examination of the opened specimen indicates corresponding mucosal and mural transition zones. Coupling of mucosal, mural and mesenteric disease is further reected in the fact that mucosal ulceration almost always commence at the mesenteric (and not the anti-mesenteric) axis of the intestinal circumference (called axial polarity). This is also the zone where the mes­entery intersects the intestinal circumference.