It is well known that complicated diverticular disease (DD), which includes Acute Uncomplicated Diverticulitis (AUD), Acute Complicated Diverticulitis (ACD) and Chronic Diverticulitis (CDiv), is characterised by profound structural changes in the colonic tissue, varying from tissue disruption to fibrosis; it has been hypothesised that an unbalanced expression of matrix metalloproteinases (MMP) and their inhibitors (TIMP) protein expression in the bowel wall might, at least in part, mediate this process.1 However, there is limited knowledge about the role of MMPs in the pathogenesis of diverticulitis. It has been reported that altered concentrations of MMPs and TIMPs may explain the structural changes found in diverticulitis.1 Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract characterised by chronic, multifocal transmural inflammation potentially affecting the whole gastrointestinal tract, particularly in the ileocolonic segment. Altadill et al 2 recently hypothesised that CD and complicated DD seem to share the same destiny: a chronic inflammation evolving towards fibrosis.

Adhesion molecules containing heparan sulfate (syndecan family) are proteo-glycans, and play a significant role in tissue repair.3 Basic fibroblast growth factor (bFGF) is a peptide able to …