Pathophysiology of Diverticular Disease: From Diverticula Formation to Symptom Generation

Abstract

Diverticular disease is a common clinical problem, particularly in industrialized countries. In most cases, colonic diverticula remain asymptomatic throughout life and sometimes are found incidentally during colonic imaging in colorectal cancer screening programs in otherwise healthy subjects. Nonetheless, roughly 25% of patients bearing colonic diverticula develop clinical manifestations. Abdominal symptoms associated with diverticula in the absence of inflammation or complications are termed symptomatic uncomplicated diverticular disease (SUDD). The pathophysiology of diverticular disease as well as the mechanisms involved in the shift from an asymptomatic condition to a symptomatic one is still poorly understood. It is accepted that both genetic factors and environment, as well as intestinal microenvironment alterations, have a role in diverticula development and in the different phenotypic expressions of diverticular disease. In the present review, we will summarize the up-to-date knowledge on the pathophysiology of diverticula and their different clinical setting, including diverticulosis and SUDD.

Keywords: ENS; SUDD; diet; diverticular disease; environment; genetic factors; inflammation; microbiota; pathophysiology.

Figure 1

Factors involved in diverticula formation and/or in symptom generation. On the basis of the available data, the figure shows which factors are likely involved in diverticula formation (i.e., in the pathophysiology of diverticulosis and SUDD) and/or in symptom generation (i.e., in the pathophysiology of SUDD).

Figure 2

Representative figure of pathophysiological mechanisms involved in SUDD. ENS, enteric nervous system; Ach, acetylcholine; ChAT, choline acetyltransferase; NO, nitric oxide; TNF-a, tumor necrosis factor alpha; IL-6, interleukin-6; NK1, neurokinin1; 5HT-4R, 5idrossitriptamina-4 receptor; ↓, decrease; ↑, increase; ↕, bidirectional interaction.