Colonic muscle in diverticular disease

The muscle abnormality in diverticular disease is seen most often in surgically excised specimens in the sigmoid colon, though a pancolonic form of the disease without muscle thickening also exists in the elderly. In terms of physiopathology, the condition has a raised intraluminal pressure operating on the wall locally, this being most readily demonstrated in symptomatic patients. In Western societies the colon loses its tensile properties throughout life. The anatomical and functional evidence is that the colon is outstandingly strong in infancy in both Africans and Europeans, but later the mechanical properties of the African colon become superior and they remain so throughout ensuing decades. The diminished tensile strength and elasticity of the wall is no different in the diverticular and non-diverticular subjects and this suggests that an additional factor, such as pressure, may be necessary in Europeans to cause the mucosal extrusion which constitutes each diverticulum. Fiber fills the colon with bulkier, moister feces, which necessitates less work, especially as it operates for most of the time as a low-pressure system, only occasionally evacuating by mass peristalsis into the rectum. Cereal fiber binds salt and water and there is evidence that this is mostly a physicochemical process, dependent on particle size. Certain types of fibers undergo chemical degradation in the cecum and increase the bacterial population of the stool. Population studies show that diverticular disease subjects consume less fiber and in countries where the fiber intake is reduced, fecal output is lessened, transit is slower, and intraluminal pressure may be rising. As a result of the adoption of high-fiber diets and the use of bulking agents elective operations for diverticular disease are less commonly performed. The number of operations in most Western countries may be increasing because of increasing longevity. Complications often arise after a relatively short history; most are explicable on the basis of sudden pressure increments. The recent important finding in this disease is the change in colonic wall compliance, which probably occurs because of a collagen failure. Contraction of the taeniae may follow elastosis, which may relate to under-filling; this produces the contracted structure seen in the excised colonic specimen. The strength of the colonic wall diminishes throughout life, due to changes in its composition; some of these changes are hastened by self-imposed stresses, which currently seem to be mainly of dietary origin.