Pathophysiology of Diverticula Formation
Diverticula form through herniation of the colonic mucosa and submucosa through weak points in the circular muscle layer of the bowel wall, specifically at sites where blood vessels (vasa recta) penetrate the colonic wall, driven by excessive intraluminal pressure. 1, 2, 3
Anatomical Mechanism
Diverticula are "false" or "pseudo" diverticula because they do not contain all layers of the bowel wall—only the mucosa and submucosa herniate through defects in the muscularis propria 2, 3
The penetration points of the vasa recta represent inherent structural weak points in the colonic wall where the circular muscle is naturally interrupted, making these sites vulnerable to herniation 2, 3, 4
The sigmoid colon is most commonly affected due to its smaller diameter and higher intraluminal pressures compared to other colonic segments 2, 4
Primary Causative Factor: Increased Intraluminal Pressure
Excessive intraluminal pressure is the fundamental mechanical force that drives mucosal herniation through the muscular weak points 1, 3, 4
Colonic segmentation and spasm create localized high-pressure zones that force the mucosa outward through the vasa recta penetration sites 4, 5
Studies using intraluminal manometry have documented elevated intracolonic pressures in patients with diverticulosis compared to controls 5
Contributing Factors
Dietary Factors
Low dietary fiber intake is strongly associated with diverticula formation, as it reduces stool bulk and increases the need for higher propulsive pressures 1, 2, 5
Western diets deficient in fiber correlate with high prevalence of diverticular disease, while African populations consuming high-fiber diets have very low rates 5
The fiber-deficiency theory, originally proposed by Painter & Burkitt in the 1970s, remains the dominant etiological explanation 1
Structural and Age-Related Changes
Alterations in colonic muscle properties occur with aging, including thickening of the muscularis propria and changes in muscle contractility 4, 5
Abnormalities in collagen metabolism and extracellular matrix components may weaken the structural integrity of the bowel wall, facilitating herniation 5
Prevalence increases dramatically with age, reflecting cumulative effects of pressure exposure and tissue remodeling over time 2, 3, 5
Lifestyle and Medication Risk Factors
Obesity, particularly central obesity, increases risk through mechanisms that may include increased intra-abdominal pressure 1, 2
Smoking is an independent risk factor for diverticula formation 1, 2
NSAIDs, corticosteroids, and opiates increase risk, potentially through effects on colonic motility and tissue integrity 1, 2
Genetic Predisposition
Approximately 40-50% of diverticular disease risk is attributable to genetic factors, as demonstrated by twin and sibling studies 1
Genome-wide association studies have identified over 30 susceptibility loci affecting genes important for connective tissue integrity, smooth muscle function, cell adhesion, and immunity 1
Clinical Pitfalls
Not all diverticula become symptomatic—most patients with diverticulosis remain asymptomatic throughout their lives, with only 10-25% developing diverticulitis 5
The presence of muscle thickening without inflammation ("spastic colon diverticulosis" or "painful diverticular disease") can cause symptoms mimicking diverticulitis even without true inflammation 4
Simple diverticulosis without muscle thickening is usually asymptomatic, distinguishing it from the symptomatic variant with muscular hypertrophy 4