Pathophysiology of Diverticulosis and Its Usual Site
Diverticulosis develops through a multifactorial process involving decreased dietary fiber intake, increased intraluminal colonic pressure, and structural weakness at specific anatomical points where blood vessels penetrate the colonic wall, with the sigmoid colon being the predominant site in Western populations. 1, 2
Pathophysiologic Mechanisms
Formation of Diverticula
The fundamental mechanism involves herniation of colonic mucosa and submucosa through the muscular layer at points of vascular penetration. 1, 2 The intraluminal pressure exerted on the colonic wall causes diverticular outpouchings at any of the three areas where the vasa recta (blood vessels) enter the wall, creating natural points of weakness. 1
Dietary factors play a central role, with Western low-fiber diets leading to decreased stool bulk, increased segmentation, and elevated intraluminal pressures during colonic contractions. 1, 2
Structural changes in the colonic wall include alterations in musculature, collagen, and elastin composition that occur with aging, making the wall more susceptible to herniation. 2
Functional changes involve motility disorders and increased intraluminal pressure, particularly in the sigmoid colon where the lumen is narrowest and pressures are highest according to Laplace's law. 2
Genetic factors contribute significantly, with approximately 50% of diverticulitis risk attributable to genetic factors, including variants in the TNFSF15 gene. 3, 4
Progression to Inflammation
The transition from asymptomatic diverticulosis to symptomatic disease involves chronic low-grade inflammation, gut dysbiosis, and altered immune response. 5, 6
Fiber deficiency causes changes in the intestinal microecology that result in decreased colon immune response and permit a low-grade chronic inflammatory process that precedes acute diverticulitis. 1
Microperforation at the fundus of the diverticulum (not an impacted fecalith as previously thought) is the key event leading to acute diverticulitis, with infection extending into pericolic tissue. 1, 2
Histamine and its receptors appear to play a role in the inflammatory process, corresponding with the therapeutic effects of probiotics and anti-inflammatory agents. 2
Anatomical Distribution
Primary Location
The sigmoid colon is the predominant site of diverticulosis in Western populations, representing the most common location for both diverticula formation and subsequent complications. 7
Acute left-sided colonic diverticulitis (ALCD) is the typical presentation, with clinical findings including acute pain or tenderness in the left lower quadrant. 7
The sigmoid location reflects biomechanical factors, as this segment has the smallest luminal diameter and therefore experiences the highest intraluminal pressures during segmentation. 2
Geographic and Demographic Variations
The prevalence of diverticulosis increases dramatically with age, affecting 32.6% of patients aged 50-59 years and up to 71.4% of patients aged 80 years in Western populations. 7, 8
Geographic differences are striking: prevalence is much lower in Africa and parts of Asia (historically 1.85% in Nigeria in 1989), though this is increasing with adoption of Western dietary patterns (10.6% in Nigeria by 2016). 7
Right-sided diverticulosis is more common in Asian populations, representing a distinct epidemiological pattern compared to Western populations. 2
Clinical Implications
Only 1-4% of patients with diverticulosis will develop acute diverticulitis in their lifetime, and approximately 85% of acute diverticulitis cases are uncomplicated. 4, 5
The lifetime risk of developing acute left-sided colonic diverticulitis is about 4% among patients with diverticulosis, with up to one-fifth of Western patients with acute diverticulitis being under 50 years of age. 7
Complications occur only after microperforation through the diverticulum wall into pericolic tissue, which may result in microabscess, phlegmon, large abscess formation, or rarely free perforation. 1
Diverticular bleeding is a distinct pathophysiologic process occurring without diverticulitis, due to eccentric rupture of the vasa recta at the neck of the diverticulum. 2
Key Pathophysiologic Distinctions
Understanding the progression from diverticulosis to diverticular disease requires recognizing three distinct stages: asymptomatic diverticulosis (75% of cases), symptomatic uncomplicated diverticular disease (SUDD), and complicated disease with acute diverticulitis or hemorrhage. 5, 6
The factors predicting symptom development remain incompletely understood but likely involve complex interactions among colonic motility, diet, lifestyle, genetic features, and intestinal microflora changes. 6
Chronic low-grade inflammation precedes acute episodes, suggesting that the pathophysiology involves ongoing inflammatory processes rather than isolated acute events. 1, 5