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Diverticular Disease of the Intestine

Q: Where does the mucous membrane most often prolapse during the formation of the "pouch"?

The mucous membrane protrudes beyond the tunica muscularis, very often penetrating directly into the tissue of the intestinal appendices epiploicae.

*Diverticulosis intestini*

For medical students2 min readUpdated 2026-10-10

Diverticular disease of the intestine is a pathological condition characterized by the formation of multiple diverticula in various parts of the digestive tract. From the perspective of pathological anatomy, the process represents the formation of specific "pouches" due to hernia-like protrusion of the mucous membrane beyond the muscular layer.

Type of lesionFalse diverticulum (mucosal herniation)

InfiltratePlasmacytic with an admixture of eosinophils

LocalizationAny parts of the digestive tract

DirectionBeyond the muscular layer (into appendices epiploicae)

Macroscopic Appearance and Formation Mechanism

Diverticular disease is a complex pathology characterized morphologically by the appearance of multiple pathological outpouchings. These formations can be localized in absolutely any part of the digestive tract, disrupting its normal anatomical structure.

A key feature and the main distinguishing sign of this disease is the formation of so-called false diverticula. To understand the essence of the pathology, it is necessary to clearly distinguish between true and false formations. A true diverticulum, which is most often congenital in origin, is a complete protrusion of the entire intestinal wall, including absolutely all its layers. In contrast, a false diverticulum is a hernia-like protrusion exclusively of the mucous membrane.

Macroscopically, this process looks like the formation of a peculiar blind "pouch." This pouch aggressively prolapses, protruding beyond the muscular layer of the intestinal wall. Very often, on gross specimens, one can observe how these mucosal hernias penetrate deep into the surrounding tissues, invading directly into the tissue of the intestinal appendices epiploicae.

Anatomical Landmarks of the Intestinal Wall

For accurate histological verification of the disease, the pathologist must navigate the microscopic anatomy of the intestinal wall. The pathological process of herniation affects strictly defined layers, disrupting their normal interrelation.

In classical histology, the following layers figure in the morphogenesis of a diverticulum:

Lamina propria (lamina propria of the mucosa) — the connective tissue framework, which serves as the main arena for the development of inflammatory reactions in the complicated course of the disease.
Lamina muscularis mucosae (muscular layer of the mucosa) — a microscopic layer of smooth muscle cells serving as the boundary between the mucosa and underlying tissues.
Submucosa (submucosal layer) — the layer providing mobility to the mucous membrane.
Tunica muscularis (muscular coat) — the robust muscular framework of the intestine. It is through defects in the tunica muscularis that the mucosal layer is extruded outward, forming the morphological substrate of a false diverticulum.

Histological Changes in Inflammation

When an inflammatory process joins the structural deformation of the wall, the microscopic picture of the biopsy specimen undergoes very characteristic changes. The main morphological impact is sustained by the lamina propria.

Detailed microscopic examination reveals the following triad of signs:

Specific cellular infiltration. A dense inflammatory infiltrate forms within the lamina propria. Its cellular composition is dominated by plasma cells (forming a plasmacytic infiltrate). A crucial diagnostic nuance is the mandatory admixture of eosinophils within this pool of cells.
Lymphoid hyperplasia. In response to the pathological process, lymphoid follicles begin to actively form in the tissues of the altered intestinal wall, serving as a striking marker of local tissue immune activation.
Destruction of the epithelial lining. Superficial defects—erosions—form on the surface of the mucous membrane. These erosive damages are not point-like; they are fairly extensive and capture several adjacent intestinal crypts at once, leading to a disruption of the normal architectonics of the glandular apparatus.

Mnemonic

To easily remember the difference between a false and a true diverticulum, use the association: "A lie is always superficial." A false diverticulum consists only of the superficial layer (mucosa), which "escapes" through the muscular layer, much like a hernia.

Frequently asked questions

In which part of the large intestine are acquired diverticula most frequently localized?

Acquired diverticula are most frequently localized in the left colon. In the "Western" type of disease, up to 95% of outpouchings are detected in the sigmoid colon, with their number decreasing in the proximal direction. Segmental involvement affecting only the sigmoid and transverse colon is also possible. In the "Eastern" type, which is significantly less common, diverticula are localized in the cecum and ascending colon.

What macroscopic complications of diverticular disease are distinguished in pathological anatomy?

Macroscopic complications of diverticular disease include inflammatory complications, fistulas, hemorrhages, and rare complications:

Fistulas (fistula) — most frequently involving the urinary bladder, forming a colovesical fistula.
Giant cyst (giant cyst) — a rare complication; represents a pseudocyst formed during the expansion of a contained subserosal perforation.
Abscess — pericolic, pelvic, intra-abdominal, retroperitoneal, or diverticular.
Peritonitis — generalized purulent or fecal.
Infiltrate — acute or chronic paraintestinal; pericolic infiltrate is also described.
Stenosis.
Hemorrhage — acute or recurrent.
Pericolic phlegmon.
Diverticular perforation.
Volvulus as a rare complication.

What pathogenetic factors lead to increased intraluminal pressure and the formation of diverticula?

The formation of diverticula is caused by structural changes in the intestinal wall, though direct data on factors increasing intraluminal pressure is limited. The pathogenesis includes the following steps:

Elastin deposition in the taeniae, causing contraction and shortening of the intestine.
Corrugation of the mucosa and circular muscle layers.
Formation of a thickened intestine with interdigitating folds.

Diverticula themselves form at anatomical "points of weakness" — sites where vasa recta penetrate through the circular muscle layer.

With which diseases must macroscopic differential diagnosis of diverticular disease be performed?

Differential diagnosis for diverticular disease and its complications includes:

Carcinoma / tumor involvement of the large intestine — CT perfusion parameters can play a role in differentiating between cancer and diverticulitis.
Duplication cyst (duplication cyst) — a differential diagnosis for a giant cyst associated with diverticular disease.
Ulcerative colitis — ulcerative colitis must be differentiated from diverticulitis and other conditions.

What is the main morphological difference between a false and a true diverticulum?

A true (congenital) diverticulum contains all layers of the intestinal wall. A false diverticulum represents a hernia-like protrusion exclusively of the mucous membrane beyond the muscular layer.

Which cells predominate in the inflammatory infiltrate in this pathology?

A predominantly plasmacytic infiltrate with a characteristic and diagnostically important admixture of eosinophils is observed in the lamina propria of the mucosa.

How does the glandular apparatus of the intestine change during diverticular inflammation?

Extensive erosions form on the mucous membrane, capturing and destroying several intestinal crypts at once. The formation of lymphoid follicles is also observed in the tissues.

Where does the mucous membrane most often prolapse during the formation of the "pouch"?

The mucous membrane protrudes beyond the tunica muscularis, very often penetrating directly into the tissue of the intestinal appendices epiploicae.

Go deeper

Pathogenesis of mucosal herniation through the tunica muscularis.
Morphological differences between congenital (true) and acquired (false) diverticula.
Role of eosinophils and plasma cells in the inflammatory infiltrate of the lamina propria.
Mechanism of erosion formation and destruction of intestinal crypts during inflammation.
Topography of appendices epiploicae and their involvement in diverticular disease.