What is Inflammatory Bowel Disease?

cross sections IBD

The simplest definition of IBD is a chronic inflammatory disease affecting the colon that leads to gastrointestinal issues, a loss of life-quality, a lifetime of drug use and possibly extensive surgery. According to the center of disease control, IBD is one of the top five most expensive gastrointestinal diseases in the United States with the cost burden reaching $1.7 billion 1. IBD can appear at any age, however, it does develop more often in two age groups: before the age of 30 and then in later life when one is 50-60 years old. IBD, however, is not just a single disease. It is actually a general name for four individual gastrointestinal diseases.

  • Crohn’s disease
  • Ulcerative colitis
  • Collagenous colitis (kuh-LAJ-uh-nus)
  • Lymphocytic colitis

Crohn’s disease (CD) and Ulcerative Colitis (UC) are the two main forms of IBD. In general, CD differs from UC in that the inflammation can be located anywhere from mouth to anus and it can extend deeply into the colon wall. In UC, inflammation is constrained to the colon and is superficial in nature. At the moment, I will just discuss these two forms. In a future post, I will discuss the other two. This article covers the following topics to help you get an idea about CD and UC.

General Pathology 2,3

Ulcerative colitis: UC is characterized by superficial inflammation in the colon and it does not usually lead to fistula formation (abnormal passageways that lead to other organs or the exterior of the body), cell wall thickening or strictures (narrowing of the intestinal passageway). When active, the intestinal lumen (inner) surface is bright red and covered with blood and mucus. There are numerous small hemorrhages caused by broken blood capillaries. Ulcers are apparent.
When examined microscopically, one can see that the patches of inflamed tissue are characterized by loss of crypt architecture with decreased crypt density. These areas are also associated with underlying infiltrating inflammatory cells in the lamina propria (a cell rich area underlying the epithelial layer of the intestine). There is a diffuse basal plasmacytosis, which is the aggregation of plasma cells under the crypts. Plasma cells are the cells responsible for producing antibodies. Goblet cells, which produce mucus, are depleted. Neutrophils are present in the inflammatory infiltrates as well eosinophils. Granulomas (aggregations of macrophages) are not present in UC but there are structures that are similar called “Cryptolytic lesions”, which form when macrophages conglomerate around a ruptured crypt.

Crohn’s disease: CD is unlike UC in that it can affect all areas of the gastrointestinal tract. Upper GI disease is present in approximately 8–40% of the cases. However, the terminal ileum and proximal colon are the most common sites for inflammation, followed by the anorectum (the anus and last 2 cm of the rectum) and colon. Like UC, inflamed areas can be characterized by ulcerations. However, the inflammation in CD is more aggressive and extends deeper into the intestinal wall (transmural disease) to include the submucosa, the muscularis propria, the subserosa and mesenteric fat. CD severity can be classified by its pathology:

  • Mild disease: inflammation only
  • Moderate disease: disease with stricturing (the narrowing of the intestinal tract)
  • Severe disease: presence of intra-abdominal or peri-anal fistulas, inflammatory masses and/or abscesses.
Granuloma Crohn's disease

Microscopic examinations of inflamed CD tissues show a feature unique to CD: granulomas. Granulomas are round patches of monocyte/macrophages that have a structure that is similar to epithelial cells. These cells are called epithelioid cells and they can be detected in the majority of patients. Like UC, immune cell infiltrates are also observed, which consist of neutrophils, macrophages and lymphocytes. Another unique characteristic of CD is the presence of “creeping fat” or “fat wrapping”. This is observed in 75% of the surgical specimens and is now considered an accomplice in the disease as it immunologically active. Creeping fat produces both pro-inflammatory mediators and houses immune cells 4. Examination of fistulas histologically shows that the walls are composed of granulation tissue and the lumen contains nuclear debris and inflammatory cells, particularly neutrophils. Granulomas are present in approximately 25% of the perianal fistulas or abscesses.

colon wallStudies of strictures reveal that in CD muscle cells are behaving abnormally. There is an irregular increase in the number of smooth muscle cells in muscularis mucosae layer, a thick layer of smooth muscle cells surrounding the intestinal wall. There are unusually large amounts of collagen (Types V and III), laminin and tenascin.

Risk factors5, 6

The factors that lead to one getting IBD are varied and include both environmental and genetic factors. Living in a northern climate, an industrialized nation and an urban area will all increase the probability of developing IBD. Those with a higher education and occupation are also more at risk. Stress plays a role. Children of small families and children with a low birth rank are also more likely to develop IBD. IBD does run in families and having a direct family member with the disease increases your risk of eventually developing it. Those of Ashkenazi Jewish descent are particularly susceptible.

Why many of these environmental factors lead to increased IBD rates may be explained by a concept called the hygiene hypothesis, which suggests that limited encounters with enteric pathogens during childhood leads to a malfunctioning immune system. In fact, studies show that increased Helicobacter pylori infection is negatively correlated with IBD incidence. Likewise, helminth (parasitic worm) infections, which have been eradicated in Western cultures in the last 50 years, are protective. Increased antibiotic use is also associated with increased rates of IBD.

However, this is not to suggest that IBD may not be the result of an opportunistic infection. Mycobacterium avium subspecies paratuberculosis (MAP), the measles virus, and adherent-invasive strains of Escherichia coli (AIEC) are candidate pathogens, however, conflicting studies have yet been able to confirm their causality. Other infections that cause gastrointestinal problems are also suspected to play roles in IBD etiology. Examples of these culprits are SalmonellaCampylobacter, psychotropic bacteria (Listeria monocytogenes and Yersinia enterocolitica) and opportunistic pathogens (Candida albicans).

Another important environmental factor to consider is diet. A Japanese and a Canadian study have shown that sugar and fat consumption can contribute to IBD development. While some studies show that fiber, fruit and vegetables consumption are protective. Breastfeeding is suggested to be protective.

Drug use and smoking are clearer in their effects on susceptibility. An association has been found with Isotretinoin use. Isotretinoin is an acne medication and was sold under the name, Accutane. Current brand names for the same drug are, Amnesteem, Claravis and Sotret. Oral contraceptives have also been clearly associated with IBD as well as childhood antibiotic use. Cigarette smoking increases Crohn’s disease susceptibility and is associated with more aggressive disease, however, this is not the case with Ulcerative Colitis.

Visit our other pages to learn more about IBD symptoms, common treatments for IBD, and basic immunology.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment.


  1. Staff. 2011. Centers for Disease Control and Prevention. Inflammatory Bowel Disease (IBD). 
  2. Staff. 2012. Mayo Clinic. Inflammatory bowel disease (IBD)..
  3. Geboes, K. 2003. Chapter 18: Histopathology of Crohn’s disease and ulcerative colitis. In Inflammatory Bowel Diseases 4th edition ed. J. Satsangi, ed. Churchill-Livingstone, New York. 255-276.
  4. Drouet, M., L. Dubuquoy, P. Desreumaux, and B. Bertin. 2012. Visceral fat and gut inflammation. Nutrition 28:113-117.
  5. Danese, S., M. Sans, and C. Fiocchi. 2004. Inflammatory bowel disease: the role of environmental factors. Autoimmun Rev 3:394-400.
  6. Molodecky, N. A., and G. G. Kaplan. 2010. Environmental risk factors for inflammatory bowel disease. Gastroenterol Hepatol (N Y) 6:339-346.


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