The Histopathological Evolution of Crohn’s Disease

Abstract

The histopathological diagnosis of Crohn’s disease rests upon the recognition of a combination of tissue changes each of which is relatively non-specific, but which together produce a characteristic histological pattern (1). Some features are always present: transmural lymphoid aggregates, mural thickening, and fissuring ulceration. In addition about 70% of cases show granulomas. Although the finding of granulomas superimposed on the above histological changes is strong supportive evidence, their presence is not essential for a diagnosis of Crohn’s disease to be made. This raises fundamental questions about the significance of the granuloma in Crohn’s disease, and indeed about the nature of Crohn’s disease itself. There are several possible explanations for the inconstant presence of granulomas in Crohn’s disease:

• 1] Crohn’s disease may be caused by several different agents, only some of which cause granuloma formation.

• 2] Granulomas may appear in Crohn’s disease in some patients following mucosal ulceration and consequent access to the diseased bowel wall by granuloma-inducing luminal agents. This theoretical possibility is rendered less likely by the observation that other diseases in which mucosal ulceration occurs are not associated with the presence of granulomas.

• 3] A single aetiological agent of Crohn’s disease may only cause granuloma formation in some patients [cf tuberculoid and lepromatous leprosy].

• 4] Granulomas may be present only in certain phases of the disease [cf sarcoid, lymphogranuloma venereum].