Classical endoscopic findings of CD in colonoscopic examination include discontinuous chronic mucosal inflammation, aphthoid ulcerations, longitudinal ulcerations, and cobblestone appearance with normal surrounding mucosa. Skipped inflammatory lesions with normal intervening bowel segment are one of the key findings that differentiate CD from ulcerative colitis. Strictures, both fibrotic and inflammatory, may also be present. More than two-thirds of CD patients have colonic involvement which is divided into pan-colonic and segmental colitis. Approximately 40 % patients with colonic CD show rectal sparing from inflammation, while whole rectal involvement is usually observed in ulcerative colitis [13].

Relatively initial characteristic finding of CD is aphthoid ulcer (Fig. 2.1). It shows as a small (less than 5 mm sized), covered with exudates (whitish or yellowish), and superficial (flat or slightly raised) punched-out ulceration with reddish border. Other colitis which needs to be distinguished from CD such as intestinal Behcet’s disease, intestinal tuberculosis, and infectious colitis can also present this aphthoid ulcer. Thus, aphthoid ulcer itself is a nonspecific finding. Multiple presentations of aphthoid ulcers are more specific findings when diagnosing CD. Aphthoid ulcerations are developed over lymphoid follicles and frequently arranged along longitudinal axis of the colon in patients with early or mild CD (Fig. 2.2). Typical longitudinal ulcers of CD are thought to arise from these aphthoid ulcers in a longitudinal direction. Not only in the early stage can these aphthoid ulcers also be seen in the advanced stage of CD, especially around the main ulcerative lesions. Spotty erythematous lesions with localized edema (Fig. 2.3) of mucosa which are considered as beginning stages of CD also can be seen in the early state of CD.

As CD progresses, ulcers tend to be bigger and deeper. Adjacent mucosa shows grossly normal appearance. The shape of ulcers varies from round (Fig. 2.4) to irregular (Fig. 2.5). These types of ulcerations often present in a way of extensive irregular geographic borders or appearance of annular ulcers (Fig. 2.6) around intestinal lumen in CD. Therefore, in this case, it is difficult to differentiate from intestinal tuberculosis. However, the typical progress directions of the ulcerations are usually parallel to the axis of the colon (Fig. 2.7). Classic deep linear ulcerations with discrete margin are seen. Longitudinal alignment of ulceration might also be seen as a railroad track appearance (Fig. 2.8). In addition to linear mucosal features, serpentine mucosal lesion also can be observed by endoscopy in patients with CD, which may be accompanied by multiple geographic ulcers (Fig. 2.9).

As the ulcerations deteriorate, they coalesce into large network of lesions. Therefore, in active CD, the colonic mucosa may be thickened and swollen because of the intermittent pattern of diseased and healthy tissues. It is called as a “cobblestone” appearance, which is a highly specific finding of CD (Fig. 2.10). Remnant mucosal islands surrounded by ulcerations show edematous hyperplastic changes and look like multiple raised lesions. It is seen usually in the distal area of stenotic colon due to inflammation (Fig. 2.11); however, the small bowel near the terminal ileum is also able to show cobblestoning.

Long-standing CD with or without acute inflammation may be characterized by the presence of various mucosal changes including mucosal bridges, scars, fistulas, inflammatory polyps, and stenosis. As a result of fibrosis or scar arising from deep undermining ulceration (Fig. 2.12) and fissures, it can lead to mucosal bridge in the colonic mucosa (Fig. 2.13). During improvement of ulcerations, scars can be found by endoscopy (Fig. 2.14). Severe scarring change of the intestinal mucosa is sometimes indistinguishable from healed ulcerative colitis or infectious colitis such as salmonellosis. Inflammatory polyps also can be seen in patients with CD. These polyps are known as benign lesions caused by long-standing erosive inflammation of the intestine. Usually they are longer in dimension than are wide (Fig. 2.15).

As a result of repeated development and healing of ulcers, cicatricial contraction of bowel wall can be formed. Excessive contraction becomes severe stricture formation with ischemic damages (Fig. 2.16). Strictures can occur in the colon or small intestine and present single or multiple lesions. Sometimes, surrounding normal mucosa nearby stricture sticks together and makes diverticulum like structure, which is called pseudodiverticulum (Fig. 2.17). Most of the severe stricture can be managed by segmental resection and anastomosis; however, noninvasive intervention such as endoscopic balloon dilation can be applied in selected cases with short (<6 cm), moderately active lesions in generally good conditioned patients [9].

Recurrent severe transmural inflammation can lead to a resultant fistula (Fig. 2.18). Primary colonic fistulae are complications of CD, and sometimes the colon is secondarily involved due to small bowel Crohn’s disease [13]. Fistula formation can develop not only bowel to bowel but to the any part of the adjacent organs. Detailed materials will be discussed in “Complication” chapter.

Endoscopic biopsy provides diagnostic clues to confirm the diagnosis of CD. Histological findings of CD (Fig. 2.19) can be summarized with transmural inflammation (span the entire depth of the intestinal wall), noncaseating granuloma (cheese-like appearance of granulomas associated with infections), chronicity, and focality. An increased cellularity of lymphocytes and plasma cells in the lamina propria implies chronic inflammations of disease. Crypt irregularity such as distortion, fibrosis extending to the muscularis mucosae, and noncaseating granuloma indicate another possibility of CD [11]. Noncaseating granulomas are observed in only 15–36 % in CD patients, whereas they are regarded as a prominent histopathologic feature of CD [21]. Histological results are just one of various diagnostic tools; therefore clinicians have to remember that biopsies are not meant to tell us everything about the disease.