The various etiological factors associated with the development of these adenomas are:

Majority of colorectal carcinomas follow the adenoma–carcinoma sequence because of following facts:

Risk factors for high-grade dysplasia and invasive carcinoma include polyp size (38.5 % for polyps more than 10 mm). Polyp size is the strongest predictor. Other factors include villous histology, age more than 60 years, and left-sided lesions.

Colonoscopic prevalence of adenoma in asymptomatic patient of more than 50 years is 24–47 %. Prevalence increases with age and is about 50–65 % in patients with more than 75 years of age.

Adenoma can occur in 30–50 % of patient 6 months to 4 years after polypectomy.

Mean age of adenoma diagnosis is 10 years earlier than carcinoma. Adenoma grows from <5 mm to 1 cm in 2–3 years, and progression from 1 cm adenoma to carcinoma takes 2–5 years. Cancer probability for lesions >1 cm is 3 %, 8 %, and 24 % at 5, 10, and 20 years, respectively. Metastasis occurs only in lesions invading the muscularis mucosa through the lymphatics close to it.

Thirty percent of these tumors can be missed if they are less than 5 mm, and 10 % of these tumors can be missed if they are 6–9 mm.

Six to nine percent of these adenomas are advanced, i.e., more than 1 cm in size, high-grade dysplasia, and appreciable villous tissue. Most adenocarcinomas arise from adenomas and removal of adenomas has been found to reduce the incidence of carcinoma.

Villous adenomas harbor malignancy in 4–40 % of cases, associated with severe degree of dysplasia, and 40 % of such tumors will recur despite complete excision (Cho et al. 2008). Invasive carcinoma is missed in 40 % cases. The risk of malignant transformation is 15–25 % and 40 % if a lesion is >4 cm.

Based on their shape, adenomas are classified as (a) sessile and (b) pedunculated. Histologically they are classified into (a) tubular [85–91 %], (b) villous [5–10 %], and (c) tubulovillous [1 %] adenomas (O’Brien et al. 1990).

Tubular adenomas typically have at least 80 % dysplastic tubules, which are packed tightly and extending into the normal appearing lamina propria and only 0–25 % of villous tissue.

Tubulovillous adenomas have more than 20 % tubular component and 25–75 % villous component.

Villous adenomas consist of at least 80 % villous fronds, which are essentially crypts elongated to twice the normal length or more. These villous fronds have a lamina propria core surrounded by adenomatous epithelium. These are rarely less than 1 cm. in size and premalignant polyps of the gastrointestinal tract. Sixty percent of adenomas >2 cm and all large flat adenomas are villous.

Complications which adenomas can undergo include hemorrhage, obstruction, bowel torsion, and malignant transformation.

Serrated polyps appear as pale, nodular, small lesions and grossly resemble hyperplastic polyps (Fig. 15.5). They are considered by some authors to be a subtype of hyperplastic polyps or adenomatous polyps, while some others consider hyperplastic polyps as a subtype of serrated polyps. They can occur as a part of the serrated polyposis syndrome and can potentially undergo malignant transformation. Microscopic examination of a serrated polyp typically shows serrated and dilated crypts which may sometimes be oriented horizontally. These dilated crypts demonstrate branching at the base, with small and normally arranged basilar nuclei and enlarged hyperchromatic nuclei. There may be focal areas of excess mucous production (Torlakovic and Snover 1996). There may also be varying degrees of atypia and dysplasia (Lu et al. 2010). The normal mucosal zone of proliferation which is at the base of the crypts is noted to be located in the middle or the upper part of the crypts (Torlakovic and Snover 1996) (Fig. 15.6).

Serrated polyps are classified into (a) traditional serrated adenoma, (b) mixed polyps, and (c) sessile serrated adenomas (Bauer and Papaconstantinou 2008). The three variants have subtle architectural variations, and all three have malignant potential (Longacre and Fenoglio-Preiser 1990). The sessile serrated adenoma is considered a precursor to dysplastic serrated adenoma and also adenocarcinoma (Goldstein et al. 2003). This transformation is thought to occur through the serrated adenoma pathway, which is distinct from the adenoma–carcinoma sequence in colorectal cancer, and involves acquired genetic mutations of the BRAF oncogene and KRAS (Chan et al. 2003).

Traditional serrated adenoma is very rare (0.5–1.3 %) of colorectal polyps and occurs as a pedunculated lesion. On microscopy, there is characteristic epithelial dysplasia and infolding, with serration of the luminal surface of the crypts. The nuclei appear elongated and centrally placed. There may also be pseudostratification and eosinophilic cytoplasm. Mixed polyps demonstrate a mixture of the serrated architecture seen in hyperplastic polyps and sessile serrated adenoma with dysplastic features seen in adenomatous polyps (Harvey and Ruszkiewicz 2007). The sessile serrated adenoma is the most common variant and constitutes about 15–20 % of serrated adenoma. They are pale, large, and sessile lesions that are usually located on the crests of the mucosal folds. Microscopic features which are characteristic of both hyperplastic polyps and traditional serrated polyps are seen, such as dilated crypts and change of the zone of proliferation (Torlakovic et al. 2003). They grow larger than the other variants, with extension parallel or through the muscularis mucosae.

Endoscopic visualization techniques such as chromoendoscopy with indigo carmine staining and narrow band imaging aid in differentiating between hyperplastic polyp and sessile serrated adenoma and also between dysplastic sessile serrated adenoma, traditional serrated adenoma, and mixed polyp. Characteristic starlike pattern of pits and honeycomb pattern of capillaries seen in hypertrophic polyp can be differentiated from the irregularly distributed pits with dilated and elongated capillaries seen in adenoma. Although rates of recurrence after resection and also rates of progression of the disease are not very clear, in view of the risk of malignant transformation, excision of these lesions is advisable. Most lesions can be removed endoscopically, the sessile lesions being resected using the saline lift technique and the pedunculated lesions using a polypectomy snare. Occasionally, extension of a sessile lesion deeper to the muscularis mucosae may result in incomplete resection, and these patients require surveillance at shorter intervals. Large polyps which are not amenable for endoscopic resection should be surgically resected (Bauer and Papaconstantinou 2008).

These are not true polyps but are identified by chromoendoscopy with indigo carmine dye. These adenomas occur with an incidence of 20 % and contain cancer more often than polypoid adenomas. Flat adenomas of >1 cm. in size have 29 % incidence of high-grade dysplasia or cancer. Treatment consists of endoscopic polypectomy or operative resection.

Hyperplastic polyps develop as a result of defective epithelial maturation and failure of apoptosis. Although they are considered to be nondysplastic and nonmalignant, transformation into an adenomatous polyp, a mixed hyperplastic and serrated polyp, or a serrated polyp can occur (Estrada and Spjut 1980). Serrated polyps are considered to be a type of hyperplastic polyp with potential for malignant transformation. Hyperplastic polyps occurring as a part of a polyposis syndrome show an increased incidence of malignant transformation.

They are usually multiple and occur most commonly in the rectosigmoid region (Fig. 15.7). These are small and nodular lesions, measuring less than 5 mm in size, appearing pale in contrast to the adjacent mucosa, and have a broad base (Estrada and Spjut 1980). Microscopic examination shows characteristic hyperplastic, elongated, and nonbranching mucosal crypts, with no atypia and containing mature goblet cells. Chromoendoscopy with indigo carmine staining and magnification reveals a starlike pit pattern which helps to distinguish it from the irregular grove pattern typically seen in adenomatous polyp. On narrow band imaging, a typical honeycomb pattern is seen (Kudo et al. 1994). One of the polyps should be endoscopically or transanally excised for confirmation of diagnosis. Patients should be advised regular colonoscopic surveillance.

Inflammatory polyps occur in a background of chronic inflammation and attempts at repair. They are pseudopolyps and are usually seen in ulcerative colitis but may be seen in Crohn’s disease and in infective colitis. They occur as multiple lesions with uniform width from their base to the head, consisting of inflamed regenerating mucosa, with adjacent areas of ulceration. Inflammatory polyps do not require any specific treatment and the underlying inflammatory disease should be treated. The adjacent mucosa should be evaluated for dysplasia.

Hamartomatous polyps, otherwise called as juvenile or retention polyps, are localized proliferation of normal and mature intestinal epithelial cells. They occur usually in children, and the incidence is more common in men (boys) than in women (girls). They can occur sporadically or as a part of a polyposis syndrome. Sporadically occurring hamartomatous polyps are considered nonmalignant, unless histological examination reveals adenomatous components (Mesiya et al. 2005). When more than three of these lesions are noted, a polyposis syndrome should be thought of. Juvenile polyposis syndrome is a rare autosomal dominant disorder, with multiple such polyps being found throughout the gastrointestinal tract. There may be a family history of the disease in 20–50 % of these patients (Rickert et al. 1979).

Patients can present with abdominal pain, sometimes with bleeding if ulceration has occurred and occasionally with diarrhea. The polyp can prolapse out through the anal canal. Hamartomatous polyps are thought to occur due to the blockage of colonic glands caused by mucosal inflammation or ulceration, leading to dilatation and proliferation of the gland with the development of granulation and connective tissue proliferation. Microscopy examination typically reveals dilated, mucous-filled, cystic-looking glands, in a highly vascularized background of fibrous stroma. Although these polyps are not premalignant, juvenile polyposis syndrome is considered to be a potentially premalignant condition (Longo et al. 1990). Treatment is by endoscopic resection followed by a thorough histological examination.

These are benign tumors of lymphoid origin. Lymphoid hyperplasia is an uncommon, benign condition that occurs in the rectum and occasionally in the anal canal, due to the presence of lymphoid follicles (Cornes 1961). The exact etiology for this occurrence is not known, but it is possibly due to an inflammatory response. However, a hereditary predisposition has also been noted. In children, it can present as an acute inflammatory response to an infective process. Since the first report of this condition in 1865, many sporadic occurrences of this condition have been reported. The tumors can occur at any age, with a higher incidence in the third and fourth decades of life. In children, a higher incidence is noted between the first and the third years of life, and the incidence in boys is twice that of girls. Because of a few reported occurrences in twins and in siblings and an association with familial polyposis, a hereditary predisposition has also been suggested. It may be asymptomatic if the location is in the rectum but can be painful when located in the anal canal, especially during defecation (Alvear 1984).

The tumor can occur as focal nodular, diffuse, or polypoidal and is noted most commonly in the distal rectum. The nodules are usually small, firm, and sessile but can occasionally be large and pedunculated. There may be an umbilication at the apex or the center of the nodule which may be helpful in making a diagnosis. Histologically, there is a thin lining of mucosa covering well-differentiated lymphoid tissue, which had whitish fibrous bands interspersed between the follicles. In the polypoidal form, the follicles have a well-defined germinal center. The macroscopic and microscopic appearance can resemble that of a malignant lymphoma (Symmers 1948). Evaluation is done by endoscopy and biopsy for histological examination, which usually confirms the diagnosis. Excision and histological examination is necessary because of its close resemblance to other malignant tumors. It is also necessary to differentiate this condition from multiple polyposis. Local excision is the treatment of choice and recurrence of disease is rare.