Non-neoplastic colonic polyps

Lesion

Many colon polyps are not tumours: some are piled-up normal cells, some come from injury, and some are inherited malformations with cancer risk.

Updated Nov 12, 2026

Key points

Hyperplastic polyp: small (often under five millimetres), left colon and rectum; serration limited to the upper crypt; no malignant potential.
Solitary rectal ulcer syndrome: rectal bleeding, mucus and an anterior rectal wall lesion from poor sphincter relaxation and prolapse; fibromuscular hyperplasia of the lamina propria.
Juvenile polyp: usually under age five, rectum, rectal bleeding; cystic mucin-filled glands in an inflamed lamina propria.
Juvenile polyposis syndrome: autosomal dominant, SMAD4 or BMPR1A (TGF-β pathway); SMAD4 cases often also have hereditary haemorrhagic telangiectasia; high colorectal cancer risk.
Peutz–Jeghers syndrome: autosomal dominant STK11; mucocutaneous pigmented macules (lips, buccal mucosa); arborizing polyps with smooth muscle, mostly small bowel; intussusception; high lifetime risk of many cancers.
Other syndromes: Cowden (PTEN), Cronkhite–Canada (non-hereditary, nail and hair loss), tuberous sclerosis.

What it is

Intestinal polyps are divided into neoplastic (adenomas) and non-neoplastic types: hyperplastic, inflammatory and hamartomatous. Hyperplastic polyps have no malignant potential but must be told apart from sessile serrated lesions. Inflammatory polyps arise from cycles of injury and repair, as in the solitary rectal ulcer syndrome. Hamartomatous polyps can be sporadic or part of inherited syndromes, several of which carry a high risk of cancer inside or outside the gut.

Non-neoplastic polyps and polyposis syndromes

Lesion	Gene or cause	Histology	Cancer risk
Hyperplastic polyp	Delayed shedding of surface cells	Serrated surface, upper third of crypts only	None
Inflammatory (solitary rectal ulcer)	Repeated abrasion and prolapse	Erosion, hyperplasia, fibromuscular lamina propria	None
Sporadic juvenile (retention) polyp	Sporadic	Cystic mucin-filled glands, inflamed stroma	Very low
Juvenile polyposis syndrome	SMAD4, BMPR1A	Many juvenile polyps; dysplasia possible	High colorectal; also gastric and small bowel
Peutz–Jeghers syndrome	STK11	Arborizing smooth muscle with normal epithelium	High: colon, pancreas, breast, lung, ovary, uterus, testis
Cowden syndrome	PTEN	Hamartomatous polyps, lipomas, ganglioneuromas	Breast and thyroid; not GI

Clinical notes

Juvenile and Peutz–Jeghers polyps can bleed, prolapse through the anus or lead an intussusception.
Pigmented macules inside the mouth distinguish Peutz–Jeghers from ordinary freckles.

Test yourself

Think of the answer, then tap the question to see it.

Which gene is mutated in Peutz–Jeghers syndrome?

STK11, a tumour suppressor regulating AMP-activated kinase pathways.

What histologic feature distinguishes a Peutz–Jeghers polyp from a juvenile polyp?

An arborizing network of smooth muscle mixed with lamina propria and normal-looking glands.

Which genes cause juvenile polyposis syndrome?

SMAD4 and BMPR1A, members of the TGF-β signalling pathway.

Why must a hyperplastic polyp be distinguished from a sessile serrated lesion?

Hyperplastic polyps have no malignant potential, whereas sessile serrated lesions can progress to cancer.

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Connections

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Peutz-Jeghers syndrome: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2025); Juvenile polyposis syndrome: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2025).

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Representative model, for educational purposes only.