A polyp is an abnormal growth of tissue that protrudes from a mucous membrane, commonly found in the colon, nose, uterus, and stomach. While most polyps are benign, their presence signals a disruption in cell growth and tissue maintenance. Understanding the specific cause is important because the mechanism of formation differs significantly depending on the body system involved. Polyps are not a single disease but a shared architectural feature resulting from diverse biological processes, including genetic mutations, chronic inflammation, or hormonal imbalances.
Colorectal Polyps: Cellular and Genetic Changes
The formation of colorectal polyps is primarily driven by acquired genetic mutations that lead to uncontrolled cell proliferation in the lining of the large intestine. The most common pathway for development is described by the adenoma-carcinoma sequence, where normal epithelial cells gradually transform into a benign growth, which may then progress to cancer. This process begins with mutations in tumor suppressor genes, such as the APC (Adenomatous Polyposis Coli) gene, which typically regulates cell division and adhesion.
Once the cell loses the function of the APC gene, a cascade of further mutations often follows, including those in the KRAS oncogene, which promotes increased cell signaling and growth. The continuous accumulation of these genetic errors provides a selective advantage to the cell, causing it to multiply faster than surrounding healthy tissue. Later in the sequence, mutations in the TP53 gene, a master regulator of the cell cycle and programmed cell death, can ultimately lead to the transformation of the advanced adenoma into invasive carcinoma.
Lifestyle factors significantly influence the acquisition of these mutations. Advanced age is the single greatest risk factor, increasing the lifetime opportunity for genetic errors to occur. A diet high in fat and red meat, low in fiber, smoking, and excessive alcohol consumption create an environment that promotes damage and rapid cell turnover in the colon lining. This environment fosters the sporadic development of adenomatous polyps, which account for the majority of colorectal cancers.
A smaller but important proportion of colorectal polyps are caused by inherited genetic syndromes. Familial Adenomatous Polyposis (FAP) is an autosomal dominant disorder caused by a germline mutation in the APC gene, leading to the development of hundreds or thousands of polyps and a near 100% lifetime risk of colorectal cancer if untreated. Lynch Syndrome, caused by mutations in DNA mismatch repair genes like MLH1 or MSH2, results in fewer polyps but a high risk of cancer due to the rapid accumulation of errors throughout the genome.
Chronic Inflammation and Nasal Polyp Development
The etiology of nasal polyps is distinct from colorectal polyps, centering on a prolonged, abnormal inflammatory response within the sinonasal mucosa. These growths are typically associated with chronic rhinosinusitis, a persistent inflammation of the nose and sinuses. The underlying trigger is often a breakdown of the mucosal epithelial barrier, allowing irritants, bacteria, or allergens to penetrate the tissue.
This breach initiates a powerful immune reaction, often characterized by a T-helper 2 (Th2) cell-driven response featuring high levels of eosinophils and the signaling molecule Interleukin-5. The sustained presence of these inflammatory cells leads to significant tissue remodeling and a localized pressure imbalance within the nasal lining. This imbalance facilitates the outflow of fluid from capillaries into the surrounding interstitial space, which the tissue cannot reabsorb effectively.
The resulting fluid buildup, or edema, causes the nasal mucosa to swell and eventually herniate outward, forming the characteristic gelatinous polyp structure. Conditions like asthma, allergies, and Aspirin-Exacerbated Respiratory Disease (AERD) are frequently associated with nasal polyps because they share this underlying eosinophilic inflammatory pattern. The mechanism is a physical consequence of immune dysregulation and fluid dynamics, rather than a defect in cell growth control.
Uterine and Cervical Polyps: Hormonal Influence and Tissue Response
Polyps found in the reproductive tract, specifically in the uterus (endometrial polyps) and on the cervix, are predominantly influenced by hormonal fluctuations. Endometrial polyps arise from an overgrowth of the glandular tissue lining the uterus, a process that is highly sensitive to estrogen. Estrogen stimulates the proliferation of this tissue, and an excess or prolonged exposure to the hormone is considered a primary driver of polyp formation.
This hormonal sensitivity explains why uterine polyps are most commonly observed during perimenopause and postmenopause, periods characterized by fluctuating or unopposed estrogen levels. Medications like Tamoxifen, used in breast cancer treatment, or certain types of hormone replacement therapy, can also increase the risk by exerting estrogen-like effects on the endometrial tissue. The excess proliferation creates a localized thickening that extends into the uterine cavity.
Cervical polyps share a link to elevated estrogen but also have a stronger association with local inflammatory processes. Chronic inflammation, often due to infection or irritation, is thought to promote congestion of local blood vessels and stimulate the overgrowth of the cervical lining. While generally benign, both uterine and cervical polyps represent a localized, exaggerated tissue response to hormonal stimulation and inflammation.