Sebaceous hyperplasia (SH) is a common, benign skin condition resulting from the enlargement of the skin’s oil-producing glands. It manifests as small, often multiple, bumps on the face, typically becoming noticeable in middle-aged and older adults. These growths represent a localized overgrowth of gland cells but are medically harmless and not associated with skin cancer. This exploration details the normal function of the oil gland and the cellular changes that cause this finding.
Understanding the Sebaceous Gland
The sebaceous gland is a microscopic structure located within the dermis, the skin layer just beneath the surface. These glands are typically connected to a hair follicle, forming a complete unit known as the pilosebaceous unit. Their primary function is to synthesize and secrete sebum, an oily mixture of lipids that lubricates and waterproofs the hair and skin, helping to maintain the skin’s barrier function.
The cells that compose this gland are called sebocytes. Sebocytes continuously produce lipids, swell, and then disintegrate to release their oily contents into the hair follicle duct. When sebaceous hyperplasia develops, the glands become enlarged, containing an increased number of sebaceous lobules attached to a central duct. The resulting lesions appear as soft, yellowish or flesh-colored papules, usually two to five millimeters in diameter. These dome-shaped bumps are most frequently found across the forehead, cheeks, and nose, often featuring a slight central indentation corresponding to the gland’s opening.
The Core Hormonal Mechanism
The fundamental cause of sebaceous hyperplasia involves the hyperproliferation of sebocyte cells, leading to an overall increase in gland size. This cellular overgrowth is linked to age-related changes in circulating sex hormones, particularly androgens. Sebaceous glands are highly sensitive to androgens, such as testosterone, and contain specific enzymes, like 5-alpha-reductase type I, that convert weaker androgens into more potent forms locally within the skin.
As individuals age, circulating levels of androgens naturally decline, which paradoxically triggers the development of sebaceous hyperplasia. This decline slows the normal life cycle of the sebocytes, specifically the rate at which they mature and disintegrate to release sebum. The slower turnover means undifferentiated sebocytes, which are smaller and have less lipid content, accumulate within the gland structure. This cellular crowding and delayed migration cause the gland and its central duct to enlarge, resulting in the clinically observed bump. The condition is a structural enlargement caused by the accumulation of immature cells rather than an overproduction of sebum, which tends to slow down with age.
Systemic Risk Factors and Triggers
Aging remains the most significant factor, with sebaceous hyperplasia most commonly observed in adults over the age of forty. This prevalence correlates strongly with the hormonal shifts that initiate cellular changes within the glands. Beyond chronological age, an individual’s genetic makeup also plays a role, as a familial tendency is often noted, suggesting a hereditary predisposition.
The use of certain medications can also directly trigger or accelerate the development of these growths. Immunosuppressive drugs, such as Cyclosporine, are strongly associated with the onset of sebaceous hyperplasia, with prevalence rates as high as 10 to 16% reported in patients undergoing long-term therapy. Cyclosporine appears to directly stimulate undifferentiated sebocytes, promoting their proliferation and causing the glands to enlarge. Chronic exposure to ultraviolet (UV) radiation is considered a secondary contributing factor, as sun damage can affect cell regulation and turnover in exposed skin areas.
Clinical Identification and Resolution
A dermatologist typically identifies sebaceous hyperplasia through a physical examination, sometimes utilizing a magnifying tool called a dermatoscope. This device allows for clear visualization of the central indentation and the fine, crown-like blood vessels surrounding the lesion, which helps distinguish it from other skin conditions. Because these lesions can sometimes resemble basal cell carcinoma, a common form of skin cancer, a biopsy may be performed in ambiguous cases to confirm the benign diagnosis.
Although sebaceous hyperplasia is harmless and requires no medical intervention, many individuals seek removal for cosmetic reasons. Treatment methods focus on destroying the enlarged gland structure. These procedures include electrocautery, which uses heat to vaporize the tissue, and various laser therapies, such as carbon dioxide laser ablation. Topical treatments, including high-concentration retinoids or photodynamic therapy, are also used to reduce the size of the sebaceous glands, though recurrence is possible.