Sebaceous glands are microscopic exocrine glands attached to hair follicles and are central to the development of acne. Their primary function is to produce sebum, a complex mixture of lipids including triglycerides, wax esters, squalene, and free fatty acids. Sebum is released into the follicular canal and spreads across the skin surface, where it helps maintain hydration, supports the skin barrier, and provides antimicrobial activity. Under normal conditions, sebum contributes to skin flexibility and protection. However, when production increases or when sebum composition changes, it can contribute to clogged pores and acne formation.
Sebaceous gland activity is strongly influenced by hormones, particularly androgens. During puberty, rising androgen levels stimulate gland enlargement and increase sebum output, which is why acne commonly begins in adolescence. In adulthood, sebaceous glands remain hormonally responsive. Even subtle shifts in androgen sensitivity can increase oil production, especially in individuals genetically predisposed to oily skin. Excess sebum alone does not cause acne, but when it combines with abnormal follicular keratinization, retained dead skin cells accumulate inside the pore. This mixture forms microcomedones that may develop into blackheads, whiteheads, or inflamed lesions.
The biology of sebaceous glands also involves a process known as holocrine secretion. As sebocytes mature, they accumulate lipids and eventually rupture, releasing their contents into the follicle. This continuous cycle means that sebaceous glands are highly active tissues. In acne-prone skin, increased sebocyte proliferation and altered lipid composition may create an environment that supports the overgrowth of Cutibacterium acnes. The interaction between excess sebum and bacterial byproducts can trigger inflammation, leading to redness, swelling, and discomfort.
Inflammatory signaling within the sebaceous gland itself has become an area of growing research. Sebocytes are not passive oil producers; they can respond to stress, environmental pollutants, and hormonal changes by releasing pro-inflammatory mediators. Oxidative stress may alter sebum components such as squalene, potentially contributing to pore irritation. These processes highlight that acne is not solely a surface-level condition but involves complex interactions within the follicle.
Skincare strategies often aim to regulate sebaceous gland activity and maintain balanced pore function. Topical retinoids are commonly recommended because they normalize follicular keratinization and may indirectly reduce comedone formation. Salicylic acid penetrates into oily pores and can help dissolve accumulated debris, while benzoyl peroxide reduces bacterial overgrowth that contributes to inflammation. Niacinamide may help regulate oil production and support the skin barrier, making it useful for individuals with both oily skin and sensitivity.
While sebaceous gland activity is partly determined by genetics and hormones, it can be influenced by skincare habits and environmental factors. Over-cleansing or harsh exfoliation may disrupt the barrier and stimulate compensatory sebum production. Humidity and heat can increase surface oiliness, while chronic stress may affect hormonal signaling. Understanding the biology of sebaceous glands provides context for why acne treatments focus on controlling oil, preventing clogged pores, and reducing inflammation rather than simply drying the skin.
Managing acne effectively involves respecting the role of sebaceous glands in overall skin health. Sebum is not inherently harmful; it becomes problematic when regulation is disrupted. With balanced, evidence-informed skincare and, when necessary, professional dermatologic guidance, it is possible to support healthier pore function while preserving the protective benefits that sebaceous glands provide
