Acne vulgaris is a widespread skin condition that affects the pilosebaceous units (hair follicles and their associated oil glands), primarily on the face, chest, and back. A lesion refers to any area of tissue that has suffered abnormal change or damage. In acne, lesions are the physical manifestations of the disease, ranging from superficial bumps to deep, painful swellings, commonly known as pimples, blackheads, or cysts.
The Underlying Mechanism of Acne Formation
The development of any acne lesion results from a four-part process occurring within the hair follicle. The first factor is the excessive production of sebum, the skin’s natural oil, which is stimulated by circulating hormones like androgens.
The second factor is follicular hyperkeratinization, where there is an abnormal shedding of dead skin cells inside the follicle. Instead of naturally sloughing off, these sticky cells accumulate and mix with the excess sebum, forming a plug that clogs the pore. This blocked follicle, known as a microcomedone, is the precursor to all visible acne lesions.
The third element involves the proliferation of a bacterium called Cutibacterium acnes (C. acnes), which is a normal resident of the skin’s microbiome. This anaerobic bacterium thrives in the oxygen-poor, oil-rich environment of the clogged follicle, feeding on the trapped sebum. The final factor is the resulting inflammation, which is the body’s immune response to the bacteria and the irritation caused by the breakdown of sebum.
Non-Inflammatory Lesions (Comedones)
The mildest forms of acne are non-inflammatory lesions known as comedones, which are simply clogged hair follicles. These lesions are classified into two distinct types based on whether the pore opening is closed or open to the air.
Closed comedones, commonly called whiteheads, form when the pore is completely blocked beneath the skin surface. They appear as small, slightly elevated, dome-shaped bumps, typically white or flesh-colored, because the trapped material remains sealed off from the air. Open comedones, or blackheads, result when the follicular opening is dilated, allowing the plug to be exposed to oxygen. The dark color is caused by the oxidation of the melanin and keratin within the plug upon air exposure, not dirt.
Inflammatory Lesions (Papules and Pustules)
When the follicular wall ruptures due to the pressure from the trapped sebum, skin cells, and bacteria, the contents spill into the surrounding dermis, triggering a noticeable inflammatory response. This immune reaction marks the transition from non-inflammatory comedones to moderate forms of acne, which appear red and tender. These lesions are generally considered superficial because the inflammation is contained near the skin’s surface.
Papules are the first stage of this inflammatory process, presenting as small, raised, solid red or pink bumps that lack a visible center of pus. Pustules are essentially papules that have progressed, characterized by a visible white or yellow center surrounded by a red ring of inflamed skin. This visible center is pus, which consists of dead white blood cells that have rushed to the site to fight the bacterial infection.
Deep and Severe Lesions (Nodules and Cysts)
The most severe and painful forms of acne occur when the follicular rupture and subsequent inflammation happen deep within the dermal layer of the skin. These deep lesions are associated with extensive tissue damage and a high risk of permanent scarring. They persist significantly longer than papules or pustules, often lasting weeks or even months.
Nodules are large, solid, hard lumps that form deep below the skin surface and are characterized by intense pain and inflammation. Unlike pustules, nodules do not typically develop a pus-filled head and feel like hard knots under the skin. Acne cysts are the deepest and largest lesions, forming soft, pus-filled sacs that are highly fluctuant, feeling like a fluid-filled pocket. Cystic lesions represent the peak of acne severity, often resembling boils and requiring professional treatment to prevent scarring.