Acne vulgaris is a widespread skin condition that manifests as various lesions commonly known as pimples. This condition affects millions of people globally. The formation of these lesions is a multi-step biological process that begins deep within the skin’s structure.
The Pilosebaceous Unit
The site of pimple formation is the pilosebaceous unit, a small anatomical structure found across most of the body’s surface. This unit includes a hair follicle, a hair shaft, and an attached sebaceous gland. The sebaceous gland’s primary function is to secrete sebum, an oily mixture of lipids. Sebum travels up the hair follicle and onto the skin surface to lubricate and protect the skin and hair.
The sebaceous gland is a holocrine gland, meaning the entire cell is destroyed and secreted as part of the sebum. When this unit malfunctions, it sets the stage for the initial blockage.
The Initial Blockage: Creating the Microcomedone
The first physical step toward a pimple involves follicular hyperkeratinization. Normally, the cells lining the hair follicle, known as keratinocytes, shed regularly and are carried away by sebum. In hyperkeratinization, these cells become abnormally sticky and fail to shed properly, leading to their accumulation. This accumulation of dead skin cells mixes with increasing sebum production.
This mixture forms a dense plug that physically obstructs the follicular opening. This tiny, non-visible blockage is called a microcomedone, the earliest precursor lesion of acne. The obstruction prevents the normal flow of sebum to the skin surface, causing the follicle to swell beneath the skin. This physical obstruction creates a sealed, oxygen-poor environment that favors the proliferation of specific microorganisms.
Bacterial Growth and the Inflammatory Response
The blocked, lipid-rich follicle provides an ideal habitat for Cutibacterium acnes (C. acnes), a type of bacteria that naturally resides on the skin. This organism is typically an anaerobic bacterium, thriving in the oxygen-deprived conditions created by the blockage. The rapid overgrowth of C. acnes is a significant factor in the progression of the lesion.
As the bacteria multiply, they secrete enzymes, such as lipases and proteases, which break down the triglycerides in the sebum into free fatty acids. These byproducts irritate the follicular wall and trigger an immune response. The immune system sends white blood cells to the area to fight the perceived threat. This signaling activates inflammatory pathways, leading to redness and swelling.
If pressure causes the follicular wall to rupture, the contents—sebum, bacteria, and dead cells—are released into the deeper layers of the skin. This rupture intensifies the immune response, as the body reacts strongly to foreign material in the dermis. This transforms the simple blockage into a noticeable, inflamed lesion.
Classifying the Blemish: From Blackhead to Cyst
The extent of the blockage and the inflammatory response determines the type of lesion that appears. Non-inflammatory lesions are called comedones.
A closed comedone, or whitehead, is a small, skin-colored bump where the follicular opening remains sealed. An open comedone, or blackhead, occurs when the blockage stretches the pore opening, exposing the keratin and sebum plug to the air. The dark color is the result of the oxidation of melanin and debris within the plug, not dirt. These are the mildest form of acne.
When inflammation is present, the lesions become red and tender.
Inflammatory Lesions
Papules are small, raised, red bumps formed when an inflamed comedone has not yet filled with pus. Pustules are papules that have accumulated pus, a substance composed of dead white blood cells and bacterial debris.
More severe forms result from deeper follicular rupture. Nodules are large, firm, and painful lumps that form deep beneath the skin when inflammation is contained in the dermis. Cysts are the most severe lesions, characterized by deep, fluid-filled sacs that can cause tissue destruction and scarring.