How does a pimple form?

Acne is an inflammatory skin disease of the pilosebaceous follicle. It is the most common dermatosis and the primary reason for consultation with a dermatologist. It generally affects teenagers during puberty, but can also occur in adulthood.

There isn't just one, but several causes behind the onset of acne. However, three main elements are significant in the pathophysiology of acne: excess sebum, the bacteria Cutibacterium acnes and hyperkeratinization.

There are several types of acne blemishes: whiteheads, papules, pustules, nodules, and cysts. These do not form in the same way on the skin.

The whiteheads, also known as closed comedones or microcysts are a form of sub-surface pre-acne. They result from an over-secretion of sebum by the sebaceous glands. This excess sebum will block the pores, forming a micro-lesion with a white appearance.

Beyond hyperseborrhea, whiteheads also result from hyperkeratinization of the cells in the follicular canal wall. In other words, the cells multiply excessively, leading to a blockage of the follicular canal that prevents the elimination of sebum.

Thus, sebum accumulates under the skin and gives rise to a localized and hardened bulge in the skin. Whiteheads can spontaneously regress or become inflamed. They are frequently observed in retentional acne.

Note : there are also open comedones, but these are not considered pimples. The open comedones or blackheads result from the same process as microcysts. When these clogged pores are open, oxidation occurs upon contact with air and the impurities trapped inside the pore darken, thus forming a blackhead.

The papules are inflammatory skin elements characterized by a swelling with a solid consistency, that is to say containing neither liquid nor pus, of small size (ranging from 1 to 4 mm) and of a pink to red color.

Papules are one of the manifestations observed ininflammatory acne. This inflammation is caused by a bacterium: Cutibacterium acnes.

Cutibacterium acnes is a commensal bacterium of the skin microbiota. It contributes to the maintenance of healthy skin balance. However, under certain conditions, Cutibacterium acnes proliferates abnormally and becomes pathogenic.

As mentioned earlier, microcysts, which are the least severe manifestation of acne, can become inflamed. Indeed, microcysts are caused, among other things, by an excess of sebum. This fat-rich environment promotes the proliferation of Cutibacterium acnes, which secretes inflammation mediators. This triggers an inflammatory response on the skin's surface. This bacterium is also responsible for a hyperkeratinization of the skin (thickening of the skin) which promotes the appearance of blemishes.

The papules observed in inflammatory acne are indicative of a superficial inflammation caused by the proliferation of Cutibacterium acnes.

The pustules are small inflammatory lesions of the skin characterized by a well-defined and circumscribed elevation of the epidermis (diameter less than 5 mm) and topped in their center by a purulent liquid of white color or yellow.

Just like papules, pustules are observed in inflammatory acne and are a sign of superficial inflammation.

When inflammation is too severe or lasts too long, a bacterial contamination comes to infect the pimple which will then fill with pus. In this case, the papule turns into a pustule.

Nodules and cysts are observed in inflammatory acne and in more severe forms of acne such as acne conglobata. They indicate a deep inflammation.

Nodules are painful solid tissue lumps larger than 5 mm. Unlike papules and pustules that appear on the skin's surface, nodules are deeper. Indeed, this indicates a progression of inflammation towards the deeper layers of the skin.

Cysts are painful deep subcutaneous lesions. Unlike nodules, cysts are filled with a semi-solid fluid (it is composed of sebum, cells, and dead skin). They result from the grouping of several nodules under the skin.

Thus, nodules and cysts are the result of a deep inflammatory reaction. Indeed, Cutibacterium acnes , which is present in pustules, continues to proliferate, thereby amplifying the inflammatory response.