What are the underlying causes of milia formation?

Primary milia are small cysts superficial keratinous lesions, most often found on the face, particularly on the eyelids and around the eyes. They result from an accumulation of trapped keratin beneath the epidermis, forming a small firm whitish papule on palpation. Unlike inflammatory acne lesions, they are not associated with bacterial infection or excessive sebum production. The cause of milia on the face is primarily due to a failure to remove keratinized cells and an obstruction of the skin’s pores.

Cause No. 1 of primary milia : Slowed cellular renewal.

One of the most common causes of primary milia is an alteration of the desquamation process. When epidermal turnover slows or becomes irregular, dead cells can accumulate and become trapped beneath the stratum corneum. This keratin retention explains the formation of small white “pearls,” often mistaken for blemishes. It is important to remember that the cause of under-eye fat bumps is generally not a lipid buildup but keratin trapped in a microcyst.

Cause No. 2 of primary milia : An individual predisposition.

Some individuals exhibit a heightened tendency toward keratin retention, promoting the spontaneous formation of milia. This predisposition may be related to genetic factors or specific characteristics of the epidermal structure, such as excessively thick skin. More rarely, primary milia can be hereditary. The inheritance pattern is generally autosomal dominant, with cases reported within the same family. In these instances, lesions may appear at birth as multiple eruptions and resolve spontaneously within a few months.

More exceptional cases of profuse milia, meaning numerous and persistent, have also been reported in association with certain genodermatoses, that is, genetic skin diseases. These include, in particular, orofacial digital syndrome type 1 and Basex-Dupré-Christol syndrome. However, these forms remain extremely rare and account for only a minority of cases observed in clinical practice.

Cause No. 3 of primary milia : The use of occlusive or comedogenic products.

Repeated application of very rich, occlusive treatments can contribute to clogging the skin’s pores. Some deeply nourishing cosmetics, or those not suited to a particular skin type, can therefore promote milia formation. For example, the coconut oil could cause milia due to its comedogenic potential for some individuals. Likewise, the makeup can be problematic when applied in heavy layers or not removed properly. Certain highly film-forming formulations, such as some sunscreens, can also exacerbate keratin retention and milia when they are too occlusive for the skin type in question.

Cause No. 4 of primary milia : The potential influence of internal factors.

Although milia are not directly linked to stress or to hormonal fluctuations such as acne, some individuals report an increased occurrence during periods of imbalance. Stress is thus sometimes cited as a cause of milia, but current scientific data do not establish a direct link. However, it is plausible that chronic stress impairs the barrier function and cellular turnover, indirectly promoting a milieu conducive to keratin retention.

Unlike primary milia, which appear spontaneously on healthy skin, secondary milia develop following an insult or a preexisting skin alteration. They are also keratin microcysts, but their formation is favored by a disrupted epidermal repair process. Any situation resulting in partial epidermal destruction, inflammation, or abnormal scarring can thus create an environment conducive to keratin retention.

Cause No. 1 of secondary milia : Cutaneous trauma.

Mechanical or chemical trauma is one of the most well-documented causes of milia. A study conducted by MONASH and his colleagues specifically showed that abrasive treatments used to diminish the appearance of acne scars could lead to the development of secondary milia. In about 25% of patients who underwent multiple sessions, milia appeared two months after the second or third treatment. Two hypotheses have been proposed: either the abrasive action causes certain hair follicles to close, or epithelial fragments become embedded in the superficial dermis during the procedure, creating a keratin inclusion. However, the study remains vague regarding the specific nature of this abrasive treatment.

More broadly, repeated microdermabrasion procedures, aggressive peels, or sometimes sessions of microneedling can lead to milia formation in some individuals. Similarly, using irritating cosmetic products or over-exfoliation of the skin can disrupt epidermal regeneration and encourage the formation of microcysts.

Cause No. 2 of secondary milia : Chronic exposure to solar ultraviolet radiation.

Exposure to UV rays can also contribute to the development of secondary milia. Indeed, UV radiation induces DNA damage in keratinocytes, promotes their apoptosis, and impairs the skin’s barrier function. Photo-damaged skin often exhibits disorganized cell turnover, which can facilitate the accumulation of keratin beneath the stratum corneum. That is why it is important to always protect your skin from the sun with sunscreen. It’s also worth noting that texture choice is not trivial, as an unsuitable product can clog pores and contribute to milia formation.

Cause No. 3 of secondary milia : Prolonged application of corticosteroids.

Prolonged use of corticosteroids topically applied are known to cause skin atrophy. These compounds induce thinning of the epidermis and an alteration of the collagen and elastin surrounding hair follicles. This tissue weakening may disrupt follicular architecture and promote keratin entrapment beneath the epidermis. Scientific data remain limited, but this mechanism is sometimes mentioned in the dermatologic literature.

Cause No. 4 of secondary milia : Certain dermatological conditions.

Secondary milia can also appear in the context of dermatological disorders characterized by a cutaneous fragility or abnormal wound healing. Epidermolysis bullosa, for example, is a rare genetic disorder involving a defect in dermo-epidermal anchoring proteins, notably type VII collagen. This fragility leads to skin detachment with minimal trauma and repeated wound repair, creating a favorable environment for milia formation. Other inflammatory or scarring dermatoses may be associated with secondary milia, although the precise mechanisms remain incompletely understood.

• MONASH S. Formation of milia following abrasive treatment for post-acne scarring. Archives of Dermatology (1953).

• TSUJI T. Milia induced by corticosteroids. Archives of Dermatology (1986).

• ROSS J. B. & al. Multiple eruptive milia: Report of a case, review of the literature, and a classification. Journal of the American Academy of Dermatology (1997).

• BERK D. R. & al. Milia: A review and classification. Journal of the American Academy of Dermatology (2008).

• BARBAROT S. & al. Les grains de milium de l’enfant. Annales de Dermatologie et de Vénéréologie (2009).

• GALLARDO AVILA P. & al. Milia. StatPearls (2023).