What are the causes of the development of milia?

Primary milia are small cysts of superficial keratinous origin, most commonly located on the face, particularly on the eyelids and around the eyes. They result from a collection of keratin trapped beneath the epidermis, forming a small firm whitish papule to the touch. Unlike inflammatory acne lesions, they are not associated with bacterial infection nor with excessive sebum production. The cause of milia on the face primarily lies in impaired desquamation of keratinised cells and obstruction of skin pores.

Cause No. 1 of primary milia : A slowed rate of cellular renewal.

One of the most frequent causes of primary milia grains is an disruption of the desquamation process. When epidermal turnover is slowed or irregular, dead cells can accumulate and become trapped beneath the stratum corneum. This keratin retention explains the formation of small white “beads,” often mistaken for blemishes. It is important to remember that the so-called fatty deposits under the eyes are generally not due to lipid accumulation but to keratin confined within a microcyst.

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

Certain individuals exhibit an increased tendency for keratin retention, favouring the spontaneous emergence of milia. This predisposition may be linked to genetic characteristics or to particular features of the epidermal structure, such as very thick skin. More rarely, the presence of primary milia can be hereditary. The inheritance pattern described is generally autosomal dominant, with cases reported within the same family. In these situations, lesions may appear from birth as multiple eruptions and resolve spontaneously within a few months.

More exceptional instances of profuse milia, i.e. numerous and persistent, have also been reported in association with certain genodermatoses, i.e. genetic skin disorders. Among these are orofaciodigital syndrome type 1 and Basex–Dupré–Christol syndrome. However, these forms remain extremely rare and represent only a minority of cases encountered in clinical practice.

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

The repeated application of very rich and occlusive treatments can contribute to pore obstruction. Some highly nourishing cosmetics, or those unsuitable for one’s skin type, may thus favour the formation of milia. For example, coconut oil could cause milia due to its comedogenic potential in certain individuals. Similarly, makeup may be implicated when applied in thick layers or when it is not properly removed. Certain very film-forming formulations, such as some sunscreens, can also exacerbate keratin retention and milia if they are too occlusive for the skin type in question.

Cause No. 4 of primary milia : The possible 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 scientific data do not permit a direct link to be established to date. It is, however, plausible that chronic stress impairs the barrier function and cellular renewal, indirectly promoting a favourable environment for keratin retention.

Unlike primary milia, which appear spontaneously on healthy skin, secondary milia develop following trauma or a pre-existing skin alteration. They also correspond to keratin microcysts, but their formation is promoted by a disrupted epidermal repair process. Any situation causing partial epidermal destruction, inflammation or abnormal scar formation can thus create a favourable context for keratin retention.

Cause No. 1 of secondary milia : Cutaneous trauma.

Mechanical or chemical traumas constitute one of the most well-documented causes of milia. A study conducted by MONASH and colleagues notably showed that abrasive treatments used to attenuate acne scars could lead to the development of secondary milia. In about 25% of patients who had undergone multiple sessions, milia appeared two months after the second or third treatment. Two hypotheses have been proposed: either the abrasive action causes occlusion of certain hair follicles, or epithelial fragments are incorporated into the superficial dermis during the procedure, forming a keratin inclusion. However, the study remains vague regarding the precise nature of this abrasive treatment.

More broadly, repeated microdermabrasion procedures, aggressive peels or sometimes even sessions of microneedling can lead to milia in certain individuals. Similarly, the use of irritating cosmetics or an over-exfoliation of the skin can disrupt epidermal regeneration and favour the formation of microcysts.

Cause No. 2 of secondary milia : Prolonged exposure to the sun’s ultraviolet (UV) radiation.

Exposure to UV radiation can also contribute to the development of secondary milia. Indeed, UV rays induce DNA damage in keratinocytes, promote their apoptosis and compromise the skin’s barrier function. Photo‐damaged skin often exhibits a disorganised cell turnover, which can facilitate the accumulation of keratin beneath the stratum corneum. That is why it is important to always protect the skin from the sun using a sunscreen. Let us once again remind ourselves that the choice of texture is not trivial, as an unsuitable product may clog pores and contribute to the formation of milia.

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

The prolonged use of corticosteroids applied topically is known to cause skin atrophy. These agents induce thinning of the epidermis and an alteration of the fibres of collagen and elastin surrounding the hair follicles. This tissue weakening may disrupt follicular architecture and favour keratin inclusion beneath the epidermis. Scientific data remain limited, but this mechanism is sometimes mentioned in the dermatological literature.

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

Secondary milia can also appear in the context of dermatological conditions characterised by a cutaneous fragility or abnormal wound healing. Epidermolysis bullosa, for example, is a rare genetic disorder linked to an alteration of dermo-epidermal anchoring proteins, notably type VII collagen. This fragility leads to skin separation at the slightest trauma and repeated healing, creating a favourable 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).