Milia are small, benign cysts that appear as tiny white or yellowish bumps on the skin, often observed on the face, eyelids, cheeks, and occasionally other parts of the body.

These cysts form when keratin, a structural protein normally found in skin, hair, and nails, becomes trapped beneath the skin’s surface.

Primary vs. Secondary Milia: Different Origins

Milia are classified into two main categories based on their origins: primary and secondary. Primary milia typically develop spontaneously, most notably in newborns, where they appear on the nose, scalp, or cheeks. These arise predominantly from abnormal keratin entrapment within the superficial layers of the skin or hair follicles without an external trigger.

In contrast, secondary milia occur as a consequence of external or internal factors that disrupt normal skin function. These factors include damage or trauma to the skin, prolonged use of certain topical medications, genetic disorders, or inflammatory skin diseases. Secondary milia frequently arise from eccrine sweat ducts or sebaceous structures due to skin injury or compromised barrier function.

Skin Damage and Trauma as a Common Cause

Physical damage to the skin, such as burns, blistering, dermabrasion procedures, or UV radiation from chronic sun exposure, is a major contributor to secondary milia formation.

These insults impair normal exfoliation and skin turnover, causing dead skin cells and keratin to accumulate beneath the epidermal layer. Such damage thickens the skin and modifies its repair mechanisms, increasing the likelihood of keratin cyst entrapment.

Moreover, persistent use of topical steroids or nonsteroidal anti-inflammatory drugs may induce skin atrophy and barrier dysfunction, predisposing to milia development. The resulting compromise in normal skin physiology limits keratin clearance, facilitating cyst formation.

Role of Genetic and Autoimmune Factors

Certain inheritable skin conditions, known as genodermatoses, exhibit milia as part of their clinical presentation. Syndromes such as Bazex-Dupre-Christol or oro-facial digital syndrome include milia among multiple dermatological signs, indicating a genetic predisposition to abnormal keratinization or follicular abnormalities.

Autoimmune responses and systemic diseases can also provoke milia by inducing chronic skin inflammation or altering normal cell turnover. These conditions influence sweat gland and follicle function, leading to cyst formation concurrently with other cutaneous symptoms.

Lifestyle and Environmental Influences

External lifestyle factors significantly impact milia occurrence. Improper skin care practices, including the excessive use of oil-based cosmetics or failure to remove dead skin cells through gentle exfoliation, can clog pores and trap keratin beneath the surface. Additionally, insufficient sleep and stress may impair the skin's natural regeneration.

Sun exposure remains a pervasive risk factor. Ultraviolet radiation damages the skin barrier, causing thickened, leathery skin that hampers dead cell shedding and increases milia risk. Regular sunscreen use and avoidance of excessive sunlight help mitigate this effect.

Dr. Neil Alan Fenske, MD, a dermatologist on milia causes: “Milia develop when bits of dead skin cells get trapped below the skin and create a really hard, little, white ball.”

Milia arise from the entrapment of keratin beneath the skin, driven by a variety of factors ranging from intrinsic genetic susceptibilities to external skin damage and lifestyle influences. Differentiating between primary and secondary milia is crucial for accurate assessment and management.

Prevention hinges on protecting skin integrity through trauma avoidance, appropriate skin care, and sun protection. Ongoing research into the molecular pathways regulating keratinization promises improved therapeutic options for persistent or recurrent milia, enhancing skin health and patient quality of life.