What are the causes of keratosis pilaris?

Keratosis pilaris is a skin condition resulting from a disruption in the keratinization process. In other words, it is due to an excessive production of keratin, leading to the blockage of hair follicles. This excess is also responsible for the accumulation of dead cells, hence the thickening and irregularity of the skin. Keratosis pilaris most often has a genetic origin and is transmitted in an autosomal dominant manner. This means that the "defective" allele is located on a non-sex chromosome and that only one copy of the gene needs to be affected for the condition to develop. This anomaly is transmitted by one of the parents, who is also affected and carries the genetic anomaly in one copy on one of their chromosomes.

Several studies have focused on the etiology of keratosis pilaris and have attempted to determine which mutation is responsible for the condition. Although research is still ongoing, it appears that the loss of function of the structural protein filaggrin leads to a major risk of developing keratosis pilaris. It is indeed commonly suggested that this condition results from a disorder of the keratinocytes caused by a mutation of the FLG gene, which codes for filaggrin. As a reminder, filaggrin is a protein associated with keratin in the epidermis and plays an essential role in the integrity of the stratum corneum.

Research tends to suggest a link between a disruption in the epithelial barrier and keratosis pilaris.

Beyond this genetic component, a hormonal influence is also suspected. Indeed, it is known that hyperandrogenism causes hyperkeratinization of the hair-sebaceous unit of terminal hairs in response to circulating androgens, a phenomenon that could lead to keratosis pilaris. Hyperandrogenism is more common in women and is characterized by high levels of testosterone. Most often associated with acne and hirsutism, it is possible that hyperandrogenism may have other less known consequences and that this condition also plays a role in the pathogenesis of keratosis pilaris.

It has also been suggested that insulin resistance could play a role in the development of keratosis pilaris. Indeed, a study showed that young patients with insulin-dependent diabetes had a higher prevalence of keratosis pilaris than healthy controls. Although the mechanisms at work have not been identified, the following hypothesis can be made: insulin resistance being associated with a low-grade chronic inflammation, this inflammation can affect the hair follicles and contribute to the development of keratosis pilaris.

Finally, studies have shown that there is a link between keratosis pilaris and certain skin conditions such as atopic eczema and ichthyosis, due to their common etiology. Indeed, atopic dermatitis is also caused by a dysfunction of the skin barrier due to an anomaly affecting the gene encoding for filaggrin. This results in a lack of sebum production, lipids, and cell adhesion molecules. Ichthyosis also develops on a particular genetic background and results in a strong dryness of the skin and the presence of scales on its surface.

Note : there are other factors that, while not causing keratosis pilaris, can intensify its symptoms. This is particularly the case with shaving, skin dryness, poor exfoliation, seasonal temperature changes, and contact with irritating substances.