Lipid Dysfunction, Sebaceous Glands and Keratosis Pilaris
In 2015 a fantastic study by Gruber et al compared 20 individuals with Keratosis Pilaris (KP) to 20 individuals with normal skin. Extensive testing was done including genetic analysis (Genotyping), skin pH, skin TEWL (trans epidermal water loss), and finally skin biopsies. Key findings to note as follows:
- All 20 individuals with KP had xerosis (significant loss of moisture from skin) "dry skin"
- Seven out of 20 who have KP had a common mutation in FLG gene (Filaggrin) whereas only 1 out of 20 of individuals without KP had any mutation in that gene
- All 20 had a "striking absence" of sebaceous glands!
No Sebaceous Glands - Why does this matter?
The lack of Sebaceous Glands leads to what I call the Lipid Dysfunction. Sebaceous glands are responsible for releasing Lipids we call "Sebum" (Free Fatty acids, Squalane, Triglyceride and Wax Esters). These critical components serve to first lubricate the hair shaft for proper hair maturation. Subsequently the lipids reach the skin surface where they serve many roles including moisture retention and skin protection.
When these lipids are not synthesized and delivered to the maturing infundibulum (the opening for hair shaft to exit), pathology ensues! The corneocytes within the infundibulum cannot shed properly leading to Hyperkeratinization... In effect this "dead" skin cells (corneocytes) cannot naturally move along due to a lack of lubricating oil. This leads to a blocked infundibulum which means the path for a hair follicle to exit is blocked! So normal hair follicle development is curtailed leading to a "plugged" orifice. These "plugs" are what we feel as the Bumpy part of KP.
1. Gruber R, et al. Sebaceous gland, hair shaft, and epidermal barrier abnormalities in keratosis pilaris with and without filaggrin deficiency. Am J Pathol. 2015 Apr
2. Giovannini et al. Zur histologie der keratosis pilaris. Archiv Dermatol Syphilis 1902