What Causes Keratosis Pilaris (Chicken Skin)
Keratosis pilaris is caused by keratin accumulation in the hair follicles, where dead skin cells plug the follicular openings, creating the characteristic rough bumps on the skin. 1, 2
Primary Pathophysiology
- Keratin buildup is the fundamental mechanism—excess keratin protein blocks hair follicles, preventing normal hair growth and creating the distinctive "plucked chicken skin" appearance 1
- The condition results in follicular hyperkeratosis with small, folliculocentric keratotic papules that may have surrounding erythema 3, 4
- Dead skin cells that normally shed become trapped and form hard plugs within the follicles 2
Genetic Factors
- Inherited mutations play a significant role, particularly in the FLG (filaggrin) gene and ABCA12 gene 3
- Keratosis pilaris is considered a common inherited disorder with genetic predisposition 4
- The condition often runs in families, though it can occur sporadically 3
Associated Conditions
- Ichthyosis vulgaris and palmar hyperlinearity are commonly associated with keratosis pilaris 3
- The association with atopic dermatitis is less likely than previously thought, though some connection exists 3
- In rare cases, keratosis pilaris can form part of specific syndromes including cardio-facio-cutaneous syndrome, where it appears as follicular hyperkeratosis of the extremities and/or face 5
Clinical Presentation
- Most commonly affects the extensor aspects of upper arms, upper legs, and buttocks 4
- The small papules create a stippled appearance resembling gooseflesh 4
- Patients are usually asymptomatic, with complaints limited to cosmetic concerns or mild pruritus 4
Important Clinical Pitfall
While keratosis pilaris is typically a benign condition, clinicians should be aware that it can occasionally signal underlying genetic syndromes or be associated with other dermatologic conditions 1. However, in the vast majority of cases, it represents a common, isolated finding requiring only reassurance and symptomatic management if desired 3, 4.