Keratosis Pilaris: Causes, Pathophysiology, and Treatment Options

KERATOSIS PILARIS
Introduction
Keratosis pilaris is a common benign skin disorder. The condition is characterized
by the appearance of sometimes itchy, tiny, goose bump like eruptions on the skin that
sometimes occur with inflammation .Gerbig, A. W,(2012) indicates that on most occasions the
eruptions appear on the lateral aspect of the upper arm,face,trunk and the surface of the
gluteus region. The appearance of Keratosis pilaris is uncommon on glabrous skin. This skin
abnormality results in spotting of the skin accompanied by irritation hence a scratching reflex.
The scratching results in inflammation, worsened by cold environment and pregnancy.
Keratosis pilaris is also common in the pediatric population especially in children with ichthyosis
vulgaris and atopic eczema (B. Mevorah, A. Marazzi, E. Frenk,2015). The occurrence in the
aged population is variable but with the elderly it is uncommon.
Etiology
The condition is caused by abnormal distribution of keratin lining the proximal
portion of the follicular infundibulum. This ends up in scale filling of the follicle limiting
physiological exfoliation. Genetic inheritance also determines the manifestation (Gerbig, A. W.,
2012). The trait is autosomal dorminant hence with exposure the penetrance in next generation
has an increased incidence of having the condition. Dermal distribution of Keratosis pilaris(KP)
is quite symmetrical and scaly spots appear red or brown and may not be sore. The clinical
expression is also determined by both environmental condition and humidity. There is strong
association between FLG mutations and Keratosis Pilaris cold regions than equatorial locales

(S.C. Cai et Al, 2012).There is also evidenced increase acquired cases of KP in underlying
diseases like diabetes, obesity and Vitamin A deficiency malnutrition.
Pathophysiology and Effect to barrier function
KP has an unknown pathogenesis. It is based on hyperkeratinization of the skin.
There is a crucial association between KP and atopic dermatitis thus a possibility of association
of KP with the FLG deficiency. The FLG protein is a major structural protein of the dermis which
aggregates keratin filaments to corneocytes and is also hydrolyzed to individual amino acids
with osmotically active properties (S. Kezic et al, 2011) . The amino acids contribute to 50% of
the moisturization of the stratum corneum and also facilitate photo protection and acidification
of the skin surface. The study done by (Khumalo et al.., 2012) indicates nonsense mutations of
the FLG protein end up in reduction of stratum corneum moisturization. More to this, the hair is
trapped beneath the keratin debris. Erythema occurs around the hair follicles because of local
inflammation. The coiled hair is visible beneath the papule, the papules being a result of
accumulation of keratin all around the follicular orifice limiting hydration, sweating and
excretion.
Chemical peel treatment of KP
KP affects the functioning of the skin and the clinical manifestation is a nuisance.
The itch, skin dryness and the inflammation on skin is uncomfortable. Management involves
resurfacing procedures which can be chemical or microdermabrasion (Klar et al,
2015 ).Microdermabrasion techniques involve use of a microcrystal spray on the stratum
corneum to remove excess keratin. There is regeneration of the stratum corneum with

increased synthesis of collagen and elastin filaments on the dermal surface. This procedure is
suitable for minute and superficial scars and procedures reliable outcomes on skin papules. In
some instances the procedure can aggravate acne and result in an hypersensitivity reaction
worsening the prognosis especially in individuals with autoimmune disorders and diabetes.
Chemical methods unlike mcrodermabrassion are suitable of deep scars and active cases of
acne. Various combinations of dermal ointments containing glycolic acid, lactic acid, retinol,
urea or salicylic acid are used. The application of chemical or peel ointments including alfa-
hydroxy acids (AHA) are productive after skin exfoliation and produce better accuracy with an
increased surface area of skin covered (Fischer et al,2010).
The specificity of a resurfacing procedure is determined by the patients’ allergic
response and the state of the dermis. In cases of erythema around affected regions, application
of chemical peels is suitable. Inflammation requires the application of steroids including
predisilone to manage the local inflammation. Microdermabrassion on the other hand is an
independent procedure. The procedure involves direction of a stream of micro-aluminum oxide
crystals to the affected dirt. A gun is placed on the individual skin at a constant emission rate
and duration. The crystals from the gun exfoliate the stratum corneum and the affected
hyperkeratinized papules. The mild suction produced results on the removal of the skin debris
and the remaining tiny aluminum crystals.
Furthermore, removal of the excess hyperkeratinized skin facilitates regeneration
of the stratum corneum from the underlying dermal epithelium .The body response mechanism
triggers synthesis of new collagen and elastin filaments reinforced with keratin. Skin therapy by

the procedure produces thick and healthy strata. Treatment involve multiple sessions for a
better outcome with a common reference of six to ten sessions on a programmed span break of
two weeks between sessions under the patients specification module and response to
treatment. Microdermapression is usually painless and a single session takes half an hour to a
full hour under sterile conditions. Treatment of KP using the set procedure causes exfoliation
and synthesis of skin and increased sensitivity to stimuli and light that should be managed.
Healing process
The skin is covered with Keratin which forms the barrier to physical, mechanical
and chemical modalities that may result in injury. There is also protection from the entry of
bacteria that would end up causing an infection .Microdermabrassion results in the exfoliation
this external surface and limits the protection mechanism. The pilosebaceous unit is also
responsible for the protection through the production of secretions including sweat that
provide the chemical barrier. The resurfacing procedure results in the removal of most of the
protective layer due to the peeling process of the hyperkeratinized skin. Initiation of the healing
process involves the stem cells in the stratum basale, which has regenerative capacity.
Stratum corneum replacement involves a physiological feedback mechanism, the
stratum corneum work in homeostasis with the underlying stratum basale. The process of
desquamation skin cells off the skin occurs in tandem with the proliferation of the new
keratinocyctes formed in the germinative layer, the stratum Basale (Hwang, S., & Schwartz, R.
A..., 2008). After the procedure of microdermapression, most of the stratum corneum is
exfoliated, the process of cornificartion ensues. Cornification involves the transformation of the