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J. Cosmet. Sci., 75.5, 339–352 (September/October 2024)
*Address all correspondence to Randy Wickett, wicketrr@ucmail.uc.edu
The Aging Skin Barrier
RANDALL WICKETT AND MARTHA TATE
James L. Winkle College of Pharmacy University of Cincinnati, Cincinnati, Ohio, USA (R.W.)
Tate Science LLC., Atlanta, Georgia, USA (M.T.)
Accepted for publication August 08, 2024.
Synopsis
It is well known that the population is aging as life spans increase, leading to both challenges and opportunities
for the cosmetic industry. There are many reviews that discuss the effect of aging and photoaging on the
dermal matrix or on the skin as a whole. The purpose of the current publication is to specifically review the
effect of age on the barrier function of the skin. After a brief discussion of the structure and formation of the
stratum corneum (SC) barrier we review the literature on the effect of age on the barrier and its function.
Observed increases in corneocyte size and lipid profiles are reviewed along with the decreasing rate of SC
turnover. The conflicting literature data on the effect of age on barrier function measured by transepidermal
water loss are discussed in detail. The effect of age on skin permeation and susceptibility to skin irritation are
also reviewed and the somewhat surprising result that both skin permeation and susceptibility to irritants
seem to decrease with age is discussed. The literature indicates that that the rate of SC turnover decreases with
age as does the rate of barrier repair after barrier disruption.
FORMATION AND STRUCTURE OF THE SKIN BARRIER
While there are previous reviews1–4 detailing the effect of aging and photoaging on the
dermal matrix or on the skin as a whole,4 here the focus is on the barrier function of the
skin, including permeation and susceptibility to irritants. Skin barrier function resides
primarily in the epidermis and barrier function is a vital function of the epidermis.5 Layers
of the epidermis are shown schematically in Figure 1.
The epidermal barrier defends the body from water loss to the environment, absorption
of noxious chemicals from the environment and microbial infection. These defensive
functions depend critically on the top layer, the SC, and are thought to be integrated with
SC formation and homeostasis.5,6
For 40 years the most common model of the SC barrier has been the “bricks and mortar”
model originally proposed by Elias.7 This model is based on the observation that corneocytes
are surrounded by the extracellular lipids of the SC and the corneocytes are modeled as
bricks and the lipids as mortar. Small, moderately hydrophobic molecules are thought to
penetrate the SC by diffusing through the extracellular lipids, winding their way around
the corneocytes.8 Harding has described an updated version of the bricks and mortar

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model that includes the presence of the desmosomes that hold SC cells together prior to
desquamation and discusses the role of natural moisturizing factor in SC function.9 This
model is illustrated in Figure 2.
The SC primarily forms in the stratum granulosum (SG), named for the granules that
appear in the cells comprised of keratohyalin granules10 composed of protein and lamellar
bodies that contain lipids.11,12 In the SG: the nucleus is digested, the cytoplasm disappears,
and the lipids that will eventually form the SC barrier are released into the intercellular
space.7,13–15 Epidermal keratins aggregate to form microfibrils16 inside the corneocytes
under the influence of filaggrin from the keratohyalin granules.17–19 The keratinocyte cell
membrane is replaced by the corneocyte cell envelope made of cross-linked protein from
the cytoplasm and keratohyalin granules and lipids that are covalently attached to its
Figure 1. Diagram showing layers of the epidermis. Illustration by Robin M. Wickett.
Figure 2. Schematic of the “bricks and mortar” model for human stratum corneum illustrating the corneocyte
“bricks,” the intercellular lipid “mortar” and the desmosomes connecting the corneocytes.