347 Aging Skin Barrier
Biniek at al.104 investigated the effect of age on the mechanical properties of isolated SC.
They reported that the SC stiffened with age, and that delamination energy increased with
age. These factors could potentially contribute to an increased tendency to form both cracks
and flakes in elderly skin.
Lactate is a component of the NMF that may be derived either from sweat105 or through
anaerobic metabolism in the upper epidermis.106 Nakagawa et al. investigated the correlation
between NMF components and SC stiffness, pH, and hydration in summer and winter with
healthy subjects.42 The only components that correlated significantly to SC stiffness and
hydration were lactate and potassium. One might expect that the slower metabolism of
aging skin reflected by the lower SC turnover rate might lead to lower levels of lactate in
the SC. However, Prahl and coworkers reported that keratinocytes from aging skin produce
higher levels of lactate ex vivo.107 It is well established that sweating rates decrease with
age108 which might lead to lower levels of lactate and thus stiffer, less well hydrated SC.
Another factor may be the decline sebum production that occurs with age109 especially
in post-menopausal women. Fluhr et al. have presented data from studies of asebic
mice, indicating that glycerol derived from the hydrolysis of sebum contributes to skin
hydration.110 Sebum production declines dramatically in women at menopause but does not
decline significantly in men before age 80109 so this may be relevant to post-menopausal
women but not to men before age 80.
It is also possible that the increased cholesterol sulfate observed in older subjects by Starr
et al.58 contributes to skin scaling. Congenital X-linked ichthyosis results from a defect in
the enzyme that convert cholesterol sulfate to cholesterol51 and there is evidence that this is
the main cause of the excessive skin scaling in this disease52 probably by inhibition of the
enzymes that break down SC desmosomes.111
Tagami’s et al. studied the dorsum of the hands of Japanese golfers who only wore a golfing
glove on one hand to compare intrinsic aging to photoaging on properties of the SC.103
Roughness of the skin surface was measured from silicon replicas. Interestingly, there was
a significant negative correlation between the difference in roughness between exposed
and covered hands and the golfer’s handicap. Better golfers (lower handicap) had larger
increases in roughness on their exposed hand. Hydration as measured by higher frequency
conductance was lower for the more exposed site. indicating a drier skin surface but there
was no difference in barrier function as measured by TEWL. Tojahn et al.112 compared sun-
exposed and protected skin on the arms of female subjects and also found no significant
difference between exposed and protected sites.
The tendency for elderly subjects to develop dry skin probably has multiple contributing
factors including lower PCA levels, the slower rate of SC renewal, lower levels of lactic acid
due to reduced sweating, possibly reduced glycerol due to reduced sebum production and
perhaps other factors that have yet to be discovered.
CONCLUSIONS
Aging and photoaging profoundly affect the structure of the dermis leading to well
characterized changes in skin structure and appearance.1–4,113 The effect of age on the
epidermal barrier is less obvious and less pronounced. Somewhat surprisingly there is little
or no decline in SC barrier function as measured by TEWL (see Table I) except for the
décolleté in women68 and one report on the forehead.69 In fact most studies indicate reduced
348 JOURNAL OF COSMETIC SCIENCE
TEWL with age on most body sites (Table 1 and Akdeniz et al.77) but while statistically
significant the observed TEWL reductions may not be clinically relevant as pointed out
above. It also appears that the immediate response of the SC barrier to applied irritants is
not greater in older skin.
One result that is likely to be of clinical significance is the significantly reduced rate of SC
barrier repair after disruption reported by Ghadially et al.85 This effect is possibly due to
the reduced turnover rate of the SC24,56 as discussed above. So, while the SC barrier may not
be easier to disrupt in elderly skin it is slower to heal once disrupted.
While the tendency of older subjects to develop dry skin is well known, the source of this
problem is not yet completely clear and deserves further study.
REFERENCES
(1) Lavker RM, Zheng PS, Dong G. Morphology of aged skin. Clin Geriatr Med. 1989 5:53–67.
(2) Gilchrest BA. Skin aging and photoaging: an overview. J Am Acad Dermatol. 1989 21:610–613.
(3) Kohl E, Steinbauer J, Landthaler M, Szeimies RM. Skin ageing. J Eur Acad Dermatol Venereol.
2011 25:873–884.
(4) Wickett RR, Tate M. Part 3.2.4 Compromised Skin in the Elderly. In: Rosen M, ed. Harry’s Cosmeticology.
9th ed. Volume 1. Gloucester, MA: Chemical Publishing Company Inc 2015:282–328.
(5) Madison KC. Barrier function of the skin: “la raison d’être” of the epidermis. J Invest Dermatol.
2003 121:231–241.
(6) Elias PM, Choi EH. Interactions among stratum corneum defensive functions. Exp Dermatol.
2005 14:719–726.
(7) Elias PM. Epidermal lipids, barrier function, and desquamation. J Invest Dermatol. 1983 80:44–50.
(8) Talreja P, Kleene N, Pickens W, Wang T, Kasting G. Visualization of the lipid barrier and measurement
of lipid pathlength in human stratum corneum. AAPS PharmSci J. 2001 3
(9) Harding CR. The stratum corneum: structure and function in health and disease. Dermatol Ther. 2004 17
Suppl 1:6–15.
(10) Odland GF. Structure of the skin. In: Goldsmith LA, ed. Physiology, Biochemistry and Molecular Biology of
the Skin. 2nd ed. New York, NY: Oxford University Press 1991:3–62.
(11) Odland GF. A submicroscopic granular component in human epidermis. J Invest Dermatol. 1960 34:11–15.
(12) Oashi M, Sawada Y, Makita R. Odland body and intercellular substances. Acta Derm Venereol Suppl
(Stockh). 1973 73:47–54.
(13) Elias PM, Grayson MA, Lampe MA, Williams ML, Brown BE. The Intercorneocyte Space. In: Marks R,
Plewig G, eds. Stratum Corneum. New York, NY: Springer-Verlag 1983:53–67.
(14) Elias PM, Menon GK. Structural and lipid biochemical correlates of the epidermal permeability barrier.
Adv Lipid Res. 1991 24:1–26.
(15) Wertz PW, Downing DT. Glycolipids in mammalian epidermis: structure and function in the water
barrier. Science. 1982 217:1261–1262.
(16) Steinert PM, North AC, Parry DA. Structural features of keratin intermediate filaments. J Invest
Dermatol. 1994 103:19S–24S.
(17) Dale BA, Holbrook KA, Kimball JR, Hoff M, Sun TT. Expression of epidermal keratins and filaggrin
during human fetal skin development. J Cell Biol. 1985 101:1257–1269.
(18) Dale BA, Presland RB, Lewis SP, Underwood RA, Fleckman P. Transient expression of epidermal
filaggrin in cultured cells causes collapse of intermediate filament networks with alteration of cell shape
and nuclear integrity. J Invest Dermatol. 1997 108:179–187.
Previous Page Next Page

Extracted Text (may have errors)

347 Aging Skin Barrier
Biniek at al.104 investigated the effect of age on the mechanical properties of isolated SC.
They reported that the SC stiffened with age, and that delamination energy increased with
age. These factors could potentially contribute to an increased tendency to form both cracks
and flakes in elderly skin.
Lactate is a component of the NMF that may be derived either from sweat105 or through
anaerobic metabolism in the upper epidermis.106 Nakagawa et al. investigated the correlation
between NMF components and SC stiffness, pH, and hydration in summer and winter with
healthy subjects.42 The only components that correlated significantly to SC stiffness and
hydration were lactate and potassium. One might expect that the slower metabolism of
aging skin reflected by the lower SC turnover rate might lead to lower levels of lactate in
the SC. However, Prahl and coworkers reported that keratinocytes from aging skin produce
higher levels of lactate ex vivo.107 It is well established that sweating rates decrease with
age108 which might lead to lower levels of lactate and thus stiffer, less well hydrated SC.
Another factor may be the decline sebum production that occurs with age109 especially
in post-menopausal women. Fluhr et al. have presented data from studies of asebic
mice, indicating that glycerol derived from the hydrolysis of sebum contributes to skin
hydration.110 Sebum production declines dramatically in women at menopause but does not
decline significantly in men before age 80109 so this may be relevant to post-menopausal
women but not to men before age 80.
It is also possible that the increased cholesterol sulfate observed in older subjects by Starr
et al.58 contributes to skin scaling. Congenital X-linked ichthyosis results from a defect in
the enzyme that convert cholesterol sulfate to cholesterol51 and there is evidence that this is
the main cause of the excessive skin scaling in this disease52 probably by inhibition of the
enzymes that break down SC desmosomes.111
Tagami’s et al. studied the dorsum of the hands of Japanese golfers who only wore a golfing
glove on one hand to compare intrinsic aging to photoaging on properties of the SC.103
Roughness of the skin surface was measured from silicon replicas. Interestingly, there was
a significant negative correlation between the difference in roughness between exposed
and covered hands and the golfer’s handicap. Better golfers (lower handicap) had larger
increases in roughness on their exposed hand. Hydration as measured by higher frequency
conductance was lower for the more exposed site. indicating a drier skin surface but there
was no difference in barrier function as measured by TEWL. Tojahn et al.112 compared sun-
exposed and protected skin on the arms of female subjects and also found no significant
difference between exposed and protected sites.
The tendency for elderly subjects to develop dry skin probably has multiple contributing
factors including lower PCA levels, the slower rate of SC renewal, lower levels of lactic acid
due to reduced sweating, possibly reduced glycerol due to reduced sebum production and
perhaps other factors that have yet to be discovered.
CONCLUSIONS
Aging and photoaging profoundly affect the structure of the dermis leading to well
characterized changes in skin structure and appearance.1–4,113 The effect of age on the
epidermal barrier is less obvious and less pronounced. Somewhat surprisingly there is little
or no decline in SC barrier function as measured by TEWL (see Table I) except for the
décolleté in women68 and one report on the forehead.69 In fact most studies indicate reduced
348 JOURNAL OF COSMETIC SCIENCE
TEWL with age on most body sites (Table 1 and Akdeniz et al.77) but while statistically
significant the observed TEWL reductions may not be clinically relevant as pointed out
above. It also appears that the immediate response of the SC barrier to applied irritants is
not greater in older skin.
One result that is likely to be of clinical significance is the significantly reduced rate of SC
barrier repair after disruption reported by Ghadially et al.85 This effect is possibly due to
the reduced turnover rate of the SC24,56 as discussed above. So, while the SC barrier may not
be easier to disrupt in elderly skin it is slower to heal once disrupted.
While the tendency of older subjects to develop dry skin is well known, the source of this
problem is not yet completely clear and deserves further study.
REFERENCES
(1) Lavker RM, Zheng PS, Dong G. Morphology of aged skin. Clin Geriatr Med. 1989 5:53–67.
(2) Gilchrest BA. Skin aging and photoaging: an overview. J Am Acad Dermatol. 1989 21:610–613.
(3) Kohl E, Steinbauer J, Landthaler M, Szeimies RM. Skin ageing. J Eur Acad Dermatol Venereol.
2011 25:873–884.
(4) Wickett RR, Tate M. Part 3.2.4 Compromised Skin in the Elderly. In: Rosen M, ed. Harry’s Cosmeticology.
9th ed. Volume 1. Gloucester, MA: Chemical Publishing Company Inc 2015:282–328.
(5) Madison KC. Barrier function of the skin: “la raison d’être” of the epidermis. J Invest Dermatol.
2003 121:231–241.
(6) Elias PM, Choi EH. Interactions among stratum corneum defensive functions. Exp Dermatol.
2005 14:719–726.
(7) Elias PM. Epidermal lipids, barrier function, and desquamation. J Invest Dermatol. 1983 80:44–50.
(8) Talreja P, Kleene N, Pickens W, Wang T, Kasting G. Visualization of the lipid barrier and measurement
of lipid pathlength in human stratum corneum. AAPS PharmSci J. 2001 3
(9) Harding CR. The stratum corneum: structure and function in health and disease. Dermatol Ther. 2004 17
Suppl 1:6–15.
(10) Odland GF. Structure of the skin. In: Goldsmith LA, ed. Physiology, Biochemistry and Molecular Biology of
the Skin. 2nd ed. New York, NY: Oxford University Press 1991:3–62.
(11) Odland GF. A submicroscopic granular component in human epidermis. J Invest Dermatol. 1960 34:11–15.
(12) Oashi M, Sawada Y, Makita R. Odland body and intercellular substances. Acta Derm Venereol Suppl
(Stockh). 1973 73:47–54.
(13) Elias PM, Grayson MA, Lampe MA, Williams ML, Brown BE. The Intercorneocyte Space. In: Marks R,
Plewig G, eds. Stratum Corneum. New York, NY: Springer-Verlag 1983:53–67.
(14) Elias PM, Menon GK. Structural and lipid biochemical correlates of the epidermal permeability barrier.
Adv Lipid Res. 1991 24:1–26.
(15) Wertz PW, Downing DT. Glycolipids in mammalian epidermis: structure and function in the water
barrier. Science. 1982 217:1261–1262.
(16) Steinert PM, North AC, Parry DA. Structural features of keratin intermediate filaments. J Invest
Dermatol. 1994 103:19S–24S.
(17) Dale BA, Holbrook KA, Kimball JR, Hoff M, Sun TT. Expression of epidermal keratins and filaggrin
during human fetal skin development. J Cell Biol. 1985 101:1257–1269.
(18) Dale BA, Presland RB, Lewis SP, Underwood RA, Fleckman P. Transient expression of epidermal
filaggrin in cultured cells causes collapse of intermediate filament networks with alteration of cell shape
and nuclear integrity. J Invest Dermatol. 1997 108:179–187.

Help

loading