Cutaneous Biophysical Characteristics of
Melasma
by
Dong Jun Lee
Major in Medicine
Department of Medical Sciences
The Graduate School, Ajou University
Cutaneous Biophysical Characteristics of
Melasma
by
Dong Jun Lee
A Dissertation Submitted to The Graduate School of Ajou
University in Partial Fulfillment of the Requirements for the
Degree of Master of Medicine
Supervised by
Hee Young Kang, M.D., Ph.D.
Major in Medicine
Department of Medical Sciences
The Graduate School, Ajou University
August, 2011
This certifies that the dissertation
of Dong Jun Lee is approved.
SUPERVISORY COMMITTEE
Hee Young Kang
Eun-So Lee
You Chan Kim
The Graduate School, Ajou University
June 23rd, 2011
감사
본 논 시작에 끝 지 심 양면 도움 주시고 지도
조언 아끼지 않 셨 지도 이신 강희 님께 감사를
드립니다. 또한 좋 연구를 할 있도 부족한 가 많 가르침
주시고 격 를 주신 이 소 님과 찬 님께도 감사
마 합니다.
그리고 연구 간 동안 도움 주신 피부 과학 실 모든
생님들과 실험 여러 과 도 주신 IEC Korea Skin Research
Center 하재 생님, 이 생님과 조직 염색과 분 도 주신
배 생님께 감사 드립니다. 언 나 아낌 없는 사랑 지원해
주시는 부모님, 가족들에게도 감사 마 합니다.
2011 6 월
자씀
i
- ABSTRACT-
Cutaneous Biophysical Characteristics of Melasma
Background: Melasma is characterized by increased pigmentation and photodamaged
skin. These features suggest that melasma patients might have a significant impact on
cutaneous biophysical characteristics.
Objective: The cutaneous biophysical characteristics in melasma were investigated.
Methods: A total of 16 Korean volunteers with melasma were enrolled. The melanin
index/erythema index, stratum corneum (SC) hydration, sebum content, and
transepidermal water loss (TEWL) were measured and compared between lesional and
perilesional normal skin. The TEWL was re-measured immediately and 5 hours after tape
stripping to investigate SC integrity and barrier recovery rate. The sebum content was
measured at 30 minutes and 5 hours after degreasing by facial washing to estimate the
sebum excretion rate. Skin biopsy was performed in 11 volunteers to measure the SC
thickness and to study the expression of lipid metabolism associated genes such as
peroxisome proliferator-activated receptor alpha (PPAR-α), and arachidonate 15-
lipoxygenase, type B (ALOX15B).
Results: The melanin index, erythema index, and SC hydration were significantly higher
in lesional skin compared to nonlesional skin, whereas the measurement of basal TEWL
showed no significant difference. However, the increased rate of TEWL after tape-
stripping was significant higher in lesional skin compared to nonlesional skin. Also,
ii
barrier recovery rate of lesional skin was significant delayed. The melanin index was
found to be inversely correlated with the barrier recovery rate. There was no significant
difference between the basal sebum content and the sebum excretion rate. The expression
between PPAR-α and ALOX15B was not significantly different, whereas SC thickness
was reduced in lesional skin, which showed correlation with the barrier recovery rate.
Conclusions: Melasma skin showed a normal hydration state and sebaceous gland
activity. However, the SC integrity and barrier function were impaired in lesional skin of
melasma. The SC thickness was reduced in lesional skin, and it positively correlated with
the barrier recovery rate. These results suggest that improving SC function should be
considered in treating melasma.
Keywords: Melasma, Stratum corneum, Barrier function, TEWL
iii
TABLE OF CONTENTS
ABSTARCT ·············································································································· i
TABLE OF CONTENTS ························································································· iii
LIST OF FIGURES ································································································· iv
LIST OF TABLES ···································································································· v
I. INTRODUCTION ································································································· 1
II. MATERIALS AND METHODS ·········································································· 3
A. Subjects ·········································································································· 3
B. Measurement of biophysical properties ··························································· 5
C. Measurement of stratum corneum thickness and immunohistochemistry ·········· 5
D. Statistical analysis ···························································································· 6
III. RESULTS ··········································································································· 8
A. Melanin index and erythema index ····································································· 8
B. Basal stratum corneum properties ····································································· 10
C. Epidermal permeability barrier function ···························································· 11
D. Sebum content ·································································································· 13
E. Expressions of PPAR-α and ALOX15B and SC thickness ································· 14
IV. DISCUSSION ··································································································· 17
V. CONCLUSION ·································································································· 22
REFERENCES ······································································································· 23
국 요약 ················································································································ 26
iv
LIST OF FIGURES
Fig. 1. Melanin/Erythema index ·················································································· 8
Fig. 2. Stratum corneum capacitance ········································································· 10
Fig. 3. Basal TEWL ·································································································· 11
Fig. 4. Barrier recovery rate ······················································································ 12
Fig. 5. Correlation between melanin index and barrier recovery rate ·························· 13
Fig. 6. Sebum contents ······························································································ 14
Fig. 7. Expressions of PPAR-α and ALOX15B and stratum corneum thickness ········· 15
Fig. 8. Stratum corneum thickness and correlation with barrier recovery rate ············· 16
v
LIST OF TABLES
Table 1. General characteristics of volunteers ····························································· 4
- 1 -
I. INTRODUCTION
Melasma is a common acquired hyperpigmentary disorder characterized by
irregular light to dark brown macules and patches on sun-exposed skin.(Kang et al., 2002) A
major histopathological feature of melasma is an increased epidermal pigmentation. Melanin
is concentrated in the basal layer but also distributed throughout the epidermis. It has been
thought that skin pigmentation is associated with multiple cutaneous functions. Stratum
corneum (SC) in black skin contains more cell layers and greater electrical resistance and
requires more tape strips to remove it than that of white skin, suggesting better intercellular
cohesion in black skin.(Berardesca and Maibach, 1996) Moreover, epidermal barrier function
is different between blacks and white skin, although the results are inconclusive. Darker skin
has been shown to recover faster after barrier damage.(Reed et al., 1995) Whereas,
Kompaore et al.(Kompaore et al., 1993) found significant higher transepidermal water loss
(TEWL) after stripping in blacks and Asians than in whites. These findings suggest that
lesional skin of melasma may have different biophysical characteristics compare to non-
lesional skin.
Additional distinguishing histological characteristics of melasma are the features of
photodamaged skin. It is reported that Melasma lesions show a higher degree of UV-induced
damage, like solar elastosis and increased vascularity.(Kang et al., 2002; Kim et al., 2007;
Hernandez-Barrera et al., 2008) Photodamaged skin has been thought to have modified
cutaneous functions. Barrier recovery is delayed in photoaged skin as compared to
chronologically aged skin.(Reed et al., 1997) Moreover, recently we found that most lipid
- 2 -
metabolism-associated genes such as peroxisome proliferator-activated receptor alpha
(PPARA) and arachidonate 15-lipoxygenase, type B (ALOX15B) were down-regulated,
accompanying a delayed barrier recovery rate in lesional skin.(Kang et al., 2011) These
findings suggest that cutaneous biophysical characteristics may have a significant impact on
melasma patients.
Therefore, in this study, I measured the cutaneous biophysical characteristics of
melasma including SC hydration, sebum content, and TEWL and made comparisons between
lesional and perilesional normal skin.
- 3 -
II. MATERIALS AND METHODS
A. Subjects
A total of 16 female Korean volunteers with melasma were recruited. The mean age
was 44.2±5.36 years old (31-55 years old), and the average of disease duration was 12.9±7.2
years. All subjects have Fitzpatrick skin type III or IV. All subjects had a washout period of
at least one month from a bleaching agent or steroid containing triple agents and a washout
period of at least one year from lasers, dermabrasion, and chemical peeling. No skin care
products had been applied to the measured sites 24 hours prior to the measurements, and the
measured sites had not been washed with soaps or surfactants for at least two hours prior to
the study. A two-millimeter punch biopsy from lesional and perilesional skin of melasma was
performed in 11 of 16 volunteers. Informed written consent was obtained. This study was
approved by the institutional review board of Ajou University Hospital (IRB number:
AJIRB-MED-DEO-10-152).
- 4 -
Table 1. General characteristics of volunteers
Age Skin type Disease duration
(yrs)
Previous Medical history Skin biopsy
1 42 IV 30 None O
2 31 IV 2.3 None O
3 44 IV 5 None O
4 55 IV 20 None O
5 46 IV 23 None O
6 42 III 10 None X
7 46 III 15 None O
8 47 III 7 None X
9 51 III 18 None O
10 39 III 15 None X
11 44 III 20 None O
12 44 III 7 Anemia, Thyroid nodule X
13 43 III 10 None X
14 48 III 20 Diabetes mellitus O
15 46 IV 14 None O
16 39 III 10 None O
- 5 -
B. Measurements of biophysical characteristics
The melanin/erythema index, SC hydration capacitance, TEWL and amount of
sebum were measured on lesional and perilesional skin by respective probes (Mexameter:
MX16®; Corneometer: CM825®; Tewameter: TM210®; Sebumeter: SM810®) connected
to MPA-5® (Courage+Khazaka electronic GmbH, Köln, Germany). SC capacitance and
melanin/erythema index were measured on the right side of the face, and the final value was
expressed as the mean of three readings. TEWL was assessed on the left side of the face.
After baseline measurement of TEWL, barrier perturbation was performed by 5 times
repeated tape stripping (D-squame®) for barrier recovery rate measurement. TEWL was
measured immediately and 5 hours after tape stripping. Sebum amount was measured at 30
minutes after facial washing and at 5 hours after degreasing to evaluate sebum excretion rate.
All measurements were performed in an environmentally controlled research facility that
maintained an ambient temperature at 22-24 and relative humidity of 50℃ -55%. All
volunteers were allowed to acclimatize for 30 minutes prior to the test in order to adapt to the
room conditions.
C. Measurement of stratum corneum thickness and immunohistochemistry
Hematoxylin and eosin staining was performed using standard protocols. Under
H&E stain, digital images were captured (SPOT Flex®, SPOT Imaging Solutions, Sterling
Heights, MI, USA) for estimating the area of SC and length of SC baseline. SC thickness
was measured by the ratio of area and length of SC baseline.
In immunohistochemial analyses, formalin-fixed and paraffin-embedded tissue was
- 6 -
serial sectioned at 4.5μm and deparaffinized and rehydrated by sequential immersion in
xylene, graded concentrations of ethanol. The deparaffinized tissue sections were incubated
for 30 minutes at room temperature in a solution of 0.5% hydrogen peroxidase in methanol
to quench endogenous peroxidase activity, followed by heated for 20 minutes with citrate
buffer at pH 6.0 in a microwave or pretreated with trypsine for 10 minutes in 42 for ℃
antigen retrieval. After washing by Tris-buffered saline (TBS, 0.1mol/L, pH7.4, Dako,
Carpinteria, CA), tissue sections were incubated with primary antibodies for 30 minutes at
38 . ℃ A monoclonal antibody to peroxisome proliferator-activated receptor-α (PPAR-α;
Abcam, Cambridge, U.K.) and arachidonate 15-lipoxygenase, type B (ALOX15B, Lifespan
Biosciences, Seattle, WA, USA) were used with 1:200 and 1:100 dilution respectively. After
incubation with secondary antibody for 10 minutes, horseradish peroxidase (HRP) complex
and AEC chromogen were added for 15 minutes and 20 minutes respectively, followed by,
counterstaing was performed with hematoxylin. The image was analyzed using Image-Pro
Plus Version 4.5 (Media Cybernetics co., Silver Spring, MD, USA).
D. Statistical analysis
The SPSS 14.0 statistics program (SPSS, Inc., Chicago, IL, USA) and the GraphPad
Prism 5 software (GraphPad Software, Inc., La Jolla, CA, USA) was used for all statistical
analysis. If the data showed normality distribution, the independent t-test was used to
analyze the statistically significant difference between the melasma-involved and
perilesional normal skin; if it does not, Mann-Whitney test was used. The relationship
between each biophysical property was tested with Spearson correlation. A value of less than
- 7 -
0.05 was considered to be statistically significant. Data are expressed as mean ± standard
deviation (SD).
- 8 -
III. RESULTS
A. Melanin index and erythema index
The melanin index was significantly higher in lesional skin than in perilesional
normal skin (221.4±54.3 vs. 150.4±29.9, p<0.001; Fig 1A). The erythema index was
significantly increased in lesional skin than perilesional normal skin (323.2±60.3 vs.
272.3±34.8, p<0.012; Fig 1B). The melanin and erythema index showed a positive
correlation (Correlation coefficient: 0.703, p<0.01; Fig 1C).
A.
- 9 -
B.
C.
Fig. 1. Melanin/Erythema index; Comparison of melanin/erythema index between lesional
skin and perilesional normal skin; A. Melanin index, B. Erythema index, C. Correlation
between melanin/erythema index; Melanin index and erythema index showed positive
correlation. (*p< 0.05)
- 10 -
B. Basal stratum corneum properties
The SC hydration was significantly increased in lesional skin compared to
perilesional normal skin (66.9±9.9 vs. 58.4±10.1; p<0.029; Fig.2). However, the basal
TEWL showed no significant difference between lesional and perilesional normal skin
(15.6±4.6 vs. 13.5±4.0, p=0.210; Fig 3).
Fig. 2. Stratum corneum capacitance; Stratum corneum capacitance was significantly
higher in melasma-involved skin than perilesional normal skin. (*p< 0.05)
- 11 -
Fig. 3. Basal TEWL: There was no significant difference between lesional skin and
perilesional normal skin. (*p< 0.05)
C. Epidermal permeability barrier function
Immediately after tape stripping, the increased rate of TEWL in lesional skin was
significantly higher than that of perilesional normal skin (%, 143.2±116.4 vs. 79.5±40.9,
p=0.014; Fig 4). Furthermore, 5 hours after 5 times of tape stripping, a significant delayed
barrier recovery rate was demonstrated in lesional skin in comparison to perilesional normal
skin (%, 62.5±22.8 vs. 76.3±12.3, p=0.043; Fig 4). The melanin level was found to be
inversely correlated with TEWL levels after tape stripping (Correlation coefficient: -0.503,
p<0.05; Fig 5).
- 12 -
Fig. 4. Barrier recovery rate: Immediately after tape-stripping 5 times, the rate of TEWL in
lesional skin was significantly higher in comparison to perilesional normal skin. In addition,
5 hours after the tape stripping, the barrier recovery rate was significantly delayed in lesional
skin in comparison to perilesional normal skin. (*p< 0.05)
- 13 -
Fig. 5. Correlation between melanin index and epidermal barrier recovery rate: There
was negative correlation between the melanin index and barrier recovery rate.
D. Sebum content
Sebum amount measurement showed no significant difference between lesional
skin and perilesional normal skin at 30 minutes after facial washing (μg/cm2, 7.9±5.8 vs.
10.6±14.5, p=0.897, Fig 6). After 5 hours for acclimatization, the amount of sebum and the
sebum excretion rate during 5 hours showed no significant difference (μg/cm2, 5 hours after
degreasing: 20.5±15.4 vs. 22.4±24.1, p=0.752, Fig 6).
- 14 -
Fig. 6. Sebum contents: There were no significant differences in sebum amount at both 30
minutes and 5 hours after facial degreasing.
E. Expressions of PPAR-α and ALOX15B and SC thickness
Because lipid metabolism related genes, such as PPARA and ALOX15B were found
to be down-regulated in melasma, we examined their protein levels.(Kang et al., 2011) There
was no significant difference in immunoreactivity of PPAR-α and ALOX15B between
lesional and perilesional normal skin (Fig 7). However, we found that the SC thickness was
reduced in the lesional skin of melasma in comparison with perilesional normal skin (µm,
10.4±2.9 vs. 14.5±5.5, p=0.052, Fig 7, 8A). The SC thickness showed positive correlation
with epidermal barrier recovery rate (Correlation coefficient: 0.721, p=0.02; Fig 8B)
- 15 -
Fig. 7. Expressions of PPAR-α and ALOX15B and stratum corneum thickness: A.
Stratum corneum thickness was lower in lesional skin compared to perilesional normal skin.
B, C. There was no significant difference of PPAR-α and ALOX15B expression between
lesional and perilesional normal skin. (N: perilesional normal skin, L: Lesional skin. original
magnification x200)
- 16 -
A.
B.
Fig. 8. Stratum corneum thickness and correlation with barrier recovery rate; A. SC of
lesional skin showed reduced tendency in comparison with perilesional normal skin. B. SC
thickness showed positive correlation between epidermal barrier recovery rate.
- 17 -
IV. DISCUSSION
The present study demonstrated that melasma skin showed a normal hydration state
and sebaceous gland activity. However, the SC integrity and barrier function were impaired
in the lesional skin of melasma. The SC thickness was reduced in lesional skin, and it
correlated with the barrier recovery rate. The melanin index was also significantly related
with delayed barrier recovery.
The mechanisms underlying abnormal barrier function in melasma are unclear, but
there are possible explanations. Recently, we found the lipid metabolism-associated genes
such as peroxisome proliferator-activated receptor alpha (PPARA), arachidonate 15-
lipoxygenase, and type B (ALOX15B) were down-regulated in the lesional skin of melasma
(Kang et al., 2011). It is well known that the lipids of SC play an important role in
maintaining cutaneous barrier homeostasis. PPAR-α is an important regulator of lipid
catabolism, mediating fatty acid oxidation, fatty acid uptake, and lipoprotein assembly and
transport.(Mao-Qiang et al., 2004) Therefore, down-regulated lipid metabolism-associated
genes may be a causal factor of the impairment of epidermal barrier function in melasma,
although we could not confirm the down-regulation of these proteins by
- 18 -
immnohistochemical staining. The reduced SC thickness may play another role in barrier
impairment in lesional skin. In our study, reduced SC thickness was significantly related with
delayed barrier recovery. SC thickness is correlated linearly to the 1/TEWL value
(Weigmann et al., 2005). Furthermore, it has been reported that SC thickness is significantly
correlated with the objective score of atopic dermatitis (Nemoto-Hasebe et al., 2009). Also,
SC thickness is significantly decreased in acute eczematous atopic skin compared to non-
lesional and control healthy skin (Voegeli et al., 2009). That means that SC thickness may
influence the epidermal barrier homeostasis. Taken together, it is speculated that reduced SC
thickness and down-regulation of lipid metabolism related genes in melasma affect the
barrier function in melasma.
Chronic UV exposure may be another possible explanation for impaired barrier
function in melasma. UV exposure is a major triggering or aggravating factor for melasma
development. Indeed, previous studies have indicated that melasma lesions show a higher
degree of UV-induced damage. Increased solar elastosis in lesional skin has been shown. It
has also been shown that melasma is characterized by increased vasculature in the lesional
skin both clinically and histologically (Voegeli et al., 2009). Expression of VEGF, a major
- 19 -
angiogenic factor of UV irradiated skin, is upregulated in melasma lesions compared to
perilesional normal skin. In literature, chronic UV exposure influences cutaneous fatty acid
metabolism and barrier function (Merle et al., 2010). Also, chronic UV irradiation reduces
the epidermal free fatty acid and triglyceride synthesis that has an important role in
epidermal barrier homeostasis (Kim et al., 2010). In addition, UVB exposure is detrimental
to the epidermal permeability barrier in a dose- and time- dependent manner (Haratake et al.,
1997). In photo-aged skin, barrier recovery is known to be significantly delayed (Reed et al.,
1997). Therefore, an altered barrier function in melasma might be a result of the chronic UV
exposure and accompanying epidermal hyperpigmentation. Interestingly, we found a
negative correlation between melanin index and barrier recovery rate. It means that patients
with severe melasma may have poor SC.
Very recently, it has been suggested that barrier function is influenced by
pigmentation in the SC (Elias et al., 2009). Gunathilake et al. (Gunathilake et al., 2009)
reported that skin type IV-V subjects have more acidic SC due to more melanosomes than
pale-skinned subjects, and these acidic conditions were attributed to enhanced SC integrity
and accelerated barrier recovery in darker skins (Bhatnagar et al., 1993; Puri et al., 2000).
- 20 -
Unfortunately, we did not measure the skin surface pH but the present study does not reveal
a positive relationship between melanin index and barrier recovery rate. Rather, there was a
negative correlation. These difference might be explained by the fact that molecules of
melanin in melasma are different from normal melanin (Moncada et al., 2009). Especially,
Raman skin spectroscopy measurements showed that melasma patients have degraded
melanin in the SC of lesional skin. Of course, there are inter-individual differences in
subjects’ race and geographic location.
The present study also demonstrated a significant increase of both the melanin and
erythema index in melasma-involved skin. Also, a positive correlation appeared between the
melanin index and the erythema index. The increased melanin index was reflected as the
hallmark of melasma in histological studies such as epidermal hyperpigmentation (Kang et
al., 2002). Furthermore, the increased erythema index in melasma-involved skin
corresponded with the results of earlier studies, which reported that melasma patients
showed higher erythema intensity and increased vascularity in the melasma lesions than that
of perilesional normal skin (Kim et al., 2007). In a histopathologic study, the number of
dermal vessels had a positive relationship with pigmentation in lesional skin (Kim et al.,
- 21 -
2007). These results have suggested that the connection between vessels and cutaneous
pigmentation. It should be further studied on a large scale in the future.
- 22 -
V. CONCLUSION
In conclusion, in the present study, I have demonstrated that the melanin index,
erythema index and SC hydration were significantly higher in lesional skin compared to
perilesional normal skin. However, the basal TEWL and sebum excretion rate showed no
significant difference. Interestingly, the epidermal barrier recovery in lesional skin is delayed,
and SC integrity is decreased in lesional skin compared to perilesional normal skin. The
melanin index showed to be inversely correlated with the barrier recovery rate. In
histopathologically, SC thickness in lesional skin decreased than perilesional normal skin
and correlated with the barrier recovery rate. These findings suggested that melasma skin
have a normal hydration state and sebaceous gland activity, whereas the SC integrity and
barrier function were impaired in melasma skin. Decreased SC integrity is one of major
biophysical characteristic of melasma.
- 23 -
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- 국 요약 -
미 피부 생 리학 특
아주 학 학원 학과
이 동
(지도 : 강 희 )
연구 경: 미는 피부 피 색소 증가 손상 피부를 특징 하는
질 이다. 이런 미 조직학 특징 미 자에 있어 피부 리학
특 변 를 야 시켰 것 생각 다.
연구목 : 따라 본 연구에 는 미 병변에 피부 리학 특 인
상 피부 하여 살펴보았다.
연구 법: 16 명 미 자를 모집하여 라닌 지 , 지 , 피 분량,
피지량, 경 피 분 손실량 미 피부 병변과 인 상 피부에 하 다.
경 피 분 손실량 경우 5 회 이프 스트리핑 법 피부 장벽에 손상
가한 직후 5 시간 동안 피부 안 취한 후 재 하여 각질 안
피부 장벽 회복 속도를 하 다. 피지량 경우 얼굴 가볍게 한
이후 각각 30 분, 5 시간 동안 피부 안 취한 후 하 다. 11 명
자에 는 2mm punch 를 이용하여 병변 인 상 피부에 피부 조직
검사를 시행하여 각질 게 지질 사 자인 peroxisome
- 27 -
proliferator-activated receptor alpha (PPAR-α), and arachidonate 15-lipoxygenase, type B
(ALOX15B) 면역조직 학염색 시행하 다.
연구결과: 라닌 지 , 지 피부 분량 인 피부에 해 미
병변에 통계 하게 증가한 면 초 경 피 분 손실량 미
상 피부 사이에 통계 한 차이는 보이지 않았다. 하지만 이프 스트리핑
법 피부 장벽에 손상 가한 직후에 한 경 피 분 손실량
증가 미 병변에 인 상 피부에 피해 통계 하게 증가 어
있었 며 5 시간 후 한 피부 장벽 회복 미 병변이 인 상 피부에
해 통계 하게 감소하는 양상 찰 었다. 또한 라닌 지 피부 장벽
회복 속도간에 상 계가 있는 것 나타났다. 미 병변과 인 상
피부 사이에 피지량 통계 한 차이를 보이지 않았다. 피부 조직에
PPAR-α ALOX15B 미 상 피부 사이에 차이를 보이지
않았 나 각질 께는 미 병변에 감소 는 양상 찰 었다. 또한 이
각질 께는 장벽 회복 속도 양 상 계가 있었다.
결 : 미 병변 상 인 분 함 량과 피지 분 를 보 다. 하지만
각질 안 장벽 능 미 병변이 인 상 피부에 해 손상 어
있 인할 있었다. 각질 께는 미 병변에 감소 어 있었 며
이는 피부 장벽 회복 속도 양 상 계가 있었다. 따라 이 연구는 피부
장벽 능 회복 또한 미 료에 있어 고 해야 한다는 것 시하는
결과라 할 있다.
핵심어: 미, 각질 , 피부 장벽 능, 경 피 분 손실량