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CURICULUM VITAE
Nama
Tempat dan tanggal lahir
Alamat Rumah
Status Kepegawaian
Jabatan
: HENDRA GUNAWAN, dr. SpKK(K), Ph.D, FINSDV
: Jakarta, 15 September 1969
: Jl. Tambak C No. 28 Jakarta Pusat 10320
: Pegawai Negeri Sipil Departemen Kesehatan
: Kepala Divisi Dermatologi Infeksi
Departemen Ilmu Kesehatan Kulit dan Kelamin
Fakultas Kedokteran Universitas Padjadjaran/
RSUP Dr. Hasan Sadikin Bandung
: Departemen Ilmu Kesehatan Kulit dan Kelamin
Faklutas Kedokteran Universitas Padjadjaran/RSHS Jl. Pasteur No. 38
Bandung
Alamat Kantor
Riwayat Pendidikan
Fakultas Kedokteran UNPAD Bandung
Diploma Course in Dermatology Bangkok, Thailand PPDS I.K.
Kulit dan Kelamin FK UNPAD, Bandung Program Doktoral
Juntendo University Tokyo, Jepang Fellowship in
Dermatopathology and Dermoscopy
Toranomon Hospital Tokyo, Jepang
Lulus tahun
Lulus tahun
Lulus tahun
Lulus tahun
Tahun 2014
1994
2002
2005
2008
Riwayat Pekerjaan
Dokter BPPKA Pertamina
Kepala Puskesmas Mapin Kebak Sumbawa
Dokter RS M.H. Thamrin Pondok Gede Jakarta
Staf Departemen I.K. Kulit dan Kelamin RSHS
Tahun
Tahun
Tahun
Tahun
1994-1995
1995-1998
1998-1999
2006-sekarang
Basic Knowledge
Hendra Gunawan
Department Dermatology and Venereology
Faculty of Medicine Universitas Padjadjaran/Hasan Sadikin Hospital Bandung
5. Manifestation of facial wrinkle
4. Histology of wrinkle
3. Pathogenesis of wrinkle
2. Factors in developing wrinkle
1. Nature of wrinkle
OVERVIEW
• When the effects of skin aging on face are addressed,
what is really being discussed is …
INTRODUCTION
• Aging  process that occurs in all organs,
but most visible in the skin
Facial
Aging
Facial Wrinkles
Wrinkle
Rhytid
CRINKLE
CREASE
Crevice
One indicator of skin aging that appear as
furrows or lines on the facial skin surface.
INTRODUCTION
Multifactorial
etiology Consequence
intrinsic &
extrinsic aging
Baumann L. Wrinled skin. In: Cosmetic dermatology.. 2009. p. 145-7.
• Fine wrinkles  flattening epidermis & atrophy
dermal papilla
Wells
(1954)
• Wrinkling  worsened by  brittleness of
horny layer with aging
Lorincz
(1960)
• Histologically  couldn’t differentiate
wrinkle from surrounding skin
Wright &
Shellow
(1965)
NATURE OF WRINKLE
Is the wrinkle a histological non-entity?
NATURE OF WRINKLE
Montagna and Carlisel (1979)
Nothing peculiar can be seen in histological
preparations of wrinkle
WRINKLE
DMS
Structure
Extrinsic
Aging
Immune
System
Genetic
Intrinsic
Aging
PARTICIPANTS IN PSORIASIS
FACTORS IN DEVELOPING WRINKLE
Genetics
Onset facial
wrinkling
Location facial
wrinkle
Severity facial
wrinkle
Progeria
Werner’s
syndrome
Cockayne
syndrome
DMS Structure
Thinning skin
Sarcopenia
Bone
resorption
Intrinsic Aging
Chronologic
age
Extrinsic Aging
Sun
exposure
FACTORS IN DEVELOPING WRINKLE
Decreased
elasticity
(recoil)
Decreased
extensibility
(stretch)
WRINKLE
FORMATION
PATHOGENESIS of WRINKLE
Both occur with AGE
1
TELOMERE
SHORTENING
2
COLLAGEN
LOSS
3
ELASTIN
DEGRADATION
PATHOGENESIS of WRINKLE
TELOMERE SHORTENING
• Telomeres:
– Terminal portions of mammmalian chromosomes
– Composed of hundreds short sequences of repeats base pairs TTAGGG
– Cap the ends of chromosomes preventing fusion
Yaar M, et al. Br J Derm 2007; 157:877
TELOMERE SHORTENING
• During cell division:
– DNA polymerase cannot
replicate terminal base pairs
of chromosome
– Continuously lost on
replication  shortening
chromosome Telomeres get “too short”
 APOPTOSIS or SENESCENCE
Play a role in AGING
“Biological Clock”
Yaar M, et al. Br J Derm 2007; 157:877
TELOMERE SHORTENING
Cytoplasm
Nucleus
PHOTOAGING
IL-1, IL-6, TNF-
Keratinocyte/
Fibroblast
Pittayapruek P, et al.. Int. J. Mol. Sci. 2016,;17,:868.
COLLAGEN LOSS
Reduced
collagen
Decreased
synthesis
Increased degradation
 High levels of
MMPs
• Abnormal collagen  Collagen Glycation
Nonenzymatic
process
Reactions
between sugar
to ECM collagen
Advanced
glycation end/
AGE product
(pentosidine)
Deposited on
collagen
Stiffer & less
susceptible to
remodeling
COLLAGEN LOSS
Interact AGEs
with receptors
Intracellular signalling
Enhanced
oxidative stress
Proinflammatory
cytokines
Breakdown collagen
COLLAGEN LOSS
ELASTIN DEGRADATION
• Solar radiation enhances fibres degradation
• UV exposure  increased elastase  ELASTOSIS !
 Structural deterioration & collapse of elastic
network  loss & resorption of fine elastic fibres
• Abnormal elastic fibres  decreased resilience 
wrinkle.
ELASTIN DEGRADATION
• Degraded elastic fibres lose their 'snap‘  when
deformed they do not recover.
– The skin consequently sags.
• Numerous fibres serve an anchoring function &
keep epidermis in tight fit with dermis
– When lost  dermis becomes more lax & surface is
then thrown into many foldings  WRINKLE.
• Skin atrophy
– Thinning epidermis
– Flattening of DEJ  telltale signs
– Dermal atrophy
• Muscle contraction
– Muscles of face are inserted into the skin itself
– Function: Open & close orifices: eyes & mouth
– Forces & repeated contraction  permanent wrinkle
• Skeletal resorption
– Maxillary resorption  excess soft tissue of upper lip 
perioral wrinkling.
DMS STRUCTURE
FACIAL MUSCULATURE
Zimbler MS, et al. Facial Plast Surg. 2001;9:179-87
•Aging of facial skeleton may be due to bone resorption
•Without structural support of bone  noticeable changes in
other layers of overlying soft tissue and skin
BONE RESORPTION
• There are no histological difference between
wrinkles and surrounding tissues.
 Histochemical stains
• Histological findings  appropriate to skin
aging subject and skin region.
HISTOLOGY OF WRINKLE
• Epidermal thinning & flattening of DEJ
• Loss collagen, elastic fibres, glycosaminoglycans (GAG)
HISTOLOGY OF AGING SKIN
Laga AC, et al. The human cutaneous photoaging. AJP. 2009;174(2):357-60
Naylor EC, et al. Molecular aspects of skin ageing. Maturitas. 2011;69:249–56.
COMPONENTS OF YOUNG SKIN
Naylor
EC,
et
al.
Molecular
aspects
of
skin
ageing.
Maturitas.
2011;69:249–56.
• Epidermis thin with age  reduced barrier repair &
 elasticity
– Causing fine lines  early signs of wrinkle
formation  being 1 to 2 millimeters in depth
Nagwa H, et al. IJD. 2012;57(3):181-6.
HISTOLOGY OF AGING SKIN
• Collagen fibers  thin, looese, and less well organized
• Collagen  undergoes chemical changes  reduce its
mechanical flexibility.
– Imperfect collagen repair  “scar-like” patches of stiff
(Masson-Trichrome ×100)
Nagwa H, et al. IJD. 2012;57(3):181-6.
HISTOLOGY OF AGING SKIN
• Elastic fiber network in dermis degrades & is replaced
by poorly organized elastin
– Loss of resiliency: ability skin to quickly return to its
original shape after distortion.
HISTOLOGY OF AGING SKIN
Nagwa H, et al. IJD. 2012;57(3):181-6.
(Orcein ×100)
Large elastin deposits:
elastosis  cause skin look
• Glycosaminoglycan (GAG) composition changes
• In aging skin with chronic photodamage   Hyaluronic acid
– These changes affect water content of dermis
HISTOLOGY OF AGING SKIN
Low hyaluronic acid
High
hyaluronic acid
• Subcutaneous fat layer  decreases markedly in thickness
HISTOLOGY OF AGING SKIN
YOUNGER SKIN AGING SKIN
Prone to
wrinkle
Thinning
Epidermis
Loss &
chemical
changing
collagen
Degrading
elastic fiber
Changing
GAG
composition
Thinning
subcutan fat
layer
FEATURES OF WRINKLE
Kligman, Contet-Audonneau, Lavker, & Tsuji:
Wrinkling
Repeated
movement skin
(facial expression)
FEATURES OF WRINKLE
PRONE
TO
WRINKLE
Thinning
Epidermis
Loss &
chemical
changing
collagen
Degrading
elastic fiber
Changing
GAG
composition
Thinning
subcutan fat
layer
It’s a configurational change  result of mechanical stresses
acting on lax & excessive skin  aged skin
Glove which heavy
duty over the years
New: Smooth
Old: Fabric grooves at
sites of stress
Fabric acquires creases
 conformational
change
No chemical or
architectural
alteration
“Like the grooves worn into an old glove”
 repeated movement
is configurational change
Type of Wrinkles
1= receding hairline
2= forehead rhytidosis
3= glabellar rhytidosis
4= brow ptosis
5= temple rhytidosis
6= upper lid redundancy and ptosis
7= lateral canthal rhytidosis
8= nasal root rhytidosis
9= lower lid redundancy and rhytidosis
10= lower lid fat pseudoherniation
11= malar bag formation
12= cheek rhytidosis
13= preauricular rhytidosis
14= nasal tip ptosis
15= cheek sagging
16= deepening nasolabial crease
17= facial rhytidosis
18= perioral rhytidosis
19= upper lip flattening and lengthening
20= thinning and atrophy of vermillion
21= chin pad ptosis
22= jowl formation
23= cervical rhytidosis
24= submental fat accumulation
25= platysmal banding
26= rhytidosis and midneck hollowing
27= submaxillary gland ptosis.
Zimbler MS, et al. Facial Plast Surg. 2001;9:179-87
Summary
• There are role of genetic, intrinsic & extrinsic aging, DMS
structures in wrinkles.
• Features of wrinkle: thinning epidermis, loss collagen,
degrading elastic fiber,, changing GAG composition,
thinning subcutan fat layer.
• Variables that influence aging:
– Repeated movement skin (facial expression)
• Much remains to be learned regarding science and
biomechanics of wrinkle  further study is needed.
• Kligman AM. The anatomy and pathogenesis of wrinkles. British J Dermat. 1985;113:37-42.
• Zimbler MS, et al. Anatomy and pathophysiology of facial aging. Facial Plast Surg. 2001;9:179-87.
• Saghari S, et al. Wrinled skin. In: Baumann L. Cosmetic dermatology. 2nd ed. McGraw Hill: New
York. 2009. p. 145-7.
• Anson G, et al. Sleep wrinkles: Facial aging and facial distortion during sleep. Aesth Surg J. 2016;
36(8): 931–40.
• Green MR. The periorbital wrinkle. In: Baran R, et al. Textbook of cosmetic dermatology. 4th ed.
Informa: London. 2010. p.242-6
• Clinical Anatomy. Plastic Surgery Key. http://plasticsurgerykey.com/clinical-anatomy.
• Makrantonaki E, et al. Genetics and skin aging. Dermato-Endocrinol. 2012;4(3):280–4.
• Laga AC, at al. The translational basis of human cutaneous photoaging. The AJP. 2009;174(2):357-
60.
• Naylor EC, et al. Molecular aspects of skin ageing. Maturitas. 2011;69:249–56.
• Nagwa H, et al. Morphometry and epidermal fas expression of unexposed aged versus young skin.
IJD. 2012;57(3):181-6.
• Pittayapruek P, et al. Role of matrix metalloproteinases in photoaging and Photocarcinogenesis.
Int. J. Mol. Sci. 2016,;17,:868.
References
1. dr. Hendra - Basic Knowledge of The Wrinkles Final A .ppt.pdf

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1. dr. Hendra - Basic Knowledge of The Wrinkles Final A .ppt.pdf

  • 1. CURICULUM VITAE Nama Tempat dan tanggal lahir Alamat Rumah Status Kepegawaian Jabatan : HENDRA GUNAWAN, dr. SpKK(K), Ph.D, FINSDV : Jakarta, 15 September 1969 : Jl. Tambak C No. 28 Jakarta Pusat 10320 : Pegawai Negeri Sipil Departemen Kesehatan : Kepala Divisi Dermatologi Infeksi Departemen Ilmu Kesehatan Kulit dan Kelamin Fakultas Kedokteran Universitas Padjadjaran/ RSUP Dr. Hasan Sadikin Bandung : Departemen Ilmu Kesehatan Kulit dan Kelamin Faklutas Kedokteran Universitas Padjadjaran/RSHS Jl. Pasteur No. 38 Bandung Alamat Kantor Riwayat Pendidikan Fakultas Kedokteran UNPAD Bandung Diploma Course in Dermatology Bangkok, Thailand PPDS I.K. Kulit dan Kelamin FK UNPAD, Bandung Program Doktoral Juntendo University Tokyo, Jepang Fellowship in Dermatopathology and Dermoscopy Toranomon Hospital Tokyo, Jepang Lulus tahun Lulus tahun Lulus tahun Lulus tahun Tahun 2014 1994 2002 2005 2008 Riwayat Pekerjaan Dokter BPPKA Pertamina Kepala Puskesmas Mapin Kebak Sumbawa Dokter RS M.H. Thamrin Pondok Gede Jakarta Staf Departemen I.K. Kulit dan Kelamin RSHS Tahun Tahun Tahun Tahun 1994-1995 1995-1998 1998-1999 2006-sekarang
  • 2. Basic Knowledge Hendra Gunawan Department Dermatology and Venereology Faculty of Medicine Universitas Padjadjaran/Hasan Sadikin Hospital Bandung
  • 3. 5. Manifestation of facial wrinkle 4. Histology of wrinkle 3. Pathogenesis of wrinkle 2. Factors in developing wrinkle 1. Nature of wrinkle OVERVIEW
  • 4. • When the effects of skin aging on face are addressed, what is really being discussed is … INTRODUCTION • Aging  process that occurs in all organs, but most visible in the skin
  • 7. One indicator of skin aging that appear as furrows or lines on the facial skin surface. INTRODUCTION Multifactorial etiology Consequence intrinsic & extrinsic aging Baumann L. Wrinled skin. In: Cosmetic dermatology.. 2009. p. 145-7.
  • 8. • Fine wrinkles  flattening epidermis & atrophy dermal papilla Wells (1954) • Wrinkling  worsened by  brittleness of horny layer with aging Lorincz (1960) • Histologically  couldn’t differentiate wrinkle from surrounding skin Wright & Shellow (1965) NATURE OF WRINKLE
  • 9. Is the wrinkle a histological non-entity? NATURE OF WRINKLE Montagna and Carlisel (1979) Nothing peculiar can be seen in histological preparations of wrinkle
  • 11. Genetics Onset facial wrinkling Location facial wrinkle Severity facial wrinkle Progeria Werner’s syndrome Cockayne syndrome DMS Structure Thinning skin Sarcopenia Bone resorption Intrinsic Aging Chronologic age Extrinsic Aging Sun exposure FACTORS IN DEVELOPING WRINKLE
  • 12.
  • 15. TELOMERE SHORTENING • Telomeres: – Terminal portions of mammmalian chromosomes – Composed of hundreds short sequences of repeats base pairs TTAGGG – Cap the ends of chromosomes preventing fusion Yaar M, et al. Br J Derm 2007; 157:877
  • 16. TELOMERE SHORTENING • During cell division: – DNA polymerase cannot replicate terminal base pairs of chromosome – Continuously lost on replication  shortening chromosome Telomeres get “too short”  APOPTOSIS or SENESCENCE Play a role in AGING “Biological Clock”
  • 17. Yaar M, et al. Br J Derm 2007; 157:877 TELOMERE SHORTENING
  • 19.
  • 21. • Abnormal collagen  Collagen Glycation Nonenzymatic process Reactions between sugar to ECM collagen Advanced glycation end/ AGE product (pentosidine) Deposited on collagen Stiffer & less susceptible to remodeling COLLAGEN LOSS
  • 22. Interact AGEs with receptors Intracellular signalling Enhanced oxidative stress Proinflammatory cytokines Breakdown collagen COLLAGEN LOSS
  • 23. ELASTIN DEGRADATION • Solar radiation enhances fibres degradation • UV exposure  increased elastase  ELASTOSIS !  Structural deterioration & collapse of elastic network  loss & resorption of fine elastic fibres • Abnormal elastic fibres  decreased resilience  wrinkle.
  • 24. ELASTIN DEGRADATION • Degraded elastic fibres lose their 'snap‘  when deformed they do not recover. – The skin consequently sags. • Numerous fibres serve an anchoring function & keep epidermis in tight fit with dermis – When lost  dermis becomes more lax & surface is then thrown into many foldings  WRINKLE.
  • 25. • Skin atrophy – Thinning epidermis – Flattening of DEJ  telltale signs – Dermal atrophy • Muscle contraction – Muscles of face are inserted into the skin itself – Function: Open & close orifices: eyes & mouth – Forces & repeated contraction  permanent wrinkle • Skeletal resorption – Maxillary resorption  excess soft tissue of upper lip  perioral wrinkling. DMS STRUCTURE
  • 26. FACIAL MUSCULATURE Zimbler MS, et al. Facial Plast Surg. 2001;9:179-87
  • 27. •Aging of facial skeleton may be due to bone resorption •Without structural support of bone  noticeable changes in other layers of overlying soft tissue and skin BONE RESORPTION
  • 28.
  • 29. • There are no histological difference between wrinkles and surrounding tissues.  Histochemical stains • Histological findings  appropriate to skin aging subject and skin region. HISTOLOGY OF WRINKLE
  • 30. • Epidermal thinning & flattening of DEJ • Loss collagen, elastic fibres, glycosaminoglycans (GAG) HISTOLOGY OF AGING SKIN Laga AC, et al. The human cutaneous photoaging. AJP. 2009;174(2):357-60
  • 31. Naylor EC, et al. Molecular aspects of skin ageing. Maturitas. 2011;69:249–56. COMPONENTS OF YOUNG SKIN
  • 32.
  • 34. • Epidermis thin with age  reduced barrier repair &  elasticity – Causing fine lines  early signs of wrinkle formation  being 1 to 2 millimeters in depth Nagwa H, et al. IJD. 2012;57(3):181-6. HISTOLOGY OF AGING SKIN
  • 35. • Collagen fibers  thin, looese, and less well organized • Collagen  undergoes chemical changes  reduce its mechanical flexibility. – Imperfect collagen repair  “scar-like” patches of stiff (Masson-Trichrome ×100) Nagwa H, et al. IJD. 2012;57(3):181-6. HISTOLOGY OF AGING SKIN
  • 36. • Elastic fiber network in dermis degrades & is replaced by poorly organized elastin – Loss of resiliency: ability skin to quickly return to its original shape after distortion. HISTOLOGY OF AGING SKIN Nagwa H, et al. IJD. 2012;57(3):181-6. (Orcein ×100) Large elastin deposits: elastosis  cause skin look
  • 37. • Glycosaminoglycan (GAG) composition changes • In aging skin with chronic photodamage   Hyaluronic acid – These changes affect water content of dermis HISTOLOGY OF AGING SKIN Low hyaluronic acid High hyaluronic acid
  • 38. • Subcutaneous fat layer  decreases markedly in thickness HISTOLOGY OF AGING SKIN YOUNGER SKIN AGING SKIN
  • 39. Prone to wrinkle Thinning Epidermis Loss & chemical changing collagen Degrading elastic fiber Changing GAG composition Thinning subcutan fat layer FEATURES OF WRINKLE Kligman, Contet-Audonneau, Lavker, & Tsuji:
  • 40. Wrinkling Repeated movement skin (facial expression) FEATURES OF WRINKLE PRONE TO WRINKLE Thinning Epidermis Loss & chemical changing collagen Degrading elastic fiber Changing GAG composition Thinning subcutan fat layer
  • 41. It’s a configurational change  result of mechanical stresses acting on lax & excessive skin  aged skin Glove which heavy duty over the years New: Smooth Old: Fabric grooves at sites of stress Fabric acquires creases  conformational change No chemical or architectural alteration
  • 42. “Like the grooves worn into an old glove”  repeated movement is configurational change
  • 43. Type of Wrinkles 1= receding hairline 2= forehead rhytidosis 3= glabellar rhytidosis 4= brow ptosis 5= temple rhytidosis 6= upper lid redundancy and ptosis 7= lateral canthal rhytidosis 8= nasal root rhytidosis 9= lower lid redundancy and rhytidosis 10= lower lid fat pseudoherniation 11= malar bag formation 12= cheek rhytidosis 13= preauricular rhytidosis 14= nasal tip ptosis 15= cheek sagging 16= deepening nasolabial crease 17= facial rhytidosis 18= perioral rhytidosis 19= upper lip flattening and lengthening 20= thinning and atrophy of vermillion 21= chin pad ptosis 22= jowl formation 23= cervical rhytidosis 24= submental fat accumulation 25= platysmal banding 26= rhytidosis and midneck hollowing 27= submaxillary gland ptosis. Zimbler MS, et al. Facial Plast Surg. 2001;9:179-87
  • 44. Summary • There are role of genetic, intrinsic & extrinsic aging, DMS structures in wrinkles. • Features of wrinkle: thinning epidermis, loss collagen, degrading elastic fiber,, changing GAG composition, thinning subcutan fat layer. • Variables that influence aging: – Repeated movement skin (facial expression) • Much remains to be learned regarding science and biomechanics of wrinkle  further study is needed.
  • 45. • Kligman AM. The anatomy and pathogenesis of wrinkles. British J Dermat. 1985;113:37-42. • Zimbler MS, et al. Anatomy and pathophysiology of facial aging. Facial Plast Surg. 2001;9:179-87. • Saghari S, et al. Wrinled skin. In: Baumann L. Cosmetic dermatology. 2nd ed. McGraw Hill: New York. 2009. p. 145-7. • Anson G, et al. Sleep wrinkles: Facial aging and facial distortion during sleep. Aesth Surg J. 2016; 36(8): 931–40. • Green MR. The periorbital wrinkle. In: Baran R, et al. Textbook of cosmetic dermatology. 4th ed. Informa: London. 2010. p.242-6 • Clinical Anatomy. Plastic Surgery Key. http://plasticsurgerykey.com/clinical-anatomy. • Makrantonaki E, et al. Genetics and skin aging. Dermato-Endocrinol. 2012;4(3):280–4. • Laga AC, at al. The translational basis of human cutaneous photoaging. The AJP. 2009;174(2):357- 60. • Naylor EC, et al. Molecular aspects of skin ageing. Maturitas. 2011;69:249–56. • Nagwa H, et al. Morphometry and epidermal fas expression of unexposed aged versus young skin. IJD. 2012;57(3):181-6. • Pittayapruek P, et al. Role of matrix metalloproteinases in photoaging and Photocarcinogenesis. Int. J. Mol. Sci. 2016,;17,:868. References