Download Aging face

Lip Teh
Decmeber 2005
AGING FACE
Characterised by
1) Skin Changes at cellular level
2) Descend of subcutaneous fat with attenuation of underlying structures
(SMAS, retaining ligaments)
3) Facial skeletal resorption
Aging factors
1) Genetic
2) Environmental – Solar, dietary
3) Gravity
4) Cellular mechanisms
a. Atrophy
b. programmed cellular death
c. exhaustion
d. cellular damage
Intrinsic Aging
 process of atrophy
 Histologically
o Epidermis
 Little change in thickness of stratum corneum but lower layers
thins – faster in men (7.2% of the original value/decade) than in
women (5.7%)
 Skin becomes more transparent
 loss of dermoepidermal papillae
 increase in skin fragility to shear
 decrease in melanocyte population but size increases
 increased susceptibility to skin cancers
 lentigines proliferation (Lentigo simplex)
 decrease in Langerhan’s cells
 reduced immune system
 proliferation of seborrheic keratoses
o Dermis - layer most affected. All components affected
 Ground substance (GAG, PG) decrease with age
 Elastic fibres diminishes after age 30
 maintains the waving of collagen bundles
 loss of recoil and laxity of skin
 Collagen
 decreased Type 1:Type 3 ratio due to impaired synthesis of
Type I
 dermal thickness decrease 6% per decade
 Blood vessel walls become more fragile
 Prone to bleeding
 campbell de morgan spots - proliferation of dilated venules.
o Skin appendages
Lip Teh
Decmeber 2005
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sebaceous glands increase in size – produce less sebum
sweat glands
 reduced production
 skin dry and shiny
 Pacinian and meissner’s corpuscles decrease in numbers
 Reduced density leads to reduced sensitivity threshold
 Villus hair
o Hypodermis – atrophy of fat
 More prone to hypothermia, trauma – less cushioning
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Skin thus becomes increasingly thin and atrophic with increasing age, affecting
both epidermis and dermis.
Aged skin becomes fragile, translucent, lax and wrinkled with a tendency to easy
bruising and telangictasia.
It has a ed resistance to shearing and tensile forces, ed laxity, ed elasticity.
Immunological changes and an ed susceptibility to UV light induced skin
cancers.
The skin also loses tissue fluid and becomes dehydrated.
woman’s skin thickness remains constant until the fifth decade, when it is affected
by the hormonal changes of menopause.
Actinic damage
hallmark – thickened skin with degraded elastic fibres
Effects are
1) Chronic photoaging
2) Tanning
3) DNA damage
Chronic photoaging
o Epidermis
 Acanthosis (thickened spinosum), parakeratosis (persistence of the
nuclei of the keratinocytes into the stratum corneum), dyskeratosis
(abnormal, premature, or imperfect keratinization of the
keratinocytes)
 heterogeneity in basal layer
 ↑ keratocyte melanosome content (solar lentigines)
o Dermis
 Dermal degradation due to UV radiation activation of
metalloproteinases – degrade collagen and elastin
 Thickened, degraded elastic fibers (elastosis/basophilic
degeneration)
 ↑ ground substance
 ↓ mature collagen (mainly type 1)
 ↑ immature type III collagen
 Telangiectasia
o Subcutaneous
 Contracted septa – wrinkles and deep furrows
Lip Teh
Decmeber 2005
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Glogau classification of photoaging groups based on wrinkling, actinic damage
and camouflage.
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Mild (typically aged 28-35 y)
o Little wrinkling or scarring
o No keratosis
o Requires little or no makeup
Moderate (aged 35-50 y)
o Early wrinkling, mild scarring
o Sallow color with early actinic keratosis
o Requires little makeup
Advanced (aged 50-65 y)
o Persistent wrinkling
o Discoloration with telangiectasias and actinic keratosis
o Wears makeup always
Severe (aged 60-75 y)
o Wrinkling - Photoaging, gravitational, dynamic
o Actinic keratoses with or without skin cancer
o Wears makeup with poor coverage
Tanning
 2 stages
1) immediate pigment darkening
due to photooxidation of existing melanin
2) delayed (after 72hours)
↑ synthesis of melanin synthesis
↑ number of melanosomes
↑ melanocytes (repeat exposure)
 Indoor tanning (high dose UVA) associated with dermal elastosis and DNA
damage
 Acute sun exposure (sunburn) - 2 mechanisms
1)
delayed release of vasoactive mediator from epidermal chromophore
2)
absorbed directly by dermal vascular endothelial cells, damaging them and
causing local vasodilatation
Fitzpatrick’s Skin types
Type
Color
I
White
II
White
III
White
IV
Moderate brown
V
Dark brown
VI
Black
Reaction
Always burn, never tan
Usually burn, tan with difficulty
Sometimes mild burn, tan average
Rarely burn, tan with ease
Very rarely burn, tan very easily
No burn, tan very easily
Black vs White skin
1)
↑ corneocyte layers in stratum corneum (20 vs 16)
Lip Teh
Decmeber 2005
↑ desquamation rate (2.5x)
↑ transepithelial water loss
↓ transcutaneous permeability to various chemicals
↑ photoprotection all wavelengths (3-4x)
same number of melanocytes and melanosomes
melanosomes dispersed individually in keratocyte vs membrane-bound
aggregates
2)
3)
4)
5)
6)
7)
DNA damage
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Types of UV
1) UVA 320-400nm
2) UVB 280-320nm
3) UVC <280nm (most absorbed by the atmosphere)
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UV damage – 2 types
1) UVC type
a. direct action
b. UVC, UVB, and UVA2 (315-340nm)
c. Usually epidermis
d. Photon energy absorbed by chromophore
(DNA, proteins, lipids, urocanic acid)
2) UVA type
a. indirect thru other active molecules
b. UVA1 (340-400nm)
c. Generation of free radicals
Dietary/ Environmental Factors in Aging
1)
Exercise
2)
Radiotherapy
3)
Drugs - HRT, exogenous thyroid replacement (suppress TSH),
glucocorticoids
4)
Caffeine
a. ↓ type 1 collagen synthesis (15%)
5)
Smoking
a. perioral wrinkles
b. ↓ collagen synthesis (40%)
Genetics
Ehlers-Danlos Syndrome (Cutis hyperelastica)
 Inadequate production of lysyl oxidase
 Defects in collagen type V or III, fibronectin
1. hypermobile joints
2. thin, friable hyperextensile skin
a. great ability to stretch and recoil
b. poor wound healing
c. poor result with rhytidectomy
Lip Teh
Decmeber 2005
3. subcutaneous hemorrhages
Cutis Laxa
 Degeneration of elastic fibres in dermis
 Stretches but does not recoil
 Normal wound healing
 Normal joint extensibility
 Good result with contouring procedures
 Inheritance pattern:
1. Autosomal dominant – less severe, involve dermis only
2. Recessive – emphysema, genitourinary diverticula and hernias
3. X-linked – lysyl oxidase deficiency
Pseudoxanthoma Elasticum
 Similar to Cutis Laxa – need biopsy to differentiate
 extensive infiltration with degenerate elastic fibers
Progeria (Hutchinson-Gilford Syndrome)
 Unlike most other "accelerated aging diseases" (like Werner's syndrome,
Cockayne's syndrome or xeroderma pigmentosum), progeria is not caused by
defective DNA repair.
 AD, most sporadic
 Mutation in lamin A protein on chromosome 1 - a protein scaffold around the
edge of the nucleus that helps organize nuclear processes such as DNA and
RNA synthesis
 distinguished by limited growth, alopecia and a characteristic appearance with
small face and jaw and pinched nose
o growth retardation
o craniofacial disproportion (premature closure of epiphyses)
o loss of subcutaneous fat
o arteriosclerosis and cardiac disease
 Premature death = no indication for surgery
Adult Progeria (Werner’s Syndrome)
 Autosomal recessive; gene that codes DNA helicase and it is located on the
short arm of chromosome 8
 typically grow and develop normally until they reach puberty.
Lip Teh
Decmeber 2005
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indurated patches of skin (like scleroderma)
baldness
aged bird-like facies
hypo- and hyper pigmentation
short stature
high pitched voice
cataracts
mild diabetes mellitus
muscle atrophy
osteoporosis
premature atherosclerosis
various neoplasms
Surgery usually not indicated
Meretoga’s Syndrome
 Excessive lax skin of the face in >20yr olds
 Systemic form of amyloidosis
 Facial polyneuropathy due to amyloid deposits in perineurium and
endoneurium
 Similar appearances to Cutis Laxa
Wrinkles
3 types of skin creases
1) Mimetic/dynamic wrinkles
 Best treated by muscle resection, botulinum toxin,
 Can be smoothened with injectable skin filler materials
a. mimetic muscle insertion
b. perpendicular to the direction of the underlying facial muscles.
c. include
i. forehead
ii. glabellar lines
iii. crows feet
iv. platysma band
v. bunny lines
vi. dimpled chin
2) Superficial/static wrinkles
 on dry crepe paper skin
 amenable to treatments like laser resurfacing, chemical peels
a. fine shallow wrinkles
i. Seem with aging
ii. Due to
1. flattening of dermoepidermal junction (loss of collagen
type VII)
2. Hypotrophy of dermis and hypodermis and loss of collagen,
GAGs and elastin
3. Changes more marked under the wrinkle
b. deep wrinkles
Lip Teh
Decmeber 2005
i. Seen in solar elastosis
1. due to deposition of thickened elastotic material
2. changes more marked on either side of the wrinkle
3) Folds
 Include
1. upper lid
2. lower lid malar bag
3. nasojugal groove
4. nasolabial fold
5. jowls
6. marionette lines
 result of overlapping skin caused by genetic laxity, intrinsic aging, loss of
tone, bony atrophy, gravity, and consequent sagging.
 requires tightening procedures such as blepharoplasty, face lift, or direct skin
excision.
 Augmentation of the bony skeleton by implants, bone grafts, or skeletal
osteotomies may also be necessary to treat folds in properly selected cases.
Classification
Soft tissues changes
Features
a) gravitation descent
b) laxity of supporting ligaments
c) overactivity of muscles – frown lines
d) fat atrophy – late
1. Brow
a. Receding hairline
b. Descent of ROOF fat
c. Overactive frontalis, glabellar muscles – frown lines
2. Upper lid
a. Dermatochalasis - Lateral hooding
b. Ptosis
c. Septal weakening – fat pad herniation
d. Overactive orbicularis – crows feet
Lip Teh
Decmeber 2005
3. Lower lid/Midface
a. Laxity of tarsal plate – scleral show/ectropion
b. Weakening of septum – herniation of orbital fat
c. SOOF descent - weakening of orbitomalar ligament (malar bag)
d. Descent of malar fat pad – deepening of nasolabial fold
e. Fat atrophy/descent – tear trough deformity (deep nasojugal fold)
f. Negative vector
Lip Teh
Decmeber 2005
Classification of midfacial morphology. (Above, left) Type I: aging confined to lower
lid. Pseudoherniation of orbital fat, minimal skin/muscle excess. (Above, right) Type
II: lower lid aging with minimal descent of lid/cheek junction and malar prominence
(aging confined to upper midface). (Below, left) Type III: lower lid aging with descent
of lid/cheek junction and malar prominence, skeletalization of the orbital rim, and
deepening of the nasolabial fold. (Below, right) Type IV: advanced orbital aging with
deepening of the nasojugal groove and presence of malar bags.
Lip Teh
Decmeber 2005
4. Lower face/neck
a. Perioral wrinkling
b. Laxity of masseteric/mandibular retaining ligaments – Jowls
c. Loss of inferior mandibular border
d. Submental fat accumulation or subplatysmal fat herniation
e. Obtuse cervicomental angle
f. Overactive plastyma
5. Nose
a. relative lengthening of the nose, resultant divergence of the medial crural
feet and columellar shortening with maxillary atrophy
b. nasal dorsum takes on a more convex character secondary to the
downward rotation of the lobule and relative columellar retraction
c. increased density of sebaceous glands, in some rhinophyma
d. Migration/separation of the lower lateral cartilage from the upper lateral
cartilage with aging.
e. Weakening or loss of suspensory ligament support with loss of medial
crural support
f. Thickening and possible ossification of the cartilages, leading to greater
prominence.
g. thickening of the overlying skin and subcutaneous tissue with concomitant
increased vascularity, leading to increased bulkiness and weight of the tip.
6. Lip
a.
b.
c.
d.
Lengthening of cutaneous upper lip
Thinning of red vermillion with inversion
Loss of white roll and philtral column definition
Sagging oral commissures
Skeletal
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Reduction in facial height - most marked in the maxilla and mandible and
correlated with loss of teeth.
modest increases in facial width and facial depth and generalized coarsening of
the bony prominences.
Lip Teh
Decmeber 2005
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clockwise rotation of the midface relative to the cranial base - narrowing of
angles at the glabella, orbital, maxillary, and piriform points (responsible for
the tear trough and negative vector deformities)