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 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 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 Glogau classification of photoaging groups based on wrinkling, actinic damage and camouflage. 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 Types of UV 1) UVA 320-400nm 2) UVB 280-320nm 3) UVC <280nm (most absorbed by the atmosphere) 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 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 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 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)