Aging face ppt

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role of uv rays, intrinsic and extrinsic causes

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  • Telomeres of human chromosomes (yellow) are shown by in situ hybridization with a telomeric probe. These structural components of chromosomes are essential for genomic stability and play a key role in cancer. In normal somatic cells telomeres shorten each cell division, a process that limits cellular lifespan. However, cancer cells overcome this proliferative blockade by activating telomerase, which elongates telomeres.
    The epidermis is one of the few regenerative tissues to express telomerase.
    © Slide from: Christopher CounterAssociate ProfessorDepartment of Pharmacology and Cancer Biology, Duke University Program in Cell and Molecular Biology.
  • Aging face ppt

    1. 1. AGING FACE: PATHOPHYSIOLOGY By Dr. D R Dhaked
    2. 2. Aging     Begins day we are born and highly individualized No single measure of how “old” a person is Proceeds at different rates in different people Gradual decline in organ functional reserves with reduction in ability to maintain homeostasis under stress
    3. 3. Facial Aging    Begins with surface and subsurface structural changes in multiple facial tissue layers, including skin, fat, muscle and bone. Facial tissue layers age interdependently, contributing to overall facial appearance. Changes in one tissue layer have an effect on the other layers.
    4. 4. Skin  With age, skin undergoes several changes. • More likely to wrinkle or sag • Reduction in collagen • Thinner • Drier • Less elastic
    5. 5. Fat -A youthful look depends on having the right amount of facial fat in right places. Redistribution, accumulation, and atrophy of fat lead to facial volume loss. • Some areas lose fat (forehead and cheeks). • Other areas gain fat (mouth and jaw). • Modification of the fat pads leads to contour deficiencies.
    6. 6. Bone •There is a significant loss of facial bone with age. •Aging of the craniofacial skeleton may be due to changes in relative dynamics of bone expansion and bone resorption. •Bone resorption leads to biometric volume loss. •Without the structural support of bone, there are noticeable changes in the other layers of overlying soft tissue and skin
    7. 7. Signs of Facial Aging • Greater visibility of bony landmarks, lines and wrinkles • Prominence of transverse forehead lines • Nasolabial folds become more prominent • Hollowing of the mid-face (loose skin) • Changes in area around the mouth (vertical wrinkles, lip thinning and flattening) • Development of prejowl depression
    8. 8. Aging   INTRINSIC SKIN AGING (chronologic aging) or normal aging EXTRINSIC AGING
    9. 9. INTRINSIC SKIN AGING (chronologic aging)      Inevitable natural aging process that occurs in all people Occurs as part of a pre-programmed degeneration within cells and extracellular matrix in all skin layers. Although begin in 20’s, visible signs are not apparent for many decades. Intrinsic aging proceeds at highly variable rates between different people Primarily determined by unique genetic make-up and underlying type of skin
    10. 10. Intrinsic Aging: Role of Telomeres
    11. 11. Telomeres   Tandem repeats of short base sequences, ...TTAGGG... in mammals, at end of each chromosome, that are required for chromosome stability. With continued cell division, telomeres are shortened, resulting in loss of ability of cells to divide.
    12. 12. Telomeres   Telomerase activity is detected in vitro and in vivo in normal human epidermis, primarily in the proliferative basal layer Not found in the dermal compartment of skin or in cultured fibroblasts Harle-Bachor, C, Boukamp, P: Telomerase activity in the regenerative basal layer of the epidermis in human skin and in immortal and carcinoma-derived skin keratinocytes. Proc Natl Acad Sci USA 1996 93: 6476– 6481,
    13. 13. Cytoskeleton and Skin aging    Aged skin has increased rigidity Due to an increase in F actin filaments Important in age related loss of elasticity of the skin.
    14. 14. Endocrine System and Aging    With aging, the levels of epidermal precursor of vitamin D3 decrease. Older individuals are more susceptible to vitamin D3 deficiency in absence of regular sun exposure. May lead to osteoporosis, psoriasis and skin cancer
    15. 15. Endocrine System and Aging    Estrogen stimulates fibroblasts to make collagen Decreased levels of estrogen are associated with loss of collagen and increased wrinkling HRT protects skin from aging Baumann, L. “A dermatologist's opinion on hormone therapy and skin aging,” Fertility and Sterility 2005 Aug;84(2):289290.
    16. 16. Age related changes in metabolic functions  Reduced oxidative phosphorylation by mitochondria  Diminished synthesis of structural, enzymatic and regulatory proteins  Decreased capacity for uptake of nutrients  Increased DNA damage and diminished repair of chromosomal damage  Accumulation of oxidative damage in proteins and lipids (eg lipofuscin pigment)  Accumulation of advanced glycosylation end products
    17. 17. Morphological alterations  Irregular and abnormally lobed nuclei  Swollen, pleomorphic and vacuolated mitochondria  Decreased endoplasmic reticulum  Distorted Golgi apparatus
    18. 18. INTRINSIC SKIN CHANGES • Epidermis • Keratinocytes demonstrate slower turnover. • Keratin sloughs more slowly with thickening of keratin layer. • Melanoctyes decrease in number and produce less melanin. • Uneven melanin pigment distribution. • Flattening of the epidermis-dermis junction. Prone to blistering.
    19. 19.  Dermis      Fibroblasts – Decreased number and less collagen production. Collagen – Decreased quantity. Abnormal, weakened structure. Elastin – Thickened fibers with less elasticity. Matrix – Decreased quantity. Blood vessels – dilated, thinned and weakened walls, prone to rupture.
    20. 20.  Subcutaneous Layer       Fat loss and thinning. Weakening of the retaining ligaments. Fewer blood vessels. Sweat glands - decreased. Sebaceous glands – Fewer with less sebum production. Hair shafts – fewer and thinner with less pigment.
    21. 21. EXTRINSIC AGING –         Outside factors that accelerate intrinsic aging. Photoaging Smoking Malnutrition Hormonal Disorders Chronic Disease States Repetitive facial expressions Gravity
    22. 22. Photoaging     Caused by harmful effects of sunlight Ultraviolet light is the prinicipal cause of photoaging UVB penetrates only into epidermis and is responsible for redness and blistering associated with sunburns. UVA penetrates more deeply into dermis, related to photoaging
    23. 23.      Photoaged skin shows deep coarse wrinkling, excessive dryness, severe brown spots dry leathery texture when compared to intrinsically aged skin
    24. 24. PHOTOAGING 3 types of reactions to UV exposure:  Free Radicals, essentially due to UVA  Direct cell death, essentially due to UVB  MMP Enzymes 24
    25. 25. FREE RADICALS Free radicals or ROS (reactive oxygen species) can lead to breakage of important molecules:  DNA (mutations, renewal failure, cell death)  collagen, elastin, GAG (skin firmness)  lipids (membrane or structural) 25
    26. 26. UV DAMAGE AND OXIDATIVE STRESS DNA effects Matrix effects DNA fragmentation MMP : TIMP ratio UV damage Membrane effects: ROS Lipids peroxidation Hydroperoxides 26 Enzymatic systems SOD Glutathion peroxidase Heme oxidase
    27. 27. DNA DAMAGE   27 UVA acts through oxidative stress forming “reactive oxygen species” (ROS) that will damage the DNA and lead to cancer UVB impact on DNA in the cell creating damages which may lead to cancer: nonmelanoma skin cancer (NMSC)
    28. 28. Advanced Glycosylation End Products  Post-translational modification of collagen by sugar (AGE products)  Non-enzymatic attachment of glucose to proteins  Formation of irreversible cross links
    29. 29. UVB DAMAGE  Following structural changes in DNA, there is an altered expression of oncogenes and tumor suppression genes, such as p53  NMSC show a high incidence of mutation in p53 gene 29
    30. 30. p 53 GENE Plays an important role in:   30 blocking the cell cycle after exposure to DNAdamaging agents e.g. UV, in order to allow for repair before duplication or killing the cell to avoid multiplication of damaged cells (formation of sunburn cells)
    31. 31. p 53 GENE The induction of detectable levels of p53 in human epidermis after UV exposure is relevant to skin carcinogenesis 31
    32. 32. Collagen & Photodamage  Major structural component of ECM   32 70% of the dry weight of skin Collagen degradation is believed to play a role in formation of wrinkles
    33. 33. Collagen Cross Links  Intermolecular cross links between lysine residues in adjacent collagen helices  Non-reducible cross links increase with age  Arise as a side effect of free radical damage
    34. 34. MMP ENZYMES     34 Collagenases (1 to 4) are specific to various collagen, Gelatinases (A & B) are non specific Stromelysins (1-3) specific of fibronectin, laminin, collagen IV, Elastase: elastin
    35. 35. Smoking   Acts primarily via vasoconstriction of blood vessels going to and through skin layers. Decreased blood flow results in     decreased nutrients, decreased oxygen supply increased inflammatory byproducts (free radical oxidation byproducts). Net effect    decreased collagen production and turnover, poor quality collagen and elastin, decreased quantity of matrix components and less gland secretions.
    36. 36. Gravity.    Constantly pulls on bodies. In 50s, when skin’s elasticity declines dramatically, effects of gravity become evident. Causes tip of nose to droop, ears to elongate, eyelids to fall, jowls to form, and upper lip to disappear while lower lip becomes more pronounced.
    37. 37. THANK YOU

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