الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
There has been rapid expansion of the population of elderly people both in
the developed and developing world. Aging is a process that affects all cells,
tissues, organs, and organisms, diminishing homeostasis and increasing organism
vulnerability. Like all other organs, skin suffers progressive morphologic and
physiologic decrement with increasing age and provides the first obvious evidence
of the aging process.
Cellular senescence can be activated by various types of stressful stimuli,
including telomere shortening, oncogenic, or tumor suppressor signals, and DNA
damage. Progressive telomere shortening in successive cell divisions induces
senescence due to the loss of terminal sequences during DNA replication.
Maintenance of the telomere sequences at human chromosome ends is essential for
immortalized cells to escape from the normal limitations of the proliferation
capacity. cutaneous aging consists of distinct processes due to either intrinsic or
extrinsic Intrinsic aging depends on time and reflects the genetic background.
Hormones are decisively involved in intrinsic aging factors. The extrinsic aging,
also know as photoaging, is clinically, biologically and molecularly distinct from
intrinsic aging. The most obvious clinical impressions of the elderly skin are
increased formation of wrinkles and deficits in elasticity.
Many dermatoses of the elderly are presented completely different than in
young persons. Like Herpes zoster, bullous pemphigoid, erysipelas and herpes
zoster and pruriginous eczema. As a human being ages, the skin thins, dries,
wrinkles, and becomes unevenly pigmented. A loss of subcutaneous fat, as well as
underlying bone and cartilage, manifests as sagging skin and fallen nasal tips.
Various inflammatory, infectious, and vascular disorders become more common.
The loss of dermal collagen and elastin makes up most of the reduction in total skin
thickness in elderly adults. Dermal thickness decreases at the same rate in both
genders. The water content of the SC decreases progressively with age. total lipid
content of the aged skin decreases by age. The most widely observed structural
change in aged skin is a flattening of the dermal–epidermal junction. Mechanical
tension or stress on dermal fibroblasts, created by a healthy collagen matrix, is
critical for the maintenance of a proper balance between the synthesis of collagen
and the synthesis of collagen degrading enzymes. In the aged dermis, collagen
fibers become thicker and collagen bundles more disorganized than in younger
skin. Physiological changes in aged skin include changes in: (i) biochemistry, (ii)
neurosensory perception, (iii) permeability, (iv) vascularization, (v) response to
injury, (vi) repair capacity, and (vii) increased incidence of some skin diseases. In
older skin, capillaries and small blood vessels regress and become more
disorganized, blood vessel density diminishes. The immune response of aged skin
is generally diminished. Possible molecular mechanisms of skin agin include :
telomere shortening , DNA damage and oxidative stress. Various extrinsic factors
may be involved in the process of extrinsic aging as: solar irradiation, tobacco
smoking, ozone defect and infra-red irradiation. The exact mechanisms by which
UV radiation causes premature skin aging is not yet clear, but a number of
molecular pathways explaining one or more of the key features of photoaged skin
have been described. Some of these models are based on irradiation protocols,
which use single or few UV exposures, whereas others take into account the fact
that photoaging results from chronic UV damage, and as a consequence employ
chronic repetitive irradiation protocols. relationship between telomere shortening
and skin aging has also been observed in several studies.
Prevention of premature skin aging is of constantly increasing importance to
the general population. Basic skin care with healthy diet, emollients and sun screen
are important steb in avoiding aging. This wide range of complexities and
variabilities is echoed in the potential dermatologic interventions that can be
employed to correct or reverse the signs of aging. Dermatologic options for such
revitalization range from nonsurgical modalities (Botox, filler substances, and
nonablative lasers) to more aggressive resurfacing procedures (chemical peels,
dermabrasion, and ablative lasers) and to more traditional, surgical procedures
(liposuction, blepharoplasty, and various types of face and neck lifting). The
application of these revitalizing tools, along with their associated risks and
expected outcomes, are explored. Among several reports, the wound-healing and
anti-ageing effects of ADSC in photo-damaged aged skin have come into attention.
ADSC injection increases dermal thickness and fibroblast number. So it can attract
our minds toward stem cells as a new therapeutic modality.