الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 280 |  |  |
| | | from | 280 | | |
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.