Difference between revisions of "Skin laxity"

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(Collagen)
(Collagen)
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Radiofrequency produces thermal effects at various depths, promoting collagen remodeling while sparing the overlying tissue.[http://www.ncbi.nlm.nih.gov/pubmed/25594130] Precise and controlled subdermal heating may promote subdermal skin tightening.[http://www.ncbi.nlm.nih.gov/pubmed/25607794] Radiofrequency may be more effective than cutaneous and subcutaneous administration of CO<sub>2</sub>[http://www.ncbi.nlm.nih.gov/pubmed/25549818]
 
Radiofrequency produces thermal effects at various depths, promoting collagen remodeling while sparing the overlying tissue.[http://www.ncbi.nlm.nih.gov/pubmed/25594130] Precise and controlled subdermal heating may promote subdermal skin tightening.[http://www.ncbi.nlm.nih.gov/pubmed/25607794] Radiofrequency may be more effective than cutaneous and subcutaneous administration of CO<sub>2</sub>[http://www.ncbi.nlm.nih.gov/pubmed/25549818]
  
[http://www.waiwiki.org/index.php?title=Maillard_reaction AGEs/ALEs] accumulate in aged skin.[http://www.ncbi.nlm.nih.gov/pubmed/24361253] AGE accumulation is associated with age, smoking and obesity.[http://www.ncbi.nlm.nih.gov/pubmed/22870350] AGEs (advanced glycation end products) and ALEs (advanced lipoxidation end products) are ingested with diet and formed endogenously. In diabetes, endogenous formation of AGEs is elevated, and may lead to 5-fold higher collagen glycation.[http://www.ncbi.nlm.nih.gov/pubmed/10221660][http://www.ncbi.nlm.nih.gov/pubmed/16955213] Creatinine is a potent precursor of specific AGEs ([http://www.waiwiki.org/index.php?title=Heterocyclic_Amines_(HCA) HCAs]), and creatinine clearance is associated with accumulation of AGEs in the skin.[http://www.ncbi.nlm.nih.gov/pubmed/22870350] Skin AGEs are robust long-term markers of microvascular disease progression.[http://www.ncbi.nlm.nih.gov/pubmed/25187362] AGEs and ALEs are associated with age-related NADH oxidase, which may generate free radicals (superoxide), creating oxidative damage leading to cross-linking of skin proteins [http://www.ncbi.nlm.nih.gov/pubmed/24906676], such as collagen and elastin.[http://www.ncbi.nlm.nih.gov/pubmed/22923173] Collagenase naturally degrades damaged collagen, but it may be unable to degrade collagen damaged by cross-linking too heavily.[http://www.ncbi.nlm.nih.gov/pubmed/24361253] Crosslinking may cause the increased age-related stiffness of the skin [http://www.ncbi.nlm.nih.gov/pubmed/23770560] and stiffening of blood vessels.[http://www.ncbi.nlm.nih.gov/pubmed/23612551]
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[http://www.waiwiki.org/index.php?title=Maillard_reaction AGEs/ALEs] accumulate in aged skin.[http://www.ncbi.nlm.nih.gov/pubmed/24361253] AGE accumulation is associated with age, smoking and obesity.[http://www.ncbi.nlm.nih.gov/pubmed/22870350] AGEs (advanced glycation end products) and ALEs (advanced lipoxidation end products) are ingested with diet and formed endogenously. In diabetes, endogenous formation of AGEs is elevated, and may lead to 5-fold higher collagen glycation.[http://www.ncbi.nlm.nih.gov/pubmed/10221660][http://www.ncbi.nlm.nih.gov/pubmed/16955213] Creatinine is a potent precursor of specific AGEs ([http://www.waiwiki.org/index.php?title=Heterocyclic_Amines_(HCA) HCAs]), and creatinine clearance is negatively associated with accumulation of AGEs in the skin.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408990/] Skin AGEs are robust long-term markers of microvascular disease progression.[http://www.ncbi.nlm.nih.gov/pubmed/25187362] AGEs and ALEs are associated with age-related NADH oxidase, which may generate free radicals (superoxide), creating oxidative damage leading to cross-linking of skin proteins [http://www.ncbi.nlm.nih.gov/pubmed/24906676], such as collagen and elastin.[http://www.ncbi.nlm.nih.gov/pubmed/22923173] Collagenase naturally degrades damaged collagen, but it may be unable to degrade collagen damaged by cross-linking too heavily.[http://www.ncbi.nlm.nih.gov/pubmed/24361253] Crosslinking may cause the increased age-related stiffness of the skin [http://www.ncbi.nlm.nih.gov/pubmed/23770560] and stiffening of blood vessels.[http://www.ncbi.nlm.nih.gov/pubmed/23612551]

Revision as of 13:11, 27 January 2015

Skin laxity may be caused by loose skin due to

  • redundant skin after rapid weight loss
  • damaged collagen and reduced collagen production in ageing
  • reduced muscle tone due to immobility

... in combination with heavy skin due to:

  • water retention in the true skin
  • subcutaneous fat accumulation

Collagen

Collagen is the most abundant protein in the extracellular matrix of the skin and due to its slow turnover rates it is a frequent target of modifications by reactive compounds.[1] Collagen is damaged by sunlight exposure, endogenous- and dietary AGEs/ALEs and free radicals in general. Elevated exposure will accelerate age-related exhaustion of collagen production. Solar UV irradiation causes photoaging, characterized by fragmentation and reduced production of type I collagen fibrils that provide strength to skin.[2] Long-term exposure to sunlight, including ultraviolet A and B, produces signs associated with photoaging and photodamage, including laxity.[3] Exposure to UV-B irradiation suppresses collagen synthesis. Daily life low-dose UV-A1 exposures promote photoaging by affecting collagen breakdown. Responsive darkening of the skin does not prevent UV-A1-induced collagenolytic changes.[4] Resveratrol has antioxidant properties and promotes autophagy, stimulating mitochondrial biogenesis. Topically applied Resveratrol (1%) in combination with vitamin E (1%) and baicalin (0.5%) may reduce skin laxity in 12 weeks.[5] Topically applied Pogostemon cablin may inhibit UV-induced photaging, due to its antioxidative property.[6] Radiofrequency produces thermal effects at various depths, promoting collagen remodeling while sparing the overlying tissue.[7] Precise and controlled subdermal heating may promote subdermal skin tightening.[8] Radiofrequency may be more effective than cutaneous and subcutaneous administration of CO2[9]

AGEs/ALEs accumulate in aged skin.[10] AGE accumulation is associated with age, smoking and obesity.[11] AGEs (advanced glycation end products) and ALEs (advanced lipoxidation end products) are ingested with diet and formed endogenously. In diabetes, endogenous formation of AGEs is elevated, and may lead to 5-fold higher collagen glycation.[12][13] Creatinine is a potent precursor of specific AGEs (HCAs), and creatinine clearance is negatively associated with accumulation of AGEs in the skin.[14] Skin AGEs are robust long-term markers of microvascular disease progression.[15] AGEs and ALEs are associated with age-related NADH oxidase, which may generate free radicals (superoxide), creating oxidative damage leading to cross-linking of skin proteins [16], such as collagen and elastin.[17] Collagenase naturally degrades damaged collagen, but it may be unable to degrade collagen damaged by cross-linking too heavily.[18] Crosslinking may cause the increased age-related stiffness of the skin [19] and stiffening of blood vessels.[20]