The depth of peeling depends not on the substance used only, but on its concentration, pH of the solution and time of application. Deep peels coagulate proteins and produce complete epidermolysis, restructure of the basal layer and restoration of the dermal architecture. An increase in collagen fiber content, water and GAG in the dermis has been reported. Nonablative skin rejuvenation is not a precise term since rejuvenation is a controlled form of skin wounding aimed at achieving a more youthful appearance after the wound heals.
Treatment of photoaged skin has been divided into treatment of ectatic vessels and erythema, irregular pigmentation, and pilosebaceous changes Type I and into the improvement of the dermal and subcutaneous senescence Type II. Lasers emitting 1,, 80 1,, 81 and 1, nm 82 using interstitial and intracellular water as target chromophores and pulsed dye lasers PDL 83 using oxyhemoglobin as the primary chromophore are now employed for Type II photo rejuvenation only. The clinical efficacy of these nonablative modalities are weaker than that of the ablative methods, however, new collagen formation and clinically observable improvement in wrinkles can be observed.
The increase in dermal collagen has also been confirmed by noninvasive ultrasonographic analysis 94 and radioimmunoassay. A before, B after one treatment with IPL with nm cut-off filter. Histological sections of skin before and after treatment with the different IPL devices have shown the formation of new collagen in the papillary and reticular dermis, as well as an increase in the number of fibroblasts and proportional decrease in the amount of solar elastosis is also usually found. Laser resurfacing has been shown to be effective in counteracting photoaging through entire epidermal ablation, collagen shrinkage, stimulation of neocollagenesis, extensive dermal remodeling, regeneration of cellular organelles and intercellular attachments but parallelly, results in long recovery time are associated with risks of severe long lasting side effects, such as persistent erythema, hypo- or hyperpigmentation, infection or scarring.
Recently, fractionated CO 2 -, erbium glass or erbium-YAG lasers have been introduced to reduce downtime and side effects. Monopolar RF is a noninvasive way to obtain skin tightening 39 and immediate collagen contraction with a single treatment. Unlike lasers, the RF technology produces electric current, which generates heat through resistance in the dermis and as deep as the subcutaneous fat.
It is obvious that different treatment modalities using visible light devices have resulted in varying clinical effects and allow to select individual treatment parameters for different indications. The goal of skin biorejuvenation is to increase the biosynthetic capacity of fibroblasts, inducing the reconstruction of an optimal physiologic environment, the enhancement of cell activity, hydration, and the synthesis of collagen, elastin and HA hyalorunic acid.
The desired effect could be achieved by the microinjections in the superficial dermis of products containing only one active ingredient or cocktails of different compounds which are perfectly biocompatible and totally absorbable: HA, vitamins, minerals, nutrients, hormones, GF, amino acids, autologous cultured fibroblasts, homeopathic products, etc. The proof of concept, including long-term efficiency, optimal injecting protocols are still lacking too. Products injected within or beneath the skin to improve its physical features by soft tissue augmentation are known as fillers.
These may be grouped into temporary, semipermanent lasting between 1—2 y , or permanent materials lasting longer than 2 y. GAG and particularly HA or hyaluronan are major components of the cutaneous extracellular matrix involved in tissue repair of all animal tissues. As a physical background material, it has functions in space filling, lubrication, shock absorption, and protein exclusion.
In addition, HA has been implicated as a regulator of cell proliferation and locomotion. Patient showing the difference of the nasolabial fold: non-treated left side with site marks for planned HA injection and right side straight after injection of only 0. Natural HA has a half-life in tissue of only 1 to 2 d before undergoing aqueous dilution and enzyme degradation in the liver to carbon dioxide and water. The long-lasting dermal fillers maintain the position 1—2 y or even more.
One of long-lasting synthetic semi-permanent dermal fillers is calcium hydroxyl apatite based filler CaHA suspended in an aqueous carboxymethylcelluose gel carrier. CaHA is biocompatible with an identical composition to bones with a low potential for antigenicity, foreign body reaction, and minimal inflammatory response.
No osteoblast activity has been observed in soft tissue. The application of poly-L-lactic acid PLA in soft tissue augmentation exploits a mechanism of action not seen in any other soft tissue filler like a treatment plan, preparation of injection material, and injection technique is distinct as well. Crystals are left behind to stimulate collagen and a granulomatous reaction. This inflammatory reaction elicits resorbtion and the formation of fibrous connective tissue about the foreign body, causing dermal fibroplasia that leads to the desired cosmetic effect.
Although subjective patient satisfaction is high in many of the studies with skin fillers and skin thickness as measured using wrinkle scale ratings of appearance, long-term efficacy and clinical safety data are lacking because patients are likely to continue to undergo subsequent cosmetic interventions. PRP is derived from fresh whole blood, which contains a high concentration of platelets.
Botulinum toxin BTX has no effect on skin texture and cannot discontinue the skin aging process. However, regular BTX injections can slow down the visible aging process by helping in the management of certain dynamic facial lines and wrinkles - Fig. Current treatment options of exaggerated frown lines, glabellar lines or crow feet such as surgery or implants, do not address the underlying cause of these lines, namely the excessive nerve stimulation.
The mechanism of action of BTX makes it an ideal agent to target the major cause of these dynamic lines. A pre-injection, B after injection with botulinum toxin. Seven constitutionally similar but antigenically distinct subtypes of neurotoxin A-G are produced by different strains of the anaerobic, gram-positive bacterium Clostridium botulinum.
BTX-A produces temporary chemical denervation by blocking the presynaptic release of acetylcholine Ach at the neuromuscular junction NMJ. This induces receptor-mediated endocytosis of the toxin. The light chain that is responsible for the toxicity splits off in the cell, and inactivates a synapse-specific protein synaptosomal-associated protein of 25 kDa SNAP which is one of several proteins required for Ach exocytosis and release into the NMJ. The toxin binds to presynaptic neurons of selected muscles rapidly under an hour and specifically.
Clinically reversible chemical denervation and selective muscle relaxation or paralysis starts after 24 to 48 h and may not be completed for up to 2 weeks. Another factor explaining the regaining of muscle function could be an increase in the area of muscle membrane sensitive to acetylcholine. Muscular changes in the form of atrophy were demonstrated in animal studies, and were completely reversible after 4—6 mo. In human muscle, no lasting atrophy could be detected even after repeated injections, only a predominance of type I fibers. Dosing of BTX-A is essential in achieving precise and predictable effects.
The biological activity given in mouse units MU and the weight of the molecule is not associated with the dosage. Several commercial preparations of BTX-A products which are produced from different strains of bacteria by different purification methods and therefore have distinct components and properties, requirements of storage, shelf-life, and dose are currently available for aesthetic uses. A thorough understanding and evaluation of the relevant anatomy and physiology of the muscles and possible alterations in the area to be injected is essential.
Dosage for the patients depends on the area, muscle mass, gender and other factors individually. Contraindications include conditions of peripheral motor neuropathic diseases or neuromuscular functional disorders, coadministration with aminoglycoside antibiotics or other agents that interfere with neuromuscular transmission and may potentiate general weakness, treatment of patients with inflammatory skin disorders at the injection site, history of reaction to toxin, pregnancy and lactation, age younger than 12 y, participation in occupations that necessitate a wide range of facial expressions.
Given the short-term and localized effects of BTX-A injections, it is reassuring that any potential adverse reactions known to date may also be short lived, localized, and reversible in a dose-dependent period of 6—8 weeks. Systemic or serious side effects in general are rare, immune-mediated disorders or other idiosyncratic reactions are unknown. The incidence of complications in many cases depends on the proper application and the qualification of the physician.
However, it has always to be considered that the benefits of this treatment are transient and repeated injections are necessary for a long-term effect. It is well known that there is a progressive decrease of hormone synthesis with age. Levels of growth hormone GH and insulin-like growth factor-1 IGF-1 , melatonin nocturnal , TSH, thyroid hormones T3 , dehydroepiandrosterone DHEA sulphated form and its urinary keto-metabolites , estrogens and testosterone are progressively decreasing. The main hormonal deficits in humans are menopause, andropause and partial androgen deficiency of the aging male.
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In a randomized and placebo-controlled study of older men and women 60—79 y of age , each subject received 50 mg of DHEA daily for a year. The women showed an improvement of the libido, skin health, and osseous density.
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The treatment led to an improved body condition, with an increase of muscle mass and osseous density and a decrease of adipose tissue. Moreover, an increase of skin thickness was observed. Melatonin has been shown to have a favorable influence on the aging process, because it has an inverse effect with regard to body weight; food restriction raises the levels of melatonin and decreases its age-related decrease.
With increasing age comes a decrease of melatonin production, which may have a connection to sleep disorders suffered by elderly people. It also has be shown that melatonin can prevent tumor development and growth. Interestingly, a study showed that patients with tumors had decreased levels of melatonin compared with healthy individuals. HRT with testosterone is absolutely indicated in older men who are either symptomatic or have a low serum testosterone level. Either a decrease of testosterone or a loss of the circadian rhythm of testosterone secretion has been observed in a high percentage of older men.
Clinical symptoms include general weakness, sexual dysfunction, diminished muscle and bone mass, and decreased erythropoiesis. A low testosterone level has been shown in epidemiological studies to lead to a higher morbidity and mortality rate and to a higher prevalence of depression, coronary heart disease, and osteoporosis. Insulin resistance has been shown to play an important role in the development of hypogonadism in older men. Thus, obese men and men with type 2 diabetes, show significantly lower testosterone levels compared with subjects in control groups.
On the contrary, HRT has been accused to have a higher cardiovascular risk and increase of the risk of breast cancer.
PATENT ANALYSIS: A LOOK AT THE INNOVATIVE NATURE OF PLANT-BASED COSMETICS
However, it has clear, positive preventive effects on osteoporosis, and an early, low-dose estrogen monotherapy can be considered to have advantages. While natural aging is genetically determined, extrinsic aging can be prevented. Previously published online: www. National Center for Biotechnology Information , U. Journal List Dermatoendocrinol v. Aikaterini I. Christos C. Author information Copyright and License information Disclaimer.
Zouboulis, Email: ed. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. This article has been cited by other articles in PMC. Abstract Skin aging is a complex biological process influenced by a combination of endogenous or intrinsic and exogenous or extrinsic factors.
Keywords: aging, anti-aging, antioxidants, laser, peeling, fillers, botulinum toxin, hormone replacement therapy, cell regulators, prevention. Skin Aging Prevention and Therapy The skin anti-aging strategies attempted to reverse the dermal and epidermal signs of photo- and chronological aging can be grouped under the following approaches Table 1.
Skin antiaging approaches. Open in a separate window. Skin Care Healthy and functioning skin barrier is important protector against dehydration, penetration of various microorganisms, allergens, irritants, reactive oxygen species and radiation. Photoprotection and Systemic Antioxidants Chronic photodamage of the skin manifests itself as extrinsic skin aging photoageing. Topical Pharmacological Agents with Anti-Aging Properties There are two main groups of agents that can be used as anti-aging cream components, the antioxidants and the cell regulators.
Chemical Peels Chemical peels are methods to cause a chemical ablation of defined skin layers to induce an even and tight skin as a result of the regeneration and repair mechanisms after the inflammation of the epidermis and dermis. Injectable Skin Rejuvenation and Dermal Fillers The goal of skin biorejuvenation is to increase the biosynthetic capacity of fibroblasts, inducing the reconstruction of an optimal physiologic environment, the enhancement of cell activity, hydration, and the synthesis of collagen, elastin and HA hyalorunic acid.
Botulinum Toxin Botulinum toxin BTX has no effect on skin texture and cannot discontinue the skin aging process. Conclusions While natural aging is genetically determined, extrinsic aging can be prevented. Disclosure of Potential Conflicts of Interest No potential conflicts of interest were disclosed. Footnotes Previously published online: www. References 1. Human models of aging and longevity. Expert Opin Biol Ther. Uitto J. Understanding premature skin aging. N Engl J Med. Scaffidi P, Misteli T. Lamin A-dependent nuclear defects in human aging. Fisher, G. The pathophysiology of photoaging of the skin.
Cutis, 75, 5—9 58— Nuclear hormone receptors in human skin. Horm Metab Res. Vitamins as hormones. Biology of estrogens in skin: implications for skin aging. Exp Dermatol. Hall G, Phillips TJ. Estrogen and skin: the effects of estrogen, menopause, and hormone replacement therapy on the skin. J Am Acad Dermatol. Estrogens and the skin. Draelos ZD. Topical and oral estrogens revisited for antiaging purposes. Fertil Steril. Kanda N, Watanabe S.
Regulatory roles of sex hormones in cutaneous biology and immunology. J Dermatol Sci. Modulation of collagen metabolism by the topical application of dehydroepiandrosterone to human skin. J Invest Dermatol.
Kligman LH. Manifestations, prevention, and treatment. Clin Geriatr Med. Intrinsic aging vs. Mathematical morphologic analysis of aging-related epidermal changes. Anal Quant Cytol Histol. Epidermal thickness, skin pigmentation and constitutive photosensitivity. Photodermatol Photoimmunol Photomed. Makrantonaki E, Zouboulis CC. William J. Cunliffe Scientific Awards. Characteristics and pathomechanisms of endogenously aged skin. Molecular mechanisms of skin aging: state of the art.
Ann N Y Acad Sci. Age-related mechanical properties of human skin: an in vivo study. Yaar M, Gilchrest BA. Aging of skin. McGraw-Hill:New York, ; — Baumann L. Skin ageing and its treatment.
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J Pathol. A short-term screening protocol, using fibrillin-1 as a reporter molecule, for photoaging repair agents. A histological study of human wrinkle structures: comparison between sun-exposed areas of the face, with or without wrinkles, and sun-protected areas.
Br J Dermatol. Inhibition of type I procollagen synthesis by damaged collagen in photoaged skin and by collagenase-degraded collagen in vitro. Am J Pathol. Ultraviolet B wavelength dependence for the regulation of two major matrix-metalloproteinases and their inhibitor TIMP-1 in human dermal fibroblasts. Photochem Photobiol. Molecular basis of sun-induced premature skin ageing and retinoid antagonism.
Pathophysiology of premature skin aging induced by ultraviolet light. Singlet oxygen induces collagenase expression in human skin fibroblasts. FEBS Lett. Oikarinen A. The aging of skin: chronoaging versus photoaging. The influence of age and sex on skin thickness, skin collagen and density. Chronic sun exposure alters both the content and distribution of dermal glycosaminoglycans. Elsner P, Maibach HI. Cosmeceuticals and Active Cosmetics: Drugs versus Cosmetics 2nd edn. Marcel Dekker: New York, NWSA J. Bayer K. Cosmetic surgery and cosmetics: redefining the appearance of age.
Holstein MB, Minkler M. Mykytyn C. Anti-aging medicine: Predictions, moral obligations, and biomedical intervention. Anthropol Q. Wollina U, Payne CR. Aging well--the role of minimally invasive aesthetic dermatological procedures in women over J Cosmet Dermatol. Vedamurthy M. Antiaging therapies. Indian J Dermatol Venereol Leprol.
Visible light treatment of photoaging. Dermatol Ther.
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Biophysical assessment of persistent effects of moisturizers after their daily applications: evaluation of corneotherapy. Evidence-based corneotherapy. Vitamin A antagonizes decreased cell growth and elevated collagen-degrading matrix metalloproteinases and stimulates collagen accumulation in naturally aged human skin. Topically applied vitamin C enhances the mRNA level of collagens I and III, their processing enzymes and tissue inhibitor of matrix metalloproteinase 1 in the human dermis.
Kockaert M, Neumann M. Systemic and topical drugs for aging skin. J Drugs Dermatol. Hyaluronic acid and dermatan sulfate are selectively stimulated by retinoic acid in irradiated and nonirradiated hairless mouse skin. Trautinger F. Mechanisms of photodamage of the skin and its functional consequences for skin ageing. Clin Exp Dermatol. Berger MM. Can oxidative damage be treated nutritionally? Clin Nutr. Marini A. Does it really work? Effects of antioxidant supplementation on the aging process. Clin Interv Aging. Active oxygen species generation and cellular damage by additives of parenteral preparations: selenium and sulfhydryl compounds.
Ferulic acid stabilizes a solution of vitamins C and E and doubles its photoprotection of skin. Topical niacinamide reduces yellowing, wrinkling, red blotchiness, and hyperpigmented spots in aging facial skin. Int J Cosmet Sci. Clinical, biometric and structural evaluation of the long-term effects of a topical treatment with ascorbic acid and madecassoside in photoaged human skin. Kerscher M, Buntrock H. What really helps? A topical antioxidant solution containing vitamins C and E stabilized by ferulic acid provides protection for human skin against damage caused by ultraviolet irradiation.
The latest cosmeceutical approaches for anti-aging. Evaluation of the antioxidant capacity and preventive effects of a topical emulsion and its vehicle control on the skin response to UV exposure. Skin Pharmacol Physiol. Cutaneous photoprotection from ultraviolet injury by green tea polyphenols.
Improvement of naturally aged skin with vitamin A retinol Arch Dermatol. Bhawan J. Short- and long-term histologic effects of topical tretinoin on photodamaged skin. Int J Dermatol. Cosmeceutical peptides. Clinical improvement following dermabrasion of photoaged skin correlates with synthesis of collagen I. Arch Dermatol. Telomerase and the cellular lifespan: implications of the aging process. J Pediatr Endocrinol Metab. Chemical peels. J Eur Acad Dermatol Venereol. Phenol-induced histological skin changes: hazards, technique, and uses.
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Comparative histological study of mini pig skin after chemical peel in an animal model after chemical peel and dermabrasion. Arch Otolaryngol. Histologic study of dermabrasion and chemical peel in an animal model after pretreatment with Retin-A. Aesthetic Plast Surg. Effects of chemical peeling in photoaged hairless mice. Quantitative and qualitative effects of chemical peeling on photo-aged skin: an experimental study. Plast Reconstr Surg.
I tell people the most important preventive thing you can do, if you can't afford treatment, is change your [style of] underwear: Wear a thong. Does diet play a big role in the amount of cellulite people get? Diet does play a role, because look, women in Asia, what do they have for breakfast? Noodles—it's a high-calorie meal, but when they go to work they burn those calories.
In contrast, we eat these calories, then go to work and sit at a desk. Think of those [fat-producing] alpha receptors just waiting to rock and roll. So, it all goes together. That's why women struggle to lose weight below the waist. From the waist up, for every four receptors that break down fat, there are five that make it, so it's almost a one-to-one ratio. From the trunk up, there's just one layer of fat, except for the triceps arm area. It's really a whole biochemistry. People tell you: Don't eat fat, don't eat sugar. It's really more than that.
It's hormone balance—you need to eat healthy, you need activity. How big a role do genes play in cellulite levels? There is a genetic component or predisposition to cellulite. But just because you have the genetic component doesn't mean you have to develop it if you do the right things: eat a healthy diet , exercise, and skip restrictive underwear.
Do creams—thigh creams, caffeine creams—really work? Most all creams will only address the fat. Caffeine creams will help by blocking the making of fats by the alpha receptors. Some creams have aminophylline, a compound in some respiratory drugs which, like caffeine, works by blocking the alpha receptors. In most creams, you find some way of targeting only the fat cells [and not addressing the connective tissue or circulation aspects of cellulite].
What other treatments are there for cellulite? There are three treatable components of cellulite: You have to address the collagen; you have to reduce the fat, and you have to increase circulation. But it depends on the grade of cellulite you have. There are four grades, ranging from zero to three: Grade zero is no visible cellulite. If you pinch the skin and see a cottage cheese—like texture—that's grade one. Grade two is if cellulite is visible on the legs of someone standing. Grade three is if you see cellulite when you look in the mirror or lie down.
I call grade three "terminal," because it's very hard to treat, although the good news is that I don't think anyone's ever died of it. Machines to treat cellulite include vacuum rolling and radio waves to break up the fat. The first one of them on the market was Endermologie. When you're vacuuming and rolling [the skin], you're increasing circulation, and the heat helps to break down the fat, which smoothes out the skin. The downside to the machines is you have to go once a month [for at least several years]. What about lasers, injections and surgery?
Laser treatments are combined with massage and rolling; they either do suction or rolling and use radio waves and heat up the fat—put fat on a stove in a frying pan, and it melts. For subcision, you anesthetize the area, then you take a special needle—a Nokor needle, which looks kind of like a little hatchet—so you can make a small incision and, moving it back and forth, you can cut the skin from the tissue holding [it] down, getting rid of the dimples. I've see women who have had fat injected into their thighs, buttocks, bellies and anyplace else they have cellulite in an attempt to even out the texture—and it was like a bump sticking out of the leg.
Other injections you have to have every few months. The bad thing about silicone [and fat-transfer] injections [that aim to fill in the dimples] that they can move and can get absorbed—and you can't get rid of it. As for liposuction [when plastic surgeons literally suck out the fat through a tube], you'll find tons of women who complain that the procedure actually made their cellulite worse. Liposuction has only been proven to work for body sculpting [changing the body's contours by removing excess fat from some areas of the body, which doesn't have much—if any—effect on the texture of fat that will remain below the skin].
If you have a doctor telling you that you can get rid of cellulite with liposuction, run out that door and don't ever look back. You have free article s left. Already a subscriber? Sign in. See Subscription Options. Read more from this special report: The Science of Beauty. Get smart. Sign up for our email newsletter.
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