dermatology nursing overview of skin aging and photoaging of skin aging and... · dermatology...

DERMATOLOGY NURSING/June 2008/Vol. 20/No. 3 177

Overview of Skin Aging andPhotoaging

DERMATOLOGY NURSING

One of the more common der-matologic concerns in pa-tients is aging skin. In a cul-ture that is often called

“youth-obsessed,” patients increas-ingly look for creams and proce-dures that can improve the appear-ance of their skin. In 2004, U.S. retailsales of cosmeceuticals, cosmeticproducts purported to have medici-nal or drug-like benefits, accountedfor over $12.4 billion. By 2010, theanti-aging market is expected toaccount for over $16.5 billion insales (Choi & Berson, 2006).Research into skin aging has alsoadvanced considerably in the past 2decades. Clinical manifestations ofskin aging, mechanisms whichunderlie these clinical changes, andapproaches to treatment will beexplored.

Clinical Signs of Aging andPhotoaging

Many of the skin changes com-monly associated with aging,changes in pigmentation, sallowness,

aging, in contrast, is characterized bylaxity and fine wrinkling, as well asdevelopment of benign growths suchas seborrheic keratoses and angio-mas, but is not associated with in-creased pigmentation or the deepwrinkles that characterize photoag-ing (Yaar et al., 2002).

Yolanda Rosi Helfrich, MD, is anAssistant Professor, University of MichiganDepartment of Dermatology, Ann Arbor, MI.

Dana L. Sachs, MD, is an AssociateProfessor of Dermatology, University ofMichigan, Ann Arbor, MI.

John J. Voorhees, MD, is Duncan andElla Poth Distinguished Professor, andChariman of the Department of Dermatology,University of Michigan Medical School, AnnArbor, MI.

Note: The authors reported no actual orpotential conflict of interest in relation to thiscontinuing nursing education article.

The Editor, Marcia J. Hill, MSN, RN, dis-closed that she is an employee of Genentech.

All other Dermatology Nursing EditorialBoard members reported no actual or potentialconflict of interest in relation to this continuingnursing education article.

Aging skin is an issue of concernto many patients. In this reviewaging and photoaging aredefined, mechanisms whichunderlie these processes explored,and available treatment optionsdiscussed.

Yolanda Rosi HelfrichDana L. SachsJohn J. Voorhees

This article and the CNE answer/evaluation form are also available

online atwww.dermatologynursing.net

OBJECTIVESThis continuing nursing educational (CNE) activity is designed for nurs-

es and other health care providers who care for and educate patients andtheir families regarding skin aging and photoaging. For those wishing toobtain CNE credit, an evaluation follows. After studying the information pre-sented in this article, the nurse will be able to:

1. Define the clinical signs of aging and photoaging.2. Describe the mechanisms of aging and photoaging.3. Discuss treatments for aging skin.

and deep wrinkling, are actually theresult of sun exposure. Sun-exposedareas of the skin, such as the face,neck, upper chest, hands, and fore-arms, are the sites where thesechanges occur most often. As early asthe 19th century, researchers notedprofound differences in the facialskin of farmers and sailors as com-pared to that of indoor workers(Urbach, Forbes, Davies, & Berger,1976). Outdoor laborers were notedto have thickening and brownish dis-coloration on light-exposed skin;these changes were also associatedwith an increased number of skincancers (Urbach et al., 1976).

The term “photoaging” was firstcoined in 1986 and describes theeffects of chronic ultraviolet (UV)light exposure on skin (Kligman &Kligman, 1986). Clinical signs ofphotoaging include dryness; irregu-lar, dark/light pigmentation; sallow-ness; either deep furrows or severeatrophy; telangiectases; premalignantlesions; laxity; and a leathery appear-ance (see Table 1) (Yaar, Eller, &Gilchrest, 2002). Other signs includeelastosis (a coarse, yellow, cobble-stoned effect of the skin) and actinicpurpura (easy bruising related to vas-cular wall fragility in the dermis)(Gilchrest, 1990). Chronologic skin

177-DNJ June 2008.ps 6/5/08 4:13 PM 77

DERMATOLOGY NURSING/June 2008/Vol. 20/No. 3178

Microscopic Findings in Aging andPhotoaging

There are microscopic differ-ences in the two aging processes aswell. In chronologically aged skin,the epidermis is atrophic, with flat-tening of the dermal-epidermal junc-tion and loss of rete pegs (Kurban &Bhawan, 1990). The dermis alsobecomes thinner, with decreasednumbers of fibroblasts and de-creased levels of collagen (Varani etal., 2000). Photoaged skin, in con-trast, can be associated with eitherincreased epidermal thickness orpronounced epidermal atrophy. Themost pronounced histologic changeis the accumulation of elastin-con-taining material just below the der-mal-epidermal junction, known assolar elastosis (Lavker, 1995). Colla-gen, which composes over 90% ofthe skin’s total proteins, becomes dis-organized (Bernstein et al., 1996).

Mechanism of PhotoagingCollagen is one of the main

building blocks of human skin, pro-viding much of the skin’s strength.Dermal fibroblasts make precursormolecules called procollagen, whichis converted into collagen. There are

two important regulators of collagenproduction: transforming growthfactor (TGF)-β and activator protein(AP)-1. TGF-β is a cytokine that pro-motes collagen production (Massagué,1998). AP-1 is a transcription factorthat inhibits collagen production andup-regulates collagen breakdown(Kang, Fisher, & Voorhees, 1997).Collagen in skin undergoes continu-ous skin remodeling and turnover,with TGF-β and AP-1 playingimportant roles. TGF-β promotescollagen formation, while AP-1 pro-motes collagen breakdown by up-regulating enzymes called matrixmetalloproteinases (MMPs).

When skin is exposed to sun-light, UV radiation is absorbed byskin molecules that can generateharmful compounds, called reactiveoxygen species (ROS), which thencause “oxidative damage” to cellularcomponents like cell walls, lipidmembranes, mitochondria, andDNA. These ROS also play animportant role in molecular path-ways. Irradiation of human buttockskin with 2 MED (two times the doseof UVA/UVB that causes barely per-ceptible skin reddening, the minimalerythema dose) causes increased

generation of hydrogen peroxide, anROS, within 15 minutes (Kang et al.,2003). Within the same time frame,AP-1, which leads to increased colla-gen breakdown, becomes elevatedand remains elevated for at least 24hours following UV irradiation(Fisher et al., 1996). Collagen-degrading MMPs, which are up-reg-ulated by AP-1, are also markedlyelevated within 24 hours of UV irra-diation (Fisher et al., 1996). Within24 hours of a single dose of UV irra-diation, increased collagen break-down can be demonstrated (Fisher etal., 1997).

To summarize, UV irradiationleads to generation of ROS andinduction of AP-1, which causesincreased MMP production, withsubsequent increased breakdown ofcollagen. In addition, UV irradiationleads to decreased expression ofTGF-β2, a member of the TGF-βfamily. As noted previously, TGF-βpromotes collagen formation; there-fore, decreased expression of TGF-βcauses decreased collagen produc-tion. Researchers have demonstrateddecreased procollagen synthesiswithin 8 hours of UV irradiation(Quan, He, Kang, Voorhees, &Fisher, 2002). Increased breakdownand decreased production of colla-gen are the cornerstones of photoag-ing. Each UV insult induces a woundresponse with subsequent imperfectrepair, leaving an invisible “solarscar.” Repetitive UV insults over alifetime eventually lead to develop-ment of a visible “solar scar,” mani-festing as a visible wrinkle (Kang,Fisher, & Voorhees, 2001) (seeFigure 1).

It is commonly accepted thatincreased innate pigmentation (dark-er skin tone) is associated with pro-tection from sun damage. Darker-skinned people are less likely todevelop a sunburn after intense sunexposure, and have a lower inci-dence of skin cancer. In addition,darkly pigmented subjects have sig-nificantly less induction of collagen

DERMATOLOGY NURSING

Table 1.Comparison of Changes Seen in Photoaging and

Chronologic Aging of Skin

Photoaging Chronologic Aging

Deep, coarse wrinkles Fine wrinkles

Mottled pigmentation Laxity

Sallowness Benign neoplasms

Dryness

Telangiectasia

Premalignant lesions

Laxity

Atrophy

Leathery appearance

Elastosis

Actinic purpura

178-DNJ June 2008.ps 6/5/08 4:13 PM Page 178


breakdown and less DNA damagethan lightly pigmented subjects(Fisher et al., 2002). These molecularfindings support the clinical observa-tion that darker-skin pigmentationprotects against photoaging.

Mechanism of Skin AgingGenerally, the molecular changes

of photoaging are considered to be anaugmentation and amplification ofthe molecular changes associatedwith chronologic skin aging (Fisher et

al., 2002). In aged skin, there is eleva-tion of AP-1 as compared to youngskin (Chung et al., 2000). MMP activ-ity is also increased in aged humanskin, and is associated with increasedlevels of degraded collagen (4-foldhigher in aged vs. young subjects )(Fisher et al., 2002). In addition, syn-thesis of types I and III procollagen isreduced in aged human skin (Varaniet al., 2000). The combination ofincreased breakdown of collagen anddecreased synthesis of new collagen

results in an overall decrease in colla-gen levels in the dermis. Thesemolecular changes in chronologicallyaged skin resemble the changes asso-ciated with photoaging. This supportsthe notion that photoaging is super-imposed upon and amplifies thechanges associated with chronologicskin aging.

Chronologic aging is thought toresult from a combination of forces.Generation of ROS is thought to playa major role. The free radical theoryof aging proposes that aging resultsfrom accumulation of oxidative dam-age over a lifetime due to excessROS, which result from aerobicmetabolism (Hensley & Floyd, 2002).ROS generation is increased in agedskin. As discussed previously, ROSgeneration is a key step in molecularpathways which eventually lead toincreased collagen breakdown. Thisfree radical theory of aging gives agood explanation of the molecularchanges associated with chronologicaging.

Treatment of Aging SkinTreatment of aging skin includes

(a) measures to prevent against UVdamage and (b) medications and pro-cedures to reverse existing damage.

Photoprotection. Photoprotectionrefers to measures that can be taken toprotect the skin from UV damage andis achieved by sunscreens, sun-protec-tive clothing, and sun avoidance.Sunscreens are broadly defined asagents that protect against UV dam-age and protect against sunburn, wrin-kles, and pigmentary changes(Gilchrest, 1996). Sun-protection fac-tor (SPF) refers to the degree of pro-tection from ultraviolet B and does notaccount for protection against ultravi-olet A. Patients should be advised tochoose a sunscreen with an SPF of 15or higher and to apply liberally andfrequently to all exposed body sites,especially the face and neck.Sunscreens should be applied every 2to 3 hours, especially if patients areengaged in outdoor activities. Because

DERMATOLOGY NURSING

Acute ultraviolet irradiation leads to generation of ROS, upregulation of AP-1, anddownregulation of TGF-β. AP-1 leads to collagen breakdown, while decreased TGF-β activity is associated with decreased collagen production. No damage to the skin isrepaired perfectly; acute solar damage leads to an invisible solar scar. Repeatedultraviolet irradiation and injury eventually leads to accumulation of damage,eventually manifesting as a visible solar scar, or a wrinkle associated with photoaging.

Figure 1.Model Depicting the Effect of Ultraviolet Radiation on Skin

AP-1

MMPs

CollagenBreakdown

TGF-β

ProcollagenProduction

ROSGeneration

Imperfect Repair

Invisible Solar Scar

Repeated UV Injury

Visible Solar Scar =“Wrinkle of Photoaging”

Sun



the SPF rating only confers protectionagainst ultraviolet B, patients shouldbe educated to look for ultraviolet Aprotection features in a sunscreen.Chemical blockers of UVA includeoxybenzone and avobenzone (Parsol1789). Some newer UVA blockershave become available in the UnitedStates including ecamsule, which isthe most photostable UVA blockeravailable and sold under the tradename Mexoryl™ (Anthelios, La RochePosay/L’Oreal), and Helioplex™, a sta-bilized form of avobenzone(Neutrogena). Sunscreens that containphysical blockers such as titaniumdioxide and zinc oxide confer protec-tion against both UVB and UVA.Newer technologies such as microniza-tion have been developed over recentyears to make these physical blockersmore cosmetically acceptable. A com-plete list of sunscreens with the SkinCancer Foundation’s Seal of Recom-mendation can be found at www.skincancer.org.

Sun-protective clothing linesexist and are widely available insporting goods stores and on theInternet. These clothing lines providehats, long-sleeved clothing, etc. andare geared towards patients who workoutdoors and are avid outdoor enthu-siasts for whom sunscreens might beless practical to use. The fabrics usedin these lines are highly engineeredand sophisticated materials that con-fer high levels of sun protection andprotect against both UVA and UVB.Solumbra, manufactured by SunPrecautions, offers an SPF 30+ andreportedly blocks 97% of UVA andUVB. Coolibar is another brand ofsun-protective clothing and hats andoffers an ultraviolet protection factor(UPF) of 50+ and reportedly blocks98% of ultraviolet A and B. UPFs aresimilar to SPFs but are typically usedfor devices such as clothing and fab-rics rather than for sunscreen.Clothing lines and other sun-protec-tive devices endorsed by the SkinCancer Foundation are listed on theirWeb site.

Finally, sun-protective behavioris achieved through patient educa-tion. Patients should be discouragedfrom using suntanning beds, whichaccelerate photoaging. Patientsshould be educated to avoid middaysun exposure when ultraviolet radia-tion is most intense, to participate inoutdoor activities early or late in theday, to avoid sunbathing (even withsunscreens), and to seek shady, cov-ered areas rather than direct sunlight.

Topical retinoids. Available topicalretinoids include prescription tretinoin(Retin-A®), adapalene (Differen®), andtazarotene (Tazorac®) and over-the-counter Retinol® and Retinol-A®.These drugs are derivatives of vitaminA which have anti-aging properties.Topical tretinoin was first observed toameliorate the clinical signs of pho-toaging by Cordero (1983) andKligman, Grove, Hirose, and Leyden(1986). The first double-blinded, ran-domized, vehicle-controlled clinicaltrials investigating the use of tretinoinfor photoaged skin were performed inthe late 1980s. In these studies, inves-tigators found that surface roughness,dyspigmentation, and fine wrinklesdemonstrated the most improvementwith topical tretinoin therapy in thefirst 4 to 10 months of therapy (Weisset al., 1988). Because epidermalchanges seen early in therapy revertedto baseline, the wrinkle-improvingeffect of tretinoin was presumed to bedue to effects on the dermis. In studies,topical tretinoin increased collagentype I in photoaged skin (Griffiths etal., 1993; Talwar, Griffiths, Fisher,Hamilton, & Voorhees, 1995). It iscommon and predictable for patientsto develop a retinoid dermatitis char-acterized by erythema and scalingafter starting a retinoid. With timeand continued use, this dermatitisimproves. A patient may use topicaltretinoin as part of a daily and ongo-ing program to reverse the signs ofclinical photoaging. Topical tretinoinis typically prescribed as a 0.05% or0.1% cream, and for patients more sen-sitive to the effects, lower strengths can

be used (0.02%, 0.025%). Tretinoincan be used indefinitely. There are notrue contraindications to its use,though some patients are not able totolerate the accompanying retinoiddermatitis.

Cosmeceuticals. Cosmeceuticalsare agents that are marketed as cos-metic products, contain biologicallyactive ingredients, and are availablewithout a prescription. Drugs exert abiologic effect, are dispensed by pre-scription, and are regulated by theU.S. Food and Drug Administration.Cosmeceuticals do not undergo therigorous testing required for drugapproval, and there are few clinicalcontrolled trials of these products. Infact, most of the work supportingtheir use is in vitro or small, open-label, industry-sponsored trials. Thecosmeceutical industry is huge andfuture projections estimate that it willexceed $16 billion by 2010 (Choi &Berson, 2006). Cosmetic productscontaining peptides, antioxidants,and botanicals are examples of cos-meceuticals. A complete review ofcosmeceuticals is beyond the scope ofthis article, so only select ones will bementioned.

Peptides are amino acid chains thatare fragments of large proteins such ascollagen. Pal-KTTS is a collagen pep-tide fragment, and there is evidence inwound healing that it may penetrateinto the dermis and stimulate collagenproduction (Katayama, Armendariz-Borunda, Raghow, Kang, & Seyer,1993). Pal-KTTS is marketed asMatrixyl™ (Sederna, France) and is aningredient in a number of cosmeceuti-cals. A tripeptide-copper complex canincrease collagen in wounds and is aningredient in a number of cosmeceuti-cals such as Procyte GHK-copperpeptide (Maquart et al., 1993).

Antioxidants are molecules thatwork in the skin to reduce ROS,which are generated by UV damageand lead to breakdown of collagen.There is much interest in the use ofantioxidants both orally and topicallyto combat aging skin, but there are

DERMATOLOGY NURSING



few published studies on the efficacyof these agents. There is reason to beoptimistic, as preliminary studiesdemonstrate that certain antioxidantsmay exert an anti-aging effect by pre-venting and even reversing sun dam-age. Idebenone is a synthetic analogof Coenzyme Q 10 with potentantioxidant activity; it reduces skinroughness, increases skin hydration,reduces fine lines, and was associatedwith an improvement in overall glob-al assessment of photoaged skin(McDaniel, Neudecker, DiNardo,Lewis, & Maibach, 2005). Topicalvitamin C 5% cream applied for 6months led to clinical improvementin the appearance of photoaged skinwith regard to firmness, smoothness,and dryness compared to vehicle(Humbert et al., 2003). Topical vita-min C stimulates the collagen-pro-ducing activity of the dermis(Nusgens, Humbert, Rougier,Richard, & Lapière, 2002).

Botulinum toxin and soft tissuefillers. Purified botulinum toxin typeA (Botox®, Allergan Inc., Irvine, CA)is a neurotoxin used to paralyze vari-ous muscle groups of the face for cos-metic improvement of wrinkles.Injection of Botox® is easily one of themost popular procedures for aestheticenhancement. Botox® is most com-monly used to treat wrinkles of theglabella, forehead, and periocularregions. Paralysis of these small mus-cle groups of the face results in a moreyouthful appearance. With time andrepeated injections, many patientswill note softening or disappearanceof particular facial lines. Botox®

works by neuromuscular inhibition ofacetylcholine and the effects last from3 to 6 months. Side effects of Botox®

injections include pain, bruising, andparalysis of the nerves that controleyelid function.

Of the 9.7 million nonsurgicalprocedures performed in the UnitedStates in 2004, nearly 10% were softtissue augmentation procedures, asreported by the American Society forAesthetic Plastic Surgery (Matarasso,

Carruthers, Jewell, & The RestylaneConsensus Group, 2006). Firstapproved in 1981, bovine collagenwas the gold standard for soft tissueaugmentation, but in recent years,non-animal stabilized hyaluronic acidgel marketed as Restylane® (MedicisPharmaceuticals, Scottsdale, AZ ) hasgained tremendous popularity amongpatients and physicians, and is cur-rently the most widely used filler inthe United States and Canada(Coleman & Carruthers, 2006). Otheravailable fillers include calciumhydoxylapatite (Radiesse®, BioFormMedical, Inc., San Mateo, CA), poly-L-lactic acid (Sculptra™, DermikLaboratories, Bridgewater, NJ), andhuman-based collagen (Cosmoderm®

and Cosmoplast®, both made byAllergan Inc., Irvine, CA). Soft tissuefillers are most commonly used toimprove the appearance of thenasolabial folds, which become morepronounced as a result of photoagingand chronological aging. They arealso injected into cheeks, periocularareas, and glabellar lines, and areoften used in combination withBotox® for maximal effect, since theyaddress different aspects of aging skin(Coleman & Carruthers, 2006). Softtissue fillers have been thought toexert their effect by volume expan-sion, but recent work investigating themechanism of action of Restylane®

suggests the filler stretches fibroblasts,leading to new collagen formation(Wang et al., 2007).

Laser procedures. Laser proceduresfor the aging face are numerous andemerging rapidly. A complete discus-sion of these is outside the realm ofthis article.

Ablative laser resurfacing is con-sidered to be the gold standard toimprove clinical features of the agingface and generally refers to treatmentwith a carbon dioxide laser (10,600nm). It improves fine and somecoarse wrinkles and overall dyspig-mentation, lightens dark under-eyecircles, and generally improves thetexture of skin; it can also be used to

ameliorate old acne scarring. Thisprocedure works by vaporizing theepidermis and portions of the papil-lary dermis so that neocollagenesiscan occur (Railan & Kilmer, 2005).

The biochemical changes associ-ated with the carbon dioxide laserhave been studied; a well-organizedwound healing response occurs,resulting in quantitatively significantincreases in production of types I andIII procollagen (Orringer et al.,2004). Due to the depth of penetra-tion of this laser, anesthesia isrequired and can be achieved by IVsedation, endotracheal sedation, or acombination of oral anxiolytics, topi-cal EMLA, and regional nerveblocks. Carbon dioxide laser resurfac-ing is performed as a single treatment,and it takes 2 weeks for the skin to re-epithelialize following the procedure.Antiviral prophylaxis is started 1 dayprior to the procedure and continuedfor 14 days, and anti-staphylococcalantibiotics are started 1 day prior andcontinued for 7 days. During thistime, wound care is frequent and timeconsuming, and patients must bemonitored closely for viral and bacte-rial skin infections. Patients withFitzpatrick skin types I and II are theideal candidates, as the procedure isassociated with skin lightening.Additionally, patients may retain apink or erythematous tone to theirskin that may last for weeks to monthsfollowing the procedure.

At our institution, an occlusiveprotective dressing is left in place for48 hours. Once the dressing isremoved, the skin is cleansed with adiluted vinegar solution and a copi-ous layer of Aquaphor® HealingOintment or Vaseline® is used tocover the resurfaced skin. Patientsneed to perform dilute vinegar soaksfor 7 to 14 days every 2 to 3 hoursduring the day and through the nightfollowed by Aquaphor or Vaselineapplication until the skin is complete-ly re-epithelialized.

Non-ablative laser resurfacingprocedures are much less invasive

DERMATOLOGY NURSING



than ablative lasers. There is muchinterest in these techniques because ofthe intense wound care, high cost,and recovery time immediately asso-ciated with ablative laser resurfacing.Select non-ablative lasers include thelong-pulsed neodymium YAG (1064nm), 1320 nm (CoolTouch®, Rose-ville, CA), radiofrequency (Therm-age®, Thermage, Inc, Hayward, CA),and Fraxel® (Reliant Technologies,Mountainview, CA). Each of thesetreatments is performed on multipleoccasions, usually several weeksapart. It is important to bear in mindthat none of the non-ablative laserscan replace the ablative procedures.

Intense pulsed light is anotherlight-based treatment but is not a truelaser as it is composed of several dif-ferent wavelengths. It is popular forfacial rejuvenation and is used tolighten lentigines and reduce telang-iectases to achieve an overall blend-ing effect. When used with a photo-sensitizer (photodynamic therapy),intense pulsed light and other light-based therapies may have a greatereffect than the light source alone(Dover, Bhatia, Stewart, & Arndt,2005). Q-switched lasers are lasersthat target pigment in skin and areuseful for removing benign pigment-ed lesions seen in photoaged andaged skin. Careful clinical assessmentis required prior to proceeding withtreatment to avoid laser treatment ofpotentially malignant skin lesionssuch as lentigo maligna or melanoma.Pulsed-dye lasers and KTP lasers areused in photoaging to target the dilat-ed blood vessels which produce aruddy and uneven appearance.Treatment with either of these vascu-lar lasers usually requires severaltreatments. Side effects includeincreased erythema immediately fol-lowing the treatment, slight discom-fort, swelling, and potential bruising.

Pre-treatment clinical assessmentand consultation are critical beforeprescribing or performing the previ-ously described treatments and pro-cedures to review the risks and com-

plications. Patient expectations mustbe gauged so that optimal improve-ment is achieved. It is of utmostimportance that patients followwound care instructions after ablativeresurfacing in order to achieve opti-mal healing. It is also crucial thatpatients understand that texturalirregularities and dyspigmentation ofskin can be improved, and that therewill be a tightening effect, but that theresults will not simulate a surgicalfacelift.

SummaryIt is important to distinguish

between natural skin aging and pho-toaging. Knowledge about the mech-anisms underlying these processescan be utilized for developing futuretherapies. Educating patients is essen-tial, as sunscreens and sun protectioncan prevent many of the changesassociated with photoaging. Manytreatments are available to treat pho-toaged skin; however, the best treat-ment is prevention.

ReferencesBernstein, E.F., Chen, Y.Q., Kopp, J.B.,

Fisher, L., Brown, D.B., Hahn, P.J., etal. (1996). Long-term sun exposurealters the collagen of the papillary der-mis. Comparison of sun-protected andphotoaged skin by northern analysis,immunohistochemical staining, andconfocal laser scanning microscopy.Journal of the American Academy ofDermatology, 34(2 Pt 1), 209-218.

Choi, C.M., & Berson, D.S. (2006). Cos-meceuticals. Seminars in CutaneousMedicine and Surgery, 25(3),163-168.

Chung, J.H., Kang, S., Varani, J., Lin, J.,Fisher, G.J., & Voorhees, J.J. (2000).Decreased extracellular-signal-regulat-ed kinase and increased stress-activatedMAP kinase activities in aged humanskin in vivo. Journal of InvestigativeDermatology, 115(2), 177-182.

Coleman, K.R., & Carruthers, J. (2006).Combination therapy with Botox® andfillers: The new rejuvenation paradigm.Dermatologic Therapy, 19, 177-188.

Cordero, A. Jr. (1983). La vitamina a acida enla piel senile. Actualizaciones TerDermatologica, 6, 49-54.

Dover, J.S., Bhatia, A.C., Stewart, B., &Arndt, K.A. (2005). Topical 5-amino-levulinic acid combined with intensepulsed light in the treatment of pho-

toaging. Archives of Dermatology, 141(10),1247-1252.

Fisher, G.J., Datta, S.C., Talwar, H.S., Wang,Z.Q., Varani, J., Kang, S., et al. (1996).Molecular basis of sun-induced prema-ture skin ageing and retinoid antago-nism. Nature, 379(6563), 335-339.

Fisher, G.J., Kang, S., Varani, J., Bata-Csorgo, Z., Wan, Y., Datta, S., et al.(2002). Mechanisms of photoaging andchronological skin aging. Archives ofDermatology, 138(11), 1462-1470.

Fisher, G.J., Wang, Z.Q., Datta, S.C., Varani,J., Kang, S., & Voorhees, J.J. (1997).Pathophysiology of premature skinaging induced by ultraviolet light. NewEngland Journal of Medicine, 337(20),1419-1428.

Gilchrest, B.A. (1990). Skin aging and pho-toaging. Dermatology Nursing, 2(2), 79-82.

Gilchrest, B.A. (1996). A review of skin age-ing and its medical therapy. BritishJournal of Dermatology, 135(6), 867-875.

Griffiths, C.E., Russman, A.N., Majmudar,G., Singer, R.S., Hamilton, T.A., &Voorhees, J.J. (1993). Restoration of col-lagen formation in photodamagedhuman skin by tretinoin (retinoic acid).New England Journal of Medicine, 329(8),530-535.

Hensley, K., & Floyd, R.A. (2002). Reactiveoxygen species and protein oxidationin aging: A look back, a look ahead.Archives of Biochemistry and Biophysics,397(2), 377-383.

Humbert, P.G., Haftek, M., Creidi, Lapière,C., Nusgens, B., Richard, A., et al.(2003). Topical ascorbic acid on pho-toaged skin. Clinical, topographical andultrastructural evaluation: Double blindstudy vs. placebo. ExperimentalDermatology, 12, 237-244.

Kang, S., Chung, J.H., Lee, J.H., Fisher, G.J.,Wan, Y.S., Duell, E.A., et al. (2003).Topical N-acetyl cysteine and genisteinprevent ultraviolet-light-induced signal-ing that leads to photoaging in humanskin in vivo. Journal of InvestigativeDermatology, 120(5), 835-841.

Kang, S., Fisher, G.J., & Voorhees, J.J. (1997).Photoaging and topical tretinoin:Therapy, pathogenesis, and prevention.Archives of Dermatology, 133(10), 1280-1284.

Kang, S., Fisher, G.J., & Voorhees, J.J. (2001).Photoaging: Pathogenesis, prevention,and treatment. Clinics in GeriatricMedicine, 17(4), 643-659.

Katayama, K., Armendariz-Borunda, J.,Raghow, R., Kang, A.H., & Seyer, J.M.(1993). A pentapeptide from type I pro-collagen promotes extracellular matrixproduction. The Journal of BiologicalChemistry, 268(14), 9941-9944.

Kligman, A.M., Grove, G.L., Hirose, R., &Leyden, J.J. (1986). Topical tretinoin for

DERMATOLOGY NURSING



photoaged skin. Journal of the AmericanAcademy of Dermatology, 15, 836-859.

Kligman, L.H., & Kligman, A.M. (1986). Thenature of photoaging: Its preventionand repair. Photodermatology, 3, 215-227.

Kurban, R.S., & Bhawan, J. (1990).Histologic changes in skin associatedwith aging. Journal of DermatologicSurgery & Oncology, 16(10), 908-914.

Lavker, R.M. (1995). Cutaneous aging:Chronologic versus photoaging. In B.Gilchrest (Ed.), Photodamage (Vol. 1, pp.123-135). Cambridge: Blackwell.

Maquart, F.X., Bellon, G., Chaqour, B.,Wegrowski, J., Patt, L.M., Tracy, R.E., etal. (1993). In vivo stimulation of con-nective tissue accumulation by thetripeptide-copper complex glycyl-L-his-tidyl-L-lysine Cu2+ in rat experimentalwounds. Journal of Clinical Investigation,92, 2368-2376.

Massagué, J. (1998). TGF-beta signal trans-duction. Annual Review of Biochemistry,67, 753-791.

Matarasso, S.L., Carruthers, J.D., Jewell,M.L., & The Restylane ConsensusGroup. (2006). Consensus recommen-dations for soft tissue augmentationwith nonanimal stabilized hyaluronicacid (Restylane). Plastic and Reconstruc-tive Surgery, 117(Suppl.), 3S-34S.

McDaniel, D.H., Neudecker, B.A., DiNardo,J.C., Lewis, J.A., & Maibach, H.I.(2005). Clinical efficacy assessment inphotodamaged skin of 0.5% and 1.0%idebenone. Journal of Cosmetic Derma-tology, 4, 167-173.

Nusgens, B.V., Humbert, P., Rougier, A.,Richard, A., & Lapière, C.M. (2002).Stimulation of collagen biosynthesis bytopically applied vitamin C. European

Journal of Dermatology, 4(12), XXXII-IV.Orringer, J.S., Kang, S., Johnson, T.M.,

Karimipour, D.J., Hamilton, T.,Hammerberg, C., et al. (2004). Con-nective tissue remodeling induced bycarbon dioxide laser resurfacing of pho-todamaged human skin. Archives ofDermatology, 140(11), 1326-1332.

Quan, T., He, T., Kang, S., Voorhees, J.J., &Fisher, G.J. (2002). Ultraviolet irradia-tion alters transforming growth factorbeta/smad pathway in human skin invivo. Journal of Investigative Dermatology,119(2), 499-506.

Railan, D., & Kilmer, S. (2005). Ablativetreatment of photoaging. DermatologicTherapy, 18, 227-241.

Talwar, H.S., Griffiths, C.E., Fisher, G.J.,Hamilton, T.A., & Voorhees, J.J. (1995).Reduced type I and type III procolla-gens in photodamaged adult humanskin. Journal of Investigative Dermatology,105(2), 285-290.

Urbach, F., Forbes, P.D., Davies, R.E., &Berger, D. (1976). Cutaneous photobiol-ogy: Past, present and future. Journal ofInvestigative Dermatology, 67(1), 209-224.

Varani, J., Warner, R.L., Gharaee-Kermani,Phan, S.H., Kang, S., Chung, J.H., et al.(2000). Vitamin A antagonizesdecreased cell growth and elevated col-lagen-degrading matrix metallopro-teinases and stimulates collagen accu-mulation in naturally aged human skin.Journal of Investigative Dermatology,114(3), 480-486.

Wang, F., Garza, L., Kang, S., Varani, J.,Orringer, J.S., Fisher, G.J., et al. (2007).In vivo stimulation of de novo collagenproduction caused by cross-linkedhyaluronic acid dermal filler injectionsin photodamaged human skin. Archivesof Dermatology, 143(2), 155-163.

Weiss, J.S., Ellis, C.N., Headington, J.T.,Tincoff, T., Hamilton, T.A., &Voorhees, J.J. (1988). Topical tretinoinimproves photoaged skin. A double-blind vehicle controlled study. JAMA,259(4), 527-532.

Yaar, M., Eller, M.S., & Gilchrest, B.A.(2002). Fifty years of skin aging. Journalof Investigative Dermatology: SymposiumProceedings, 7(1), 51-58.

DERMATOLOGY NURSING

Need additional CNE credits?Visit the Dermatology Nursing

Web site for online CNE articles.

www.dermatologynursing.net

Look for free CNE courtesy of Abbott Laboratories.

Ask Your Patients to Participate in “Patients' Perspectives: Living With...”Dermatology nurses and other health care professionals may

sometimes fail to appreciate and recognize the physical and emotionalchallenges faced by patients with a particular chronic dermatologic dis-ease or condition. To better bring patients’ feelings and perceptions intofocus, the Dermatology Nursing Editorial Board is introducing a newseries, “Patients’ Perspectives: Living With...,” and we need your help.

If you know of a patient who would be interested in sharing his/herexperiences with the dermatology health care community, please askhim/her to briefly answer (3-5 sentences) for each of the following 10questions.1. When were you diagnosed with your disease/condition?2. When and how did you find out you had the disease/condition?3. How would you describe your appearance?4. What kind of education and support were you given at the time of

your diagnosis?5. How has your disease/condition affected your life, physically and

emotionally?6. What would you like health care providers to know about treating

people with your disease/condition?

7. What worked for you and what didn’t (treatments, emotional sup-port, etc.)?

8. What do you wish society knew about your disease/condition?9. What would you tell other people who are newly diagnosed with

this disease/condition?10. How do you think living with this disease/condition will affect your

life in the future?To put a “face” on these insights, we also ask that patients include

a color photo (headshot) of themselves. (Photos are optional; nameswill also be withheld upon request.) Our goal is that these importantpatient views and comments will improve patient care. Please considerasking interested patients to share their perspectives with dermatologynurses.

Submissions can be sent via e-mail to the journal office [email protected] or mailed to Patients’ Perspectives, DermatologyNursing, East Holly Avenue Box 56, Pitman, NJ 08071-0056.

Thank you for helping us in our efforts to improve dermatologicpatient care.


dermatology nursing overview of skin aging and photoaging of skin aging and... · dermatology...

Documents