| Abstract|| |
Vitamin A-containing products have been used topically since the early 1940s to treat various skin conditions. To date, there are four generations of retinoids, a family of Vitamin A-containing compounds. Tretinoin, all-trans-retinoic acid, is a first-generation, naturally occurring, retinoid. It is available, commercially, as a gel or cream. The authors conducted a complete review of all studies, clinical- and basic science-based studies, within the literature involving tretinoin treatment recommendations for impending facial procedures. The literature currently lacks definitive recommendations for the use of tretinoin-containing products prior to undergoing facial procedures. Tretinoin pretreatment regimens vary greatly in terms of the strength of retinoid used, the length of the pre-procedure treatment, and the ideal time to stop treatment before the procedure. Based on the current literature and personal experience, the authors set forth a set of guidelines for the use of tretinoin prior to various facial procedures.
Keywords: Facial resurfacing, retinoic acid, retinoids, tretinoin
|How to cite this article:|
Buchanan PJ, Gilman RH. Retinoids: literature review and suggested algorithm for use prior to facial resurfacing procedures. J Cutan Aesthet Surg 2016;9:139-44
|How to cite this URL:|
Buchanan PJ, Gilman RH. Retinoids: literature review and suggested algorithm for use prior to facial resurfacing procedures. J Cutan Aesthet Surg [serial online] 2016 [cited 2021 Oct 22];9:139-44. Available from: https://www.jcasonline.com/text.asp?2016/9/3/139/191653
| Introduction|| |
The quest for more youthful, younger-looking skin is of paramount concern amongst the ageing population. Reversing the visible signs of skin ageing, such as wrinkles, pigmentation and lack of elasticity, is of importance to a woman's quality of life. These reasons represent a common reason for seeking a dermatologic referral.,
Retinoids are a family of compounds derived from Vitamin A. First-generation agents include both retinol and tretinoin. These compounds have been used topically and systemically since the 1940s for various skin conditions, particularly acne. Over a quarter century ago, female acne patients reported that their skin subjectively felt smoother and had less wrinkles after treatment with retinoid-containing products. In the 1980s, Kligman et al. first published a report showing that tretinoin rejuvenated the epidermis.,,, Subsequently, a clinical trial proved that patients treated with tretinoin had improvement in sunlight-induced epidermal atrophy and dyspigmentation. Tretinoin has since become the gold standard for the treatment of photoaged skin.,
In addition to prolonged sun exposure, numerous other intrinsic factors, such as diabetes and hypothyroidism, have been shown to cause epidermal atrophy, reduced fibroblast proliferation and decrease matrix synthesis. Lateef et al. demonstrated that these effects can be reversed with retinoid treatment, specifically noting an increase in epidermal thickness and collagen production. Ultimately, the Food and Drug Administration (FDA) has approved the use of tretinoin for photo-damaged skin. Retinol, a metabolic precursor of tretinoin, is also widely included in multiple over-the-counter “anti-wrinkle” cosmetic products.
Despite the FDA approval, the use of tretinoin and retinol-containing products are associated with certain adverse effects. These side effects include pruritus, burning sensation, erythema and desquamation. Collectively, this side effect profile is termed the “retinoid reaction” and is more common with the use of tretinoin than with retinol.,, The retinoid reaction is dose dependent and subsides over time.,
For patients who are sensitive to tretinoin-containing products or with a severe retinoid reaction, the use of an adapalene, marketed under the brand name of Differin, may be used as there is a lower incidence of retinoid dermatitis. Adapalene is a third-generation retinoid with many of the same properties as tretinoin. However, unlike tretinoin, adapalene is a synthetic compound with a longer half-life. This longer half-life causes a delay in maximal effectiveness and requires an earlier initiation period for adapalene prior to resurfacing procedures.,,
In contrast to the irritancy potential of the classical, prescription tretinoin therapy, cosmetic anti-wrinkle formulations using retinol are well tolerated. Despite the literature being devoid of studies directly comparing tretinoin to retinol, it is presumed that retinol anti-wrinkle products are not as clinically efficacious as prescription strength tretinoin therapies., Therefore, the question remains: What is the optimal dosing and duration of topical tretinoin application prior to facial resurfacing procedures?
| Mechanism of Action|| |
Retinoids' primary action is on the upper papillary dermis where collagen content is increased by collagen degradation inhibition. Topical tretinoin increases Type I collagen production by 80% in photoaged skin and increases wrinkle effacement through epidermal hyperplasia with compaction of the stratum corneum and thickening of the granular layer., Tretinoin binds to specific nuclear receptors thereby inducing a conformational change and exposing a DNA-binding site. The activated nuclear receptor controls cellular function by binding to specific DNA sites that can either stimulate or repress gene expression. When bound, tretinoin produces a 70% repression of AP-1 transcription factor binding to DNA. This repression decreases the overall activation of metalloproteinases.,,, Likewise, matrix metalloproteinase production and collagen degradation are prevented with topical treatment of tretinoin prior to ultraviolent irradiation.
| Retinoid Therapy|| |
Multiple studies within the literature have sought to determine the optimal concentration of tretinoin to balance its beneficial and deleterious effects. The standard treatment dose of tretinoin cream is 0.05%, applied nightly. This administration protocol shows an improvement in fine wrinkle effacement in approximately 3 months., Changes in the dermal layer were seen after 12 months of continued treatment, at which point new collagen fibre formation and elastic material reduction were seen, histologically.
To date, there have been two randomised, controlled, double-blinded studies performed with both studies showing a more significant improvement in epidermal wrinkle effacement using a 0.05% over a 0.01% concentration of tretinoin., In other studies, 0.1% was compared with a 0.025% concentration of tretinoin and followed over an 8-month period. In looking at epidermal changes, no statistically significant difference was seen between the two concentrations., Other studies have investigated lower tretinoin concentrations for longer durations. Olsen et al. studied the daily application of 0.05% and 0.01% versus a placebo for 11 months. Statistically significant improvements of both concentrations over the placebo were seen. Nyirady et al. studied the daily application of 0.02% and 0.05% tretinoin cream for 24 months and found no statistically significant difference in clinical outcomes. In a porcine model, Hung et al. treated eight animals with 0.05% tretinoin cream daily for 10 days prior to partial-thickness skin wounding. This study concluded that continued treatment with topical tretinoin before wounding caused an acceleration of epithelial wound healing but continued treatment after wounding retarded reepithelialisation.
Other studies have looked at higher concentrations of tretinoin cream for shorter durations. Kligman et al. noted that the use of 0.25% tretinoin cream, used every other night for 14 days, yielded similar clinical and histological improvement after 4–6 weeks that a 0.05% concentration did after 12 months. This use of higher concentrations over a shorter course of therapy was later termed 'rapid retinisation'. Multiple other studies noted that discontinuation and/or truncation of tretinoin therapy resulted in the reversal of the epidermal effects.,,
Retinol-containing products have been in use, cosmetically, since 1984. The use of retinol was widely accepted after Kang et al. published a study showing that retinol induces epidermal thickening in a similar manner as retinoic acid, but with minimal side effects, unlike tretinoin. Retinol causes less transepidermal water loss, irritancy, erythema and scaling compared to tretinoin. Likewise, clinical studies proved retinol's relative capacity in monotherapy to produce fine wrinkle effacement.,,
| Clinical Studies|| |
The depth of dermal injury is what classifies chemical peels into a superficial peel, medium peel or deep peel. Superficial peels, such as alpha-hydroxy acids, beta-hydroxy acids and Jessner solution, injure the epidermal layer without deeper penetration. Medium peels, trichloroacetic acid (TCA) 20–35%, penetrate into the papillary dermis. Deep peels, including phenols with or without croton oil and TCA 45–50%, affect the reticular dermis.,
Hevia et al. studied the effects of pretreatment with 0.1% tretinoin cream, used 14-day prior to a 35% TCA peel of the face. The reduced stratum corneum caused by the tretinoin cream application resulted in earlier, more intense, frosting, and a statistically significant increase in reepithelised skin area after 7 days.
Kim et al. used guinea pig skin to show morphological and histological changes with tretinoin pretreatment prior to a TCA chemical peel. The peak epidermal hypertrophy occurred after 7 days of tretinoin application. This hypertrophy climax was shown to reverse towards normal epidermis after 14 days of continued treatment.
Dermabrasion and microdermabrasion
Microdermabrasion utilises inert aluminium oxide or sodium chloride crystals to debride the superficial epidermal layer. Unlike other resurfacing procedures, dermabrasion can be performed on all skin types to address photodamage, superficial rhytides, hyperpigmentation and/or scarring.,, Surgical dermabrasion usually involves the use of a power-driven rotating diamond rasp where the skin is pared mechanically. Depth is determined by the operator and can vary from superficial epidermal to deep reticular dermal. The technique is not often used because of the risk to operative personnel by skin and blood aerosolised by the procedure.
In one study, patients were pretreated using 0.5% tretinoin cream for 14 days prior to undergoing either a full or half-face dermabrasion. These pretreated faces were completely reepithelialised 2 days earlier than the control group. These findings were further solidified in an animal model, wherein animals pretreated with tretinoin attained reepithelialisation earlier than their control counterparts, both clinically and histologically.,
Laser resurfacing comes in three forms: Ablative, non-ablative and a combination of ablative and non-ablative. Within these categories, the energy can be delivered either as full-field or fractionated. Ablative lasers penetrate into the dermis and treat fine and deep rhytids, telangiectasias, actinic keratosis and scarring. Such ablative lasers include the carbon dioxide and erbium: yttrium-aluminium-garnet lasers.,,,,,,,, Non-ablative lasers include the long pulse dye, pulsed pulse dye, pulsed potassium titanyl phosphate, erbium: yttrium-aluminium-garnet, diode and erbium laser. These lasers heat the tissue without ablating, thereby having a more favourable side effect profile compared to the ablative lasers.,, Fractional lasers whether ablative or non-ablative deliver thermal injury in columnar zones leaving untouched tissue in between. This avoidance of confluent injury allows for faster recovery with a reduced side effect profile when compared to the full-field lasers.,
Animal studies were conducted looking at the effects of pretreating guinea pigs with tretinoin prior to undergoing carbon dioxide laser resurfacing. This tretinoin pretreatment resulted in faster reepithelialisation and healing. Despite these results, Orringer et al. showed no benefit in terms of reepithelialisation when pretreating photo-damaged forearm skin with 0.05% tretinoin cream. This is likely due to the fact that after 21 days of tretinoin treatment, only the epidermis is affected, which is ablated by carbon dioxide resurfacing.
| Discussion|| |
The question remains, “Do all facial resurfacing procedures necessitate skin pretreatment with tretinoin?” Each resurfacing modality causes various levels of dermal injury. Harnessing the technical ability to control the level of injury while performing these resurfacing procedures is paramount for efficacy and safety. Stegman proved histologically that the rate of reepithelialisation is proportional to the depth of injury caused by the resurfacing procedure. Therefore, the use of tretinoin would provide the most benefit when used prior to therapies that cause deep wounds when compared to those procedures that cause only superficial epidermal injury.
In regards to retinoid dermatitis, the best prevention method when using higher strength retinoids is to start treatment at a lower concentration and gradually increase the concentration. The concomitant use of skin moisturisers also helps hydrate and protect the skin from a dermatitis reaction. Furthermore, synthetic retinoids such as adapalene and tazarotene may be used in patients with sensitivity to tretinoin. Likewise, retinoids can be safely used in darker skin types, Fitzpatrick Type IV+, in the same manner as with lighter skin types. Gel or solution formulations may be of benefit for very oily skin types while creams are better for drier skin types.,,,,,,,
Pretreatment with tretinoin products has been deemed essential to expedite reepithelialisation and epidermal healing; however, much of this seems to be based on anecdotal evidence. Pretreatment regimens have varied greatly in terms of the strength of tretinoin used, length of the pre-procedure treatment and ideal time to stop treatment before the procedure., We, therefore, have derived tretinoin pretreatment guidelines prior to specific facial resurfacing procedures.
Based on the available literature exploring the mechanism of action of tretinoin, as described above, as well as published observational studies and personal experience, we propose the following algorithm for the pre-operative use of tretinoin in facial resurfacing [Figure 1]. For ablative lasers, the authors recommend using 0.1% tretinoin cream applied nightly for 3 months prior to, and discontinuing 24 h before, the planned procedure. For non-ablative laser resurfacing, this dose should be decreased to 0.05%. Tretinoin pretreatment is not recommended for microdermabrasion since this procedure only affects the superficial epidermis. A 0.1% tretinoin concentration pretreatment is recommended for a surgical dermabrasion, with initiation starting 3 months prior to the planned procedure date.
|Figure 1: Tretinoin pretreatment recommendations prior to laser, dermabrasion and chemical peel facial resurfacing|
Click here to view
In regard to chemical peel resurfacing, tretinoin concentration recommendations are divided into three categories, depending on the level of depth of the peel. For a superficial chemical peel, it is recommended to use a 0.05% concentration, starting 1 month prior to the procedure, daily and halting 24 h before the treatment. For a medium chemical peel, use a 0.1% concentration daily starting 1 month prior to the procedure and discontinuing 24 h prior to the chemical peel. A deep chemical peel requires the use of 0.1% tretinoin concentration, daily, starting 3 months prior to the procedure and stopping 24 h prior.
To date, no data within the literature support the notion that discontinuing the use of tretinoin prior to a resurfacing procedure is deemed necessary. However, the authors recommend not starting the use of tretinoin-containing products sooner than 3–4 weeks prior to a facial resurfacing procedure. Treatment with products containing tretinoin initiated within 3–4 weeks of a resurfacing procedure causes symptomatic dryness and exfoliation as the facial skin has not yet had time to accommodate to its effects. Likewise, the improvement in fine wrinkle effacement reverses once tretinoin application ceases, and therefore, there are no data available that show usage of these products leading into a resurfacing procedure interferes with healing.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Bouloc A, Vergnanini AL, Issa MC. A double-blind randomized study comparing the association of Retinol and LR2412 with tretinoin 0.025% in photoaged skin. J Cosmet Dermatol 2015;14:40-6.
Ooe M, Seki T, Miura T, Takada A. Comparative evaluation of wrinkle treatments. Aesthetic Plast Surg 2013;37:424-33.
Hubbard BA, Unger JG, Rohrich RJ. Reversal of skin aging with topical retinoids. Plast Reconstr Surg 2014;133:481e-90e.
Kligman AM, Grove GL, Hirose R, Leyden JJ. Topical tretinoin for photoaged skin. J Am Acad Dermatol 1986;15(4 Pt 2):836-59.
Kligman LH. Effects of all-trans-retinoic acid on the dermis of hairless mice. J Am Acad Dermatol 1986;15(4 Pt 2):779-85, 884-7.
Kligman LH, Duo CH, Kligman AM. Topical retinoic acid enhances the repair of ultraviolet damaged dermal connective tissue. Connect Tissue Res 1984;12:139-50.
Kang S, Fisher GJ, Voorhees JJ. Photoaging and topical tretinoin: Therapy, pathogenesis, and prevention. Arch Dermatol 1997;133:1280-4.
Weiss JS, Ellis CN, Headington JT, Tincoff T, Hamilton TA, Voorhees JJ. Topical tretinoin improves photoaged skin. A double-blind vehicle-controlled study. JAMA 1988;259:527-32.
Buchanan PJ, Kung TA, Cederna PS. Evidence-based medicine: Wound closure. Plast Reconstr Surg 2014;134:1391-404.
Lateef H, Abatan OI, Aslam MN, Stevens MJ, Varani J. Topical pretreatment of diabetic rats with all-trans retinoic acid improves healing of subsequently induced abrasion wounds. Diabetes 2005;54:855-61.
Mukherjee S, Date A, Patravale V, Korting HC, Roeder A, Weindl G. Retinoids in the treatment of skin aging: An overview of clinical efficacy and safety. Clin Interv Aging 2006;1:327-48.
Basak PY, Eroglu E, Altuntas I, Agalar F, Basak K, Sutcu R. Comparison of the effects of tretinoin, adapalene and collagenase in an experimental model of wound healing. Eur J Dermatol 2002;12:145-8.
Leyden J. Adapalene in clinical practice. Cutis 2001;68 4 Suppl: 7-9.
Nyirady J, Grossman RM, Nighland M, Berger RS, Jorizzo JL, Kim YH, et al.
A comparative trial of two retinoids commonly used in the treatment of acne vulgaris. J Dermatolog Treat 2001;12:149-57.
Fu JJ, Hillebrand GG, Raleigh P, Li J, Marmor MJ, Bertucci V, et al.
A randomized, controlled comparative study of the wrinkle reduction benefits of a cosmetic niacinamide/peptide/retinyl propionate product regimen vs. a prescription 0.02% tretinoin product regimen. Br J Dermatol 2010;162:647-54.
Bruce S. Cosmeceuticals for the attenuation of extrinsic and intrinsic dermal aging. J Drugs Dermatol 2008;7 2 Suppl: s17-22.
Griffiths CE, Russman AN, Majmudar G, Singer RS, Hamilton TA, Voorhees JJ. Restoration of collagen formation in photodamaged human skin by tretinoin (retinoic acid). N Engl J Med 1993;329:530-5.
Herbig K, Trussler AP, Khosla RK, Rohrich RJ. Combination Jessner's solution and trichloroacetic acid chemical peel: Technique and outcomes. Plast Reconstr Surg 2009;124:955-64.
Rohrich RJ, Herbig KS. The role of modified Jessner's solution with 35% trichloroacetic acid peel. Plast Reconstr Surg 2009;124:965-6.
Stegman SJ. A study of dermabrasion and chemical peels in an animal model. J Dermatol Surg Oncol 1980;6:490-7.
Vagotis FL, Brundage SR. Histologic study of dermabrasion and chemical peel in an animal model after pretreatment with Retin-A. Aesthetic Plast Surg 1995;19:243-6.
Jurzak M, Latocha M, Gojniczek K, Kapral M, Garncarczyk A, Pierzchala E. Influence of retinoids on skin fibroblasts metabolism in vitro
. Acta Pol Pharm 2008;65:85-91.
|23.|Bhawan J, Andersen W, Lee J, Labadie R, Solares G. Photoaging versus intrinsic aging: A morphologic assessment of facial skin. J Cutan Pathol 1995;22:154-9
Caputo R, Monti M, Motta S, Barbareschi M, Tosti A, Serri R, et al.
The treatment of visible signs of senescence: The Italian experience. Br J Dermatol 1990;122 Suppl 35:97-103.
Weinstein GD, Nigra TP, Pochi PE, Savin RC, Allan A, Benik K, et al.
Topical tretinoin for treatment of photodamaged skin. A multicenter study. Arch Dermatol 1991;127:659-65.
Griffiths CE, Kang S, Ellis CN, Kim KJ, Finkel LJ, Ortiz-Ferrer LC, et al.
Two concentrations of topical tretinoin (retinoic acid) cause similar improvement of photoaging but different degrees of irritation. A double-blind, vehicle-controlled comparison of 0.1% and 0.025% tretinoin creams. Arch Dermatol 1995;131:1037-44.
Olsen EA, Katz HI, Levine N, Nigra TP, Pochi PE, Savin RC, et al.
Tretinoin emollient cream for photodamaged skin: Results of 48-week, multicenter, double-blind studies. J Am Acad Dermatol 1997;37(2 Pt 1):217-26.
Nyirady J, Bergfeld W, Ellis C, Levine N, Savin R, Shavin J, et al.
Tretinoin cream 0.02% for the treatment of photodamaged facial skin: A review of 2 double-blind clinical studies. Cutis 2001;68:135-42.
Hung VC, Lee JY, Zitelli JA, Hebda PA. Topical tretinoin and epithelial wound healing. Arch Dermatol 1989;125:65-9.
Kligman DE, Sadiq I, Pagnoni A, Stoudemayer T, Kligman AM. High-strength tretinoin: A method for rapid retinization of facial skin. J Am Acad Dermatol 1998;39(2 Pt 3):S93-7.
Kligman DE, Draelos ZD. High-strength tretinoin for rapid retinization of photoaged facial skin. Dermatol Surg 2004;30:864-6.
Bhawan J, Olsen E, Lufrano L, Thorne EG, Schwab B, Gilchrest BA. Histologic evaluation of the long term effects of tretinoin on photodamaged skin. J Dermatol Sci 1996;11:177-82.
Ellis CN, Weiss JS, Hamilton TA, Headington JT, Zelickson AS, Voorhees JJ. Sustained improvement with prolonged topical tretinoin (retinoic acid) for photoaged skin. J Am Acad Dermatol 1990;23(4 Pt 1):629-37.
Olsen EA, Katz HI, Levine N, Nigra TP, Pochi PE, Savin RC, et al.
Sustained improvement in photodamaged skin with reduced tretinoin emollient cream treatment regimen: Effect of once-weekly and three-times-weekly applications. J Am Acad Dermatol 1997;37(2 Pt 1):227-30.
Kang S, Duell EA, Fisher GJ, Datta SC, Wang ZQ, Reddy AP, et al.
Application of retinol to human skin in vivo
induces epidermal hyperplasia and cellular retinoid binding proteins characteristic of retinoic acid but without measurable retinoic acid levels or irritation. J Invest Dermatol 1995;105:549-56.
Fluhr JW, Vienne MP, Lauze C, Dupuy P, Gehring W, Gloor M. Tolerance profile of retinol, retinaldehyde and retinoic acid under maximized and long-term clinical conditions. Dermatology 1999;199 Suppl 1:57-60.
Gold MH, Kircik LH, Bucay VW, Kiripolsky MG, Biron JA. Treatment of facial photodamage using a novel retinol formulation. J Drugs Dermatol 2013;12:533-40.
Varani J, Warner RL, Gharaee-Kermani M, Phan SH, Kang S, Chung JH, et al.
Vitamin A antagonizes decreased cell growth and elevated collagen-degrading matrix metalloproteinases and stimulates collagen accumulation in naturally aged human skin. J Invest Dermatol 2000;114:480-6.
Nguyen AT, Ahmad J, Fagien S, Rohrich RJ. Cosmetic medicine: Facial resurfacing and injectables. Plast Reconstr Surg 2012;129:142e-53e.
Hevia O, Nemeth AJ, Taylor JR. Tretinoin accelerates healing after trichloroacetic acid chemical peel. Arch Dermatol 1991;127:678-82.
Kim IH, Kim HK, Kye YC. Effects of tretinoin pretreatment on TCA chemical peel in guinea pig skin. J Korean Med Sci 1996;11:335-41.
Bernard RW, Beran SJ, Rusin L. Microdermabrasion in clinical practice. Clin Plast Surg 2000;27:571-7.
Karimipour DJ, Karimipour G, Orringer JS. Microdermabrasion: An evidence-based review. Plast Reconstr Surg 2010;125:372-7.
Mandy SH. Tretinoin in the preoperative and postoperative management of dermabrasion. J Am Acad Dermatol 1986;15(4 Pt 2):878-9, 888-9.
Stuzin JM. Discussion. A randomized controlled trial of skin care protocols for facial resurfacing: Lessons learned from the Plastic Surgery Educational Foundation's Skin Products Assessment Research study. Plast Reconstr Surg 2011;127:1343-5.
Roy D. Ablative facial resurfacing. Dermatol Clin 2005;23:549-59, viii.
Stuzin JM, Baker TJ, Baker TM. CO2 and erbium: YAG laser resurfacing: current status and personal perspective. Plast Reconstr Surg 1999;103:588-91.
Stuzin JM, Baker TJ, Baker TM, Kligman AM. Histologic effects of the high-energy pulsed CO2 laser on photoaged facial skin. Plast Reconstr Surg 1997;99:2036-50.
Alster TS, Nanni CA, Williams CM. Comparison of four carbon dioxide resurfacing lasers. A clinical and histopathologic evaluation. Dermatol Surg 1999;25:153-8.
Aslam A, Alster TS. Evolution of laser skin resurfacing: From scanning to fractional technology. Dermatol Surg 2014;40:1163-72.
Nanni CA, Alster TS. Complications of cutaneous laser surgery. A review. Dermatol Surg 1998;24:209-19.
Nanni CA, Alster TS. Complications of carbon dioxide laser resurfacing. An evaluation of 500 patients. Dermatol Surg 1998;24:315-20.
West TB, Alster TS. Effect of botulinum toxin type A on movement-associated rhytides following CO2 laser resurfacing. Dermatol Surg 1999;25:259-61.
Alexiades-Armenakas MR, Dover JS, Arndt KA. The spectrum of laser skin resurfacing: Nonablative, fractional, and ablative laser resurfacing. J Am Acad Dermatol 2008;58:719-37.
Brightman LA, Brauer JA, Anolik R, Weiss E, Karen J, Chapas A, et al.
Ablative and fractional ablative lasers. Dermatol Clin 2009;27:479-89, vi-vii.
Tierney EP, Kouba DJ, Hanke CW. Review of fractional photothermolysis: Treatment indications and efficacy. Dermatol Surg 2009;35:1445-61.
Metelitsa AI, Alster TS. Fractionated laser skin resurfacing treatment complications: A review. Dermatol Surg 2010;36:299-306.
Narurkar VA. Nonablative fractional laser resurfacing. Dermatol Clin 2009;27:473-8, vi.
McDonald WS, Beasley D, Jones C. Retinoic acid and CO2 laser resurfacing. Plast Reconstr Surg 1999;104:2229-35.
Orringer JS, Kang S, Johnson TM, Karimipour DJ, Hamilton T, Hammerberg C, et al.
Tretinoin treatment before carbon-dioxide laser resurfacing: A clinical and biochemical analysis. J Am Acad Dermatol 2004;51:940-6.
Anthony J, Miller L, Dinehart SM. Topical tretinoin decreases healing times of electroepilation-induced wounds. Dermatologica 1991;183:129-31.
Francz PI, Conrad J, Biesalski HK. Modulation of UVA-induced lipid peroxidation and suppression of UVB-induced ornithine decarboxylase response by all-trans-retinoic acid in human skin fibroblasts in vitro
. Biol Chem 1998;379:1263-9.
Griffiths CE. The role of retinoids in the prevention and repair of aged and photoaged skin. Clin Exp Dermatol 2001;26:613-8.
Leyden J, Lowe N, Kakita L, Draelos Z. Comparison of treatment of acne vulgaris with alternate-day applications of tazarotene 0.1% gel and once-daily applications of adapalene 0.1% gel: A randomized trial. Cutis 2001;67 6 Suppl: 10-6.
Nyirady J, Lucas C, Yusuf M, Mignone P, Wisniewski S. The stability of tretinoin in tretinoin gel microsphere 0.1%. Cutis 2002;70:295-8.
Robert H Gilman
Section of Plastic Surgery, 2130 Taubman Center, SPC 5340, 1500 East Medical Center Drive, Ann Arbor, MI 48109
Source of Support: None, Conflict of Interest: None