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Plastic and Reconstructive Surgery - Global Open:
doi: 10.1097/GOX.0b013e31828ed1da
Special Topics

The Science and Theory behind Facial Aging

Farkas, Jordan P. MD; Pessa, Joel E. MD; Hubbard, Bradley MD; Rohrich, Rod J. MD

Open Access
United States
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Author Information

From the Department of Plastic Surgery, University of Texas Southwestern Medical Center, Dallas, Tex.

Disclosure: The authors have no financial interest to declare in relation to the content of this article. The Article Processing Charge was paid for by the authors.

Jordan P. Farkas, Department of Plastic Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75390-9132, E-mail: jpfarkasmd@gmail.com.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/3.0. American Society of Plastic Surgeons

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Abstract

Summary: The etiology of age-related facial changes has many layers. Multiple theories have been presented over the past 50–100 years with an evolution of understanding regarding facial changes related to skin, soft tissue, muscle, and bone. This special topic will provide an overview of the current literature and evidence and theories of facial changes of the skeleton, soft tissues, and skin over time.

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INTRODUCTION

The etiology of age-related facial changes has many layers. Multiple theories have been presented over the past 50–100 years with an evolution of understanding regarding facial changes related to skin, soft tissue, muscle, and bone.110 Historically, facial dystrophic changes were attributed to gravity on the soft tissues over time and the descent of the facial bony scaffolding.1114 Gonzalez-Ulloa and Flores15 presented their theory on facial aging and “senility of the face” almost 50 years ago. They first described facial aging in relation to changes of the skin, descent of the soft tissues, attrition of the facial septa, and craniofacial resorption based on observation. Plastic surgeons have searched to uncover the true myths behind facial aging in their quest to restore attractive, youthful facial characteristics in their patients. External environmental factors such as body mass index, hormones, alcohol consumption, cigarette smoking, and unprotected sun exposure have all been associated with contributing to an accelerated appearance of facial aging.1 Pessa and Rohrich et al6,1526 have spent 3 decades in evaluating and studying the anatomical facial changes that occur in the facial skeleton and overlying soft tissues over time. Earlier dogma of facial aging has only been recently supplanted after careful adiographical and scientific evidence of the tangible changes to facial skeleton, soft tissue, and skin and the three-dimensionality of facial changes with time. This special topic will provide an overview of the current literature and evidence and theories of facial changes of the skeleton, soft tissues, and skin over time.

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FACIAL SKELETON

Original theories behind facial aging have focused on soft-tissue laxity, ptosis, and descent of the envelope over time on account of gravity. Anatomical observational studies evaluating skeletal morphological changes of the midface, mandible, and orbit over time by authors such as Hellman, Lambros et al, Pessa et al, and Shaw and Langstein et al confirm bony facial remodeling over the course of one’s life.7,20,25,27,28 Hellman7 identified that facial shape continued to change throughout life and outlined morphological differentiation of the facial skeleton. Three-dimensional stereolithography and facial computer topographic scanning provided radiological evidence of the facial remodeling in young and old, looking at specific changes to the maxilla, mandible, pyriform, glabella, and orbits.20,21,25,28 Lambros and Pessa et al uncovered the clockwise rotation of the midface in relation to the cranial base in separate younger and older individuals (Fig. 1). These studies highlighted the characteristic changes in the aging facial skeleton, concentrating on the posterior displacement of the maxilla, lateral inferior shifting of the lateral and inferior orbital rim, creating a larger orbital aperture, and shrinking of the mandible in a vertical and a horizontal plane. Pessa et al23 further expanded on Hellman’s work confirming facial skeletal “differentiation” with time, showing an increase in mandibular size and shape over time and the sexual dimorphism in lower facial shape (Fig. 2). These skeletal changes create dramatic shifting of the overlying soft tissue and retaining ligaments of the face, and when combined with fat atrophy and volume loss, these provide a tangible explanation behind the complex, multifaceted etiology of facial aging. Obviously, limitations to these studies are use of different younger and older individuals in their comparison; however, their findings should not be dismissed. These landmark studies opened new doors in understanding the complexities of facial aging and the pivotal role of facial bony resorption and remodeling. Changes to the bony scaffolding with time inarguably lead to significant facial change and act in concert with soft-tissue atrophy and laxity, creating the appearance of aging.

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A graduated level of understanding of these changes leads to the development of specific treatment modalities designed to address the bony attrition with techniques such as focused midface and chin implantation and subperiosteally placed calcium hydroxyapatite filler (ie, Radiesse).

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FACIAL SOFT TISSUE AND FAT COMPARTMENTS

The recent description of the superficial and deep fat compartments of the face by Rohrich and Pessa20 and radiological confirmation by Gierloff et al29 not only reinforced the soft-tissue compartmentalization of the face but also provided further support of the theory of facial deflation and volume changes to these compartments over time (Figs. 3 and 4). Defined anatomical boundaries of the nasolabial, medial, middle, lateral superficial cheek, deep medial cheek, suborbicularis, buccal, and periorbital fat compartments provide evidence of the compartmentalization of the facial soft issues. Further, injection studies performed by Pessa, Rohrich, and Ristow et al highlighted the powerful topographical changes that occur with limited volumetric changes in these specific areas of the face (Figs. 5 and 6).26 Attenuation of the zygomatic-cutaneous, orbitomalar, and mandibular retaining ligaments of the face gives the appearance of descent of the facial soft tissue, and as anatomical studies have confirmed, it acts as a hammock to the atrophied fat compartments and soft tissues of the face, contributing to the morphological appearance of the tear trough deformity, malar bags, and jowling.5,6,11,12,17,29–33 The deflation and loss of the normal anatomic subcutaneous facial fat compartments gives off the appearance of increased skin laxity or prominent folds around the nasolabial region, periorbital region, and jowl.1519,3242 It was once thought that along with atrophy and changes of the facial fat over time, the mimetic musculature and periosteum of the face also underwent similar changes. However, using magnetic resonance imaging, Gosain et al26 found that although facial soft tissues underwent ptosis and subcutaneous hypertrophy in the deep cheek over time, the mimetic musculature was unchanged in volume and length.

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The uncovering of fat compartmentalization of the face has revolutionized the approach to facial rejuvenation. Focused localized fat injection and/or soft-tissue filler into discrete compartments, such as the deep medial, and middle fat pads of the cheek, has a dramatic effect on facial volume and reshaping the soft tissues of the face into an anatomically more youthful position.1518 Fat injection techniques in combination with the resuspension of the facial and neck soft tissues through rhytidectomy, release of the retaining ligaments, and/or superficial musculo-aponeurotic system and platysma repositioning address specific soft-tissue changes on an individualized basis. Increasing anatomical understanding of facial soft-tissue morphological changes over time allows for tailoring of the rejuvenation techniques to specific deficiencies uncovered with detailed facial analysis.

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FACIAL SKIN

The skin is the envelope or canvas of the face, revealing the deflation and atrophic changes of the underlying bone and soft-tissue compartments as previously discussed. However, in addition, the skin also goes through intrinsic changes over time on account of external and internal factors.43,44 Some suggest that repetitive dynamic muscle contractions result in the appearance of superficial and deep rhytids over areas of habitual muscle contractions such as the orbicularis oculi and oris, risorius, frontalis, and corrugators on account of fascial partitioning and connections of the dermis and periosteum between the different facial muscle groups. Smoking and photodamage result in increased production of intracellular reactive oxidative intermediates and species and cause a multitude of facial skin changes resulting in epidermal thinning, solar elastosis, and dermal collagen disorganization, leading to characteristics consistent with aging skin (Fig. 7).1,43,45,46

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Solar elastosis is the term used to describe the histologic appearance of the photoaged dermal extracellular matrix. This condition is characterized by an accumulation of amorphous, abnormal elastin material surrounding a decreased volume and disorganized array of wavy collagen fibrils.47–50 It is hypothesized that the abnormal elastin results from overproduction of normal elastin, which is subsequently degraded by the chronic inflammatory state.47 The other major components of extracellular matrix, glycoproteins and glycosaminoglycans (GAGs), tend to diminish with age, but they are ironically increased in photoaged skin.4346,4953

Ultra violet A (UVA) and ultra violet B (UVB) radiation causes direct and indirect damage to skin through absorption of the Ultra violet (UV) energy. The two most significant UV spectrum chromophores in skin are DNA and urocanic acid. Although UVA has been shown to directly induce DNA changes, its main route of cell damage is indirect, that is, through the creation of reactive oxygen species and free radicals.4655 Several matrix metalloproteinases combine to degrade the collagen extracellular framework, leading to an increase in oxidative stresses contributing to the degradation of the surrounding collagen and increased elastin production. The epidermis undergoes characteristic histological changes with sun damage, leading to increased thickness, slower keratinocyte turnover, and decreased melanocyte counts. However, there are also regions of increased melanocyte concentration, with increased capacity for melanin production and deposition to keratinocytes, which present as solar lentigines.46,5458

It is important to remember that UVB light is almost completely absorbed by the epidermis, and thus dermal photodamage is solely caused by UVA. In unprotected skin, there is an increase in all cells and extracellular matrix contents, elastin, and GAGs, and in fibroblast and Langerhans cells.4851 UV radiation has also been shown to increase angiogenesis and likely accounts for the telangiectases seen in sun-exposed skin.

In contrast to the epidermis, the histologic picture of photoaged dermis on the cellular level is one of chronic inflammation. Fibroblast and Langerhans cells are decreased and surrounded by abundant inflammatory infiltrate. Fibroblasts are morphologically abnormal and produce less collagen due to impaired signaling (lessened response to transforming growth factor beta). Langerhans cells decrease in number and undergo functional and morphologic changes. Interestingly, other major components of extracellular matrix, glycoproteins and GAGs, tend to diminish with age, but they are increased in photoaged skin.4459 However, the increased GAGs are not found in the papillary dermis as usual; instead they are deposited in the reticular dermis within the elastotic material and are not able to regulate dermal hydration, leading to dry and leathery-appearing skin.

There is unquestionably a powerful genetic component to facial skin aging, which in turn plays a significant role in overall skin appearance over time. This is likely the most powerful intrinsic factor of the appearance of skin aging.4459

Of all topical treatment modalities and gimmicks for skin wrinkle improvement and rejuvenation, there is substantial level 1 evidence behind the success of tretinoin in the treatment of photoaged and damaged skin. Actions of tretinoin, which is the active form of retinol, include prevention of the activation of matrix metalloproteinases and oxidative stress, and stimulation of regeneration of the ever-important extracellular matrix. Retinoids also inhibit keratinocyte differentiation and stimulate epidermal hyperplasia with increased keratinocyte turnover (Fig. 8). The addition of retinoids with various resurfacing procedures has proven to be impressively beneficial in the improvement of mild-to-moderate facial rhytids.43,4752,6062

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CONCLUSIONS

To adequately restore youthful facial characteristics, adequate understanding of facial morphological changes over time in its entirety is essential. Over the past 20–30 years, sound scientific data and tangible evidence have provided a foundation for understanding the changes to the facial skin, soft tissue, and bony scaffolding that have been theorized to contribute to facial aging. However, understanding of facial changes over time is still in its infancy, and facial changes can only truly be understood when comparing the changes of the facial components in a single individual at variable time points over the course of a life as first instituted almost a century ago with the Bolton-Brush longitudinal growth study at Case Western Reserve School of Dentistry.7,23 Obviously, the evaluation of radiographical and/or anatomical changes of the same person over time is quite difficult. However, the historical theories of facial aging being attributed to the descent of soft tissues have now not only been validated by sound anatomical and radiographical observational studies but also expanded on advancing our understanding of the complexities of overall facial morphological change with time.8–10 The recent uncovering of anatomical facial fat compartment anatomy has revolutionized the concept and approach of adding volume to specific deflated soft-tissue compartments, creating a more individualized youthful restoration to the face. The outstanding improvement in understanding has compartmentalized the treatment strategy to facial rejuvenation. Restoring youthful characteristics starts from the skeletal framework and builds progressively to the canvas of the face. With proper diagnosis and facial analysis, specific age-related changes can be addressed. By improving the skeletal proportions of the midface with calcium hydroxyapatite, or implants, or restoring proper position and volume of the soft tissues with fat grafting and manipulation of the superficial musculo-aponeurotic system and lid structures, or lastly through skin rejuvenation with tretinoin, botulinum injections, or resurfacing, youthful characteristics of the face can be restored in a stepwise organized fashion that is tailored to the specific changes in the individual.

Morphological changes to the facial skeletal framework, soft tissue, retaining ligaments, fat compartments, and skin envelope all contribute to facial aging in variable degrees depending on the intrinsic and extrinsic factors highlighted in this report. To provide our patients with the best possible rejuvenation strategy, appropriate diagnosis of the physiological changes of each of the elements of facial aging is imperative.

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PATIENT CONSENT

Patients provided written consent for the use of their images.

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REFERENCES

1. Guyuron B, Rowe DJ, Weinfeld AB, et al. Factors contributing to the facial aging of identical twins. Plast Reconstr Surg. 2009;123:1321–1331

2. Lande JH. Growth behavior of the human bony facial profile as revealed by serial cephalometric roentgenology. Angle Orthod. 1952;22:78

3. Nanda SR. The rates of growth of several facial components measured from serial cephalometric roentgenograms. Am J Orthod. 1955;41:658

4. Little JW. Three-dimensional rejuvenation of the midface: volumetric resculpture by malar imbrication. Plast Reconstr Surg. 2000;105:267–285; discussion 286

5. Stuzin JM, Baker TJ, Gordon HL. The relationship of the superficial and deep facial fascias: relevance to rhytidectomy and aging. Plast Reconstr Surg. 1992;89:441

6. Reece EM, Pessa JE, Rohrich RJ. The mandibular septum: anatomical observations of the jowls in aging-implications for facial rejuvenation. Plast Reconstr Surg. 2008;121:1414–1420

7. Hellman M. Changes in the human face brought about by development. Int J Orthod. 1927;13:475

8. Israel H, Fierro-Benitez R, Garces J. Skeletal and dental development in the endemic goitre and cretinism areas of Ecuador. J Trop Med Hyg. 1969;72:105–113

9. Perrett KI, May KA, Yoshikawa S. Facial shape and judgments of female attractiveness. Nature. 1994;368:239

10. Perrett KI, Lee KJ, Penton-Voak I, et al. Effects of sexual dimorphism on facial attractiveness. Nature. 1998;393:884

11. Furnas DW. The retaining ligaments of the cheek. Plast Reconstr Surg. 1989;83:11–16

12. Barton FE Jr. The SMAS and the nasolabial fold. Plast Reconstr Surg. 1992;89:1054

13. Pitanguy I, Pamplona D, Weber HI, et al. Numerical modeling of facial aging. Plast Reconstr Surg. 1998;102(1):200–204

14. Furnas DW. Festoons, mounds, and bags of the eyelids and cheek. Clin Plast Surg. 1993;20:367–385

15. Gonzalez-Ulloa M, Flores ES. Senility of the face—basic study to understand its causes and effects. Plast Reconstr Surg. 1965;36:239–246

16. Rohrich RJ. Ethical approval of clinical studies, informed consent, and the Declaration of Helsinki: what you need to know. Plast Reconstr Surg. 2007;119:2307–2309

17. Rohrich RJ, Pessa JE, Ristow B. The youthful cheek and the deep medial fat compartment. Plast Reconstr Surg. 2008:2107–2112

18. Rohrich RJ, Ahmad J, Hamawy AH, et al. Is intraorbital fat extraorbital? Results of cross-sectional anatomy of the lower eyelid fat pads. Aesthet Surg J. 2009;29:189–193

19. Rohrich RJ, Arbique GM, Wong C, et al. The anatomy of sub–orbicularis oculi fat: implications for periorbital rejuvenation. Plast Reconstr Surg. 2009;124:946–951

20. Rohrich RJ, Pessa JE. The retaining system of the face: histologic evaluation of the septal boundaries of the subcutaneous fat compartments. Plast Reconstr Surg. 2008;121:1804–1809

21. Pessa JE. An algorithm of facial aging: verification of Lambros’s theory by three-dimensional stereolithography, with reference to the pathogenesis of midfacial aging, scleral show, and the lateral suborbital trough deformity. Plast Reconstr Surg. 2000;106(2):479–488

22. Pessa JE, Zadoo VP, Yuan C, et al. Concertina effect and facial aging: nonlinear aspects of youthfulness and skeletal remodeling, and why, perhaps, infants have jowls. Plast Reconstr Surg. 1999;103(2):635–644

23. Pessa JE, Desvigne LD, Lambros VS, et al. Changes in ocular globe-to-orbital rim position with age: implications for aesthetic blepharoplasty of the lower eyelids. Aesthetic Plast Surg. 1999;23:337–342

24. Pessa JE, Slice DE, Hanz KR, et al. Aging and the shape of the mandible. Plast Reconstr Surg. 2008;121:196–200

25. Pessa JE, Zadoo VP, Adrian EK, et al. Anatomy of a “black eye”: a newly described fascial system of the lower eyelid. Clin Anat. 1998;11:157–161

26. Gosain AK, Klein MH, Sudhakar PV, et al. A volumetric analysis of soft-tissue changes in the aging midface using high-resolution MRI: implications for facial rejuvenation. Plast Reconstr Surg. 2005;115(4):1143–1152

27. Shaw RB Jr, Katzel EB, Koltz PF, et al. Aging of the facial skeleton: aesthetic implications and rejuvenation strategies. Plast Reconstr Surg. 2011;127(1):374–383

28. Lambros V. Observations on periorbital and midface aging. Plast Reconstr Surg. 2007;120(5):1367–1376

29. Gierloff M, Stöhring C, Buder T, Gassling V, Acil Y, Wiltfang J. Aging changes of the midfacial fat compartments: a computed tomographic study. Plast Reconstr Surg. 2012;1:263–273

30. Kikkawa DO, Lemke BN, Dortzbach RK. Relations of the superficial musculoaponeurotic system to the orbit and characterization of the orbitomalar ligament. Ophthal Plast Reconstr Surg. 1996;12:77–88

31. Camp M, Filip ZA, Wong W, et al. A novel three-dimensional analysis of periorbital facial aging. Plast Reconstr Surg. 2009;124(4S):41–42

32. Moss CJ, Mendelson BC, Taylor GI. Surgical anatomy of the ligamentous attachments in the temple and periorbital regions. Plast Reconstr Surg. 2000;105:1475–1490; discussion 1491

33. Mendelson BC. Surgery of the superficial musculoaponeurotic system: principles of release, vectors, and fixation. Plast Reconstr Surg. 2001;107:1545

34. Mendelson BC, Muzaffar AR, Adams WP Jr. Surgical anatomy of the midcheek and malar mounds. Plast Reconstr Surg. 2002;110:885–896; discussion 897

35. Byrd HS. The extended browlift. Clin Plast Surg. 1997;24:233–246

36. Aiache AE, Ramirez OM. The sub-orbicularis oculi fat pads: an anatomic and clinical study. Plast Reconstr Surg. 1995;95:37

37. Shaw RB Jr, Katzel EB, Koltz PF, et al. Aging of the mandible and its aesthetic implications. Plast Reconstr Surg. 2010;125(1):332–342

38. Gosain AK, Yousif NJ, Madiedo G, et al. Surgical anatomy of the SMAS: a reinvestigation. Plast Reconstr Surg. 1993;92:1254–1263; discussion 1264

39. Yousif NJ, Gosain A, Matloub HS, et al. The nasolabial fold: an anatomic and histologic reappraisal. Plast Reconstr Surg. 1994;93:60

40. Glat PM, Jelks GW, Jelks EB, et al. Evolution of the lateral canthoplasty: techniques and indications. Plast Reconstr Surg. 1997;100:1396–1405; discussion 1406

41. Hester TR, Codner MA, McCord CD. The “centrofacial” approach for correction of facial aging using the transblepharoplasty subperiosteal cheek lift. Aesthetic Surg Q. 1996;16:51

42. Hester TR, Codner MA, McCord CD. Trans-orbital lower-lid and midface rejuvenation. Oper Tech Plast Reconstr Surg. 1998;5:163

43. Hinderer UT. Correction of weakness of the lower eyelid and lateral canthus. Personal techniques. Clin Plast Surg. 1993;20:331–349

44. Schlessinger J, Kenkel J, Werschler P. Further enhancement of facial appearance with a hydroquinone skin care system plus tretinoin in patients previously treated with botulinum toxin Type A. Aesthet Surg J. 2011;31:529–539

45. Kovacs D, Cardinali G, Aspite N, et al. Role of fibroblast-derived growth factors in regulating hyperpigmentation of solar lentigo. Br J Dermatol. 2010;163:1020–1027

46. Varani J, Spearman D, Perone P, et al. Inhibition of type I procollagen synthesis by damaged collagen in photoaged skin and by collagenase-degraded collagen in vitro. Am J Pathol. 2001;158:931–942

47. Elias PM, Ghadially R. The aged epidermal permeability barrier: basis for functional abnormalities. Clin Geriatr Med. 2002;18:103–120, vii

48. Babamiri K, Nassab R. Cosmeceuticals: the evidence behind the retinoids. Aesthet Surg J. 2010;30:74

49. Lewis KG, Bercovitch L, Dill SW, et al. Acquired disorders of elastic tissue: part I. Increased elastic tissue and solar elastotic syndromes. J Am Acad Dermatol. 2004;51:1–21; quiz 22

50. El-Domyati M, Attia S, Saleh F, et al. Intrinsic aging vs. photoaging: a comparative histopathological, immunohistochemical, and ultrastructural study of skin. Exp Dermatol. 2002;11:398–405

51. Berlett BS, Stadtman ER. Protein oxidation in aging, disease, and oxidative stress. J Biol Chem. 1997;272:20313–20316

52. Rittié L, Fisher GJ. UV-light-induced signal cascades and skin aging. Ageing Res Rev. 2002;1:705–720

53. Young IS, Woodside JV. Antioxidants in health and disease. J Clin Pathol. 2001;54:176–186

54. Fisher GJ, Datta SC, Talwar HS, et al. Molecular basis of sun-induced premature skin aging and retinoid antagonism. Nature. 1996;379:335–339

55. Leyden JJ. Clinical features of aging skin. Br J Dermatol. 1990;122:1–3

56. Reenstra WR, Yaar M, Gilchrest BA. Aging affects epidermal growth factor receptor phosphorylation and traffic kinetics. Exp Cell Res. 1996;227:252–255

57. Gilchrest BA, Blog FB, Szabo G. Effects of aging and chronic sun exposure on melanocytes in human skin. J Invest Dermatol. 1979;73:141–143

58. Montagna W, Hu F, Carlisle K. A reinvestigation of solar lentigines. Arch Dermatol. 1980;116:1151–1154

59. Tanaka H, Okada T, Konishi H, et al. The effect of reactive oxygen species on the biosynthesis of collagen and glycosaminoglycans in cultured human dermal fibroblasts. Arch Dermatol Res. 1993;285:352–355

60. Edwards DR, Leco KJ, Beaudry PP, et al. Differential effects of transforming growth factor-beta 1 on the expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in young and old human fibroblasts. Exp Gerontol. 1996;31:207–223

61. Ho ET, Trookman NS, Sperber BR, et al. A randomized, double-blind, controlled comparative trial of the anti-aging properties of non-prescription tri-retinol 1.1% vs. prescription tretinoin 0.025%. J Drugs Dermatol. 2012;11:64–69

62. Mukherjee S, Date A, Patravale V, et al. Retinoids in the treatment of skin aging: an overview of clinical efficacy and safety. Clin Interv Aging. 2006;1:327–348

63. Lee CJ, Park JH, Ciesielski TE, et al. Retinoids, 585-nm laser, and carbon dioxide laser: a numeric comparison of neocollagen formation in photoaged hairless mouse skin. Aesthetic Plast Surg. 2008;32:894–901

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