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Concepts in a Multiprong Approach to Photoaging

Z. D. Draelos, MD
Department of Dermatology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, and Dermatology Consulting Services, High Point, North Carolina, USA

ABSTRACT

Photoaging is a multisystem degenerative process that involves the skin and the skin support systems, including the bone, cartilage, and subcutaneous compartments. These structures provide the architectural support for the dermis, epidermis, and stratum corneum. A multiprong approach to photoaging involves reversing the undesirable changes in each of these structures. Dermatologists should become adept at treating all of the visible manifestations of photoaging.

Key Words: photoaging, multiprong approach

Photoaging is a multisystem degenerative process that involves the skin and the skin support systems, including the bone, cartilage, and subcutaneous compartments. These structures provide the architectural support for the dermis, epidermis, and stratum corneum. A multiprong approach to photoaging involves reversing the undesirable changes in each of these structures. Dermatologists should become adept at treating all of the visible manifestations of photoaging.

Dermatologic Approach to Facial Rejuvenation

The compartments of the face that require attention include:
  • Bony architecture
  • Cartilage architecture
  • Subcutaneous compartment
  • Viable dermis and epidermis
  • Nonviable epidermis
  • Stratum corneum

Bony Architecture

One of the most important areas for consideration is the bony architecture over which the skin lies. Without a strong framework, the skin hangs formless over the face. Bone demineralization begins earlier than thought, at around age 25 in fair-complected females. It is this bone loss that leads to dulling of the facial features.

Unfortunately, published results outlining the risks and benefits of hormone replacement therapy1 lead many women to discontinue estrogen supplementation due to concerns about coronary disease; however, bone replacement therapy, such as bisphosphonates, is usually not begun until overt evidence of osteoporosis is present. Furthermore, many fair-complected women are Vitamin D deficient according to the new revised laboratory normal values.2 Dermatologists should become proficient at advising patients regarding facial bone health.

Instituting therapy for anticipated or existing osteopenia or osteoporosis is not difficult. Women who are at risk for facial bone loss should probably have a hip or spine Dexascan yearly to chart the success of therapy. Vitamin D therapy should be initiated at 50,000 IU for 2 weeks followed by 800 IU daily as a nutraceutical. Calcium carbonate should be given as a supplement at 1gm daily accompanied by a bisphosphonate administered once weekly. At least 30 minutes of weight-bearing exercise should be undertaken 3 times weekly. Patients should be reminded that swimming and cycling do not constitute weight-bearing exercise.

Cartilage Architecture

The architecture of the cartilage of the face, in addition to the bony architecture, defines the shape of the face. The most important facial structure dependent on cartilage is the nose. The cartilage does not disappear with advancing age, but does change shape.

Much of the change occurs during pregnancy due to the relaxins that are secreted at high levels during the final trimester to allow childbirth. I believe these relaxins also cause the tip of the nose to droop, which contributes to a more mature appearance of the female face. At present, there is no research regarding the preservation of the youthful nasal shape during pregnancy. Perhaps the use of hyaluronic acid fillers during pregnancy could preserve the up-turned, youthful female nose.

Subcutaneous Compartment

The subcutaneous compartment undergoes much of the change that contributes to the aged appearance of the face. It is presently unclear why subcutaneous fat from all over the body is removed, including the facial fat, and redeposited intrabdominally. Some researchers who study anti-aging have advocated the notion that these changes are due to lower growth hormone levels and recommended supplementation.3 This recommendation is certainly outside current mainstream medicine. Others point to the fat redistribution on the body that occurs with menopause.4,5 In postmenopausal women fat is typically redistributed to the breast, arms, waist, thighs, and buttock with loss of facial fat.

At present, the best way to replace large amounts of fat that are lost from the face, resulting in prominent nasolabial and melolabial folds, is through autologous fat transfer. The fat is removed from the hips or thighs and moved to the face for insertion on the bone, in the muscle, and below the skin. This dermatologic technique can result in a more youthful appearance without the downtime and scarring of a face-lift. I believe that autologous fat transfer is preferable to a face-lift because it does not change the essence of the individual's face.
Many women lose their characteristic appearance after a face-lift because the skin has been stretched and repositioned over the fat-devoid bones creating an angular, gaunt appearance. Although the skin folds have been removed, the youthful curves of the face have not been recreated.

Viable Epidermis and Dermis

The viable epidermis and dermis are the essence of the skin. It is the loss of dermal collagen that leads to wrinkling and the increased appearance of muscular attachments. Irregular melanization leads to lentigines, melasma, and poikiloderma, and prominent telangiectasias lead to erythema. It is in this area that many new developments have occurred.

Fillers, deep chemical peeling, and laser resurfacing can replace or encourage regeneration of lost dermal collagen. Botulinum toxin can be used to minimize the appearance of hyperkinetic muscles. Medium depth chemical peeling, cryosurgery, and intense pulsed light can be used to even out pigmentation abnormalities. Light sources, electrocautery, and sclerotherapy can be used for telangiectasias. This is an area of treatment where dermatology has much to offer.

Nonviable Epidermis

Dermatology also excels at treating the nonviable epidermis. It is in this area where desquamatory failure leads to retained corneocytes and poor skin texture. Superficial glycolic and salicylic acid chemical peels and microdermabrasion can enhance desquamation. Actinic keratoses can also contribute to poor skin texture, but are readily treated with 5-fluorouracil, diclofenac (VoltarenŽ, Novartis), imiquimod (AldaraŽ, 3M), or cryosurgery.

Stratum Corneum

The last area to consider is the stratum corneum. This is really the area of the cosmeceutical. It is the stratum corneum that is impacted by most of the creams for aging skin sold at the cosmetic counter. The most common treatable stratum corneum problem that leads to fine wrinkling is dehydration. In addition, the skin barrier may be in need of repair. A well-constructed moisturizer, e.g., CetaphilŽ (Galderma) or CeraVeŽ (Coria Laboratories), creates an environment for healing in which the corneocytes and intercellular lipids can be restored to their normal brick-and-mortar lamellar organization. The stratum corneum also provides an opportunity to prevent photodamage through the application of sunscreens.

Conclusion

Dermatologists should consider a multiprong approach to photoaging by considering its effect on all of the facial structures, including the bone, fat, dermis, epidermis, nonviable epidermis, and stratum corneum. The best long-lasting solutions for the prevention and treatment of photoaging can be achieved through this multisystem approach.

References

  1. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women's Health Initiative randomized controlled trial. JAMA 288(3):321-33 (2002 Jul).
  2. Kratz A, Ferraro M, Sluss PM, Lewandrowski KB. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Laboratory reference values. N Engl J Med 351(15):1548-63 (2004 Oct 7).
  3. Johannsson G, Bengtsson BA. Growth hormone and the metabolic syndrome. J Endocrinol Invest 22(5 Suppl):41-6 (1999).
  4. Carr MC. The emergence of the metabolic syndrome with menopause. J Clin Endocrinol Metab 88(6):2404-11 (2003 Jun).
  5. van Seumeren I. Weight gain and hormone replacement therapy: are women's fears justified? Maturitas 34 Suppl 1:S3-8 (2000 Jan).

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