Causes of changes in skin texture and fine lines

Modern cosmetic medicine demands accurate recognition of all types of rhytids and their molecular causes to tailor treatment for improving aging skin appearance. This article examines the causes and treatment of fine rhytids. The underlying cause of fine lines, also known as atrophic rhytids , is dermal thinning. Myriad molecular mechanisms have been identified in the loss of dermal strength and architecture. Dermal thinning is caused by a loss of collagen and elastin in the dermis. After reviewing the histopathology of the role of dermal atrophy in the creation of fine rhytids, practitioners can better understand the prevention and treatment of fine lines. Although fine “crinkles” and lines appear superficial, the epidermis does not significantly contribute to wrinkle formation. In reality, the fine atrophic rhytids of the face are caused by molecular changes deeper in the underlying dermis. Therefore, laser rejuvenation therapies that penetrate the dermis and induce neocollagenesis and dermal remodeling are effective against the stigmata of mature skin.

As the skin ages, changes in the color, texture, and quality of the skin become apparent. Aged skin develops four different types of wrinkles: atrophic rhytids (fine lines), solar elastosis (permanent lines), dynamic expression lines, and gravitational folds. The skin becomes dry (asteatosis), yellow, rough, and leathery, with increased laxity and decreased turgor. Periorbital comedones often develop. A generalized decrease in the skin adnexal occurs, including sebaceous glands, sweat glands, and hair follicles. Changes in pigmentation may also occur, including irregular hyperpigmentation, such as sun spots or liver spots. Hypopigmentation may develop in the form of white macules called pseudoscars from excessive sun exposure. Vascular changes in the skin associated with aging include actinic purpura secondary to weak, leaky capillary beds in the dermis, and telangiectasias.

The causes of cutaneous aging can be divided into intrinsic and extrinsic causes. The intrinsic causes are simply the passage of time and genetic programming that leads to thinning of the dermis from decreased collagen and elastic dermal support systems. Normal skin aging is first noted as early as the third decade of life, with the first signs of skin fragility seen as fine shallow lines of epidermis draped over the thinning dermis. These fine lines, or atrophic rhytids, are often the first type of skin wrinkle to develop, and are a harbinger of further signs of aging skin.

Extrinsic causes of aging skin are multifactorial, and include the sequelae of environmental, behavioral, and general medical assaults on the skin. The worst offender is photoaging, also called dermatoheliosis . Signs of sun-induced skin damage may be visible as early as 15 years of age in cases of heavy childhood sun exposure. Photoaging, which certainly accelerates the normal aging process of dermal thinning and atrophic rhytid formation, is not analogous to normal aging. Photoaging also leads to a host of additional molecular and histopathologic changes in the skin architecture. For example, photoaging leads to epidermal thickening, causing a rough, dry, leathery texture. The hallmark of dermatoheliosis is elastosis, a process of haphazard hypertrophy of elastic fibers that leads to heaped-up wrinkles with deep, crisscrossing, permanent furrows. Most mature skin pigment alterations, such as hyperpigmented macules and telangiectasias, are from photoaging.

Histopathology of fine lines

Histologically, skin is a complex layered organ. The outermost layer is the epidermis, supported by the underlying dermis, which sits on subcutaneous fat that makes up the hypodermis. The epidermis is further divided into five layers, from superficial to deep: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. The dermis has two main components. First are the papillary ridges that reach up to provide a sort of scaffolding under the epidermis. Deep to the papillary ridges lies the reticular dermis, an elastic bed supporting the skin.

The texture of the skin is largely because of the microrelief of fine furrows caused by the ridges of papillary dermis and the edges of corneocytes of the stratum corneum. Quatresooz and colleagues studied the microrelief of youthful skin and aged skin. Although young skin is commonly regarded as smooth, it is perhaps more accurately described as velvety. Young skin is, in fact, not really smooth at all. Instead, the microrelief is a fine velvety polygonal crisscross of very fine furrows each measuring approximately 200 μm in depth. As the dermis atrophies with age and environmental insults, the papillary ridges become less polygonal and more parallel. The resulting appearance is that of atrophic rhytids, which are fine lines that smooth out easily when stretched but have poor elasticity to return to a taut position. These atrophic rhytids have the appearance of crumpled tissue paper or crepe paper, and are a pesky contributor to facial aging.

In summary, the causes of fine lines are

• •
  

  Intrinsic (genetic) and extrinsic (environmental) dermal thinning

  
  
• •
  

  Loss of oxytalan elastic fibers in the dermoepithelial junction and papillary dermis

  
  
• •
  

  Atrophy of the collagen VII bundles in the reticular dermis and hypodermis

  
  
• •
  

  Decrease in glucosaminoglycans surrounding dermal collagen bundles

  
  
• •
  

  Ultraviolet radiation–induced increase in cellular expression of matrix metalloproteinases that degrade dermal collagen, elastin, and the surrounding matrix at an accelerated rate.

Solar elastosis often occurs in conjunction with atrophic rhytids, because photoaging leads to both types of wrinkles. Other wrinkle types include dynamic expression lines, which are most successfully treated with botulinum toxin injection, and gravitational rhytids, which are best treated with surgical lifting.

Histopathology of fine lines

Histologically, skin is a complex layered organ. The outermost layer is the epidermis, supported by the underlying dermis, which sits on subcutaneous fat that makes up the hypodermis. The epidermis is further divided into five layers, from superficial to deep: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. The dermis has two main components. First are the papillary ridges that reach up to provide a sort of scaffolding under the epidermis. Deep to the papillary ridges lies the reticular dermis, an elastic bed supporting the skin.

The texture of the skin is largely because of the microrelief of fine furrows caused by the ridges of papillary dermis and the edges of corneocytes of the stratum corneum. Quatresooz and colleagues studied the microrelief of youthful skin and aged skin. Although young skin is commonly regarded as smooth, it is perhaps more accurately described as velvety. Young skin is, in fact, not really smooth at all. Instead, the microrelief is a fine velvety polygonal crisscross of very fine furrows each measuring approximately 200 μm in depth. As the dermis atrophies with age and environmental insults, the papillary ridges become less polygonal and more parallel. The resulting appearance is that of atrophic rhytids, which are fine lines that smooth out easily when stretched but have poor elasticity to return to a taut position. These atrophic rhytids have the appearance of crumpled tissue paper or crepe paper, and are a pesky contributor to facial aging.

In summary, the causes of fine lines are

• •
  

  Intrinsic (genetic) and extrinsic (environmental) dermal thinning

  
  
• •
  

  Loss of oxytalan elastic fibers in the dermoepithelial junction and papillary dermis

  
  
• •
  

  Atrophy of the collagen VII bundles in the reticular dermis and hypodermis

  
  
• •
  

  Decrease in glucosaminoglycans surrounding dermal collagen bundles

  
  
• •
  

  Ultraviolet radiation–induced increase in cellular expression of matrix metalloproteinases that degrade dermal collagen, elastin, and the surrounding matrix at an accelerated rate.

Solar elastosis often occurs in conjunction with atrophic rhytids, because photoaging leads to both types of wrinkles. Other wrinkle types include dynamic expression lines, which are most successfully treated with botulinum toxin injection, and gravitational rhytids, which are best treated with surgical lifting.

In-office evaluation of fine line– and skin texture–related complaints

The in-office evaluation of patients seeking improvement of facial aesthetics should begin with a complete history and physical. This evaluation should include a detailed cosmetic history, including past cosmetic procedures, such as laser treatment, dermabrasion, chemical peels, botulinum toxin, and filler injections, and past facial plastic surgeries. Patient response and any unforeseen or undesirable outcomes should be noted. Any past medical problems that could impede wound healing, such as immunosuppression, cancer, smoking, or diabetes, must be noted and discussed with the patient as risk factors for a potentially suboptimal outcome. The ( Box 1 ) indicates specialized elements of the medical history for patients considering laser treatment.

The patient encounter should then focus on the skin and cosmetic concerns. A general dermatologic examination begins with visual inspection in natural light, or artificial light that mimics natural light, to prevent color distortion. The color, moisture, temperature, mobility, and turgor of the skin must be evaluated. The hair and nails should be inspected, and any cutaneous lesions carefully noted. Many factors contribute to skin color, such as melanin (genetic and environmental secondary to sun exposure), carotene (most visible on the palms and soles), oxyhemoglobin (arterial capillary beds), deoxyhemoglobin (venous capillary beds), and the light scatter through the skin itself and opaque vessel walls. Hyperpigmentation, hypopigmentation, scars, and telangiectasias should be recorded. The skin texture and moisture should be evaluated. The skin should be lifted gently to assess skin turgor, distensibility, and laxity. Fine lines tend to have a “crepe paper” appearance, disappear easily when the skin is stretched, and return to their crinkled appearance when released.

During the physical examination, a high index of suspicion should be maintained for potentially malignant lesions, such as malignant melanoma (caused by genetic predisposition and early childhood sunburns) and the common skin cancers of chronically sun-exposed areas, such as basal cell carcinoma (pearly, raised edges) and squamous cell carcinoma (erythematous, often pruritic patches).

As part of the visit documentation, standardized digital photodocumentation of before and after assessments is recommended to track progress of treatments. Using consistent camera equipment, lighting, and background helps minimize variability of photos and increases the fidelity of the images.

Possibly the most important part of the in-office evaluation is the skin-type analysis. The time it takes to perform an in-depth dermatologic history will likely help the physician predict cosmetic outcomes and tailor treatments to each individual patient’s skin. The Fitzpatrick scale remains the gold standard and classifies patients into six skin types based on the skin’s reaction in the sun. Lasers are ideal for patients who have Fitzpatrick skin types I through III, although consideration for safe laser practices has been described for darker skin types.

The cosmetic skin evaluation can be expanded to document wrinkles in a standardized fashion, such as using the Glogau Photoaging Classification ( Table 1 ). This scale describes degrees of wrinkling and photoaging.

Table 1

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