Skin Disorders in Older Adults: Cutaneous Signs of Normal Aging

Noah S. Scheinfeld, MD, JD
Columbia University

Dr Scheinfeld is assistant clinical professor of dermatology at Columbia University and assistant attending physician at St Luke’s–Roosevelt and Beth Israel Hospitals in New York. 


ABSTRACT: Skin aging results from both intrinsic factors (ie, alterations of cutaneous function) and extrinsic factors (eg, ultraviolet radiation that induces photoaging). Age-related thinning of the epidermis and dermis and a decrease in subcutaneous fat manifest as wrinkles (rhytides), lines, and furrows. The severity of these changes in an individual patient depends on genetic tendency, underlying skin color, and exposure to extrinsic factors (eg, ultraviolet radiation, tobacco smoke). Treatment of aged skin involves the use of moisturizers, particularly those with alpha-hydroxy acids; relaxation of the muscles underlying the skin with botulinum toxin; and injection of collagen, hyaluronic acid, calcium salts, silicone, and other substances. 

Aging leads to many changes in the skin and its appendages (nerves, glands, hair, and nails). The causes of skin aging can be classified as intrinsic (subtle but important alterations of cutaneous function) or extrinsic (eg, ultraviolet radiation that induces photoaging). Much of the appearance of older skin results from extrinsic aging, but even elderly persons with no history of exposure to the sun or other extrinsic factors of aging have skin that looks “old.”

No preventive regimen can stop time from working visible changes on the skin. Therapies for aged skin are directed toward moisturizing the skin, injecting substances into the skin to replace those that age has removed, and relaxing the underlying muscles to flatten the overlying skin.

Here, in part 1 of this 2-part series, I discuss the normal changes in the skin that occur with aging. In a coming issue, I will address changes in the hair and nails of the elderly, some of which are related to aging and others to systemic disease.


The aged (older than 60 years) epidermis is different from its younger counterpart. The rate of keratinocyte proliferation declines 30% to 50% between the ages of 30 and 80. The epidermis thins by about 5% to 30% by age 60 and the dermalepidermal junction flattens because of a reduction in the number and size of epidermal rete ridges and dermal papilla that interface—decreasing the dermal and epidermal connection.1 Linear growth rates for hair and nails also decline, and healing times for epidermal wound repair increase.

By age 60, the dermis is 20% thinner than it was at its peak thickness, and it is even thinner in areas where the skin has sustained photodamage. Even in skin that has not been exposed to ultraviolet radiation, cellularity and vascularity are relatively decreased. In elderly skin, there is a 50% decrease in mast cells and a 30% decrease in venular cross sectional area. Basal and peak cutaneous blood flow decreases by 60%, which compromises vascular responsiveness. The dermal vascular plexi involute with age. Adnexal structures decrease in size and number.

In the elderly, there is a degradation of the integrity and functionality of the connective tissue stroma and mucopolysaccharides that make up the ground substance of the skin and a decrease and dysregulation of collagen synthesis and collagen degradation. Elastic fibers decrease in number and diameter with age. Fragmentation, progressive crosslinkage, and calcification of elastin and collagen manifest and contribute to the decrease in skin turgor and elasticity.

In men and women, the total volume of subcutaneous fat decreases with age. However, the proportion of body fat as a percentage of total weight actually increases until age 70. Aging manifests with a redistribution of fat from the face and hands to the thighs and abdomen. At the same time the muscle mass of the body decreases with age and is marked in old age. The reasons for this are complex and involve metabolic and hormonal homeostatic changes.



Cutaneous changes. The thinning of the epidermis and dermis and the decrease in subcutaneous fat manifest physically as wrinkles (rhytides), lines, and furrows. The severity of these changes in an individual depends on genetic tendency, underlying skin color, and exposure to extrinsic factors (eg, ultraviolet radiation). Fine lines and wrinkles arise because of irregular thickening of the dermis and because of a decrease in the amount of water held by the epidermis. They are mainly caused by extrinsic aging factors, such as photodamage and exposure to environmental toxins, such as tobacco smoke. Physical factors that increase the number of facial lines and wrinkles are muscle movement, gravity, injury, surgery, acne, and scarring skin diseases.

The Fitzpatrick classification sets forth 3 classes that rate the degree of wrinkling around the mouth and eyes2:
•Class I: Fine wrinkles (Figure
•Class II: Fine to moderately deep wrinkles and moderate number of lines (Figure 2).
•Class III: Fine to deep wrinkles, numerous lines, and possibly redundant folds (Figure 3).

Treatment of aged skin involves the use of moisturizers, particularly those with alphahydroxy acids; relaxation of the muscles underlying the skin with botulinum toxin; and injection of collagen, hyaluronic acid, calcium salts, silicone, and other substances. These treatments are most effective for class I wrinkles but are generally ineffective for class III wrinkles. Class II and class III wrinkles can be treated by surgical removal of redundant skin with so- called “face lifts” and various “plasty” procedures. 





Specific changes occur around the eyes and on the face that relate to thinned epidermis and dermis, decreased subcutaneous fat, and atrophic muscle. These include: •Eyelid ptosis (the upper eyelid drops, sometimes obscuring the pupil).
•Brow ptosis (the forehead sags so that the eyebrows drop over the eyelids, which then feel heavy).
•Dermatochalasis—baggy eye lids (Figure 4).
•Sagging lower eyelids, revealing the reddened mucosal surface (ectropion) (Figure 5).
•Hollow appearance of the eyes (Figure 6).
•Tired-looking eyes with a prominent groove beside the nose (teartrough deformity).
•Jowls (loss of jaw line).
•Loss of neckline. •Elongated earlobes.
•Dropping of the tip of the nose.
•Thinning of the upper lip.

The following are some colloquial names that have been given to wrinkles based on their location and appearance:

•Crow’s feet around the eyes are due to smiling and activity of the eyelid muscles (orbicularis oculi).
•Worry lines on the forehead result from contraction of the frontalis muscle when raising the eyebrows.
•Frown lines between the eyebrows are caused by contraction of corru- gator supercilii muscles and procerus muscle during concentration or anger.

Skin atrophy can take place on any part of the body and results in the sagging of tissue into folds. It is often marked on the chest and arms of patients over 70 years of age (Figure 7).

Muscle atrophy. Beginning after 29 years of age, the number and size of muscle fibers progressively decline. These effects cause a decrease in skeletal muscle mass and thus lean body mass referred to as sarcopenia. Decreased exercise and physical exertion; a loss of motor units, possibly beginning during middle age; and reduced skeletal muscle protein synthesis underlie these effects.3

In the average young person, 30% of body weight is muscle, 20% is adipose tissue, and 10% is bone. Muscle accounts for 50% of lean body mass and about 50% of the total amount of body nitrogen. By age 75, 50% of the muscle mass has disappeared; 15% of body weight is muscle, 40% is adipose tissue, and 8% is bone. The atrophy of muscle is usually initially and most prominently noticeable on the hands and feet (Figure 8). Later such atrophy affects the arms and the legs. 



1. Makrantonaki E, Zouboulis CC. Molecular mechanisms of skin aging: state of the art. Ann NY Acad Sci. 2007;1119:40-50.
2. Fitzpatrick RA. Facial resurfacing with the pulsed carbon dioxide laser. A review. Facial Plast Surg Clin North Am. 1996;4(2):236.
3. Barohn RJ. Muscle diseases. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia: Saunders Elsevier; 2007: chap 447.