The final article in this series on the anatomy and physiology of ageing discusses the effects of ageing on the skin
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Citation: Nigam Y, Knight J (2008) Exploring the anatomy and physiology of ageing: Pprt 11 - the skin. Nursing Times; 104: 49, 24-25.
Authors: Yamni Nigam and John Knight are both lecturers in biomedical science, School of Health Science, Swansea University.
The skin is the largest organ of the body, comprising approximately 7% of total body weight (Montague et al, 2005). Structurally, it consists of two main parts - the epidermis and the dermis, below which is the hypodermis, a layer of subcutaneous tissue. Together these three layers protect the underlying muscles, bones and internal organs and perform a number of other functions including:
- Thermoregulation: the body temperature can be adjusted in response to environmental factors by the control of blood flow in the dermis;
- Storage and synthesis: lipids and water are stored, and vitamin D is synthesised;
- Cutaneous sensation: A variety of nerve endings in the skin sense touch, vibration, warmth, coolness and pain.
Like all organs, the skin is subject to the degenerative process of chronological and intrinsic ageing. However, its exposed interface with the environment also makes it subject to photoageing - ageing due to exposure and damage from the sun and its ultraviolet light rays.
Chronological skin ageing
Chronological ageing of the skin comprises changes that result from the passage of time. These are believed to occur mainly due to the action of reactive oxygen species (ROS), molecules (ions) generated during normal cellular metabolism. ROS destroy skin cell membranes, DNA and enzymes (Gilchrest and Krutmann, 2006). With advancing age, ROS levels increase and the ability to mop these up (via antioxidant defence systems) declines.
There is also a reduction in hormones and chemical signals, which are important in skin growth and repair, as well as a decline in the receptors detecting them - for example the amount of receptors for vitamin D decreases with age.
The top layer of skin is mainly protective keratinised squamous epithelial tissue, with an outer barrier of dead skin cells (stratum corneum). Underneath this, numerous layers of epidermal cells end in the basal layer of rapidly dividing cells, adjacent to the basement membrane and dermis. Keratinocytes (cells making keratin) and melanocytes (cells in the basal layer, which produce the photoprotective pigment melanin) are in the epidermis, as are Langerhans cells - immune dendritic cells, which form the ‘front door’ of the immune system in the epidermis. These prevent unwanted foreign micro-organisms from penetrating the skin. Because it has no blood supply, the epidermis gains its nutrition through its contact with the dermis.
With age, there is a substantial loss of melanocytes and Langherhans cells. There is also a reduction in surface contact between the epidermis and dermis, resulting in a reduced exchange of nutrients and metabolites between the two layers. In addition, the epidermis atrophies, as a result of decreased epidermal cell turnover (rates decrease by up to 50% between the 20s and 70s). The stratum corneum is not replaced quickly, skin appears rough, has a decreased barrier function and healing takes longer.
This thickest layer of skin contains blood capillaries, which provide oxygen and nourishment to all skin cells. It comprises largely of an extracellular matrix containing a mesh of collagen and elastin fibres, which give the skin its strength, elasticity and resilience. Key cells in the dermis are fibroblasts (which synthesise collagen, elastin and other structural molecules of the matrix), and mast cells (immune cells that produce histamine). Sebaceous and sweat glands, hair follicles and sensory organs of touch and pressure are also found in the dermis.
Dermal tissue atrophies with age and dermal thickness decreases by about 20% in older people. There is a 50% decrease in mast cells and due to a 60% decrease in cutaneous blood flow, there is a substantial decrease in the release of histamine. Such changes compromise the response to injury or infection.
The collagen content of the dermis decreases by 1% per year through adult life (Rigel et al, 2004). Fibroblasts appear shrivelled and those derived from older people have decreased levels of (epidermal growth factor) receptors. There is a drop in collagen synthesis, atrophy of collagen bundles, and an increase in levels of metalloproteinases and enzymes which degrade collagen. In addition, there is some resorption of the elastic fibre network.
Ageing sees a drastic reduction in dermal blood vessels, and a shortening of capillary loops in the dermal papillae. This results in the pallor, decreased temperature and impaired thermoregulation often found in the skin of older people.
The density of organs responsible for pressure and touch - Pacinian and Meissner’s corpuscles - decreases with age. There is also a loss of sensory nerve endings in the epidermis and dermis. This makes older people less able to detect changes in environmental stimuli and thus more prone to injury.
This layer underlying the skin consists mainly of fat, and acts as a shock absorber and insulator.
The volume of subcutaneous fat diminishes with age, which means its role in thermoregulation by limiting conductive heat loss is impaired. The distribution of subcutaneous fat also changes with age. For example, it decreases in parts of the face and hands and increases in the thigh and abdomen. Over bony areas, this reduction in fat may increase the risk of pressure ulcers or fractures in older people.
Clinical manifestations of chronologically aged skin include dryness (xerosis), laxity, slackness and wrinkles. These are most easily observed on the face as it is the most exposed area of the skin.
Wrinkles and skin sagging
Several factors contribute to the formation of wrinkles, including:
- Persistent gravitational forces;
- Loss of subcutaneous fat;
- Repeated traction exerted by facial muscles over expression lines.
Repeated traction can result in deep creases over the forehead, between the eyebrows, periorbitally and in the nasolabial folds.
Like all striated muscles, facial muscles show an accumulation of lipofuscin, often known as the ‘age pigment’, which is a marker of muscle cell damage. This damage, along with diminished neuromuscular control, contributes to wrinkle formation.
Skin becomes increasingly lax with age, and as a result soft tissue support diminishes. Gravity, depletion and redistribution of facial fat collaborate to form sagging, loose skin. In contrast to the appearance of a young face, where fat is diffusely dispersed, in ageing facial skin, fat tends to accumulate in pockets, for example in the nasolabial folds and submandibular regions (the jowls).
Photoageing occurs as a result of cumulative damage from ultraviolet (UV) radiation, and superimposes changes to the skin caused by chronological ageing. Actinic exposure (UV radiation) affects the epidermis, causing irreparable damage to cellular DNA. It also induces the generation of ROS, one of the earliest measurable responses to UV rays. Investigations have shown that in less than 30 minutes following UV irradiation, the level of a potent ROS (hydrogen peroxide) more than doubles in human skin.
In the dermis and epidermis, ROS, via other signalling pathways, cause the activation of collagenases and enzymes which degrade collagen and other proteins comprising the extra cellular matrix, impairing the structural integrity of the dermis. In addition, UV exposure disrupts ongoing collagen synthesis, leading to acute collagen loss in the skin. Along with increased skin pigmentation, actinic damage stimulates melanocyte proliferation.
The formation of benign skin lesions, such as seborrhoeic keratoses or solar lentigines (age spots) are regarded as the best indicators of skin ageing. These typically appear between the third and fifth decade of life and become more numerous thereafter. Due to chronic sun exposure, the likelihood of malignant skin cancers also increases with age.
Like all the other organ systems discussed in this series on the anatomy and physiology of ageing, the skin is affected by the passage of time. Ageing is widely known to be the consequence of genetic programming and cumulative ‘wear and tear’ damage and these effects are to a large extent unavoidable. With advancing age, the biochemical composition of tissues changes, physiological capacity is progressively reduced, and the ability to respond to environmental stimuli is decreased. All these changes lead to the increased probability of disease and death.
However, while ageing is the natural and unavoidable consequence of life, the extent to which it can affect an individual can be minimised, particularly in two ways. Regular weight-bearing exercise and eating a diet rich in fibre and antioxidants - for example from fresh fruit and vegetables - may reduce many of the effects that occur with ageing
Gilchrest, B.A., Krutmann, J. (2006) Skin Aging. Berlin: Springer.
Montague, S.E. et al (2005) Physiology for Nursing Practice. Oxford: Bailli貥 Tindall.
Rigel, D.S. et al (2004) Photoaging. London: Informa Health Care.