Protection from Environment
The dense, adhered structure of the skin provides protection from the environment by preventing the penetration of some microbes and other foreign bodies, absorbing shock as a result of the cushioning hypodermis, serving as a barrier to excessive water absorption or loss, and by containing specialized structures and cells with other protective functions. When the skin is damaged by disease or lost as a result of injury, its functions are compromised and can have detrimental, even fatal, effects on the body.
Sensation is both informative and protective. Stimuli received in the skin and transmitted to the brain can initiate a motor response that moves the person away from noxious stimuli. Embedded in the dermis are numerous nerve endings, illustrated and summarized in FIGURE 1-5. The most prevalent diagnosis resulting in the loss of tactile, pressure, and pain sensation in the skin is diabetic polyneuropathy, a major contributing factor to the formation of diabetic foot wounds. The lack of sensation allows trauma, even repeated trauma, to occur unnoticed and thereby results in wounds that are difficult to heal. This is just one example of how the failure of the skin sensory function may be a primary cause of wounds.
Sensory nerves within the dermal reticular layer (Used with permission from Mescher AL. Chapter 18. Skin. In: Mescher AL. eds. Junqueira's Basic Histology: Text & Atlas, 13th ed. New York, NY: McGraw-Hill; 2013. http://accessmedicine.mhmedical.com/content.aspx?bookid=574&Sectionid=42524604. Accessed November 12, 2014.)
Free nerve endings—unencapsulated nerve endings resembling the roots of a tree that are in the stratum basale of the epidermis; function as thermoreceptors, nociceptors, or cutaneous mechanoreceptors. The nerves lose the Schwann cell covering when they cross the dermal/epidermal junction into the stratum basale.
Tactile or Merkel disc—unencapsulated nerve ending close to the dermal/epidermal junction that is a receptor for light touch.
Meissner corpuscle—encapsulated unmyelinated nerve ending in the dermal papillae that responds to any deformation by pressure. The corpuscle is a single nerve fiber surrounded by lamella of flattened connective tissue cells, giving it a bulbous appearance. Meissner corpuscles are located most densely in glabrous skin.
Pacinian corpuscle—oval-shaped mechanoreceptor that consists of a single unmyelinated nerve fiber in a fluid-filled cavity surrounded by lamella of thin, flat, modified Schwann cells and wrapped in a layer of connective tissue, giving it the appearance of an onion. Pacinian corpuscles detect deep pressure and high-frequency, fast vibration.
Krause bulb—encapsulated nerve fiber located in the middle dermal layer; both a mechanoreceptor and a thermoreceptor, detecting light pressure, soft low vibrations, and cold.
Ruffini corpuscle—encapsulated elongated dendritic nerve ending located in the deep dermis and hypodermis; both a mechanoreceptor and thermoreceptor, detecting sustained pressure, stretching, and heat.
Root hair plexus—a network of sensory fibers around the root of the hair follicles in the deep dermis; detects and transmits any hair movement.
The dense, extensively cross-linked lipid and protein matrix in the stratum corneum serves as a barrier to fluid loss, thereby helping to maintain homeostasis. This protection is enhanced in the palms and soles by the presence of the stratum lucidum. In addition, “natural moisturizing factors,” including free amino acids, lactic acid, urea, and salts, attract and hold water in the stratum corneum (which is normally approximately 30% water).11 This property of maintaining the water content is termed hygroscopy. The amino acids are a result of filaggrin degradation by proteolytic enzymes.11 Injury to the skin or atmospheric conditions that result in loss of water can cause dry skin or irritant dermatitis, and moisturizers that rehydrate and repair the skin can use the same chemicals that are in normal skin.8
In addition to the physical barrier to environmental microbes, the skin has three properties that contribute to its role in the body's immune system: Langerhans cells, pH, and antimicrobial peptides and lipids.
Langerhans cells are dendritic cells primarily in the stratum spinosum that are alerted by any foreign microbes that enter the epidermis. Subsequently they bind, process, and present the antigens to the T-lymphocytes that are also in the epidermis, thereby initiating an immune response.1 Antimicrobial peptides are innate protein fragments that prick the microbe cell membrane and destroy its integrity, rendering it inactive. Some antimicrobial peptides are present in both healthy and infected tissue (eg, human β-defensin or HBD 1 and RNase 7), whereas others are present only in the event of epidermal penetration by the microbes (eg, psoriasin S100A7, HBD 2, and HBD 3). Lysozyme, dermcidin, and LL-37 are antimicrobial peptides found in the hair follicles and eccrine glands.2 These same peptides signal and recruit the immune cells (eg, T-lymphocytes, macrophages, neutrophils, and other dendritic cells) needed to phagocytose the attacked microbes or present antigens to the host immune system. See Chapter 2 for a more detailed discussion of peptides and their role in wound healing.
The skin has a slightly acidic pH (4.2–6) that serves as a barrier to exogenous bacteria. The “acid mantle” of the stratum corneum is a result of free fatty acids, oils (sebum) produced by the sebaceous glands, secretions from the eccrine sweat glands, and proton pumps (by pumping H+ ions out of cells onto the skin).12 This acidic layer is a hostile environment for the bacteria, inhibiting their replication and thus serving as a natural immune mechanism.
Thermoregulation as a response to changes in the environmental temperature is maintained by the dermal vasculature and by the sweat glands. When a person is inactive, normal skin blood flow is 30–40 mL/min/100 g of skin. During cold stress, the arterioles and the arteriovenous anastomoses (AVAs) constrict and thereby reduce the flow of blood to the skin and preserve inner body heat. In extreme conditions, the flow can be reduced almost to zero, at which point the AVAs will dilate to maintain tissue temperature and viability. (Examples are when the skin turns erythematous upon application of a cold pack or when the nose turns red in extremely cold weather.) On the contrary, during times of heat stress, the same vessels will dilate to allow more blood to circulate near the skin surface and thereby dissipate the heat. The catalyst for the vasoconstriction or vasodilation is a dual sympathetic neural control. Glabrous skin arterioles have sympathetic, norepinephrine innervation; nonglabrous (hairy) skin has both noradrenergic and cholinergic innervation. Nonglabrous skin vasculature also responds to the effects of local temperature changes (eg, with application of hot or cold packs).13
During periods of heat stress due to exercise or when the environmental temperature is higher than the blood temperature, thermoregulation is enhanced by the evaporation of fluid from the eccrine sweat glands. Initially the fluid produced is isotonic, but as it progresses toward the outer layer of the skin it becomes hypotonic by the reabsorption of the Na+ ions.11
Protection from Ultraviolet Rays
The presence of melanin in the skin provides color variation among individuals and protects the underlying tissue from the effects of ultraviolet rays. This is accomplished through the activity of the epidermal-melanin unit, composed of the melanocytes that produce melanin and keratinocytes that store melanin. In the stratum basale, there is one melanocyte for every 5–6 keratinocytes, located within 600–1200/mm2 of skin surface.1 Melanocytes synthesize melanin through a multistep process in which tyrosinase converts tyrosine into dihydroxyphenylalanine (DOPA) that is further transformed into melanin. The melanin migrates into the dendrites of the melanocytes. The dendritic ends of the keratinocytes phagocytose the melanocyte tips, allowing the melanin to enter into the keratinocyte where it is stored as melanosomes in quantities sufficient to absorb and reflect UV rays, thereby protecting the cellular DNA from the harmful effects of UV radiation. Increases in both melanin production and accumulation result from increased exposure to sunlight, and is evidenced by the darker color of ethnic groups who originated in geographical areas near the equator.1,14
Synthesis and Storage of Vitamin D
Vitamin D is necessary for calcium metabolism and bone formation; vitamins D2 and D3are both secosteroids (vitamin D2 is ergocalciferol; vitamin D3is cholecalciferol). The skin is the primary source of vitamin D3synthesis in the stratum basale and stratum spinosum.15 Keratinocytes express vitamin D hydroxylase enzymes that convert provitamin D3 (7-dehydrocholesterol) to vitamin D3. This process is stimulated by exposure to sunlight, occurs rapidly, and peaks within hours of exposure. Vitamin D3 is bound to a vitamin D–binding protein that carries it from the epidermis through the bloodstream and to the liver and kidneys where it is hydroxylated into an active form for calcium metabolism.
Vitamin D also contributes to the role of the epidermis in immunity by up-regulating the expression of antimicrobial peptides, and when the vitamin is lacking in the epidermis, there is a concordant increase in infection.16
Aesthetics and Communication
Skin color, texture, and hyper/hypopigmentation are a major component of an individual's appearance and contribute to sexual attraction. Apocrine sweat glands, located primarily in the axillary and perineal regions, are dependent upon sex hormones for development and their secretions contain sex pheromones that can influence social behavior.