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invaginates into it, by attachment via collagen and elastin. The hypodermis predominantly consists of adipocytes. 2.1.4. Skin appendages Skin appendages are structures derived from the skin that serve particular functions. The appendages are: Hair follicles Sweat glands ○ Eccrine glands ○ Apocrine glands Sebaceous glands. Hair follicles are found in skin covering the entire surface of the body except for the palms, soles and glans penis. The face and scalp have the greatest densities of hair follicles. Each hair shaft is composed of a medulla, a cortex of keratinocytes and an outer cuticle. Each follicle consists of two root sheaths which surround the hair bulb. The inner root sheath is derived from the epidermis and the outer root sheath from the dermis. The follicles are lined by germinative cells and melanocytes, which produce keratin and pigment, respectively. Erector pili muscles are associated with each hair shaft. These muscles function to erect the hair follicles by contracting in the cold or during times of fear and emotion, leading to goose bumps. They also aid drainage of sebaceous glands into the hair follicles. There are over 2.5 million sweat glands in the dermis over most of the body. Eccrine glands are found in the skin covering all body surfaces and secrete an odourless hypotonic fluid under sympathetic control. They are particularly abundant in the forehead, palms, soles and axillae. Apocrine glands are larger than eccrine glands and emit thicker, odourless secretions, which are metabolised by skin bacteria to produce body odour. They are found in the axilla, the anogenital region and areolar tissue and emit secretions in response to heat, under sympathetic control. Sebaceous glands are holocrine glands derived from the epidermis. They are closely associated with hair follicles and are therefore absent in hairless skin. In response to androgenic stimulation, sebaceous glands secrete cells which break down to release their lipid cytoplasm directly onto the skin (sebum). The functions of sebum include: 6 Textbook of Plastic and Reconstructive Surgery Antimicrobial action Provision of vitamin E to superficial skin layers Maintain integrity of skin barrier Thermoregulation. 3. WOUND HEALING Wound healing is classically divided into four phases: haemostatic, inflammatory, proliferative and remodelling. It is worth noting, however, that some authors currently consider the haemostatic phase to be part of the inflammatory phase. This simplified categorisation incorporates a wide array of immune cells, signalling pathways and chemical mediators, which contribute to the formation of a healed wound. When wounds penetrate the full thickness of the skin, they always produce a scar. The haemostatic phase is typically an immediate and short-lived phase, lasting only from seconds to minutes. In response to injury, prostaglandins are released from endothelial cells and platelets, leading to vasoconstriction. Collagen exposed in the damaged vessel walls is adhered to by platelets, which then release chemoattractant substances that help to initiate the coagulation cascade. The result is formation of a fibrin–platelet matrix, which functions to control haemorrhage, concentrate growth factors at the site of damage and form the scaffold required for subsequent wound healing processes (Martin, 1997). Hairy Skin Hairless Skin Epidermis Hair shaft Opening of sweat duct Dermal papillae Erector pili muscle Sebaceous gland Hair follicle Eccrine sweat duct Eccrine sweat gland Dermis Hypodermis Superficial arteriovenous plexus Papillary dermis Reticular dermis Meissener’s Corpuscle Sweat Duct Deep arteriovenous plexus Subcutaneous fat Figure 1.1. The skin with its separate layers and appendages. Principles of Reconstructive Surgery 7 The inflammation phase typically lasts between 3 and 5 days. It is important for limiting wound contamination and induction of the proliferative phase of healing. Vasodilatation and increased capillary leakiness occur, promoting delivery of nutrients and immune cells to the site of injury and thus causing tissue oedema. The stimulus for this is provided by prostaglandins, kinins, histamine, serotonin and bacterial components. Inflammatory cytokines and other mediators (e.g. platelet-derived growth factor, tumour necrosis factor α, interleukin-1) attract granulocytes to the site of injury soon after the injury has occurred. Neutrophils act by phagocytosing debris and microorganisms. These actions are facilitated by the release of proteases to break down damaged tissue and debris and the use of cellular reactive oxygen species to eliminate pathogens. Other immune cells involved in this phase are macrophages, which are terminally differentiated monocytes present in tissues. Monocytes migrate to the wound from local sites to become macrophages within 24–48 hours of injury. Macrophages participate in phagocytosis and are essential in the wound healing process via the release of growth factors. Regulation of the inflammatory phase is important because overstimulation or prolonged stimulation can damage local tissues and, in severe cases, can trigger the systemic inflammatory response syndrome. Conversely, insufficient inflammation and failure to induce proliferation can lead to development of a chronic wound. The proliferative phase begins soon after an
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