Gartner_BRS Cell Biology & Histology, 9e

BRS Cell Biology and Histology

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The incidence of malignant melanoma is rapidly increasing in the United States. According to the Ameri can Cancer Society, 97 610 new cases of invasive cutaneous melanoma are estimated to be diagnosed and to result in 7 990 deaths in the United States in 2023. A single-nucleotide polymorphism in the gene coding for the MC1R is responsible for the formation of loss-of-function MSH receptors, which results in the synthesis of pheomelanin and the lack of induction of DNA repair and antioxidant-forming pathways. Mutations in a number of tumor suppressor genes such as CDKN2A (p16), CDK4, RB1, CDKN2A (p19), PTEN/MMAC1 , and ras are also implicated in sporadic and hereditary melanoma. 2. Epidermal dendritic cells ( Langerhans cells ) originate in the bone marrow as monocytes that circulate the bloodstream. The monocytes that enter the dermis and then migrate into the epi dermis to take residence primarily in the stratum spinosum differentiate into epidermal den dritic cells. These independent cells make no adhesive junctions with keratinocytes. a. Epidermal dendritic cells express various immune-related transmembrane proteins, such as CD1a, major histocompatibility complex (MHC) I and MHC II, C3b receptors, and immuno globulin G (IgG) receptors that, once bound to ligands, initiate immune responses. b. These cells also function as antigen-presenting cells in immune responses to contact an tigens ( contact allergies ) and some skin grafts. They phagocytose antigens and travel to a lymph node where they present the epitope to T cells and thereby initiate a delayed-type hypersensitivity reaction . 3. Tactile epithelial cells ( Merkel cells ) are present in small numbers in the stratum basale , near areas of well-vascularized, richly innervated connective tissue. a. They are believed to be of neural crest origin but, because they possess desmosomes and keratin filaments, a nonneural ectodermal origin has also been suggested. b. Their pale cytoplasm contains small dense-core granules that are consistent with those in some cells of the diffuse neuroendocrine system and are presumed to house neurosecretory products. c. They synapse with axon terminals of myelinated sensory neurons that form Merkel cell-­ neurite complexes that probably function as mechanoreceptors . These mechanoreceptors appear to be more abundant in areas that require more acute sensory perception, as at the tips of fingers. D. Thick and thin skin are distinguished on the basis of the epidermal thickness . 1. Thick skin has an epidermis that is 400 to 600 μ m thick with a prominent stratum corneum, a well-developed stratum granulosum, and often a distinct stratum lucidum. It lines the palms of the hands and the soles of the feet. It lacks hair follicles, sebaceous glands, and arrector pili muscles. 2. Thin skin has an epidermis that is 75 to 150 μ m thick with a much less prominent stratum cor neum. Thin skin lacks stratum lucidum and sometimes also stratum granulosum, although it contains individual cells that are similar to the cells of these layers. Thin skin covers most of the body and contains hair follicles, sebaceous glands, and arrector pili muscles. PEARLS Epidermolysis bullosa (EB) is a group of hereditary diseases of the skin characterized by blister formation following minor trauma to the skin. These conditions are associated with weakening of the hemidesmosomes, resulting in fragile attachment between the epidermis and the dermis. The four major types of EB are EB simplex, junctional EB, dystrophic EB, and EB acquisita. They vary in the degree of severity and the locus of the genetic defect. More than 90% of EB is of the EB simplex type, in which the genetic defect occurs in the genes for keratin 5 and keratin 14, resulting in the formation of defective intermediate filaments that anchor and stabilize hemidesmosomes. In this condition, blistering occurs in the region of trauma, namely, on the hands and feet. The second most prevalent form is dystrophic EB (about 5% of the cases) in which the genetic defect involves type VII collagen that forms the anchoring fibrils. The number of anchoring fibrils is greatly reduced and results in numerous blisters throughout, not only in the skin but also in the epithelial lining of the esophagus. The skin and esophagus of affected individuals display severe scarring resulting from infections and lack of adequate healing. Many patients with dystrophic EB develop SCC, which is one of the principal causes of death in these individuals before they reach age 30 years. Clinical

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