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Anatomy, physiology, and histology of the skin
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
This epidermal layer is exclusively found in areas of thick skin, such as the soles of the feet. It is a transparent layer of dead epidermal cells characterised by the presence of densely packed granules of the protein eleidin, an intermediate product between keratin and keratohylin. Keratohylin is crucial in the keratinisation of epithelial cells, causing keratin molecules to aggregate and cross-link whilst simultaneously dehydrating the cells themselves. This allows for the formation of the tough and waterproof outer layers of epidermal cells.
Introduction to dermatological treatment
Published in Richard Ashton, Barbara Leppard, Differential Diagnosis in Dermatology, 2021
Richard Ashton, Barbara Leppard
Wound healing occurs in three stages: An influx of inflammatory cells to aid reabsorption of necrotic cells and prevent infection. This causes erythema and exudate.The formation of granulation tissue and revascularisation. At this stage there is a reduction in exudate.Migration of epidermal cells to cover the wound and growth of new connective tissue underneath.
Comparative Anatomy, Physiology, and Biochemistry of Mammalian Skin
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
The epidermis is composed of two primary cell types, the keratinocytes and the nonkeratinocytes, which include melanocytes, Merkel cells, Langerhans’ cells, and indeterminate cells. The epidermis is separated from the underlying dermis by the basement membrane. Epidermal keratinocytes can be classified in layers above the basement membrane; starting with the stratum basale and continuing upward to the stratum spinosum, stratum granulosum, stratum lucidum, and ending with the outermost stratum corneum. The differences in cell structure seen among these layers primarily relate to the process of keratinization and formation of the complex stratum corneum barrier. When investigators generically refer to epidermal cells, they are generally speaking of the stratum basale cells (basal keratinocytes). Biochemically, these are the most active cells in the epidermis and form the precursors which ultimately form the intracellular protein and extracellular lipid components of the stratum corneum barrier.
Epigenetic control of skin immunity
Published in Immunological Medicine, 2023
The skin is an organ that is constantly exposed to external stimuli and functions as the first-line of defense against invasion to initiate immune responses [1]. It maintains homeostasis by rapidly responding to external environmental signals that are sensed by the outermost layer of the skin, the epidermis. Upon receiving external stimuli, epidermal cells are first activated by themselves, and then, activate surrounding epidermal cells and immune cells [2–4]. This strengthens both the structural and immunological barriers of the skin, and preemptively prepares the skin for a putative invasion by external stimuli. The activated epidermal cells and responding immune cells also possess a rapid recovery system that enables a quick return to the steady state after exposure to external stimuli. The plasticity of epidermal and immune cells, which can flexibly shift between steady and activated states, is therefore responsible for the maintenance of skin homeostasis [1,5]. Crosstalk with immune cells is also active in other non-immune skin cells, including fibroblasts, nerve cells, and vascular endothelial cells. Thus, non-immune cells as well as immune cells support skin immunity through the reciprocal production of immune-regulatory factors. Disruption of the appropriate crosstalk between these cells results in prolonged inflammation as well as abnormal activation and differentiation of skin component cells, which may manifest as chronic inflammatory skin diseases, such as psoriasis and atopic dermatitis [1,5].
Occupational exposure assessment with solid substances: choosing a vehicle for in vitro percutaneous absorption experiments
Published in Critical Reviews in Toxicology, 2022
Catherine Champmartin, Lisa Chedik, Fabrice Marquet, Frédéric Cosnier
As shown in Figure 1, the epidermis is a coating epithelium. The viable epidermis, with a thickness varying roughly from 30 to 100 µm, consists of the stratum basale, the stratum spinosum, and the stratum granulosum (SG). It is separated from the dermis by the basement membrane. The viable epidermis is innervated but not vascularized, and its nutritional needs are met through diffusion from the basement membrane. One of its functions is as a barrier against environmental aggression. The majority (80%) of epidermal cells are the keratinocytes; the other cell types found in the epidermis are melanocytes, Langerhans cells, and Merkel cells. Specialized junctions called corneodesmosomes or desmosomes (to which the tonofilaments are tethered) (Prost-Squarcioni 2006) link keratinocytes together and contribute to the outside-in epidermal barrier. The highly protective outermost layer of the epidermis – the stratum corneum (SC) – is constantly renewed. It is about 10–40 µm thick and composed of 15–25 layers of corneocytes, i.e. dead and keratinized cells resulting from the terminal differentiation of keratinocytes that have migrated to the skin’s surface.
Co-encapsulation of metformin and ginger into the liposomes: in vitro characterization and in vivo anti-psoriasis evaluation
Published in Drug Development and Industrial Pharmacy, 2021
Kiana Jenabikordi, Behzad Sharif Makhmal Zadeh, Anahita Rezaie
Histopathologic evaluation of the IMQ-treated group (G14) revealed different lesions including thickening of the epidermis due to hyperplasia of keratinocytes (acanthosis) and infiltrations of inflammatory cells in the dermis around vessels and between the collagen fibrils. Inflammatory cells were seen on the surface of the epidermis and between epidermal cells. Also increasing keratin layers on the epidermis (hyperkeratosis) and dilation of capillaries were happened (Figure 5(A)). Described microscopic characteristics indicated psoriasis lesion formation and resistance 7, 21, and 28 days after IMQ treatment. These features in IMQ- treated mouse skin previously were reported by Lin et al. All groups showed time-dependent different degrees of healing effects. After 1 week of treatment (Figure 5(B,E)), G1 showed a better healing effect in comparison with others. The thickness of epidermis and keratin layers were thinner and less inflammatory cell infiltration was observed in G1 (Figure 5(B)). After a one-week treatment, the mentioned lesions in all groups except G1 and G2 were the same as the positive control (Figure 5(H)). Described lesions demonstrated different degrees of healing after 21 and 28 days of treatment (Figure 5(C,D)). The best healing effect provided by G1 followed by G2 that after 21 days of treatment, no psoriatic lesions were found. Microscopic evaluations of the skin in other groups G3-G10 show different degrees of psoriasis lesions healing during treatment (Figure 5(B–G)). Liposomal groups provided better healing properties than non-liposomal ones.