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Skin sloughing is the process of shedding dead surface cells from the skin. It is most associated with cosmetic skin maintenance via exfoliation, but can also occur biologically or for medical reasons.
Keratinocytes are the main cell type of the epidermis. They form several layers of the skin. Life for a keratinocyte begins at the stratum basale layer. Cells here proliferate and move through the stratum spinosum and stratum granulosum. The topmost layer is called the stratum corneum. During sloughing, it is this layer that is removed. [1] As cells progress through the various layers to reach the stratum corneum, they undergo a process called cornification which transforms keratinocytes to corneocytes, effectively killing them. The resulting cell is flat, has no nucleus, and is surrounded by a cellular envelope. [2]
Calcium is the main regulator of keratinocytes and cornification. [3] A calcium concentration gradient differentiates the layers of skin with the lowest concentration being in the stratum basale. Calcium is also involved in different signaling pathways within skin cells. Phospholipase C triggers the release of intracellular calcium through inositol trisphosphate (IP3) and diacylglycerol (DAG). This increase of calcium then induces Protein Kinase C (PKC) which can alter keratinocyte transcription and further contribute to differentiation of the epidermis. Various other calcium channels and pathways are also used to form the skin.
Ultimately, the most superficial layer of the epidermis is designed[ by whom? ] as a barrier of dead keratinocytes which can then be sloughed away with little impact on the lower skin layers for many different reasons.
Intentional skin sloughing usually occurs as a result of cosmetic exfoliation, however, skin sloughing can also be the result of a medical condition or disease.
Common, nonthreatening skin conditions can cause sloughing.
Dry skin can medically be considered xeroderma. Although many forms of xeroderma exist, an individual need not be diagnosed with a disease to experience skin sloughing from dry skin. Dry skin can be a result of genetics. Harsh environments can lead to dry skin. These include exposure to excessively hot or cold temperatures and lack of humidity in the air.
Hyperhidrosis, or excessive sweating, can result in the peeling or sloughing of skin.
Sunburns transmit UVB to keratinocytes which causes them to undergo apoptosis.[ citation needed ] UVB radiation is dangerous as it can lead to DNA damage as well as damage of tumor-suppressor pro-apoptotic signaling pathways. The formation of sunburn cells is in response to the damage done by UVB exposure. Sunburned cells are those which have initiated apoptosis. The programmed cell death prevents the activity of damaged DNA or pathways that could otherwise lead to cancer. In the process, however, keratinocytes are killed. If the keratinocytes that apoptose are in the lowest layer of the skin, this can be an issue. Typically, however, keratinocytes in higher layers are able to slough away normally. The skin peeling that occurs as sunburns heal is due to this process.
Fungal infections that lead to this condition include ringworm, athlete's foot, and jock itch. Most fungal infections related to skin sloughing are caused by dermatophytes.[ citation needed ] Because this type of fungi require keratin to grow, they target the epidermis. The more superficial layers of the dermis often serve as a protective barrier against these fungi because they are dry and typically dead. If fungi are able to infect, however, it can cause inflammation in the skin and patches similar to psoriasis.
Bacterial infections include toxic shock syndrome, staph infection, and scarlet fever.[ citation needed ]
Dermatitis, or skin inflammation, involves skin peeling. Atopic dermatitis (or eczema) is the most common inflammatory skin disease. Skin may slough in a peeling fashion. Contact dermatitis arises from contact with a skin irritant. The ensuing irritation can cause sores and skin sloughing. and Seborrheic dermatitis which is associated with skin shedding through dandruff.
Psoriasis is the proliferation of keratinocytes. There are several factors that can contribute to the development of psoriasis. A prevalent mechanism of disease expression involves the malfunction and dysregulation of Receptor tyrosine kinase, whose abnormal hyper-activity activates other cell signaling pathways and eventually MAP kinase. This increases transcription and results in cell proliferation.[ citation needed ] Generally, psoriasis affects innate and adaptive immune system cells. Cells that are impacted in psoriasis include dendritic cells, T lymphocytes, and keratinocytes. Depending on the stage of the disease, the impacts may be larger on different cell types.[ citation needed ] The proliferation of epidermal cells is associated with an increase in skin sloughing.
Cutaneous T cell lymphoma and non-Hodgkin's lymphoma may include skin sloughing as a side effect. Cutaneous T cell lymphoma is a varying category of cancers in the lymph system. The effects of these lymphomas on the skin typically progress with the disease. It is most common to experience patches or plaques on the skin. The initial sloughing of the skin in this lymphoma can be confused for nonthreatening inflammatory conditions due to the lack of cancer cells in the affected areas.[ citation needed ]
Also known as toxic epidermal necrolysis, Stevens Johnson Syndrome causes entire sheets of skin to be lost. Apoptosis of associated cells in the epidermis initiates the process. [4]
Certain conditions should be treated with medication, but skin sloughing caused by dry skin may be treated without medical intervention. Dry skin can be treated with moisturizers.[ citation needed ] The least irritating to the skin are typically unscented.
Individuals prone to dry skin or skin sloughing may use a number of methods to prevent the condition in the first place. Decreasing exposure to harsh environments can decrease dry, peeling skin.
If professional help is necessary, individuals can visit a dermatologist.
Skin is the layer of usually soft, flexible outer tissue covering the body of a vertebrate animal, with three main functions: protection, regulation, and sensation.
7-Dehydrocholesterol (7-DHC) is a zoosterol that functions in the serum as a cholesterol precursor, and is photochemically converted to vitamin D3 in the skin, therefore functioning as provitamin-D3. The presence of this compound in human skin enables humans to manufacture vitamin D3 (cholecalciferol). Upon exposure to ultraviolet UV-B rays in the sun light, 7-DHC is converted into vitamin D3 via previtamin D3 as an intermediate isomer. It is also found in the milk of several mammalian species. Lanolin, a waxy substance that is naturally secreted by wool-bearing mammals, contains 7-DHC which is converted into vitamin D by sunlight and then ingested during grooming as a nutrient. In insects 7-dehydrocholesterol is a precursor for the hormone ecdysone, required for reaching adulthood. 7-DHC was discovered by Nobel-laureate organic chemist Adolf Windaus.
The integumentary system is the set of organs forming the outermost layer of an animal's body. It comprises the skin and its appendages, which act as a physical barrier between the external environment and the internal environment that it serves to protect and maintain the body of the animal. Mainly it is the body's outer skin.
Psoriasis is a long-lasting, noncontagious autoimmune disease characterized by patches of abnormal skin. These areas are red, pink, or purple, dry, itchy, and scaly. Psoriasis varies in severity from small localized patches to complete body coverage. Injury to the skin can trigger psoriatic skin changes at that spot, which is known as the Koebner phenomenon.
A blister is a small pocket of body fluid within the upper layers of the skin, usually caused by forceful rubbing (friction), burning, freezing, chemical exposure or infection. Most blisters are filled with a clear fluid, either serum or plasma. However, blisters can be filled with blood or with pus.
Keratinocytes are the primary type of cell found in the epidermis, the outermost layer of the skin. In humans, they constitute 90% of epidermal skin cells. Basal cells in the basal layer of the skin are sometimes referred to as basal keratinocytes. Keratinocytes form a barrier against environmental damage by heat, UV radiation, water loss, pathogenic bacteria, fungi, parasites, and viruses. A number of structural proteins, enzymes, lipids, and antimicrobial peptides contribute to maintain the important barrier function of the skin. Keratinocytes differentiate from epidermal stem cells in the lower part of the epidermis and migrate towards the surface, finally becoming corneocytes and eventually being shed, which happens every 40 to 56 days in humans.
The epidermis is the outermost of the three layers that comprise the skin, the inner layers being the dermis and hypodermis. The epidermis layer provides a barrier to infection from environmental pathogens and regulates the amount of water released from the body into the atmosphere through transepidermal water loss.
A skin condition, also known as cutaneous condition, is any medical condition that affects the integumentary system—the organ system that encloses the body and includes skin, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment.
The stratum corneum is the outermost layer of the epidermis. Consisting of dead tissue, it protects underlying tissue from infection, dehydration, chemicals and mechanical stress. It is composed of 15–20 layers of flattened cells with no nuclei and cell organelles.
Desquamation, or peeling skin, is the shedding of dead cells from the outermost layer of skin.
Ceramides are a family of waxy lipid molecules. A ceramide is composed of sphingosine and a fatty acid joined by an amide bond. Ceramides are found in high concentrations within the cell membrane of eukaryotic cells, since they are component lipids that make up sphingomyelin, one of the major lipids in the lipid bilayer. Contrary to previous assumptions that ceramides and other sphingolipids found in cell membrane were purely supporting structural elements, ceramide can participate in a variety of cellular signaling: examples include regulating differentiation, proliferation, and programmed cell death (PCD) of cells.
The stratum spinosum is a layer of the epidermis found between the stratum granulosum and stratum basale. This layer is composed of polyhedral keratinocytes. These are joined with desmosomes. Their spiny appearance is due to shrinking of the microfilaments between desmosomes that occurs when stained with H&E. Keratinization begins in the stratum spinosum, although the actual keratinocytes begin in the stratum basale. They have large pale-staining nuclei as they are active in synthesizing fibrillar proteins, known as cytokeratin, which build up within the cells aggregating together forming tonofibrils. The tonofibrils go on to form the desmosomes, which allow for strong connections to form between adjacent keratinocytes. The stratum spinosum also contains Langerhans cells, which functions as a macrophage by engulfing bacteria, foreign particles, and damaged cells that occur in this layer.
UV-induced apoptosis UV-induced apoptosis is an adequate (physiological) reaction of a cell damaged by UV radiation (UVR) in a sufficiently large (lethal) dose and it prevents the disordered destruction of UV damaged cells by help necrosis. Cell elimination by apoptosis occurs when UV-induced cell damage which cannot be repaired by the intracellular repair system exceeds at it certain limit. Through apoptosis, the cells are self-disassembled into compartments with their subsequent utilization. The first time sign of the beginning of the apoptosis system is working in a UV damaged cell is the activation of restriction enzymes, which divide cell DNA into fragments convenient for utilization. But too large a dose of UVR can lead to breakdown (inactivation) of the energy-dependent mechanism of apoptosis. In this case, cell destruction occurs randomly, not orderly, and during a significantly longer time interval. UV-irradiated cells do not change their appearance for a long time [1, 6], as a result of which the researchers may make the erroneous conclusion that “revealed an unexpected response to a dose at which a higher dose of UV increased the viability of keratinocytes” [2]. The fact that UV-induced apoptosis at high doses of UVR begins to be replaced by necrosis was established in 2000 [3]. For keratinocytes, the proportion of cells that have elimination by help apoptosis, with an increase in UVR dose can reach to achieve 45%, but with a further increase in the dose of UVR, destruction of damaged cells by help necrosis and the part of cells that eliminated by apoptosis begins to decrease [4, 11]. In the dose range of UVR from “lethal” to “super-lethal”, “pro-inflammatory” apoptosis can be manifested, which was experimentally discovered in 2003 [5]. This may be the result of partial damage to the apoptosis mechanism by UV radiation [1]. If at moderate doses “pure” apoptosis does not cause an inflammatory reaction, then at sufficiently large doses, an inflammatory reaction arises due to pro-inflammatory apoptosis, which leads to the appearance of “fast” erythema for UV irradiated skin keratinocytes. Kinetic of “fast” erythema is much faster by the time of development of UV erythema caused by necrosis of UV damaged keratinocytes [6]. The most erythemogenic is UVB the spectral range of UVR, since radiation in this range is less absorbed by the outer layers of the skin, which allows UVB radiation, in contrast to UVC, to reach more deep layers skin and act on keratinocytes of the deep-lying basal layer of the epidermis of the skin. The ability to induce apoptosis for UVB and UVC radiation is due to the fact that the DNA of the nucleus [7] and / or mitochondria [8] of the cell absorbs UVR well in the UVC and UVB spectral range. Keratinocytes of the skin are in a state of programmed apoptosis, during which the keratinocytes of the basal layer are removed from it and during the transition through all layers of the epidermis within 28 days turn into flakes of the outer stratum corneum, which are subsequently desquamated. It is clear that the keratinocyte response to UV exposure will depend on what phase of programmed apoptosis the keratinocyte experienced UV exposure, and this is the main reason for the difference of the UV effect for UVC and UVB on the skin. There are also differences in the initiation of mitochondrial (internal) and caspase-dependent (external) apoptosis for the UVC and UVB spectral ranges [9]. Sunburn cells (SBS) are the keratinocytes in the process of UV-induced apoptosis. The appearance of SBC may be not associated with an inflammatory reaction, but the role of UV-induced apoptosis of skin keratinocytes in the development of UV erythema of the skin has been established, which allowed the development of a patent-protected METHOD FOR QUANTITATIVE ASSESSMENT OF APOPTOSIS SYSTEM [10], in which “the brightest lamp of skin display "(photoerythema) is used to diagnose the state of the body systems involved in the elimination of UV-induced damage. Such systems include the immune system, the intracellular repair system, the microcirculation system and not only.
The human skin is the outer covering of the body and is the largest organ of the integumentary system. The skin has up to seven layers of ectodermal tissue guarding muscles, bones, ligaments and internal organs. Human skin is similar to most of the other mammals' skin, and it is very similar to pig skin. Though nearly all human skin is covered with hair follicles, it can appear hairless. There are two general types of skin: hairy and glabrous skin (hairless). The adjective cutaneous literally means "of the skin".
Corneocytes are terminally differentiated keratinocytes and compose most of the stratum corneum, the outermost layer of the epidermis. They are regularly replaced through desquamation and renewal from lower epidermal layers and are essential for its function as a skin barrier.
Keratohyalin is a protein structure found in cytoplasmic granules of the keratinocytes in the stratum granulosum of the epidermis. Keratohyalin granules (KHG) mainly consist of keratin, profilaggrin, loricrin and trichohyalin proteins which contribute to cornification or keratinization, the process of the formation of epidermal cornified cell envelope. During the keratinocyte differentiation, these granules maturate and expand in size, which leads to the conversion of keratin tonofilaments into a homogenous keratin matrix, an important step in cornification.
Photoaging or photoageing is a term used for the characteristic changes to skin induced by chronic UVA and UVB exposure. Tretinoin is the best studied retinoid in the treatment of photoaging.
Poikiloderma vasculare atrophicans (PVA), is a cutaneous condition characterized by hypo- or hyperpigmentation, telangiectasia and skin atrophy. Other names for the condition include prereticulotic poikiloderma and atrophic parapsoriasis. The condition was first described by pioneer American pediatrician Abraham Jacobi in 1906. PVA causes areas of affected skin to appear speckled red and inflamed, yellowish and/or brown, gray or grayish-black, with scaling and a thinness that may be described as "cigarette paper". On the surface of the skin, these areas may range in size from small patches, to plaques, to neoplasms.
The epidermal differentiation complex (EDC) is a gene complex comprising over fifty genes encoding proteins involved in the terminal differentiation and cornification of keratinocytes, the primary cell type of the epidermis. In humans, the complex is located on a 1.9 Mbp stretch within chromosome 1q21. The proteins encoded by EDC genes are closely related in terms of function, and evolutionarily they belong to three distinct gene families: the cornified envelope precursor family, the S100 protein family and the S100 fused type protein (SFTP) family.