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Phytomedicines Targeting Antibiotic Resistance through Quorum Sensing and Biofilm Formation Associated with Acne Vulgaris
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Isa A. Lambrechts, Namrita Lall
There is a range of theories about the sequence of these pathogenic factors and their contribution to the progression of acne vulgaris, which have not yet been fully answered. It is believed that follicular hyperkeratinization (the abnormal shedding of the skin) is the first step in the pathogenic pathway, blocking the pilosebaceous unit and leading to excess sebum accumulation. Comedone formation is a combined effect between the overproduction of keratinocytes and a reduction in the shedding of keratocytes due to the skin cells’ inability to separate from one another. Comedones form when keratinocytes block the pilosebaceous unit that results in the accumulation of sebum in the unit. Several factors contribute to hyperkeratinization. These factors include the lack of linoleic acid in the sebum due to hyperseborrhea, resulting in abnormal keratinocyte differentiation. Cytokines such as cytokine interleukin-1 alpha (IL-1α) present in the follicle are believed to induce hyperkeratinization. Furthermore, it was recently discovered that the acne-inducing bacteria Cutibacterium acnes secrete a glycocalyx polymer that is a component of the bacterial biofilm. This secretion is incorporated in the sebum, which increases cohesion between the keratinocytes. This results in a blockage in the pilosebaceous unit and results in the formation of a comedone. It is therefore plausible that the initial step of acne pathogenesis could be the colonization and biofilm formation of C. acnes instead of hyperkeratinization (Dessinioti and Katsambas, 2010; James, Burkhart, and Morrell, 2009; Pawin et al., 2004).
Dermal and Transdermal Drug Delivery Systems
Published in Tapash K. Ghosh, Dermal Drug Delivery, 2020
Kenneth A. Walters, Majella E. Lane
Calluses, corns and warts generally manifest as hyperkeratinization of the skin. It follows that actives which are keratolytic or which dissolve the intracellular keratin should be useful in the management of such conditions. The formulations currently available to treat these skin problems are predominantly topical solutions, gels or creams of salicylic acid or DTPs in the form of adhesive (rubber or karaya) matrices containing salicylic acid, which are applied as pads or disks to the affected area. Salicylic acid collodion preparations, which are nitrocellulose solutions that dry on the skin to leave a film, are also available. Salicylic acid may be formulated alone or with other components that also promote keratolysis (most commonly lactic acid). Podophyllotoxin is available as an alcohol-based topical solution or cream for warts affecting the genital areas. Imiquimod is also available in cream form for the same indication.
Hidradenitis Suppurativa
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
HS is a disease of follicular hyperkeratinisation in apocrine gland bearing skin. The exact pathophysiology of HS development is uncertain; however, HS has several key contributing factors. There is a definite role for genetic predisposition as well as hormonal abnormalities and immune dysregulation in the development of HS. However, further research is required to determine how these factors can be related back to patient treatment. Conservative management has been studied for mild HS disease, including the use of antibiotics, but these do not alter the natural history of disease progression and should be avoided for long periods of time. Surgery, in particular WLE, offers the best chance at cure during long-term follow-up, yet carries a significant morbidity.
Transfollicular elimination of sebaceous glands in a patient with disseminate and recurrent infundibulofolliculitis
Published in Baylor University Medical Center Proceedings, 2021
Mahmud Alkul, Travis S. Dowdle, Jay Truitt, Michelle B. Tarbox
Differential diagnoses for DRIF include bacterial and fungal folliculitis, follicular eczema, keratosis pilaris, and truncal acne, among others.3 Although rare Pityrosporum yeast were demonstrated on biopsy, their presence in only some of the follicles make this diagnosis less likely. Follicular eczema is characterized by inflammatory infiltrate not limited to the infundibulum of the hair follicle.2 Keratosis pilaris is clinically significant for hyperkeratinization.2 Lesions may be differentiated from truncal acne vulgaris by histopathology revealing follicular dilation, increased sebum production, and accumulation of keratin.4 DRIF has been associated with other dermatologic conditions such as hidradenitis suppurativa, a chronic inflammatory disease of the pilosebaceous unit, especially in patients with trisomy 21.5
Effects of Type 2 Diabetes Mellitus on Gene Expressions of Mouse Meibomian Glands
Published in Current Eye Research, 2020
Erdost Yıldız, Noushin Zibandeh, Berna Özer, Afsun Şahin
Lastly, we have also investigated the effects of these genes on various protein groups and pathways. Several important protein groups were affected from type 2 DM, like ribosome, proteasome, cytoskeleton and aldehyde dehydrogenase-related proteins were up-regulated; on the other hand, like cornified envelope and histone-related proteins were down-regulated. Up-regulation of cornified envelope-related gene expressions also has been observed in human subjects.22,29 Up-regulation of cornified envelope-related genes could lead to keratinization and proliferation of human keratinocytes in ocular surface. The hyperkeratinization process could be one of the main components of MG dysfunction. We also have shown a significant decrease in gene related with WNT signaling and pentose phosphate pathways in MGs of type 2 DM mice. Both pathways have certain roles in complications of type 2 diabetes mellitus, but their roles in MG dysfunction and dry eye disease are still unknown.30,31
Pharmacotherapeutic approaches for transportation of anticancer agents via skin
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Pravin Shende, Jai Vaidya, R. S. Gaud
The largest and the most heterogeneous organ of our body, skin is made up of three layers: epidermis, dermis and hypodermis. Epidermis, the outermost avascular layer made up of keratinocytes, plays a key role in delivering substances across the skin. (Figure 2) The differentiation of epidermis from inside to outside towards the outer surface of skin gives rise to stratum corneum which forms the prime barrier for the delivery of drugs due to its composition. The stratum corneum is made up of packed layer of corneocytes with the lipid matrix composed of cholesterol, free fatty acids and ceramides. These lipids are present in two co-existing lamellar phases: one is long (with repeat distance of 13 nm) and second is short (with constant distance of 6 nm). The space between two head and tail domains is less than 5 nm. The deep within the keratinocytes, several melanocytes (produce melanin) and Langerhans cells (antigen presenting cells) are embedded which are involved mainly in development of skin tumours [22]. The exposure to environmental factors such as UV-rays causes tumour lesions ensuing into hyperkeratinization, which impedes the delivery of drug through the skin [23]. To initiate the immune response to treat actinic keratosis, it is imperative to pass the anti-cancer or immunomodulator drugs through this hyperkeratotic stratum corneum, which further act on Langerhans cells to release pro-inflammatory mediators. Hence, it is necessary to optimize the topical formulations, which will penetrate through the deep layers of skin to reach the tumours.