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Diagnosing Skin Disease
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
The replacement rate of the cornified cells in the stratum corneum, the outermost layer of the epidermis, is approximately 2 weeks with some variation by body site and age. This turnover normally occurs incrementally through the shedding of individual cornified cells throughout the course of daily life. This process is largely imperceptible in healthy skin, but it can become apparent when the process of normal keratinization is disrupted. Should this occur, a significant scale can form on the surface of the skin, which results in visual and textural changes. This disruption of skin function can be the result of a variety of underlying conditions that can range from genetic abnormalities, such as ichthyosis, to inflammatory changes, such as psoriasis, to the exogenous influence of factors, such as medication application and repetitive friction.
Comparative Anatomy, Physiology, and Biochemistry of Mammalian Skin
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
Keratinization is the process by which epidermal cells differentiate. Keratin filaments, keratohyalin, and membrane-coating granules are formed in large numbers during keratinization. As the basal epithelial cells migrate upward, the volume of the cytoplasm increases, and organelles and tonofilaments are prominent. The tonofilaments are opaque and measure 5 nm in diameter. They aggregate into dense tonofibrils and filamentous substance between them may, at times, be visible. Loose tonofibrils may also be present. In the spinosum layers, membrane-coating granules are found, along with bundles of tonofibrils which usually have a compact appearance. Some tonofibrils may resemble those of the stratum basale layer.
The skin
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The outermost layer of the skin, the epidermis, is a constantly self-renewing structure composed primarily of keratinocytes along with melanocytes, Langerhans cells, and Merkel cells. Keratinocytes are cells that produce keratin, a polymer of intermediate filaments that forms the intracellular cytoskeleton, providing structural integrity. The process of keratinization is a highly regulated process that results in terminally differentiated, anucleate, largely impermeable keratinocytes on the skin surface. The epidermal keratinocytes are organized into 4 distinct layers from bottom to the top: (a) the basal layer (stratum basale), (b) the spinous/squamous/prickle cell layer (stratum spinosum), (c) the granular layer (stratum granulosum), and (d) the cornified layer (stratum corneum) (Figure 19.1B).
Higher degree of keratinization correlated with severe bone destruction in acquired Cholesteatoma
Published in Acta Oto-Laryngologica, 2023
Yisi Feng, Zhuohao Li, Wuhui He, Ying Xiong, Yu Si, Zhigang Zhang
In this study, we identified highly keratinized ectopic epidermis in cholesteatoma matrix as a potential inducer of bone erosion. Keratinization is known to be a process involving keratinocyte differentiation, during which proliferative basal cells expressing K5 and K14 are keratinized and transit to the postmitotic suprabasal layer with upregulated K1 and K10. In stratified squamous epithelium, epithelial cells are gradually cornified and die as they move to the superficial cell layer, forming the stratum corneum [13]. Therefore, the expression levels of K1 and K10, as well as the thickness of the stratum corneum, can be regarded as markers of epidermal keratinization. K1 and K10 were also detected in clinical samples of cholesteatoma [14,15]. In the present study, high K10 expression and a thicker stratum corneum in the cholesteatoma matrix correlated with more severe bone resorption induced by cholesteatoma. Animal experiments also supported these findings. The implantation of highly keratinized skin from mouse tails resulted in more damage to mice calvaria. It was suggested that in cholesteatoma, these highly differentiated keratinocytes were induced by fibroblasts from the perimatrix [16]. Furthermore, K1, the ligand of K10, can maintain the integrity and mechanical stress of the epidermis and is involved in decreasing the release of IL-18, which is known to synergize with IL-12 and IFN-γ and inhibit osteoclast formation [17]. Therefore, it was implied that K1 could promote the process of osteoclastogenesis, which suggested that bone destruction tended to be caused by the epidermis that was more keratinized.
Postoperative Complications of Dermis-Fat Autografts in the Anophthalmic Socket
Published in Seminars in Ophthalmology, 2018
Victoria Starks, Suzanne K. Freitag
If the epidermis is not completely removed from the graft, dermal appendages and keratin may grow in the socket. Graft hirsutism or retained cilia are a common complication, noted in 3.8–25% of dermis-fat grafts, although often self-limited and asymptomatic.4,5,19,20 If retained cilia are noted prior to epithelialization of the graft, they may be simply epilated. Once the conjunctival epithelium has covered the dermis, retained cilia may be noted below the conjunctiva. Fortunately, in most such cases, the follicle degrades. Keratinization of the socket was noted in 3% of patients in a large series.11 Keratinized epithelium appears as flat, white plaques on or adjacent to healthy conjunctiva and produces a thick, white keratin discharge. Keratinization is a cosmetic issue, but may also lead to irritation and poor tolerance of a prosthesis. Large areas of keratinized epithelium may be excised and the underlying dermis may be left to re-epithelialize from the freshened conjunctival edges. Prevention of these complications is possible with attention to detail when de-epithelializing the graft at the time of surgery.
Diagnosis and management of limbal stem cell deficiency, challenges, and future prospects
Published in Expert Review of Ophthalmology, 2021
C. Maya Tong, Bonnie He, Alfonso Iovieno, Sonia N. Yeung
Ocular exposure can also be minimized by correcting eyelid malposition and reconstructing the conjunctiva and fornices [15,58]. Adnexal abnormalities seen with LSCD might include fornix foreshortening, symblepharon, ankyloblepharon, conjunctival scarring, lagophthalmos, ectropion, entropion, distichiasis, trichiasis, and keratinization of the lid margin and ocular surface [58]. Before adnexal reconstruction is attempted, ocular surface keratinization may be addressed. Squamous metaplasia associated keratinization is thought to be caused by a local vitamin A deficiency [78]. This may be from impaired delivery in cicatrized tissues, or incapacity of the cicatrized tissues to transform vitamin A into the active form required by epithelial tissues, all-trans retinoic acid [78]. Topical vitamin A or retinoic acid supplementation may cause reversal of ocular surface keratinization and improve regulation and differentiation of corneal epithelial cells [57,78,79]. It may also aid in the recovery of goblet cells, contributing to overall improvement of the tear film [57]. Once keratinization has been maximally regressed and tissues are stable, a variety of reconstructive procedures are available [57]. In general, cicatricial adhesions should be lysed. Fornices can be reconstructed with tissue substitutes including conjunctiva, oral or nasal mucosa, or amniotic membrane grafts. Mucous membrane grafts can be used to correct lid margin keratinization. Procedures for eyelid correction and reconstruction should be addressed in a multidisciplinary manner, involving otolaryngology and oculoplastic specialists where appropriate, and staged to minimize ocular exposure and maximally improve the ocular surface before consideration of limbal stem cell transplantation (LSCT) [57,58].