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Comparative Anatomy, Physiology, and Biochemistry of Mammalian Skin
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
The last component of the epidermal-dermal junction is the sub-basal lamina containing three types of fibrous structures; anchoring fibrils, microfibrils in bundles, and single collagen fibers. Anchoring fibrils (Figure 12) extend from the basal lamina to the dermis, where they can end in a reticular network. The midportion of these fibrils have a banded appearance with an irregular periodicity. Anchoring fibrils are usually more numerous beneath hemidesmosomes. Fibrils arranged in bundles usually extend from the finger-like projections of the basal lamina into the dermis. Each fiber is approximately 8 to 11 nm in diameter, with a beaded periodicity. In cross-section, it resembles a hollow tubular structure which is similar to the microfibrils found near the elastic fibers. No proper term has been designated for these fibrils. Briggaman and Wheeler suggest that they should be called microfibril bundles. The collagen fibers lie near the basal lamina, occur singly, and are randomly oriented. They are not arranged into bundles like those of the deeper dermis.192
Dermal manifestations of diabetes
Published in Robert A. Norman, Geriatric Dermatology, 2020
There are three types of diabetic bullae. The most common type has a non-inflammatory base, contains clear, sterile fluid, and heals without scarring35. Another unusual type heals with scarring, and with dystrophic epidermolysis bullosa, by forming a cleavage line below the dermo-epidermal junction by destroying the anchoring fibrils33,36. The third, and most unusual, type forms subepidermal bullae that mimic porphyria cutanea tarda. It occurs primarily in a photo-distribution7. These lesions measure about 0.5 cm to 1 cm, appear suddenly, and occur bilaterally with tense bullae primarily on the legs and feet. Occasionally they can be found on the hands as well4. It is important to keep in mind the differential for bullous diseases. This includes bullous impetigo, bullous pemphigoid, pemphigus vulgaris, epidermolysis bullosa acquisita, porphyria cutanea tarda, bullous erythema multiforme and insect bite reaction2.
Dermatitis herpetiformis
Published in Lionel Fry, Atlas of Bullous Diseases, 2020
tTG plays an important role in the cross-linking of connective-tissue fibers. This enzyme is found throughout the body and plays an active role in wound healing. tTG is synthesized by fibroblasts and keratinocytes and its primary role is stabilizing extracellular protein assemblies such as collagen fibrils, microfibrils, pericellular fibronectin matrix and basement membrane. In the healing skin, tTG is active in the dermal papillae and anchoring fibrils at the dermoepidermal junction. Interestingly, these are the sites of IgA deposition in DH. Type VII collagen is the major connective-tissue component of anchoring fibrils and is a potential substrate for tTG.
Skin proteomics – analysis of the extracellular matrix in health and disease
Published in Expert Review of Proteomics, 2020
Jörn Dengjel, Leena Bruckner-Tuderman, Alexander Nyström
One EB subtype with a particularly severe and interesting phenotype is recessive dystrophic EB (RDEB). It is caused by mutations in the COL7A1 gene that encodes collagen VII, the major protein constituent of the anchoring fibrils [150] (Figure 3). Although RDEB is monogenic, i.e. mutations in a single gene cause the disease, the consequences at tissue level are progressive and remarkably complex. Loss of collagen VII leads to lack of functional anchoring fibrils and to the separation of the epidermis from the dermis upon mechanical stress, clinically manifesting as skin blistering. But the loss of anchoring fibrils also destabilizes the dermal tissue architecture, and the blisters heal with scarring [151]. Repeated cycles of blistering and scarring become associated with generalized soft tissue fibrosis with advancing course of the disease. Although the clinical picture has been long known, the disease mechanisms remained elusive for a long time. Recent global proteomic analyses have delivered novel cues on molecular and cellular events contributing to the phenotype and on promising therapeutic targets.
Impairment of wound healing by reactive skin decontamination lotion (RSDL®) in a Göttingen minipig® model
Published in Cutaneous and Ocular Toxicology, 2020
Jessica M. Connolly, Robert S. Stevenson, Roy F. Railer, Offie E. Clark, Kimberly A. Whitten, Robyn B. Lee-Stubbs, Dana R. Anderson
Antibodies included (1) pan-laminin (Sigma L9393, dilution 1:100), (2) fibronectin (Sigma F6140, dilution 1:100), (3) collagen type VII (Sigma C6805, dilution 1:100) and (4) laminin 332 (Millipore MAB19562, dilution 1:40). Pan-laminin localises the lamina lucida of the basement membrane zone and appears consistently across the basement membrane zone when migration of the basal epithelium is almost completed and the cells are stationary. Fibronectin is a provisional matrix for wound healing that is expressed in the wound bed during early wound healing as a wide amorphous, dispersed material. It is tightly localised in the upper papillary dermis during basal epithelial cell migration (5–10 days). During later phases of wound-healing expression, it is more dispersed, amorphous and less intensely expressed. Collagen type VII, which demonstrates anchoring fibrils, is used to indicate dermal/epidermal adhesion and appears as a late event in wound healing. Laminin 332 is located in the lamina lucida and associated with hemidesmosomes. Disruption of laminin 332 localisation can represent poor basal epithelial cell adhesion.
Surgical management of hand deformities in patients with recessive dystrophic epidermolysis bullosa
Published in Journal of Plastic Surgery and Hand Surgery, 2020
Xianyu Zhou, Yan Zhang, Mengmeng Zhao, Yuluo Jian, Jinny Huang, Xusong Luo, Jun Yang, Di Sun
Epidermolysis bullosa (EB) is a group of rare genetic disorders characterized by increased skin fragility, blistering and scarring in response to minor mechanical injury [1]. Based on the location of the fragility and the level of skin cleavage, EB is classified into four major types: EB simplex (EBS), junctional EB (JEB), dystrophic EB (DEB) and Kindler syndrome [2]. DEB is caused by a mutation in the COL7A1 gene. This gene encodes type VII collagen, which makes up the anchoring fibrils in the sublamina densa. The defective anchoring fibrils allow easy epidermal detachment from the dermis, thus resulting in blisters [3,4]. DEB is categorized into two main subtypes: autosomal dominant DEB (DDEB) and recessive DEB (RDEB). These two subtypes are further mainly classified into DDEB generalized, DDEB acral, DDEB pretibial, DDEB pruriginosa, RDEB generalized severe, RDEB generalized intermediate, RDEB inversa, RDEB localized, RDEB pretibial and RDEB pruriginosa [2,5]. For DEB patients, mortality rates during infancy or early childhood are low if meticulous pediatric and dermatologic intensive care was provided.