Peer-reviewed veterinary case report
Skin fragility and scarring in a young dog with cutaneous asthenia
By Bellini, M H et al.·Published in Veterinary dermatology·2009·Energy and Nuclear Research Institute, Brazil·View original on PubMed →
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Original publication title: Increased elastic microfibrils and thickening of fibroblastic nuclear lamina in canine cutaneous asthenia.
- Species:
- dog
Plain-English summary
An 8-month-old female crossbreed dog was brought in with multiple skin lacerations and irregular scars, along with very stretchy skin that tore easily with minor trauma. This condition, known as cutaneous asthenia, is a genetic disorder that affects the skin's connective tissue, making it fragile and prone to injury. Upon examination, the dog's skin showed abnormal collagen structure, which contributed to its hyperextensibility and poor healing. Unfortunately, there is no cure for this condition, but managing the dog's environment to prevent injuries and providing supportive care can help improve her quality of life.
People also search for: dog skin problems · cutaneous asthenia in dogs · managing dog skin injuries · dog stretchy skin treatment
Abstract
Cutaneous asthenia is a hereditary connective tissue disease, primarily of dogs and cats, resembling Ehlers-Danlos syndrome in man. Collagen dysplasia results in skin hyperextensibility, skin and vessel fragility, and poor wound healing. The purpose of this study was to describe the histological findings in a dog with a collagenopathy consistent with cutaneous asthenia. An 8-month-old crossbreed female dog presented with lacerations and numerous atrophic and irregular scars. The skin was hyperextensible and easily torn by the slightest trauma. Ultrastructurally, the dermis was comprised of elaunin and oxytalan microfibrils. These are immature fibres in which the fibrillar component is increased but elastin is reduced. Collagen fibres were profoundly disorganized. The fibrils had a highly irregular outline and a corroded appearance when viewed in cross-section, and were spiralled and fragmented in a longitudinal view. Dermal fibroblasts displayed a conspicuous thickening of the nuclear lamina. Nuclear lamins form a fibrous nucleoskeletal network of intermediate-sized filaments underlying the inner nuclear membrane. Mutations in lamins or lamin-associated proteins cause a myriad of genetic diseases collectively called laminopathies. Disruption of the nuclear lamina seems to affect chromatin organization and transcriptional regulation of gene expression. A common link among all laminopathies may be a failure of stem cells to regenerate mesenchymal tissue. This could contribute to the connective tissue dysplasia seen in cutaneous asthenia.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/19192263/