Apoptosis as a Mechanism for Keratinocyte Death in Canine Toxic Epidermal Necrolysis

• Published in: Veterinary pathology Vol. 54; no. 2; pp. 249 - 253
• Main Authors: Banovic, F., Dunston, S., Linder, K. E., Rakich, P., Olivry, T.
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01-03-2017
• Subjects: Animals; Apoproteins - physiology; Caspase 3 - genetics; Caspase 3 - metabolism; Deoxyuracil Nucleotides - metabolism; DNA Nucleotidylexotransferase - metabolism; Dog Diseases - pathology; Dogs; Gene Expression Regulation, Enzymologic; In Situ Nick-End Labeling; Keratinocytes - pathology; Stevens-Johnson Syndrome - pathology; Stevens-Johnson Syndrome - veterinary; skin; apoptosis; erythema multiforme; toxic epidermal necrolysis
• ISSN: 0300-9858; 1544-2217
• DOI: 10.1177/0300985816666609

In humans and dogs, toxic epidermal necrolysis (TEN) is a life-threatening dermatosis characterized by sudden epidermal death resulting in extensive skin detachment. There is little information on the pathogenesis of keratinocyte cell death in canine TEN. We studied the occurrence of apoptosis in skin lesions of dogs with TEN to determine if apoptosis contributes to the pathogenesis of this disease. Immunostaining with antibodies to activated caspase-3 and the terminal deoxynucleotidyl-transferase (TdT)–mediated deoxyuridine triphosphate (dUTP) nick-end labeling technique revealed positive apoptotic keratinocytes in basal and suprabasal epidermal compartments in 17 biopsy specimens collected from 3 dogs with TEN and 16 from 3 dogs with erythema multiforme (EM). There was no significant difference in the number of positively stained epidermal cells between TEN and EM. These results suggest that apoptosis of epidermal keratinocytes and lymphocytic satellitosis represent one of the early steps in the pathogenesis of canine TEN, as in the human disease counterpart.