Primary follicular dystrophy with scarring dermatitis in C57BL/6 mouse substrains resembles central centrifugal cicatricial alopecia in humans.
Document Type
Article
Publication Date
2011
Keywords
Alcohol-Oxidoreductases, Alopecia, Animals, Granuloma, Hair-Follicle, Immunohistochemistry, Mice-Inbred-C57BL, Rodent-Diseases, Species-Specificity, Vitamin-A
JAX Location
see Reprint Collection (a pdf is available)
JAX Source
Vet Pathol 2011 Mar; 48(2):513-24.
First Page
513
Last Page
524
Abstract
A number of C57BL/6 (B6) substrains are commonly used by scientists for basic biomedical research. One of several B6 strain-specific background diseases is focal alopecia that may resolve or progress to severe, ulcerative dermatitis. Clinical and progressive histologic changes of skin disease commonly observed in C57BL/6J and preliminary studies in other closely related substrains are presented. Lesions develop due to a primary follicular dystrophy with rupture of severely affected follicles leading to formation of secondary foreign body granulomas (trichogranulomas) in affected B6 substrains of mice. Histologically, these changes resemble the human disease called central centrifugal cicatrical alopecia (CCCA). Four B6 substrains tested have a polymorphism in alcohol dehydrogenase 4 (Adh4) that reduces its activity and potentially affects removal of excess retinol. Using immunohistochemistry, differential expression of epithelial retinol dehydrogenase (DHRS9) was detected, which may partially explain anecdotal reports of frequency differences between B6 substrains. The combination of these 2 defects has the potential to make high dietary vitamin A levels toxic in some B6 substrains while not affecting most other commonly used inbred strains.
Recommended Citation
Sundberg JP,
Taylor D,
Lorch G,
Miller J,
Silva KA,
Sundberg BA,
Roopenian D,
Sperling L,
Ong D,
King LE,
Everts H.
Primary follicular dystrophy with scarring dermatitis in C57BL/6 mouse substrains resembles central centrifugal cicatricial alopecia in humans. Vet Pathol 2011 Mar; 48(2):513-24.