Annals of the rheumatic diseases · 2006
Sexual dimorphism, but not testosterone itself, is responsible for ankylosing enthesitis of the ankle in B10.BR (H-2k) male mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Capkova J, Ivanyi P, Rehakova Z
Аннотация
BACKGROUND: Ankylosing enthesopathy (ANKENT) with progressive stiffening of ankle and tarsal joints of the hind limbs is a naturally occurring arthropathy in B10.BR mice. Some features are similar to those of the spondyloarthropathies in humans.
OBJECTIVE: To study the role of sexual dimorphism and testosterone in the development of ANKENT.
METHODS: The incidence of ANKENT was observed in non-castrated, castrated, and testosterone substituted castrated male mice, and in control and testosterone treated female mice.
RESULTS: ANKENT occurred only in males; it did not develop in males castrated at age 2-3 months but occurred in castrated males injected with testosterone. Females injected with testosterone did not develop ANKENT.
CONCLUSION: Testosterone can replace what castration eliminates, at least in the postpubertally castrated males, but is itself not sufficient to induce joint disease.
OBJECTIVE: To study the role of sexual dimorphism and testosterone in the development of ANKENT.
METHODS: The incidence of ANKENT was observed in non-castrated, castrated, and testosterone substituted castrated male mice, and in control and testosterone treated female mice.
RESULTS: ANKENT occurred only in males; it did not develop in males castrated at age 2-3 months but occurred in castrated males injected with testosterone. Females injected with testosterone did not develop ANKENT.
CONCLUSION: Testosterone can replace what castration eliminates, at least in the postpubertally castrated males, but is itself not sufficient to induce joint disease.