Sexual dimorphism, but not testosterone itself, is responsible for ankylosing enthesitis of the ankle in B10.BR (H-2k) male mice

B10.BR (H-2k) 雄性小鼠踝关节强直性附着点炎的病因是性二态性,而非睾酮本身。

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Abstract

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.

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