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

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Sexual dimorphism, but not testosterone itself, is responsible for ankylosing enthesitis of the ankle in B10.BR (H-2k) male mice
  1. J Capkova1,
  2. P Ivanyi2,
  3. Z Rehakova3
  1. 1Institute of Molecular Genetics of the Academy of Sciences of the Czech Republic, Prague, Czech Republic
  2. 2Institute of Clinical and Experimental Medicine, Prague, Czech Republic
  3. 3University of Defence, Faculty of Military Health Sciences, Hradec Králové, Czech Republic
  1. Correspondence to:
    Dr J Capkova
    Institute of Molecular Genetics, Academy of Sciences, Videnska 1083, 142 20 Prague 4, Czech Republic; capkova{at}biomed.cas.cz

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.

  • ANKENT, ankylosing enthesopathy
  • AS, ankylosing spondylitis
  • MHC, major histocompatibility complex
  • SpA, spondyloarthropathies
  • spondyloarthropathy
  • ankylosing enthesopathy
  • ankylosing spondylitis
  • testosterone

https://doi.org/10.1136/ard.2005.039800

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