Development of scleroderma-like syndrome in Tsk/+ mice is not enhanced by silicone administration

Curr Top Microbiol Immunol. 1996:210:299-306. doi: 10.1007/978-3-642-85226-8_31.

Abstract

The possible role of silicone in the pathogenesis of a scleroderma-like syndrome is still unresolved. It has been proposed that silicone escaping from breast implants potentiates the progression of the disease. To clarify whether silicone enhances development of fibrotic skin lesions and autoantibodies, we tested its effect on tight skin (TSK/+) mice. TSK/+ mice spontaneously develop skin fibrosis and characteristic autoantibodies which resemble human scleroderma. The results of the present study indicate that silicone administration does not enhance development of skin fibrosis nor synthesis of autoantibodies to RNA polymerase and topoisomerase in TSK/+ mice.

MeSH terms

  • Animals
  • Autoantibodies / blood
  • Mice
  • Scleroderma, Systemic / etiology*
  • Silicones / toxicity*
  • Skin / pathology

Substances

  • Autoantibodies
  • Silicones