Adult mice lacking the type 2 iodothyronine deiodinase have increased subchondral bone but normal articular cartilage.

ABSTRACT:

Background

Although osteoarthritis (OA) is the commonest joint disorder and has a rising prevalence as the population ages, no drugs are available that prevent or delay the onset and progression of disease. Recent studies identified the DIO2 gene encoding type 2 deiodinase (D2) as a susceptibility locus for OA, and further data suggest deiodinase-regulated local availability of triiodothyronine (T3) in the joint plays an important role in cartilage maintenance and repair. To investigate the hypothesis that reduced tissue T3 availability protects joints from development of OA, the joint phenotypes of adult mice lacking D2 (D2KO) or lacking both D1 and D2 (D1D2KO), the only enzymes that catalyze conversion of the prohormone thyroxine to active T3, were determined.

Methods

Knee

SUBMITTER: Waung JA 

PROVIDER: S-EPMC4361410 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature