Hereditary joint disorder in progressive ankylosis (ank/ank) mice. II. Effect of high-dose hydrocortisone treatment on inflammation and intraarticular calcium hydroxyapatite deposits.
Mice homozygous for the progressive ankylosis trait develop an inflammatory joint disorder associated with the intraarticular deposition of calcium hydroxyapatite. When affected (ank/ank) mice were treated with high doses of hydrocortisone, synovitis receded, development of cartilaginous and bony osteophytes halted, and calcium hydroxyapatite accumulated in and distended the synovial spaces. No changes, however, occurred in the joint morphology of hydrocortisone-treated normal (ank/+) mice. Since inhibition of inflammation by hydrocortisone treatment did not block apatite accumulation, intraarticular deposition of hydroxyapatite occurs independent of inflammation in progressive ankylosis.
D000818:Animals; D000844:Ankylosis / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D001168:Arthritis / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D017886:Durapatite; D006854:Hydrocortisone / Q000008:administration & dosage* / Q000627:therapeutic use; D006882:Hydroxyapatites / Q000378:metabolism*; D007596:Joints / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D051379:Mice; D008817:Mice, Mutant Strains
D006882:Hydroxyapatites; D017886:Durapatite; D006854:Hydrocortisone