Hereditary joint disorder in progressive ankylosis (ank/ank) mice. I. Association of calcium hydroxyapatite deposition with inflammatory arthropathy.
Progressive ankylosis (ank), a murine autosomal recessive mutation, produces an inflammatory joint disorder associated with intraarticular calcium hydroxyapatite deposition and culminates in fusion of the joints. Joints in the feet become stiffened and swollen with milky white fluid containing polymorphonuclear leukocytes, large mononuclear macrophage-like cells, and calcium hydroxyapatite. The joints develop a proliferative synovitis, sometimes associated with marginal erosions of the articular cartilage and periosteal bone. Subsequently, cartilaginous osteophytes, extending outward from the subchondral bone, bridge the margins of the joint and undergo ossification. The progressive ankylosis mutation provides a useful system for investigating calcium hydroxyapatite-associated arthropathies.
D000818:Animals; D000844:Ankylosis / Q000235:genetics*; D001168:Arthritis / Q000378:metabolism*; D017886:Durapatite; D005528:Foot / Q000033:anatomy & histology; D006882:Hydroxyapatites / Q000378:metabolism*; D007592:Joint Diseases / Q000235:genetics*; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics*; D009154:Mutation; D013582:Synovial Fluid / Q000166:cytology; D013717:Tenosynovitis / Q000473:pathology
D006882:Hydroxyapatites; D017886:Durapatite