[Prevention of joint destruction by osteoclast-targeting therapy in search of new tools, such as OPG or cathepsin K inhibitor].
We should consider not only controlling disease activity using DMARDs and biologics as a matter of course, but also preventing against joint destruction, in the treatment for rheumatoid arthritis. Although we can indirectly regulate bone erosion via controlling disease activity, the osteoclast-targeting therapy might be more effective to stop joint destruction. We are waiting for new drugs directly targeting osteoclasts, such as OPG which is the natural inhibitor of RANKL, or cathepsin K inhibitor which reduces degeneration of bone matrix.
Kadono
Yuho
Y
Orthopaedic Surgery, University of Tokyo Hospital.
Tanaka
Sakae
S
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D001381:Azepines; D001713:Biphenyl Compounds; D056657:Cathepsin K; D002403:Cathepsins / Q000037:antagonists & inhibitors*; D002454:Cell Differentiation; D015195:Drug Design; D006801:Humans; D007596:Joints / Q000473:pathology; D010010:Osteoclasts / Q000166:cytology; D053244:Osteoprotegerin / Q000494:pharmacology / Q000627:therapeutic use*; D011725:Pyridines; D053245:RANK Ligand / Q000037:antagonists & inhibitors; D013450:Sulfones
D001381:Azepines; D001713:Biphenyl Compounds; D053244:Osteoprotegerin; D011725:Pyridines; D053245:RANK Ligand; C524569:SB-553484; D013450:Sulfones; C509706:relacatib; D002403:Cathepsins; C534130:CTSK protein, human; D056657:Cathepsin K; C527128:odanacatib