Modulation of chondrocyte production of extracellular inorganic pyrophosphate. Curr Opin Rheumatol 2004 May;16(3):268-72
Date
04/23/2004Pubmed ID
15103256DOI
10.1097/00002281-200405000-00017Scopus ID
2-s2.0-1942531958 (requires institutional sign-in at Scopus site) 21 CitationsAbstract
PURPOSE OF REVIEW: Extracellular inorganic pyrophosphate (ePPi) both inhibits and promotes different forms of pathologic mineralization. Basic calcium phosphate (BCP) deposition results from depressed levels of ePPi while excess levels of ePPi leads to calcium pyrophosphate dihydrate crystal deposition (CPPD) disease. These crystals are also often identified in patients with osteoarthritis, the most prevalent form of arthritis causing significant morbidity.
RECENT STUDIES: The two primary hypotheses for generation of ePPi, export of inorganic pyrophosphate through the multipass transmembrane protein ANK and generation of ePPi by ectoenzyme activity, continue to be supported and better understood through animal models and study of families with CPPD deposition disease.
SUMMARY: As the pathophysiology of crystal formation in both articular cartilage and synovial fluid is better understood, the opportunity for prevention and treatment of pathologic mineralization increases. In particular, a more complex understanding of the ank gene, ectoenzyme PC-1, and the transglutaminase enzyme family may eventually translate into therapeutic application for both BCP deposition and CPPD deposition disease.
Author List
Costello JC, Ryan LMMESH terms used to index this publication - Major topics in bold
Calcium PhosphatesCalcium Pyrophosphate
Cartilage, Articular
Chondrocalcinosis
Chondrocytes
Crystallization
Diphosphates
Extracellular Space
Humans
Phosphoric Diester Hydrolases
Pyrophosphatases
Synovial Fluid
Transglutaminases
