Molecular regulation of cartilage and bone mineralization

Thorsten Kirsch

Research output: Contribution to journalReview articlepeer-review


Biomineralization is a cell-regulated process. Matrix vesicles, which are released from mineralization-competent cells, initiate the mineralization process. These particles contain channel-forming annexins II, V and VI, and an Na+/Pi symport system, which enable Ca2+ and inorganic phosphate (Pi) influx into the vesicles. Rapid Ca2+ and Pi influxes are required for the formation of the first mineral phase inside the vesicles. Furthermore, matrix vesicles contain plasma cell membrane glycoprotein 1 (PC-1), an enzyme which generates pyrophosphate (PPi). Extracellular PPi is also regulated by ank, a transmembrane protein that transports intracellular PPi to the extracellular milieu. PPi is an inhibitor of mineralization; however, matrix vesicle-associated alkaline phosphatase (TNAP) may degrade PPi and thus may not only provide Pi but more importantly remove an inhibitor of mineralization. The release of mineralization-competent matrix vesicles is regulated by annexin-mediated alteration of Ca2+ homeostasis, suggesting that targeting annexin functions might provide a novel therapeutic strategy to prevent pathological mineralization. Furthermore, the possible inhibitory function of other factors, such as matrix gla protein (MGP), in mineralization and cell differentiation is discussed.

Original languageEnglish (US)
Pages (from-to)382-387
Number of pages6
JournalCurrent Opinion in Orthopaedics
Issue number5
StatePublished - Oct 2002

ASJC Scopus subject areas

  • Surgery


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