Lovisa Hessle

TL;DR: The results suggest that inhibiting PC-1 function may be a viable therapeutic strategy for hypophosphatasia, and interfere with TNAP activity may correct pathological hyperossification because of PPi insufficiency.

TL;DR: In this article, the authors crossbred Akp2−/− mice to ank/ank mice and found a partial normalization of the mineralization phenotypes and PPi levels.

TL;DR: The data suggest that hypomineralization in TNAP-deficient mice results primarily from an inability of initial mineral crystals within MVs to self-nucleate and to proliferate beyond the protective confines of the MV membrane, which may be caused by an excess of the mineral inhibitor pyrophosphate in the extracellular fluid around MVs.

TL;DR: The data provide evidence that osteoblasts in TNAP null mice differentiate normally but are unable to initiate mineralization in vitro, and provides a rationale for the presence of bone disease in carriers of hypophosphatasia.

TL;DR: It is reported that extracellular PPi deficiency promotes osteopontin deficiency and correction of osteoponin deficiency prevents hypercalcification, suggesting synergistic inhibition of hydroxyapatite deposition.