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PTH treatment converts inactive lining cells to active osteoblasts



DOI:10.1038/bonekey.2012.251

This study investigated the in vivo effects of parathyroid hormone (PTH) on bone formation by using an inducible gene system to explore the impact of intermittent PTH on the murine osteoblast lineage. Transgenic mice were first created by crossing Dmp1-CreERt2 mice with ROSA26R reporter mice. Mice chosen for experimentation had mature osteoblasts, osteoblast descendents, osteocytes and lining cells that were detectable using 5-bromo-4-chloro-3-indolyl-β-d-galactopyranoside (X-gal) staining.

On days 3, 5, 7, 14 and 21 after birth, the mice were injected with 4-OH-tamoxifen (4-OHTam) and later injected with human PTH for three consecutive days, starting on day 43 (22 days after the last 4-OHTam injection).

Histology in combination with X-gal staining revealed that PTH treatment led to an increase in the thickness of osteoblast descendents at the surface of the periosteum of the tibia and calvaria. Hormone treatment did not increase the rate of osteoblast proliferation; it converted quiescent lining cells into active osteoblasts.

Editor’s comment: This finding is not surprising; it has long been known that although the most prominent effects of PTH are on bone remodeling, the hormone also acts directly on quiescent osteoblasts lining modeling surfaces, triggering de novo bone formation. However, the elegant experimental approach in this study provides a further level of evidence that PTH exerts such effects in vivo.


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