Histological assessments for anabolic effects in teriparatide/abaloparatide administered rodent models.

Abstract

Parathyroid hormone (PTH) is thought to induce remodeling-based bone formation by promoting osteoclastic activity, a process known as cellular coupling. Our research has shown that the frequency of PTH administration affects trabecular number and thickness. High-frequency PTH administration induced remodeling-based bone formation, while less frequent administration induced both remodeling-based and modeling-based bone formation. Additionally, we found that specific bone sites influence whether remodeling-based or modeling-based bone formation is more likely to occur. Additionally, while PTH significantly increases trabecular bone, it also causes cortical porosis. Our research on the femoral diaphysis showed that PTH administration resulted in the invasion of blood vessels and osteoclasts into the cortical bone. Abaloparatide acts similarly to teriparatide through the parathyroid hormone receptor type 1 (PTH1R) but may have a wider anabolic window due to its lesser impact on bone resorption. Our mouse studies with abaloparatide showed similar results to those seen in human patients, with increased preosteoblastic cell populations and wider anabolic windows when compared with teriparatide. Abaloparatide-induced bone formation cannot be explained solely by remodeling-based bone formation, indicating the need for further research into modeling-based bone formation.