Disruption of the fibroblast growth factor-2 gene results in decreased bone mass and bone formation

TLDR

Basic fibroblast growth factor (FGF‑2) is a key regulator of cartilage and bone growth, expressed in osteoblastic cells. The study aimed to determine the role of FGF‑2 in bone by examining mice lacking the Fgf2 gene. The authors compared bone architecture and formation in Fgf2⁺/⁺ and Fgf2⁻/⁻ adult mice using micro‑CT, dynamic histomorphometry, and bone marrow stromal cultures. Loss of FGF‑2 markedly reduced trabecular bone volume, impaired mineral apposition and bone formation rates, and decreased mineralization of marrow stromal cultures, demonstrating FGF‑2’s essential role in bone mass and formation.

Abstract

Basic fibroblast growth factor (FGF-2), an important modulator of cartilage and bone growth and differentiation, is expressed and regulated in osteoblastic cells. To investigate the role of FGF-2 in bone, we examined mice with a disruption of the Fgf2 gene. Measurement of trabecular bone architecture of the femoral metaphysis of Fgf2+/+ and Fgf2–/– adult mice by micro-CT revealed that the platelike trabecular structures were markedly reduced and many of the connecting rods of trabecular bone were lost in the Fgf2–/– mice. Dynamic histomorphometry confirmed a significant decrease in trabecular bone volume, mineral apposition, and bone formation rates. In addition, there was a profound decreased mineralization of bone marrow stromal cultures from Fgf2–/– mice. This study provides strong evidence that FGF-2 helps determine bone mass as well as bone formation.