We examined the effect of parathyroid hormone (PTH) on basic fibroblast growth factor‐2 (FGF‐2) and FGF receptor (FGFR) expression in osteoblastic MC3T3‐E1 cells and in neonatal mouse calvariae. Treatment of MC3T3‐E1 cells with PTH(1–34) (10^–8M) or forskolin (FSK; 10^–5M) transiently increased a 7 kb FGF‐2 transcript with a peak at 2 h. The PTH increase in FGF‐2 mRNA was maintained in the presence of cycloheximide. PTH also increased FGFR‐1 mRNA at 2 h and transiently increased FGFR‐2 mRNA at 1 h. FGFR‐3 and FGFR‐4 mRNA transcripts were not detected in MC3T3‐E1 cells. In cells transiently transfected with an 1800‐bp FGF‐2 promoter‐luciferase reporter, PTH and FSK increased luciferase activity at 2 h and 4 h. Immunohistochemistry showed that PTH and FSK increased FGF‐2 protein labeling in the nuclei of MC3T3‐E1 cells. PTH also increased FGF‐2 mRNA, and FGFR‐1 and FGFR‐2 mRNA levels within 30 minutes in neonatal mouse calvarial organ cultures. We conclude that PTH and cAMP stimulate FGF‐2 mRNA abundance in part through a transcriptional mechanism. PTH also regulated FGFR gene expression. We hypothesize that some effects of PTH on bone remodeling may be mediated by regulation of FGF‐2 and FGFR expression in osteoblastic cells.