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AIM: To investigate mediating and regulatory effects of osteoblastic gap junctional intercelinlar communication(GJIC) on low-dose parathyroid hormones(PTH) -stimulated bone formation activities in vitro. METHODS: Rat calvarial osteoblasts (ROBs) in cultures were divided into three groups according to the different mode of exposure. Group A: vehicle (sodium acetate, SA) -treated group; Group B: 1 × 10-8 mol/L hPTH(1 -34) intermittent exposure group; Group C: 1 × 10-8 mol/L hPTH(1 - 34) + 1 × 10-7mol/L TPA exposure group. 48 h incubation cycles in three groups were repeated for eignt times. GJIC and mineralized bone nodules formation in three groups were detected using Lucifer Yellow (LY) scrape loading dye transfer (SLDT) and mineralized nodule staining together with nodule index, respectively. RESUITS: At various measuring time points of SA × 6 h in group A, PTH × 6 hin group B, PTH×6h+1 hingroupBandPTH×6h+TPA×1 bin group C, LY( + ) cell numbers were 6. 8 ±2.5, 19.5 ±6.5, 14.0 ± 3.6 and 5.7 ± 2.4, respectively. Diffusion and transfer of LY fluorescent probe was much more noticeably discerned in group B than in group A and C( P ＜ 0.01 ) Mineralized bone nodule indices were 45.2 ± 12.5, 88.0 ± 15.3 and 38. 5 ± 17.9 in group A, B and C respectively. Bone formation activity was much better reveaied in group B than in group A and C ( P ＜ 0. 01 ),whereas no statistically significant difference of bone formation activities were found in group A compared with group C( P =0. 465) . CONCLUSION:Mediations aod regulations of the coordinating signals in ostooblastic network via GJIC essentially contribute to PTH-stimulated bone anabolism. However, disruption of GJIC not only hinders ostooblastic intercellular coordination but also frustrates PTH-induced bone formation activities in vitro. Therefore, GJIC may evidently play important roles in regulations on low-dose PTH-induced bone formation.