Objective: It is well known that periodontal ligament cells (HPDL) produces PGE₂ by application of orthodontic force. PGE₂ is a pro-inflammatory agent and one of the potent osteoclast-inducing factors. It is known that RANKL is essential for osteoclastgenesis and is induced by PGE₂. In our previous study, HPDL harvested from variant aged donors were stimulated PGE₂ production in response to mechanical stress in age-dependent manner, however, HPDL expressed little RANKL. Therefore, RANKL produced by not HPDL, but osteoblasts may induce osteoclastgenesis, and PGE₂ produced by HPDL in response to mechanical stress may be a mediator of RANKL production from osteoblasts. The aim of this study was to investigate the functional difference of HPDL and normal human osteoblast cells (NHOB) by application of PGE₂ which was equal amount produced by HPDL in response to mechanical stress.
Method: HPDL and NHOB were cultured, and 48h after PGE₂ (10^-11~10^-5M) application, the expression of RANKL, OPG and M-csf was examined.
Results: RANKL expression of NHOB and HPDL were increased in dose-dependent manner, however the maximum expression of RANKL in NHOB was 10-fold higher compared with that in HPDL. In constant, the expression of OPG in HPDL was higher compared with that in NHOB.
Conclusion: These results suggest that HPDL does not directly produce RANKL in response to mechanical stress, but stimulates RANKL production from osteoblasts via PGE₂ production.