Influence of mechanical stress on the expression of osteopontin in human periodontal ligament cells.

• Main Authors: Prasit Pavasant, Tussanee Yongchaitrakul
• Other Authors: Chulalongkorn University. Faculty of Dentistry
• Format: Technical Report
• Language: English
• Published: Chulalongkorn University 2009
• Subjects: Osteopontin; Periodontal ligament; mechanical stress; compressive force; periodontal ligament cells; Rho kinase
• Online Access: http://cuir.car.chula.ac.th/handle/123456789/8943
• Institution: Chulalongkorn University

Background: Mechanical stress such as orthodontic forces can produce mechanical damage and inflammatory reaction in periodontium. Osteopontin (OPN) is a multifunctional cytokine that found to be correlated with periodontal disease progression. As periodontal ligaments (PDL) can be affected by stress and PDL cells are involved in periodontal destruction and remodeling, we aimed to investigate the influence of mechanical stress on the expression and regulation of OPN in human PDL (HPDL) cells. Methods: The mechanical stress was generated by continuous compressive force and the expression of OPN was examined by reverse transcription polymerase chain reaction (RT-PCR) and Western analysis. The application of inhibitors was used to examine the mechanism involved. Results: Both mRNA and protein expression of OPN significantly increased in a force-dependent manner. Increase of receptor activator of nuclear factor kappa B ligand (RANKL) was also observed. Interestingly, application of indomethacin could abolish the induction of RANKL but not that of OPN, suggesting the cyclooxygenase (COX)-independent mechanism for stress-induced OPN expression. In addition, the up-regulation of OPN was diminished by Rho kinase inhibitor, but not by cytochalasin B. Conclusions: Mechanical stress affects OPN expression in HPDL cells via Rho kinase pathway. Since OPN participates in bone resorption and remodeling induced by mechanical and biological signals, these results suggest the significance of stress-induced OPN in HPDL cells in alveolar bone resorption and remodeling.