The exact mechanism by which focal adhesion kinase (FAK) translates mechanical signals into osteogenesis differentiation in force-subjected cells has not been elucidated. The responses to different forces differ according to the origin of cells and the type of stress applied. Therefore, the recruitment of osteoclast and osteoblast progenitor cells, and the balanced activation of these cells around and within the periodontal ligament (PDL) are essential for alveolar bone remodeling. Cells within the PDL and MG63 cells were subjected to tensile forces of -100 kPa for different periods of time. At various times during the tensile force application, they were processed for the purpose of analyzing cell viability, cell cycle, and osteogenic protein. The effect of small interfering RNA transfection targeting FAK was also evaluated. Tensile force enhanced a rapid increase in the phosphorylation of FAK and up-regulated osteogenic protein expression in PDL cells, but not in MG63 cells. Transfecting PDL cells with FAK antisense oligonucleotide diminished alkaline phosphatase and osteocalcin secretion. These findings suggest that tensile force activates FAK pathways in PDL cells, which down-regulate immune cytokine and up-regulate osteogenic protein.

Objective: The purpose of this study was to analyze proliferation, inflammation, and osteogenic effects on periodontal ligament (PDL) cells after low-level laser therapy (LLLT) under simulated orthodontic tension conditions. Background data: Low-level lasers affect fibroblast proliferation and collagen synthesis and reduce inflammation. Few studies have focused on the LLLT changes in the PDL caused by moving teeth. Materials and methods: A human PDL cell line was cultured in a -100 kPa tension incubator. The PDL cells were treated with a 670 nm low-level diode laser, output power of 500 mW (continuous wave modus) for 2.5 or 5 sec, spot area 0.25 cm 2 , corresponding to 1.25 and 2.5 J at an energy density of 5 or 10 J/cm 2 , respectively. PDL cell viability was assayed by detecting the ability of the cells to cleave tetrazolium salt to formazan dye. Inflammation and osteogenic markers were analyzed by Western blot analysis. Results: PDL cell viablity increased in the experimental group, based on the ability of the cells to cleave tetrazolium salt at day 7 ( p < 0.05). The experimental group showed no difference in PDL cellular morphology compared with the control group. The inflammation markers inducible NO synthase (iNOS), cyclooxygenase (COX)-2 and interleukin (IL)-1 showed stronger expression in 5 and 10 J/cm 2 therapy at days 1 and 5, but decreased in expression at day 7. The osteogenic marker osteocalcin (OC) expression level was significantly higher at day 7 ( p < 0.05) than in the control cells. Conclusions: LLLT significantly increased PDL cell proliferation, decreased PDL cell inflammation, and increased PDL OC activity under the tension conditions used in this study.

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