RESUMEN
OBJECTIVE@#To determine the effect of continuously compressive pressure (CCP) on the expression of receptor activator of nuclear factor kappa B ligand (RANKL) in human periodontal ligament cells (HPDLCs) and to investigate the role of RANKL in alveolar bone rebuilding during orthodontic tooth movement.@*METHODS@#The primary HPDLCs were isolated from human periodontal ligament by explanting enzymatic digestion with trypsin and collagenase to establish a pressure model. Top-bottom axial pressures (1, 2, and 3 g/cm(2)) were laid on HPDLCs for 0.5, 1.5, 6, 12, 24, and 48 h, respectively. The RANKL expression was identified by the reverse transcription-polymerase chain reaction (RT-PCR) at the mRNA level.@*RESULTS@#The expression of RANKL mRNA significantly increased in a time-dependent manner (P<0.01), so did the value of pressure, especially in the 2 g/cm(2) group (P<0.05).@*CONCLUSION@#CCP can up-regulate the expression of RANKL mRNA in human periodontal ligament cells.
Asunto(s)
Humanos , Fuerza Compresiva , Ligamento Periodontal , Biología Celular , Metabolismo , Ligando RANK , Genética , ARN Mensajero , Genética , Receptor Activador del Factor Nuclear kappa-B , Genética , Metabolismo , Estrés MecánicoRESUMEN
<p><b>OBJECTIVE</b>To study the role of microfilament polymerization in menchanotransduction by human periodontal ligament fibroblast (hPDLFs).</p><p><b>METHODS</b>In tension-force group, hPDLFs were treated by tension-force values of 18% for 8 h, 16 h, 24 h. In tension-force and inhibitor group, the sample was treated with 5 microg/mL cytochalasin B before using tension-forece. Each sample was collected and the expression of cyclooxygenase-2 was measured by using immunohistoche staining.</p><p><b>RESULTS</b>In tension-force group, the expression of cyclooxygenase-2 enhanced with the extension of loading time. In tension-force and inhibitor group, cyclooxygenase-2 expression was depressed and had no relation with loading time.</p><p><b>CONCLUSION</b>Tension-force induced cyclooxygenase-2 expression is mediated by microfilament, disruption of the microfilament polymerization will destroy mechanotransduction in hPDLFs.</p>