The Effect Of Light Compressive And Tensile Orthodontics Forces On Sclerostin And Periostin Expressions In Human Periodontal Ligament Cells: An Invitro Study

Abstract

BackgroundOrthodontic treatment induces bone resorption on the compression side while on the tension side stimulates bone formation. The process involves a complex interaction of signalling molecules. The aim of the present study is to assess the expression of key regulatory proteins associated with bone remodeling, cell proliferation and apoptosis in response to different types of orthodontic forces at varied time points in periodontal ligament (PDL) cells. Materials and methods and ResultsPDL cells were isolated from extracted teeth and were divided into two groups based on the type and time of applied forces: Group 1 exposed to compressive forces for 0, 6, 24, 48, 72 hours and group 2 imposed to equi-axial tension forces in 1Hz frequency and 10% elongation in 0, 24, 48, 72 hours. Real-Time Quantitative Reverse Transcription PCR (qRT-PCR) was applied to evaluate the gene expression. The secretion of Sclerostin and Periostin was assessed using Enzyme-Linked Immunosorbent Assay (ELISA). 4′,6-diamidino-2-phenylindole staining (DAPI) was used to evaluate apoptosis.The expression of Sclerostin(SOST) elevated at protein and gene levels under compression force while the application of tensile force induced the expression of Periostin(POSTN), Runt-related transcription factor 2(RUNX2) and reduced SOST expression in a time-dependent manner. Proliferating cell nuclear antigen (PCNA), the marker of proliferation increased under tensile force. The compression forces induced apoptosis and increased gene expression of apoptotic regulators, Caspase9, and B-cell lymphoma 2(BCL2). ConclusionThe periostin and sclerostin play important role in orthodontic loads and their expressions under compressive and tensile forces are affected by both variables of time and type of applied forces. Application of compressive stress increases apoptosis while tensile force induces cell proliferation.