Periodontal ligament‑associated protein‑1 delays rat periodontal bone defect repair by regulating osteogenic differentiation of bone marrow stromal cells and osteoclast activation
- Xijiao Yu
- Shuang Liu
- Wei Wang
- Shu Li
Published online on: December 6, 2017
The aim of the present study was to assess the roles of periodontal ligament‑associated protein‑1 (PLAP‑1) in the osteogenic differentiation of rat bone marrow stromal cells (rBMSCs) and in osteoclast activation during the repair of rat periodontal bone defects. Male, 6‑week‑old, Wistar rats treated with periodontal bone defects were randomly assigned to 3 groups: The PLAP‑1‑transfected rBMSC group (PLAP‑1 group), the empty vector‑transfected rBMSC group (vector group) and the normal rBMSC group (control group). Specimens were obtained at 2, 4 and 6 weeks post‑surgery. Histological observation and micro‑computed tomography were applied to evaluate the repair effect. The bone defect areas of the mandible were dissected for western blotting and reverse transcription-quantitative polymerase chain reaction (RT‑qPCR). Osteogenesis‑associated proteins, including alkaline phosphatase (ALP), bone sialoprotein (BSP), runt-related transcription factor 2 (Runx2), Osterix (Osx) and osteocalcin (OC), as indicators of rBMSC‑induced osteogenesis, were examined by RT-qPCR and western blotting. Osteoclasts were identified and quantified using tartrate‑resistant acid phosphatase staining. Meanwhile, the receptor activator of nuclear factor κΒ ligand (RANKL)/οsteoprotegerin (OPG) ratio was quantified to assess osteoclast activation by western blotting. Τhe repair effect of the PLAP‑1 group was significantly worse than that of the vector and control groups. In the PLAP‑1 group, newly formed and mineralized bones were significantly less in quantity than that in the other two groups (P<0.05), and the expression of osteogenic proteins (ALP, BSP, Runx2, Osx and OC) was also reduced (P<0.01). However, there was no significant difference between the vector and control groups. The RANKL/OPG ratio was upregulated in the PLAP‑1 group due to decreased OPG protein expression and a simultaneous increase in RANKL protein expression (P<0.01), and more osteoclasts were activated in the PLAP‑1 group (P<0.01). In conclusion, the present study found that PLAP‑1 delays rat periodontal bone defect repair by inhibiting osteogenic differentiation and promoting osteoclast activation, mainly dependent on the upregulation of the RANKL/OPG ratio.