PEEK‑biphasic Bioceramic Composites Promote Mandibular Defect Repair and Upregulate BMP‑2 Expression in Rabbits

The present study aimed to investigate whether bone morphogenetic protein‑2 (BMP‑2) was involved in the repair of mandibular defects using polyether‑ether‑ketone biphasic bioceramic (PEEK‑BBC) composites in rabbits. PEEK‑BBC composites with abundant and interconnected pores were prepared by calcination and characterized by scanning electron microscope. A mandibular defect model in rabbits was established using dental grinder to produce a square hole. A total of 60 rabbits were divided into four groups: Control, sham, surgery, and PEEK. In the PEEK group, the holes were filled with the PEEK‑BBC composite stents. In the surgery group, the holes were produced but not filled with the composite stents. In the sham group, only the molar grooves were exposed and grinding was not performed. Animals without any treatment served as the control group. The success rate of model establishment was 100%. At 4, 8, and 16 weeks after the model was established, samples were collected from the molding sites. Bone repair was evaluated by H&E staining and Goldner trichrome staining. Bone structures in both control and sham groups were intact. A small number of osteocytes were observed in the surgery group. However, in the PEEK group, osteocytes were already evidently present in the composites at 4 weeks after surgery. At 8 and 16 weeks, there were large numbers of osteocytes in the pores of the composites. The mRNA and protein expression levels of BMP‑2 were determined by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The mRNA and protein expression levels of BMP‑2 between the control and sham groups were similar and were continuously stable. However, following defect treatment, BMP‑2 mRNA and protein expression was upregulated, which was enhanced by the PEEK‑BBC composites. In conclusion, PEEK‑BBC composites promoted the growth of osteocytes and repaired mandibular defects in rabbits, potentially via the upregulation of BMP‑2 expression.