Purpose: Osteoporosis, due to bone loss and structural deterioration, is a risk factor for dental implant failure, as it impedes initial stability and osseointegration. We aim to assess the effects of calcium phosphate polymer-induced liquid precursor (CaP-PILP) treatment, which significantly increases bone density and improves early implant osseointegration in ovariectomized rats. Methods: In this study, CaP-PILP was synthesized and characterized through TEM, FTIR and XRD. A rat model of osteoporosis was generated by ovariectomy. CaP-PILP or hydroxyapatite (HAP, negative control) was injected into the tibia, and the resulting changes in bone quality were determined. Further, implants were installed in the treated tibias, and implantation characteristics were assessed after 4 weeks. Results: The CaP-PILP group had superior bone repair. Importantly, CaP-PILP had excellent properties, similar to those of normal bone, in terms of implant osseointegration. In vivo experiment displayed that CaP-PILP group had better bone contact rate (65.97± 3.176) than HAP and OVX groups. Meanwhile, a mound of mature and continuous new bone formed. Moreover, the values of BIC and BA showed no significant difference between the CaP-PILP group and the sham group. Conclusion: In summary, CaP-PILP is a promising material for application in poor-quality bones to improve implant success rates in patients with osteoporosis. This research provides new perspectives on the application of nano-apatite materials in bone repair.

Dental pulp inflammation is a widespread public problem usually caused by caries or trauma. Alleviating inflammation is critical to inflamed pulp repair. Human β-defensin 1 short motif Pep-B is a cationic peptide that has anti-inflammatory, antibacterial, and immunoregulation properties, but its repair effect on human dental pulp stem cells (hDPSCs) under inflammation remains unclear. In this study, we aimed to investigate anti-inflammatory function of Pep-B and explore its therapeutic potential in lipopolysaccharide-(LPS-) induced hDPSCs. CCK-8 assay and transwell assay evaluated effects of Pep-B on hDPSC proliferation and chemotaxis. Inflammatory response in hDPSCs was induced by LPS; after Pep-B application, lactate dehydrogenase release, intracellular ROS, inflammatory factor genes expression and possible signaling pathway were measured. Then, osteo-/odontoblast differentiation effect of Pep-B on LPS-induced hDPSCs was detected. The results showed that Pep-B promoted hDPSC proliferation and reduced LPS-induced proinflammatory marker expression, and western blot result indicated that Pep-B inhibited inflammatory activation mediated by NF-κB and MAPK pathways. Pep-B also enhanced the expression of the osteo-/odontogenic genes and proteins, alkaline phosphatase activity, and nodule mineralization in LPS-stimulated hDPSCs. These findings indicate that Pep-B has anti-inflammatory activity and promote osteo-/odontoblastic differentiation in LPS-induced inflammatory environment and may have a potential role of hDPSCs for repair and regeneration.