Retracted: Role of toll‐like receptor 2 in inflammation and alveolar bone loss in experimental peri‐implantitis versus periodontitis
Authors: Yu X. , Hu Y. , Freire M. , Yu P. , Kawai T. , Han X. 
Published: September 2017

Background and Objective

Peri‐implantitis and periodontitis are different entities in immune characteristics even though they share similar features in clinical and radiologic signs. Toll‐like receptor 2 (TLR‐2), one of the key pathogen‐recognition receptors in the innate immune system, plays an important role in the progression of periodontitis. However, the role of TLR‐2 in peri‐implantitis remains unclear. The objective of this study was to investigate the role of TLR‐2 in inflammation and alveolar bone loss in a murine model of ligature‐induced peri‐implantitis and to compare it with ligature‐induced periodontitis.

Material and Methods

Smooth‐surface titanium implants were placed in the alveolar bone of the left maxillary molars of wild‐type (WT) and Tlr2 knockout (Tlr2‐KO) mice 6 weeks after tooth extraction. Silk ligatures were applied to the left implant fixtures and the right maxillary second molars to induce peri‐implantitis and periodontitis 4 weeks after implant placement. Two weeks after ligation, bone loss around the implants and maxillary second molars was analysed by micro‐computed tomography (micro‐CT), and inflammation around the implants and maxillary second molars was assessed at the same time point using histology and TRAP staining, respectively. Expression of mRNA for proinflammatory cytokines (interleukin‐1β [Il1β], tumor necrosis factor‐α [Tnfα]), an anti‐inflammatory cytokine (interleukin‐10 [Il10]) and osteoclastogenesis‐related cytokines (Rankl, osteoprotegerin [Opg]) were evaluated, in gingival tissue, using real‐time quantitative PCR (RT‐qPCR).

Results

The success rate of implant osseointegration was significantly higher in Tlr2‐KO mice (85.71%) compared with WT mice (53.66%) (P = .0125). Micro‐CT revealed significantly decreased bone loss in Tlr2‐KO mice compared with WT mice (P = .0094) in peri‐implantitis. The levels of mRNA for Il1β (P = .0055), Tnfα (P = .01) and Il10 (P = .0019) in gingiva were significantly elevated in the peri‐implantitis tissues of WT mice, but not in Tlr2‐KO mice, compared with controls. However, the gingival mRNA ratios of Rankl/Opg in peri‐implant tissues were significantly upregulated in both WT (P = .0488) and Tlr2‐KO (P = .0314) mice. Ligature‐induced periodontitis exhibited similar patterns of bone loss and inflammatory cytokine profile in both groups of mice, except that the level of Il10 was elevated (P = .0114) whereas the Rankl/Opg ratio was not elevated (P = .9755) in Tlr2‐KO mice compared with control mice. Histological findings showed increased numbers of TRAP‐positive cells and infiltrated inflammatory cells in ligature‐induced peri‐implantitis in both WT (P < .01) and Tlr2‐KO mice (P < .05), and the numbers of both types of cell were significantly higher in WT mice than in Tlr2‐KO mice (P < .01).

Conclusion

This study suggests that TLR‐2 mediates bone loss in both peri‐implantitis and periodontitis. However, different molecular features may exist in the pathogenesis of the two diseases.