PMID- 28872184 OWN - NLM STAT- MEDLINE DCOM- 20180905 LR - 20210126 IS - 1600-0765 (Electronic) IS - 0022-3484 (Print) IS - 0022-3484 (Linking) VI - 53 IP - 1 DP - 2018 Feb TI - Role of toll-like receptor 2 in inflammation and alveolar bone loss in experimental peri-implantitis versus periodontitis. PG - 98-106 LID - 10.1111/jre.12492 [doi] AB - 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-1beta [Il1beta], tumor necrosis factor-alpha [Tnfalpha]), 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 Il1beta (P = .0055), Tnfalpha (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. CI - (c) 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. FAU - Yu, X AU - Yu X AD - Department of Periodontology, The Affiliated Hospital of Qingdao University, College of Stomatology, Qingdao University, Qingdao, Shandong, China. AD - Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA. FAU - Hu, Y AU - Hu Y AD - Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA. FAU - Freire, M AU - Freire M AD - Department of Applied Oral Sciences, The Forsyth Institute, Cambridge, MA, USA. FAU - Yu, P AU - Yu P AD - State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China. FAU - Kawai, T AU - Kawai T AD - Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA. FAU - Han, X AU - Han X AUID- ORCID: 0000-0001-8357-1471 AD - Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA. LA - eng GR - R00 DE023584/DE/NIDCR NIH HHS/United States GR - R21 DE021837/DE/NIDCR NIH HHS/United States GR - R56 DE023807/DE/NIDCR NIH HHS/United States GR - L30 DE020037/DE/NIDCR NIH HHS/United States GR - R01 DE025255/DE/NIDCR NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Retracted Publication DEP - 20170905 PL - United States TA - J Periodontal Res JT - Journal of periodontal research JID - 0055107 RN - 0 (Cytokines) RN - 0 (Dental Implants) RN - 0 (Osteoprotegerin) RN - 0 (RANK Ligand) RN - 0 (RNA, Messenger) RN - 0 (Tnfsf11 protein, mouse) RN - 0 (Toll-Like Receptor 2) SB - IM RIN - J Periodontal Res. 2021 Jan;56(1):203. PMID: 33496961 MH - Alveolar Bone Loss/*pathology MH - Animals MH - Cytokines/genetics/metabolism MH - Dental Implants/adverse effects MH - Disease Models, Animal MH - Mice, Knockout MH - Osseointegration MH - Osteoprotegerin/genetics/metabolism MH - Peri-Implantitis/metabolism/*pathology MH - Periodontitis/metabolism/*pathology MH - RANK Ligand/genetics/metabolism MH - RNA, Messenger/metabolism MH - Toll-Like Receptor 2/genetics/*physiology PMC - PMC5760345 MID - NIHMS892882 OTO - NOTNLM OT - bone resorption OT - inflammatory cytokine OT - peri-implantitis OT - periodontitis OT - toll-like receptor 2 COIS- The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article. EDAT- 2017/09/06 06:00 MHDA- 2018/09/06 06:00 PMCR- 2019/02/01 CRDT- 2017/09/06 06:00 PHST- 2017/07/07 00:00 [accepted] PHST- 2017/09/06 06:00 [pubmed] PHST- 2018/09/06 06:00 [medline] PHST- 2017/09/06 06:00 [entrez] PHST- 2019/02/01 00:00 [pmc-release] AID - 10.1111/jre.12492 [doi] PST - ppublish SO - J Periodontal Res. 2018 Feb;53(1):98-106. doi: 10.1111/jre.12492. Epub 2017 Sep 5.