{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T17:03:56Z","timestamp":1790442236011,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,9,5]],"date-time":"2017-09-05T00:00:00Z","timestamp":1504569600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000072","name":"NIH NIDCR","doi-asserted-by":"crossref","award":["DE023807"],"award-info":[{"award-number":["DE023807"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000072","name":"NIH NIDCR","doi-asserted-by":"crossref","award":["DE025255"],"award-info":[{"award-number":["DE025255"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2018,2]]},"abstract":"<jats:sec><jats:title>Background and Objective<\/jats:title><jats:p>Peri\u2010implantitis and periodontitis are different entities in immune characteristics even though they share similar features in clinical and radiologic signs. Toll\u2010like receptor 2 (<jats:styled-content style=\"fixed-case\">TLR\u2010<\/jats:styled-content>2), one of the key pathogen\u2010recognition receptors in the innate immune system, plays an important role in the progression of periodontitis. However, the role of <jats:styled-content style=\"fixed-case\">TLR\u2010<\/jats:styled-content>2 in peri\u2010implantitis remains unclear. The objective of this study was to investigate the role of <jats:styled-content style=\"fixed-case\">TLR\u2010<\/jats:styled-content>2 in inflammation and alveolar bone loss in a murine model of ligature\u2010induced peri\u2010implantitis and to compare it with ligature\u2010induced periodontitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>Smooth\u2010surface titanium implants were placed in the alveolar bone of the left maxillary molars of wild\u2010type (WT) and <jats:italic>Tlr2<\/jats:italic> knockout (<jats:italic>Tlr2<\/jats:italic>\u2010KO) mice 6\u00a0weeks after tooth extraction. Silk ligatures were applied to the left implant fixtures and the right maxillary second molars to induce peri\u2010implantitis and periodontitis 4\u00a0weeks after implant placement. Two weeks after ligation, bone loss around the implants and maxillary second molars was analysed by micro\u2010computed tomography (micro\u2010CT), 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\u20101\u03b2 [<jats:italic>Il1\u03b2<\/jats:italic>], tumor necrosis factor\u2010\u03b1 [<jats:italic>Tnf\u03b1<\/jats:italic>]), an anti\u2010inflammatory cytokine (interleukin\u201010 [<jats:italic>Il10<\/jats:italic>]) and osteoclastogenesis\u2010related cytokines (<jats:italic>Rankl<\/jats:italic>, osteoprotegerin [<jats:italic>Opg<\/jats:italic>]) were evaluated, in gingival tissue, using real\u2010time quantitative PCR (RT\u2010qPCR).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The success rate of implant osseointegration was significantly higher in <jats:italic><jats:styled-content style=\"fixed-case\">Tlr2<\/jats:styled-content><\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice (85.71%) compared with <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice (53.66%) (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.0125). Micro\u2010<jats:styled-content style=\"fixed-case\">CT<\/jats:styled-content> revealed significantly decreased bone loss in <jats:italic><jats:styled-content style=\"fixed-case\">Tlr<\/jats:styled-content>2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice compared with <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.0094) in peri\u2010implantitis. The levels of m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> for <jats:italic><jats:styled-content style=\"fixed-case\">Il<\/jats:styled-content>1\u03b2<\/jats:italic> (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.0055), <jats:italic><jats:styled-content style=\"fixed-case\">Tnf<\/jats:styled-content>\u03b1<\/jats:italic> (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.01) and <jats:italic><jats:styled-content style=\"fixed-case\">Il<\/jats:styled-content>10<\/jats:italic> (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.0019) in gingiva were significantly elevated in the peri\u2010implantitis tissues of <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice, but not in <jats:italic><jats:styled-content style=\"fixed-case\">Tlr2<\/jats:styled-content><\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice, compared with controls. However, the gingival m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> ratios of <jats:italic><jats:styled-content style=\"fixed-case\">Rankl<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">Opg<\/jats:styled-content><\/jats:italic> in peri\u2010implant tissues were significantly upregulated in both <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.0488) and <jats:styled-content style=\"fixed-case\"><jats:italic>Tlr2<\/jats:italic>\u2010KO<\/jats:styled-content> (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.0314) mice. Ligature\u2010induced periodontitis exhibited similar patterns of bone loss and inflammatory cytokine profile in both groups of mice, except that the level of <jats:italic>Il10<\/jats:italic> was elevated (<jats:italic>P\u00a0<\/jats:italic>=\u00a0.0114) whereas the <jats:italic><jats:styled-content style=\"fixed-case\">Rankl<\/jats:styled-content>\/Opg<\/jats:italic> ratio was not elevated (<jats:italic>P\u00a0=<\/jats:italic>\u00a0.9755) in <jats:italic>Tlr2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice compared with control mice. Histological findings showed increased numbers of <jats:styled-content style=\"fixed-case\">TRAP<\/jats:styled-content>\u2010positive cells and infiltrated inflammatory cells in ligature\u2010induced peri\u2010implantitis in both <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> (<jats:italic>P\u00a0<\/jats:italic>&lt;\u00a0.01) and <jats:italic>Tlr2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice (<jats:italic>P\u00a0<\/jats:italic>&lt;\u00a0.05), and the numbers of both types of cell were significantly higher in <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice than in <jats:italic>Tlr2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice (<jats:italic>P<\/jats:italic> &lt; .01).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This study suggests that <jats:styled-content style=\"fixed-case\">TLR\u2010<\/jats:styled-content>2 mediates bone loss in both peri\u2010implantitis and periodontitis. However, different molecular features may exist in the pathogenesis of the two diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.12492","type":"journal-article","created":{"date-parts":[[2017,9,5]],"date-time":"2017-09-05T10:52:15Z","timestamp":1504608735000},"page":"98-106","source":"Crossref","is-referenced-by-count":39,"title":["<i>Retracted:<\/i> Role of toll\u2010like receptor 2 in inflammation and alveolar bone loss in experimental peri\u2010implantitis versus periodontitis"],"prefix":"10.1111","volume":"53","author":[{"given":"X.","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Periodontology The Affiliated Hospital of Qingdao University College of Stomatology Qingdao University  Qingdao Shandong China"},{"name":"Department of Immunology and Infectious Diseases The Forsyth Institute  Cambridge MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Immunology 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