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The recognition of microbial factors, such as lipopolysaccharide from <jats:italic><jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>.\u00a0actinomycetemcomitans<\/jats:italic> (<jats:sub><jats:italic>Aa<\/jats:italic><\/jats:sub><jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>), in the oral environment is made mainly by surface receptors known as <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>oll\u2010like receptors (<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>). <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 is the major <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> receptor. This interaction leads to the production of inflammatory cytokines by myeloid differentiation primary\u2010response protein 88 (<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88) \u2010dependent and \u2010independent pathways, which may involve the adaptor <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>oll\/interleukin\u20101 receptor\u2010domain\u2010containing adaptor inducing interferon\u2010\u03b2 (<jats:styled-content style=\"fixed-case\">TRIF<\/jats:styled-content>). The aim of this study was to assess the involvement of <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88 in alveolar bone loss induced by <jats:sub><jats:italic>Aa<\/jats:italic><\/jats:sub><jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> in mice. C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>6\/<jats:styled-content style=\"fixed-case\">J<\/jats:styled-content> wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) mice, <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88, <jats:styled-content style=\"fixed-case\">TRIF<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">TRIF<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88 knockout mice received 10 injections of <jats:sub><jats:italic>Aa<\/jats:italic><\/jats:sub><jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> strain <jats:styled-content style=\"fixed-case\">FDC Y<\/jats:styled-content>4 (5\u00a0\u03bcg in 3\u00a0\u03bcl), in the palatal gingival tissue of the right first molar, every 48\u00a0h. Phosphate\u2010buffered saline was injected in the opposite side and used as control. Animals were sacrificed 24\u00a0h after the 10th injection and the maxillae were removed for macroscopic and biochemical analyses. The injections of <jats:styled-content style=\"fixed-case\"><jats:sub><jats:italic>Aa<\/jats:italic><\/jats:sub>LPS<\/jats:styled-content> induced significant alveolar bone loss in <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice. In the absence of <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88 or <jats:styled-content style=\"fixed-case\">TRIF<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88 no bone loss induced by <jats:sub><jats:italic>Aa<\/jats:italic><\/jats:sub><jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> was observed. In contrast, responses in <jats:styled-content style=\"fixed-case\">TRIF<\/jats:styled-content><jats:sup>\u2212\/\u2212<\/jats:sup> mice were similar to those in <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice. Diminished bone loss in the absence of <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88 was associated with fewer <jats:styled-content style=\"fixed-case\">TRAP<\/jats:styled-content>\u2010positive cells and increased expression of osteoblast markers, <jats:styled-content style=\"fixed-case\">RUNX<\/jats:styled-content>2 and osteopontin. There was also reduced tumor necrosis factor\u2010\u03b1 production in <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88<jats:sup>\u2212\/\u2212<\/jats:sup> mice. There was less osteoclast differentiation of hematopoietic bone marrow cells from <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88<jats:sup>\u2212\/\u2212<\/jats:sup> mice after <jats:sub><jats:italic>Aa<\/jats:italic><\/jats:sub><jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> stimulation. Hence, the signaling through <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88 is pivotal for <jats:sub><jats:italic>Aa<\/jats:italic><\/jats:sub><jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced osteoclast formation and alveolar bone loss.<\/jats:p>","DOI":"10.1111\/omi.12034","type":"journal-article","created":{"date-parts":[[2013,7,30]],"date-time":"2013-07-30T08:25:16Z","timestamp":1375172716000},"page":"415-424","source":"Crossref","is-referenced-by-count":34,"title":["My<scp>D<\/scp>88 is essential for alveolar bone loss induced by <i><scp>A<\/scp>ggregatibacter actinomycetemcomitans<\/i> lipopolysaccharide in mice"],"prefix":"10.1111","volume":"28","author":[{"given":"M.F.M.","family":"Madeira","sequence":"first","affiliation":[{"name":"Departamento de Microbiologia ICB Universidade Federal de Minas Gerais (UFMG) Belo Horizonte MG Brazil"},{"name":"Departamento 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