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Authordc.contributor.authorSilva, Nora 
Authordc.contributor.authorAbusleme Ramos, Loreto Andrea 
Authordc.contributor.authorBravo, Denisse 
Authordc.contributor.authorDutzan Muñoz, Nicolás 
Authordc.contributor.authorGarcía Sesnich, Jocelyn 
Authordc.contributor.authorVernal Astudillo, Rolando 
Authordc.contributor.authorHernández, Marcela 
Authordc.contributor.authorGamonal Aravena, Jorge Antonio 
Cita de ítemdc.identifier.citationJournal of Applied Oral Science 2015; 23(3): 329-55en_US
Identifierdc.identifier.otherDOI: 10.1590/1678-775720140259
General notedc.descriptionArtículo de publicación ISIen_US
Abstractdc.description.abstractPeriodontal diseases usually refer to common inflammatory disorders known as gingivitis and periodontitis, which are caused by a pathogenic microbiota in the subgingival biofilm, including Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Treponema denticola that trigger innate, inflammatory, and adaptive immune responses. These processes result in the destruction of the tissues surrounding and supporting the teeth, and eventually in tissue, bone and finally, tooth loss. The innate immune response constitutes a homeostatic system, which is the first line of defense, and is able to recognize invading microorganisms as non-self, triggering immune responses to eliminate them. In addition to the innate immunity, adaptive immunity cells and characteristic cytokines have been described as important players in the periodontal disease pathogenesis scenario, with a special attention to CD4(+) T-cells (T-helper cells). Interestingly, the T cell-mediated adaptive immunity development is highly dependent on innate immunity-associated antigen presenting cells, which after antigen capture undergo into a maturation process and migrate towards the lymph nodes, where they produce distinct patterns of cytokines that will contribute to the subsequent polarization and activation of specific T CD4+ lymphocytes. Skeletal homeostasis depends on a dynamic balance between the activities of the bone-forming osteoblasts (OBLs) and bone-resorbing osteoclasts (OCLs). This balance is tightly controlled by various regulatory systems, such as the endocrine system, and is influenced by the immune system, an osteoimmunological regulation depending on lymphocyte- and macrophage-derived cytokines. All these cytokines and inflammatory mediators are capable of acting alone or in concert, to stimulate periodontal breakdown and collagen destruction via tissue-derived matrix metalloproteinases, a characterization of the progression of periodontitis as a stage that presents a significantly host immune and inflammatory response to the microbial challenge that determine of susceptibility to develop the destructive/progressive periodontitis under the influence of multiple behavioral, environmental and genetic factors.en_US
Patrocinadordc.description.sponsorshipScientific and Technologic Investigation Resource, Chile 1090046 1130570en_US
Publisherdc.publisherUniv Sao Paulo Fac Odontologia Bauruen_US
Type of licensedc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
Link to Licensedc.rights.uri*
Keywordsdc.subjectPeriodontal diseasesen_US
Keywordsdc.subjectProgressive periodontitisen_US
Títulodc.titleHost response mechanisms in periodontal diseasesen_US
Document typedc.typeArtículo de revistaen_US

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Atribución-NoComercial-SinDerivadas 3.0 Chile
Except where otherwise noted, this item's license is described as Atribución-NoComercial-SinDerivadas 3.0 Chile