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      Enfermedad periodontal e infección por VIH: estado actual Translated title: Periodontal disease and HIV infection: Up to date

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          Abstract

          La infección por el virus de la inmunodeficiencia humana (VIH) puede tener influencia a nivel periodontal. El deterioro del sistema inmune por una disminución de los linfocitos TCD4+ puede comprometer las defensas del huésped a nivel sistémico por lo que se puede aumentar la susceptibilidad a padecer diferentes patologías en la cavidad oral. En este trabajo de revisión se recoge el estado actual de la enfermedad periodontal en pacientes VIH+ y trata de abordar como el VIH puede influir en la microbiota subgingival aumentando el riesgo de padecer periodontitis. La presencia de otros factores coadyuvantes podría favorecer la aparición de patología o incluso agravarla independiente de la presencia del VIH.

          Translated abstract

          Human immunodeficiency virus (HIV) infection can be related with the periodontal status. The damage of the immunological system by decreasing TCD4+ lymphocytes may compromise host defences therefore the susceptibility of suffering from several diseases in the oral cavity can also be increased. This review manuscript adresses the current aspects concerning to the periodontal disease in HIV infected patients and tries to explain how HIV may influence the subgingival microflora, increasing the risk of suffering periodontal problems. Others concomitant factors, not related with HIV infection, might help either the onset or increase the severity of the disease.

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          Periodontal diseases: pathogenesis.

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            Development of a classification system for periodontal diseases and conditions.

            G Armitage (2015)
            Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classification system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics. Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology. These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings, including: (1) considerable overlap in disease categories, (2) absence of a gingival disease component, (3) inappropriate emphasis on age of onset of disease and rates of progression, and (4) inadequate or unclear classification criteria. The 1993 European classification lacked the detail necessary for adequate characterization of the broad spectrum of periodontal diseases encountered in clinical practice. The need for a revised classification system for periodontal diseases was emphasized during the 1996 World Workshop in Periodontics. In 1997 the American Academy of Periodontology responded to this need and formed a committee to plan and organize an international workshop to revise the classification system for periodontal diseases. The proceedings in this volume are the result of this reclassification effort. The process involved development by the Organizing Committee of an outline for a new classification and identification of individuals to write state-of-the-science reviews for each of the items on the outline. The reviewers were encouraged to depart from the preliminary outline if there were data to support any modifications. On October 30-November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions was held and a new classification was agreed upon (Figure 1). This paper summarizes how the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics. In addition, an analysis of the rationale is provided for each of the modifications and changes.
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              Role of cytokines and inflammatory mediators in tissue destruction.

              Colonization or emergence of microbial pathogens may result in tissue destruction by activation of one or more of five distinct host degradative pathways (matrix metalloproteinase pathway, plasminogen-dependent pathway, phagocytic pathway, PMN-serine proteinase pathway and osteoclastic bone resorption) or by direct cleavage of extracellular matrix constituents by microbial proteinases. Activation of endogenous destructive pathways may be mediated by immune responses resulting in expression of degradative cellular phenotypes among both immigrant and resident cell populations. In addition, expression of degradative phenotypes may be triggered by direct influences on host cells of microbial products (LPS, enzymes, toxins). A body of evidence suggests that each of these mechanisms involves local production of proinflammatory cytokines and growth factors. The matrix metalloproteinase pathway is centrally involved in dissolution of all unmineralized connective tissues and perhaps in resorption of bone as well. The matrix metalloproteinase family consists of nine or more genetically distinct Zn++ endopeptidases which collectively cleave all of the constituents of the extracellular matrix. Recent studies have uncovered many essential elements of a complex, but still incomplete, regulatory network that governs tissue destruction. Proinflammatory cytokines and growth factors induce signalling pathways several of which are dependent on protein kinase C and result in transient expression of the transcription factors c-jun and c-fos. Initiation of transcription of most matrix metalloproteinase genes requires binding of the transcription factor AP-1 (c-jun/c-fos) to a specific promoter sequence but attainment of maximal transcription rates is dependent on interaction with other promoter elements as well. Several matrix metalloproteinases have been detected in crevicular fluids and tissues of inflamed human gingiva as have the proinflammatory cytokines (IL-1 and TNF-alpha) which regulate their transcription. Although the mere presence of enzymes and cytokines does not necessarily impart function per se, these observations suggest that some level of spatial or temporal linkage exists between metalloproteinase/cytokine expression and gingival inflammation.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                peri
                Avances en Periodoncia e Implantología Oral
                Avances en Periodoncia
                Ediciones Avances, S.L. (Madrid, Madrid, Spain )
                1699-6585
                2340-3209
                December 2006
                : 18
                : 3
                : 135-147
                Affiliations
                [01] Madrid orgnameUniversidad Complutense de Madrid orgdiv1Facultad de Odontología
                Article
                S1699-65852006000300003
                10.4321/s1699-65852006000300003
                c43da094-96fe-4413-89f3-b0ba20f2551d

                This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 International License.

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                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 83, Pages: 13
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                SciELO Spain


                VIH,enfermedad periodontal,SIDA,situación inmunológica,higiene oral,HIV,periodontal disease,AIDS,immunologic status,oral higiene

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