Perdida ósea y defectos intraoseos por periodontitis crónica
Date
2017-09-12
Authors
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Publisher
Universidad Inca Garcilaso de la Vega
Abstract
La etiopatogenia de la periodontitis crónica se ha centrado tradicionalmente en la infección bacteriana, pero en las dos últimas décadas ha aumentado el interés en la respuesta del huésped. La respuesta inicial a la infección bacteriana, es una reacción inflamatoria local que activa el sistema inmune innato y la amplificación de esta respuesta produce la liberación de citocinas y otros mediadores inflamatorios dando como resultado la destrucción del tejido conectivo y el hueso alveolar. Pero el hueso es un órgano metabólicamente activo que constantemente se reabsorbe pero a su vez se remodela y en estos procesos participan células principales como osteoblastos, osteocitos y osteoclastos. La pérdida ósea es mediada por osteoclastos pero a su vez controlada por el sistema RANK, RANK-L, OPG.
A menudo la destrucción ósea en la periodontitis forma un cráter con destrucción del hueso alveolar a esto se conoce como defecto intraoseo o infraoseo. Existen diferentes clasificaciones de defectos intraoseos que le servirán de ayudada al especialista para un adecuado tratamiento. Según Papapanou & Tonetti lo clasifican en defectos supraoseos, infraoseos y de furcación. Golman y Cohen lo dividen en defectos de una pared, dos paredes y tres paredes.
The etiopathogenesis of chronic periodontitis has traditionally focused on bacterial infection, but interest in host response has increased over the past two decades. The initial response to bacterial infection is a local inflammatory reaction that activates the innate immune system and the amplification of this response results in the release of cytokines and other inflammatory mediators resulting in the destruction of connective tissue and alveolar bone. But bone is a metabolically active organ that is constantly reabsorbed but in turn remodels and in these processes involved major cells like osteoblasts, osteocytes and osteoclasts. Bone loss is mediated by osteoclasts but in turn controlled by the RANK system, RANK-L, OPG. Often bone destruction in periodontitis forms a crater with destruction of the alveolar bone. This is known as an intraosseous or infraosus defect. There are different classifications of intraosseous defects that will help you to the specialist for an appropriate treatment. According to Papapanou & Tonetti, they classified it into supraoseos, infraoseos and furcación defects. Golman and Cohen divide it into defects of one wall, two walls and three walls
The etiopathogenesis of chronic periodontitis has traditionally focused on bacterial infection, but interest in host response has increased over the past two decades. The initial response to bacterial infection is a local inflammatory reaction that activates the innate immune system and the amplification of this response results in the release of cytokines and other inflammatory mediators resulting in the destruction of connective tissue and alveolar bone. But bone is a metabolically active organ that is constantly reabsorbed but in turn remodels and in these processes involved major cells like osteoblasts, osteocytes and osteoclasts. Bone loss is mediated by osteoclasts but in turn controlled by the RANK system, RANK-L, OPG. Often bone destruction in periodontitis forms a crater with destruction of the alveolar bone. This is known as an intraosseous or infraosus defect. There are different classifications of intraosseous defects that will help you to the specialist for an appropriate treatment. According to Papapanou & Tonetti, they classified it into supraoseos, infraoseos and furcación defects. Golman and Cohen divide it into defects of one wall, two walls and three walls
Description
Keywords
Hueso, Pérdida ósea, Defecto intraoseo, Periodontitis crónica, Mediadores inflamatorios, Bone, Bone loss, Intraosseous defect, Chronic periodontitis, Inflammatory mediators