Publication: Efecto de la periodontitis asociada a la obesidad en el perfil plasmático bioquímico. Estudio en ratas Wistar
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2017
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Abstract
Antecedentes: En la última década, numerosos estudios epidemiológicos y clínicos han demostrado una asociación entre la obesidad y una prevalencia aumentada de periodontitis. Sin embargo, muchos aspectos relacionados con las inferencias causales y con los mecanismos moleculares involucrados tienen que ser evaluados.
Objetivos: Analizar el desarrollo de periodontitis en relación a un consumo de dieta alta en grasa y las posibles modificaciones en parámetros pro-inflamatorios y metabólicos.
Métodos: Se utilizaron 28 ratas Wistar macho que fueron divididas en 4 grupos: 1. ratas con dieta control (CON); 2. ratas con dieta alta en grasa (HFD); 3. ratas con dieta control y periodontitis inducida (CON-Perio); 4. ratas con dieta alta en grasas y periodontitis inducida (HFD-Perio). La periodontitis se indujo a través de lavados orales con P. gingivalis y F. nucleatum. Se evaluaron índices clínicos periodontales y se analizaron los niveles circulantes de citoquinas, de adipocitoquinas y de lípidos.
Resultados: Los animales expuestos a una dieta hipercalórica presentaron un incremento de peso estadísticamente significativo (p<0,05) respecto a los controles. Los grupos con periodontitis inducida mostraron un incremento de PPD, BOP y MGI estadísticamente significativos (p<0,05) respecto a los grupos sin periodontitis, siendo los valores más elevados el grupo HFD-Perio. Las citoquinas pro-inflamatorias interleucina-1 (IL-1proteína quimioatractante de monocitos (MCP-1) y factor de necrosis tumoral- (TNF- y los niveles de ácidos grasos libres y de triglicéridos exhibieron niveles estadísticamente más elevados (p<0,05) en los grupos con periodontitis respecto a los grupos sin periodontitis Las concentraciones plasmáticas de leptina, de visfatina y resistina mostraron tendencia a aumentar en las ratas con periodontitis inducida, mientras que los niveles de adiponectina se redujeron en los grupos con periodontitis.
Conclusiones: Se puede afirmar que el estado dismetabólico e inflamatorio sistémico producido por el desarrollo de la obesidad es un factor que puede modificar la incidencia y la progresión de la periodontitis. Además, el tener periodontitis, también independientemente de la obesidad, se correlaciona a un desbalance en los niveles sistémicos de adipocitoquinas y de lípidos plasmáticos.
Background: In the last decade, several epidemiological studies have found an association between obesity and increased prevalence of periodontitis. Although, several issues regarding the temporal association and the molecular mechanisms involved still need to be addressed. Objective: To evaluate the effects of a high fat diet on the clinical onset of periodontitis and the plasmatic determinants of inflammation and metabolism dysregulation. Methods: 28 male Wistar rats were randomly divided into four different groups: 1. rats fed with control diet (CON); 2. rats fed with high fat diet (HFD); 3. rats fed with control diet and periodontitis (CON-Perio); 4. rats fed with high fat diet and periodontitis (HFD-Perio). Periodontitis was induced through oral gavages with P. gingivalis and F. nucleatum. A periodontal examination was performed and the plasmatic levels of cytokines, adipocytokines and lipids were estimated. Results: A significant mean increase in body weight (p<0.05) was observed in animals fed with a hypercaloric diet compared to controls. Groups with induced periodontitis displayed statistically significant increases in PPD, BOP and MGI compared to control groups without periodontitis, with the HFD-Perio group exhibiting the highest values. Plasma levels of pro-inflammatory cytokines interleukin-1IL-1monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-TNF- and the concentration of free fatty acids and triglycerides revealed statistically significant increases (p<0.05) in the groups with periodontitis, compared to non-periodontitis groups. Plasma levels of leptin, visfatin and resistin showed an increasing trend in rats with periodontitis, while adiponectin levels were reduced. Conclusions: It may be asserted that obesity induced through a high fatty diet increases the incidence and severity of periodontal breakdown in a Wistar rat model. In addition, the complex proinflammatory and dysmetabolic state brought about by obesity and periodontitis can bolster the deleterious effects of the two diseases.
Background: In the last decade, several epidemiological studies have found an association between obesity and increased prevalence of periodontitis. Although, several issues regarding the temporal association and the molecular mechanisms involved still need to be addressed. Objective: To evaluate the effects of a high fat diet on the clinical onset of periodontitis and the plasmatic determinants of inflammation and metabolism dysregulation. Methods: 28 male Wistar rats were randomly divided into four different groups: 1. rats fed with control diet (CON); 2. rats fed with high fat diet (HFD); 3. rats fed with control diet and periodontitis (CON-Perio); 4. rats fed with high fat diet and periodontitis (HFD-Perio). Periodontitis was induced through oral gavages with P. gingivalis and F. nucleatum. A periodontal examination was performed and the plasmatic levels of cytokines, adipocytokines and lipids were estimated. Results: A significant mean increase in body weight (p<0.05) was observed in animals fed with a hypercaloric diet compared to controls. Groups with induced periodontitis displayed statistically significant increases in PPD, BOP and MGI compared to control groups without periodontitis, with the HFD-Perio group exhibiting the highest values. Plasma levels of pro-inflammatory cytokines interleukin-1IL-1monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-TNF- and the concentration of free fatty acids and triglycerides revealed statistically significant increases (p<0.05) in the groups with periodontitis, compared to non-periodontitis groups. Plasma levels of leptin, visfatin and resistin showed an increasing trend in rats with periodontitis, while adiponectin levels were reduced. Conclusions: It may be asserted that obesity induced through a high fatty diet increases the incidence and severity of periodontal breakdown in a Wistar rat model. In addition, the complex proinflammatory and dysmetabolic state brought about by obesity and periodontitis can bolster the deleterious effects of the two diseases.
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