Eje inflamatorio, genético y endotelial entre la periodontitis y la enfermedad cardiovascular: mecanismos compartidos y perspectivas clínicas
DOI:
https://doi.org/10.16921/pfr.v10i3.393Palabras clave:
periodontitis; enfermedades cardiovasculares; inflamación sistémica; disfunción endotelial; biomarcadores; microARN; aterosclerosis; salud oral sistémica.Resumen
Las enfermedades cardiovasculares son la principal causa de muerte a nivel mundial y su desarrollo se relaciona estrechamente con procesos inflamatorios crónicos. La periodontitis, una enfermedad inflamatoria multifactorial que afecta a los tejidos de soporte dental, ha sido reconocida como un posible factor de riesgo cardiovascular. Este artículo revisa la evidencia reciente sobre los mecanismos inflamatorios, moleculares y genéticos que vinculan ambas patologías, así como los efectos del tratamiento periodontal sobre los biomarcadores sistémicos.
La evidencia sugiere que las bacterias periodontales y sus endotoxinas pueden ingresar al torrente sanguíneo, activar receptores tipo Toll 2 y 4, y desencadenar la vía del factor nuclear kappa B con liberación de citoquinas proinflamatorias. Esta cascada favorece la disfunción del endotelio y la formación de placa aterosclerótica. Destacan como marcadores compartidos la proteína C reactiva, la metaloproteinasa 9 y la dimetilarginina asimétrica; también se observa la participación de pequeñas moléculas de ácido ribonucleico no codificante con función reguladora, así como de variantes genéticas en genes de la respuesta inmune innata. Los ensayos clínicos indican que el tratamiento periodontal reduce la inflamación sistémica y mejora los parámetros vasculares, aunque la causalidad directa aún no está plenamente demostrada.
En conjunto, la periodontitis debe considerarse un cofactor modificable del riesgo cardiovascular y su abordaje integrado puede fortalecer las estrategias de prevención de enfermedades crónicas no transmisibles.
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