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Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

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Autoinmunidad y Periodontitis

Massimo Costalonga¹, Vivek Thumbigere-Math², Mark C Herzberg¹

¹Division of Basic Sciences, Department of Diagnostic and Biological Sciences, School of Dentistry, University of Minnesota, Minneapolis, Minnesota, USA.

Journal of periodontal research

|January 7, 2026

Resumen

Este resumen es generado por máquina.

La autoinmunidad sistémica ocurre cuando falla la tolerancia inmunitaria, lo que lleva a que las células T y B autorreactivas ataquen los tejidos del huésped. La periodontitis exacerba esto al promover la citrulinación y la diseminación de epítopos, activando células autorreactivas latentes y provocando enfermedades autoinmunes.

Palabras clave:

Autoinmunidad Periodontitis Tolerancia inmunitaria Citrulinación Diseminación de epítopos Enfermedades autoinmunes Células T autorreactivas Células B autorreactivas Porphyromonas gingivalis Artritis reumatoide

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Área de la Ciencia:

Inmunología
Autoinmunidad
Enfermedad periodontal

Sus antecedentes:

La autoinmunidad resulta del fallo de la tolerancia inmunitaria, permitiendo que los linfocitos autorreactivos ataquen los tejidos del huésped.
La periodontitis implica inflamación y modificaciones proteicas que pueden desencadenar o empeorar condiciones autoinmunes.

Objetivo del estudio:

Revisar los mecanismos inmunitarios que vinculan la periodontitis con la autoinmunidad sistémica.
Explicar cómo los patobiontes periodontales contribuyen al desarrollo y exacerbación de enfermedades autoinmunes.

Principales métodos:

Esta revisión narrativa sintetiza la evidencia actual sobre la tolerancia inmunitaria, la activación de células T y B, y las modificaciones postraduccionales en la autoinmunidad.
Examina el papel de patógenos periodontales como Porphyromonas gingivalis en la iniciación y amplificación de respuestas autoinmunes.

Principales resultados:

Las células T autorreactivas latentes pueden ser activadas por autoantígenos modificados o péptidos microbianos durante la periodontitis.
La periodontitis promueve la citrulinación y la diseminación de epítopos, ampliando la respuesta autoinmune.
Los patobiontes periodontales contribuyen a la autoinmunidad sistémica a través de la mímica molecular y la inflamación.

Conclusiones:

La periodontitis no solo causa destrucción tisular local, sino también autoinmunidad sistémica.
Mecanismos como la citrulinación y la diseminación de epítopos en la periodontitis pueden iniciar o exacerbar enfermedades autoinmunes como la artritis reumatoide, la EII y la AD.