Stress and inflammation in periodontal disease: a review of the basic biological mechanisms

DOI: https://doi.org/10.25241/stomaeduj.2020.7(2).art.5


Background Periodontitis is a multifactorial infectious disease influenced by a myriad of other conditions and factors amongst which, psychosocial stress has emerged as a potential risk indicator. In order to establish this link in a generally accepted theory, we need to better understand the physiological pathways of stress on immune response with implications in the periodontal disease.
Objective This article aims at synthesizing the current knowledge on the effect of the psychological factors on the periodontal disease and to provide an insight into the bidirectional links between stress-related disorders and periodontitis via psychoneuroimmunology studies.
Data sources A search was performed in 2 databases – PubMed and Google Scholar, supplemented by a manual search in peer-reviewed journals and cross-referenced with the articles accessed. The key terms used were: periodontal disease, periodontitis, stress, psychosocial stress, inflammation.
Study selection The inclusion criteria were all published potentially relevant articles on relationship between stress, inflammation and periodontitis on human and animal models. The exclusion criteria were articles with non-available full text and articles that were not written in English.
Data extraction Two reviewers extracted information regarding the quality and study characteristics independently. The studies were assessed for their methodology, statistical analysis, characteristics of the periodontal outcome measures, and psychological measurements.
Data synthesis Considerable evidence documents the link between psychosocial stress and periodontitis. This should redirect the attention of researchers and clinicians towards a multidisciplinary approach to periodontitis where psychosocial disturbances might be a key component into the rebus of disease progression and treatment results.

Periodontitis; Stress; Psychosocial Stress; Inflammation; Glucocorticoids.