Stress, Cortisol, and Periodontitis in a Population Aged 50 Years and Over

Stress, Cortisol, and Periodontitis in a Population Aged 50 Years and Over
2006
J.B. Hilgert1,*, F.N. Hugo2, D.R. Bandeira3, and M.C. Bozzetti1
Journal of Dental Research

© 2006 International and American Associations for Dental Research

1 Post-graduate Program in Epidemiology, Faculty of Medicine, Federal University of Rio Grande do Sul, Rua Ramiro Barcelos, 2600/414 Porto Alegre, RS 90035-003, Brazil;
2 Department of Physiological Sciences, Faculty of Dentistry of Piracicaba, State University of Campinas, Piracicaba, SP, Brazil; and
3 Psychology Institute, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil

* corresponding author, juhilger@terra.com.br

ABSTRACT

Periodontitis and its relationship with psycho-neuro-immunological variables, such as psychological stress and cortisol, have been little explored. The objective of this study was to evaluate the extent and severity of chronic periodontitis and its association with the levels of salivary cortisol and the scores obtained with a stress questionnaire in a population aged 50 years and over. We studied 235 individuals in a cross-sectional study. They answered the LippÌs Inventory of Stress Symptoms for Adults, were instructed to collect three saliva samples for cortisol analysis, and were examined for evaluation for periodontitis. Based on logistic regression, cortisol levels were positively associated with the following outcomes: means of clinical attachment level (CAL) > = 4 mm [OR = 5.1, 95%CI (1.2, 20.7)]; 30% of sites with CAL > = 5 mm [OR = 6.9, 95%CI (1.7, 27.1)]; and 26% of sites with probing depth > = 4 mm [OR = 10.7, 95%CI (1.9, 54.1)] after adjustment for confounding variables. The results suggest that cortisol levels were positively associated with the extent and severity of periodontitis.


KEY WORDS: stress Ô periodontitis Ô glucocorticoids

INTRODUCTION

Stress has been defined as either stimulus or response. Stimulus definitions focus on events in the environment. Response definitions, which have been prevalent in biology and medicine, refer to state stress. This definition of stress, however, has some drawbacks, and a more modern definition emphasizes the relationship between the person and the environment, taking into account characteristics of the person and the stressful event (Lazarus and Folkman, 1984).

An organismÌs functions are regulated by the nervous system and the endocrine system, which are interrelated. It is known that two pathways link the brain and the immune system, one of which is the hypothalamus-pituitary-adrenal axis (Guyton and Hall, 2000).

It has been known for several decades that stressÛwhether inflammatory, traumatic, or psychologicalÛis associated with concurrent activation of the hypothalamus-pituitary-adrenal axis. In the early 1990s, it also became apparent that cytokines and other humoral mediators of inflammation are potent activators of the central stress response (Tsigos et al., 1997). On the one hand, the glucocorticoids released via the activation of the hypothalamus-pituitary-adrenal axis seem to be important, due to their ability to regulate the recruitment of immune cells into inflamed tissues, as well as to skew the Th1/Th2 balance toward a Th2-dominant response (Breivik and Thrane, 2001). Also, a negative feedback, with the activation of the immune system, associated with the increase of circulating cytokines, increases the activity of the corticotropine-releasing hormone, activating the hypothalamus-pituitary-adrenal axis and causing an elevation of the levels of cortisol. When the inflammatory action is sufficiently long and profound, systemic manifestations of the disease may become evident, as could happen with periodontitis (LeResche and Dworkin, 2002).

There are several studies that have demonstrated a relationship between psychological stress and inflammatory diseases such as rheumatoid arthritis (Zautra et al., 1997) and periodontitis (da Silva et al., 1995; Breivik et al., 1996; Aurer et al., 1999; Genco et al., 1999). However, why and how these factors are associated with increased periodontal disease susceptibility are poorly understood. The field of brain-neuroendocrine-immune interactions, therefore, is an important field to be explored (Breivik and Thrane, 2001).

Even though investigators have studied the impact of the immune response and of psychosocial components on the extent and severity of periodontitis, few studies have evaluated the impact of relationships among psychosocial well-being, status of the immune system, and the health of the periodontium. Our hypothesis was that stress elicits hypothalamus-pituitary-adrenal axis hyperactivation and leads to periodontitis. Thus, the purpose of this study was to evaluate the extent and the severity of chronic periodontitis and its association with the levels of cortisol and the scores of an inventory of stress symptoms in a population aged 50 years or older.

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