Anxiety, exhaustion and depression in relation to periodontal diseases
Abstract: Periodontal diseases (gingivitis and periodontitis), are inflammatory processes of the gingiva and supporting structures of the teeth induced by a microbial biofilm. In periodontitis this inflammatory process causes tissue degradation and eventually tooths loss. Initiation and progression of periodontitis are due to a combination of genetic factors and environmental factors e.g, neglect of oral hygiene, stress/anxiety/depression, smoking and systemic diseases. The present thesis includes four studies which all aim at increased understanding of the influence of anxiety and depression on periodontal diseases. The first specific aim of these studies was to investigate the influence of anxiety on gingival inflammation and periodontal disease in non-smokers and smokers (Study I). Secondly we wanted to determine if self-reported anxiety had an association with gingival inflammation and attachment level (AL), as well as with the levels of prostaglandin E2 (PGE2), interleukin 1beta (IL-1beta) and elastase in gingival crevicular fluid (GCF) in subjects with periodontitis (Study II). The third aim was to investigate the importance of stress for the development of periodontitis by comparing oral health status, pro-inflammatory markers, and cortisol in GCF and saliva in patients with stress-related mental depression and in non-depressed controls (Study III). The final aim was to investigate periodontal status in relation to inflammatory markers and cortisol in GCF and saliva in women on longterm sickleave for job-stress related depression compared to non-depressed women (Study IV). The findings of all of these studies revealed that the gingival inflammation was significantly elevated in anxious subjects (Studies I , II) and in the depressed patients (Studies III, IV). Anxious smokers with periodontitis had significantly more sites with pockets > 5 mm than nonanxious smokers with periodontitis (Study I). Furthermore, anxious subjects with aggressive periodontitis showed more sites with probing depth > 5 nun compared to non-anxious subjects in the same group. Anxious smokers with periodontitis exhibited a significantly higher degree of loss of attachment than the nonanxious smokers with periodontitis (Study II). The levels of PGE2, IL-10 and elastase in the GCF of these two groups did not differ significantly. The depressed women in Study III had significantly more amount of dental plaque and the depressed women in Study IV had significantly more deep pockets compared to the non-depressed women. The levels of interleukin-6 (IL6) in GCF were significantly higher in the patients in both studies compared to controls, while the levels of IL-1beta did not differ between the groups. In Study III, the cortisol level in GCF was increased, whereas the patients in Study IV surprisingly showed lower cortisol values in GCF than the controls. The level of cortisol in saliva was similar in both groups. Neither did the levels of matrix metalloproteinases-8, -9 (MMP-8, MMP- 9) differ from the control group (Study IV), however, the control group reported unexpectedly higher levels of MMP-9 than the depressed patients in Study III. In conclusion, the present thesis findings altogether strengthen the hypothesis that anxiety and depression play an important role in the progression of periodontal diseases. We suggest that this influence is due not only due to behavioural changes, but also to a direct influence on the immune system.
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