Armin Herforth

Stress, oral health behaviour and clinical outcome

OBJECTIVE Several studies indicate that stress adversely affects various health behaviours. Oral hygiene behaviour, however, has been rarely studied in this context. The present study thus aims to assess the effects of stress on oral hygiene behaviour and clinical outcome. DESIGN In a prospective matched controlled design 12 pairs of medical students, each consisting of 1 student participating in a major academic exam and 1 student not participating in any exams (control) were studied. METHODS A professional tooth cleaning was performed 4 weeks prior to exams to obtain plaque levels of 0 at all sites. Immediately prior to professional tooth cleaning and 4 weeks after exams plaque levels (as indicator of oral hygiene behaviour) and bleeding on probing (an indicator of gingivitis) were assessed. RESULTS No group differences were observed at the beginning of the exam period; after exams significant higher rates of plaque (p=.0005, d=1.74) and gingivitis (p=.016, d=1.01) were observed in exam students as compared with controls. CONCLUSIONS The study illustrates the clinical significance of stress effects on health behaviour. Stress should be included as a factor in models of patient compliance and health behaviour.

Acute Stress Induces Proinflammatory Signaling at Chronic Inflammation Sites

Objectives: To analyze in a randomized controlled study whether acute psychological stress alters local proinflammatory signals in a human model of chronic inflammation, i.e., gingivitis. Chronic inflammation represents a crucial factor in a variety of diseases and factors that contribute to the onset and progression of disease. Psychological stress is assumed to represent such a factor. However, experimental human research in this area is rare. Methods: A total of 25 students (n = 11 females, 14 males) suffering from gingivitis were subjected to a stress (public-speaking task) and to a control condition in randomized order. Local concentrations of interleukin (IL)-8 were quantified as an indicator of proinflammatory activity at sites of inflammation. IL-8 is a strong proinflammatory mediator and involved in a variety of disease processes. Samples were taken at sites of inflammation before stress versus control condition and 0, 45, and 90 minutes afterward. Results: A significant main effect (p = .03) of acute stress on local IL-8 was found. Stress induced an increase of IL-8-concentrations; univariate effect sizes varied between d = 0.23 and d = 0.36. Conclusion: This is the first human experimental in vivo study demonstrating that psychological stress alters the local concentrations of IL-8 under conditions of chronic inflammation. It provides direct evidence acute stress is involved in the regulation of local proinflammatory responses in chronic inflammation. Future studies should now explore the effects of more enduring stress conditions and the factors mediating stress effects on inflammatory signals. IL = interleukin; GCF = gingival crevicular fluid; CRH = corticotrophin-releasing hormone; SP = substance P.

Effects of acute stress on local IL-1β and IL-8 in a human in vivo model of chronic inflammation

(1–3 h), whereas a 10.0 mg/kg dose of heroin produced hypothermia during the same period of time. These effects are similar to effects of morphine at comparatively similar doses. Furthermore, the results showed that both doses of heroin inhibited LPS-induced hyperthermia, which occurs 4–8 h after administration. The results indicate an inhibitory effect of heroin on the LPS-induced fever that is not dependent on the nature of initial heroin-induced alterations in body temperature, as evidenced by the fact that both early hypothermia and hyperthermia reduced LPSinduced fever. Previous research has supported the hypothesis that LPS-induced fever is prostaglandin E2 (PGE2)-mediated. Further experimentation will investigate if heroin has similar effects on other PGE2-mediated fevers, such as fever induced by glycoprotein 120 (gp120), which has been implicated in the development of HIV-associated dementia. The investigation of opioid-induced alterations of fever could lead to a greater understanding of the mechanisms that promote infection in opioid users.