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  • 1
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Journal of clinical periodontology 29 (2002), S. 0 
    ISSN: 1600-051X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Clinical observations and epidemiological studies suggest that experiences of negative life events, especially those manifested as depression, may contribute to an increased susceptibility to periodontal disease.Objective: In the present study, the prevalence of some negative life events and psychological factors and their relation to periodontal disease were investigated. The sample consisted of individuals 50–80 years of age from an extensive cross-sectional epidemiological study performed in 1993 in the city of Jönköping, Sweden.Method: 298 dentate individuals from the Jönköping study were randomly selected. Clinical and radiographic examinations included registration of the number of existing teeth, plaque index, gingival index, pocket depth, and alveolar bone loss. In addition, a questionnaire about socioeconomic status, life events, and psychological and stress-related factors was used.Results: The results revealed that, in addition to the well-documented periodontal disease risk factors such as increased age, oral hygiene status, and smoking, the loss of a spouse (being a widow or widower) and the personality trait of exercising extreme external control were also associated with severe periodontal disease.Conclusion: The findings support recent studies suggesting that traumatic life events such as the loss of a spouse may increase the risk for periodontal disease. Above all, the present results indicate that an individual's ability to cope with stressful stimuli (coping behavior), as measured by the beliefs of locus of control of reinforcements may play a role in the progression of periodontal disease.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Munksgaard International Publishers
    Journal of periodontal research 37 (2002), S. 0 
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The hippocampus, which is a brain structure involved in learning and memory processes, plays a key role in the feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis and autonomic sympathetic nervous system, and the subsequent secretion of immuno-modulatory hormones in response to pathogenic microorganisms. Dysregulation of these brain-neuroendocrine-immune regulatory networks, which act in concert to maintain homeostasis, is found to be of critical importance to the host defence against pathogens, as well as susceptibility to diseases, including periodontal disease. The present study was designed to determine the effects of hippocampal lesioning on the progression of periodontitis. Experimental ligature-induced periodontitis was induced in 16 Wistar rats, which were bilaterally lesioned in their hippocampal region with an aspiration technique that is well documented to impair learning and memory, as well as in 15 sham-operated control rats. The disease progression was evaluated radiographically and histometrically. The results revealed that the hippocampal lesioned rats developed significantly more destruction of the periodontium than did the sham-operated controls. This finding supports recent studies that indicate that inappropriate brain-neuroendocrine regulation of inflammatory responses to infectious agents may play an important role in disease susceptibility and progression.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Journal of periodontal research 35 (2000), S. 0 
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Inappropriate hypothalamic–pituitary–adrenal (HPA) axis regulation of immune responses to bacterial challenges has been found to play an important role in infections and inflammatory disease susceptibility and progression. In the present study we investigated the tissue effects of experimental periodontitis in Fischer 344 rats, which were subcutaneously (s.c.) injected with 20 mg/kg of the glucocorticoid receptor antagonist and active antiglucocorticoid agent RU 486 every second day over a period of 14 d. Periodontitis was induced by placing a bacterial plaque retentive silk ligature in the gingival sulcus around the neck of maxillary right 2nd molar teeth 1 d after the first injection in 10 RU 486-treated and 10 vehicle (1,2-propanediol)-treated control animals. The contralateral maxillary left 2nd molars served as internal control teeth for naturally occurring periodontitis. Disease progression was evaluated radiographically and histometrically. The average level of corticosterone in blood at sacrifice was significantly lower in the RU 486-treated animals as compared to controls. The experimental animals also developed significantly less periodontal breakdown at both experimental and control teeth compared to the vehicle-treated control animals. The results support our recent findings showing that HPA hyper-reactivity, either genetically determined or experimentally induced, stimulates periodontal disease susceptibility. These findings suggest that central nervous regulation of inflammatory responses to dental plaque microorganisms in the gums may modulate periodontal disease susceptibility and progression.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Journal of periodontal research 36 (2001), S. 0 
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Organisms respond to inflammatory conditions by mounting a co-ordinated complex series of adaptive responses involving the immune, nervous and endocrine systems that are aimed at restoring the homeostatic balance. We have recently shown in a rat model that inappropriate hypothalamic-pituitary-adrenal (HPA) axis regulation and a subsequent inability to mount a suitable glucocorticoid response to gingival inflammation may influence susceptibility to periodontal disease. This study was designed to investigate whether ligature- and bacterial lipopolysaccharide (LPS)-induced inflammation in the gingival connective tissues may activate this physiological axis, and to further explore the significance of HPA regulation in periodontal disease. Experimental periodontal disease was induced in major histocompability complex (MHC)-identical but HPA low (LEW) and high (F344) responding rat strains. We tested (1) whether ongoing periodontal disease activates the HPA axis as measured by corticosterone levels, and (2) whether genetic differences in HPA regulation modulate periodontal disease progression. In the F344 strain, the periodontal tissue destruction was more severe. This observation was associated with a significant increase of corticosterone levels in F344 rats only. Addition of LPS at the gingival inflammatory site led to a further increase of corticosterone levels and disease severity in F344 rats. These findings illustrate a positive feedback loop between the HPA axis and periodontal disease: the disease activates the HPA axis, and a genetically determined high HPA responsitivity further increases disease susceptibility.
    Type of Medium: Electronic Resource
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