Abstract:Objective. To evaluate the effects of psychological stress on periodontitis healing in rats and the contribution of basic fibroblast growth factor (bFGF) expression to the healing process. Methods. Ninety-six rats were randomly distributed into control group, periodontitis group, and periodontitis plus stress group. Then, the rats were sacrificed at baseline and week(s) 1, 2, and 4. The periodontitis healing condition was assessed, and the expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), … Show more
“…Proinflammatory cytokines, such as interleukin‐1 and tumor necrosis factor‐alpha, are critical in the early healing events, and thus any stress‐induced alterations may impair wound healing, especially in the early stages. A recent experimental periodontitis study in rats also demonstrated decreased expression of basic fibroblast growth factor and slower recovery of expression of basic fibroblast growth factor in the stress group . Finally, reduced blood flow, as a result of increased catecholamine levels in response to stress, can, in turn, affect oxygen‐dependent healing mechanisms, such as angiogenesis, collagen synthesis and epithelialization .…”
Plaque-induced periodontal diseases occur in response to the accumulation of dental plaque. Disease manifestation and progression is determined by the nature of the immune response to the bacterial complexes in plaque. In general, predisposing factors for these periodontal diseases can be defined as those factors which retain or hinder the removal of plaque and, depending upon the nature of the immune response to this plaque, the disease will either remain stable and not progress or it may progress and result in chronic periodontitis. In contrast, modifying factors can be defined as those factors that alter the nature or course of the inflammatory lesion. These factors do not cause the disease but rather modify the chronic inflammatory response, which, in turn, is determined by the nature of the innate and adaptive immune responses and the local cytokine and inflammatory mediator networks. Chronic inflammation is characterized by vascular, cellular and repair responses within the tissues. This paper will focus on how common modifying factors, such as smoking, stress, hormonal changes, diabetes, metabolic syndrome and HIV/AIDS, influence each of these responses, together with treatment implications. As treatment planning in periodontics requires an understanding of the etiology and pathogenesis of the disease, it is important for all modifying factors to be taken into account. For some of these, such as smoking, stress and diabetic control, supportive health behavior advice within the dental setting should be an integral component for overall patient management.
“…Proinflammatory cytokines, such as interleukin‐1 and tumor necrosis factor‐alpha, are critical in the early healing events, and thus any stress‐induced alterations may impair wound healing, especially in the early stages. A recent experimental periodontitis study in rats also demonstrated decreased expression of basic fibroblast growth factor and slower recovery of expression of basic fibroblast growth factor in the stress group . Finally, reduced blood flow, as a result of increased catecholamine levels in response to stress, can, in turn, affect oxygen‐dependent healing mechanisms, such as angiogenesis, collagen synthesis and epithelialization .…”
Plaque-induced periodontal diseases occur in response to the accumulation of dental plaque. Disease manifestation and progression is determined by the nature of the immune response to the bacterial complexes in plaque. In general, predisposing factors for these periodontal diseases can be defined as those factors which retain or hinder the removal of plaque and, depending upon the nature of the immune response to this plaque, the disease will either remain stable and not progress or it may progress and result in chronic periodontitis. In contrast, modifying factors can be defined as those factors that alter the nature or course of the inflammatory lesion. These factors do not cause the disease but rather modify the chronic inflammatory response, which, in turn, is determined by the nature of the innate and adaptive immune responses and the local cytokine and inflammatory mediator networks. Chronic inflammation is characterized by vascular, cellular and repair responses within the tissues. This paper will focus on how common modifying factors, such as smoking, stress, hormonal changes, diabetes, metabolic syndrome and HIV/AIDS, influence each of these responses, together with treatment implications. As treatment planning in periodontics requires an understanding of the etiology and pathogenesis of the disease, it is important for all modifying factors to be taken into account. For some of these, such as smoking, stress and diabetic control, supportive health behavior advice within the dental setting should be an integral component for overall patient management.
“…These biomarkers include: measuring salivary cortisol levels, standardized stress scales and questionnaires, and the community index of periodontal care needs (CIPC) [18]. From there, studies conducted on animals [19][20][21] and on people, whether it be cohort, cross-sectional, case-control or clinical trials [6,15,28,22] showed a positive correlation between stress and the occurrence of periodontal disease. According to several recent literature reviews, the evidence is currently sufficient to suggest that stress is a risk factor for the occurrence of periodontal disease in the presence of pathogens as well as the worsening of pre-existing periodontal diseases [8,12,15,17,[23][24][25][26].…”
Section: Progressive Establishment Of the Link Between Chronic Stressmentioning
confidence: 99%
“…In the case of a normal healing process, the production of cytokines, interleukins (IL-1b, IL-6, IL-8), and TNF-a decreased significantly. In a stressed subject with periodontitis, the production rate is high, resulting in an increase in the severity of periodontal damage [19]. Stress can also burden some aspects of the immune response such as mitogen stimulation, antibody and cytokine production, and NK cell activity [54].…”
Section: Blood Flow To the Gingivamentioning
confidence: 99%
“…bFGF has multiple effects on cell proliferation, differentiation, and angiogenesis [58]. Animal studies have shown a link between stress, decreased bFGF, and the severity of periodontal disease [19]. Rats with artificially created periodontitis show a greater bone and attachment loss when subjected to stress [20].…”
--Introduction: Periodontal diseases are caused by pathogenic microorganisms that induce increases in of local and systemic proinflammatory cytokines, resulting in periodontal damage. The onset and evolution of periodontal diseases are influenced by many local and systemic risk factors. Educational objective: In this article, we aim to review the results of the research on the impact of chronic stress on the occurrence, development, and response to periodontal disease treatments and on the pathophysiological mechanisms of periodontal disease. Conclusion: Chronic stress has a negative impact on the occurrence, development, and response to the treatment of periodontal disease via indirect actions on the periodontium. This can result from behavioral changes caused by stress (poor dental hygiene, smoking, etc.) and a direct neuroimmunoendocrinological action related to the consequences (particularly immunological) of the secretion of certain chemicals (e.g., cortisol) induced by the activation of the hypothalamus and the autonomic nervous system in response to stress. These factors necessitate multidisciplinary management (e.g., physician, oral surgeon, and psychologist) of patients to identify subjects with chronic stress and to employ countermeasures to decrease the impact of stress on the periodontium.
“…7 Many studies have drawn attention to the role of the increase in local proinflammatory cytokine levels caused by these risk factors and their effects on the pathogenesis of periodontitis. 8,9 It has been reported that obesity, which is characterized by abnormal and excessive fat accumulation in the adipose tissue and has been shown to be one of the most important societal health problems today, affects the pathogenesis of periodontitis in a destructiveprovocative way. [10][11][12][13] Nishada et al 14 reported that obesity is the second most important risk determinant, following smoking, in the pathogenesis of inflammatory periodontal diseases.…”
Background and aims. The aim of this study was to evaluate the possible effects of obesity on the local (salivary) and systemic TNF-α and IL-6 levels in patients with chronic periodontitis (CP). Materials and methods. This study included 88 subjects assigned to four groups of 22 subjects each, as follows: group O+P+ (patients with obesity and CP), group O-P+ (patients with normal weight and CP), group O+P- (periodontally healthy patients with obesity), and the control group, group O-P- (periodontally healthy patients with normal weight). Serum and salivary samples were obtained a week before the recording of clinical periodontal parameters. Local and systemic TNF-α and IL-6 levels were determined biochemically. Results. In serum and saliva, both TNF-α and IL-6 levels were the lowest in O-P- group (P < 0.05). The highest TNF-α and IL-6 levels were observed in O+P+ group, while only IL-6 levels were statistically significant (P < 0.05). Conclusion. Obesity upregulated the salivary and serum levels of TNF-α and IL-6. In patients with periodontitis, who were also obese, the serum and saliva levels of IL-6 were significantly high. Obesity might play a destructive and provocative role in the pathogenesis of periodontitis by negatively affecting IL-6 levels.
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