| Objective:Studies have shown that psychological stress plays a significant role in the outcome of manydiseases. The present study is designed to investigate the effect of psychological stress onexperimental ligature-induced periodontal disease in rats by means of a variable moderatechronic stress. The stress indicators including blood glucose and serum adrenocorticotropichormone (ACTH) are detected in this study. The interleukin-1β(IL-1β) and interleukin-17(IL-17)expressions in periodontal tissues are measured by means of immunohistochemistry（IHC）toobserve the impact of the psychological stress on periodontal immune function. The serumconcentration of lactate dehydrogenase (LDH) and isoenzymes lactate dehydrogenase1(LDH1)are measured to assess the degree of hypoxia, which can help to analyze the impact of thepsychological stress on the oxygen metabolism of periodontitis. The findings will provide insightinto understanding the relationship between psychological stress and periodontal disease, andprovide new treatment ideas for periodontal disease.Methods:Eighty male Wistar rats in specific pathogen-free grades were randomly divided into fourgroups:1) normal control group, naive rats;2) experimental periodontitis group, the periodontitiswas induced by wrapping3/0silk ligature inoculated with putative periodontopathic bacteriaaround the left second maxillary molar of the rats;3) psychological stress-stimulation group, therats were only treated with stress-stimulation;4) experimental periodontits plusstress-stimulation group, the periodontitis were induced by wrapping3/0silk ligature inoculatedwith putative periodontopathic bacteria around the left second maxillary molar of the rats, andthen treated with stress-stimulation. The rats were sacrificed at week2,4,6and8respectivelyafter the ligature. Stresses were imposed by means of restraint stress immersions of cold-waterand iced water stress, and rat refoulement stress. Five rats from each group were sacrificed at thedesignated time points under deep anesthesia by ether inhalation. The tail vein blood sampleswere collected before the rats were euthanized to measure blood glucose level, serum ACTH,LDH and isoenzyme LDH1. The histopathologic changes and the alveolar bone absorption ofperiodontia stained with hematoxylin and eosin were observed under a microscope. The expression of IL-1β and IL-17were measured by immunohistochemistry, the average positivecell rate of IL-1β and IL-17was calculated to assess the degree of expression.Results:1) The level of blood glucose and ACTH in the stress-stimulation group and the experimentalperiodontits plus stress-stimulation group was significantly higher than that of the control groupand experimental periodontitis groups at weeks2and4(p＜0.01); however, the level of bloodglucose in the stress-stimulation group turned normal at weeks6and8(p＞0.05); the level ofblood glucose in the experimental periodontits plus stress-stimulation group was significantlyhigher than that of the control group (p＜0.01）and the experimental periodontitis group（p＜0.05） at weeks6and8. The level of ACTH in the experimental periodontits plusstress-stimulation group was decreased at weeks6and8, but it was still significantly higher thanthat of the control group and the experimental periodontitis groups at weeks6and8（p＜0.05）.2) The serum level of LDH in the experimental periodontits plus stress-stimulation group wassignificantly higher than that of the control group and experimental periodontitis group (p＜0.01)at any time points. The level of serum LDH in stress-stimulation group was significantly higherthan that of the control group and experimental periodontitis group at weeks2（p＜0.01);however, it showed no significant difference from that of the control group and experimentalperiodontitis group at weeks4,6and8（p＞0.05）. The serum level of LDH1in experimentalperiodontits plus stress-stimulation group was significantly lower than that of the control groupand experimental periodontitis group (p＜0.01)at any time points. The level of serum LDH1instress-stimulation group was significantly lower than that of the control group and experimentalperiodontitis group at weeks2（p＜0.01）, but it showed no significant difference from that of thecontrol group and experimental periodontitis group at weeks4,6and8（p＞0.05）.3) There were no significant differences of tooth morphologic changes of gross specimenobservation between the control group and the stress-stimulation group, e.g., gingival attachmentsites appeared normal, without periodontal attachment loss. Moderate gingival atrophy andperiodontal attachment loss were observed in the experimental periodontitis group. The grossspecimen of the experimental periodontitis plus stress-stimulation group showed severe gingivalatrophy, obvious periodontal pocket, and severe periodontal attachment loss. In addition, thefurcation of tooth root was exposed, involving both sides of the adjacent teeth. 4) Histologically, there were no differences of junctional epithelium, periodontal ligamentfibers, and morphology of alveolar bone among the normal control and stress-stimulation groups;severer inlfamatory change and alveolar bone destruction were observed in the experimentalperiodontits plus stress-stimulation group than the experimental periodontitis group. Serioustissue damage, attachment loss and destruction involving adjacent tooth tissue were observed inthe experimental periodontits plus stress-stimulation group at weeks4,6and8.5) The average rate of positive cells for IL-1β and IL-17in the normal control andstress-stimulation groups showed no significant difference at all time points（p＞0.05）; theaverage rate of positive cells for IL-1β and IL-17in experimental periodontitis group andexperimental periodontits plus stress-stimulation group was significantly higher than that ofnormal control and stress-stimulation groups at all time points(p＜0.05); the average rate ofpositive cells for IL-1β and IL-17in experimental periodontits plus stress-stimulation group wassignificantly higher than that of the experimental periodontitis group at weeks4,6and8(p＜0.05).Conclusions:1). Stress-stimulation cannot cause periodontitis.2). Stress-stimulation can aggravate the inflammation and destruction of periodontitis.3). Stress-stimulation may aggravate the inflammation and destruction of the periodontal tissueby increasing the expressing of IL-1β and IL-17.4). Stress-stimulation may aggravate periodontal disease in rats by reducing the level ofperiodontal tissue oxygen metabolism.In this study, we have provided data suggesting a correlation of periodontitis severity withpsychologic stress and periodontal tissue hypoxia in an animal model. Furthermore, the evidencesuggests that reduced psychological stress expression may play an important role in maintainingthe oral health. To the best of our knowledge, this work is the first evidence indicating that thepsychological stress induces a hypoxic tissue microenvironment, IL-1β and IL-17expression inexperimental periodontitis animal models. The mechanisms of how stress affects periodontaldisease will be studied further. |
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