Diazepam reverses the alveolar bone loss and hippocampal interleukin‐1beta and interleukin‐6 enhanced by conditioned fear stress in ligature‐induced periodontal disease in rats

Abstract

Our results suggest that diazepam treatment reduces bone loss in rats submitted to conditioned fear stress. In addition, diazepam treatment led to decreased IL-1β and IL-6 levels in the hippocampus.

Chronic stress accelerates ligature-induced periodontitis by suppressing glucocorticoid receptor-α signaling

“… 27 , 28 Several studies have investigated the possible relationship between psychological stress and periodontitis in rats and have suggested that stress may play a role in the development of periodontal disease. 29 , 30 In the present study, we showed that CS applied over a period of 4 weeks accelerates the progression of ligature-induced periodontitis, as shown by clinical indications, histological changes and radiographic examination. CS in conjunction with periodontitis also increased serum levels of IL-1β, IL-6 and IL-8 and increased the expression of TLR4 in periodontal tissue.…”

Fluoxetine reduces periodontal disease progression in a conditioned fear stress model in rats

“…On the other hand, fluoxetine did not affect local expression of the proinflammatory cytokines IL-1b and IL-6. In the same way, diazepam also did not affect local expression of the proinflammatory cytokines IL-1b and IL-6 (15). Recently, it was demonstrated that fluctuations in mood can influence inflammation by affecting cytokine production (31).…”

“…On the other hand, in a different study model (28), the nonspecific antidepressant tianeptine significantly inhibited periodontal bone loss in rats (29). Recently we demonstrated that diazepam could also reverse bone loss in the same study model (15). In the same way, it was demonstrated that fluoxetine reduces bone loss in the experimental periodontal disease model, but the animals were not stressed (13).…”

Effect of chronic stress on implant osseointegration into rat's mandible

“…As indicated by the literature, after a repair period of 28 days, pro-inflammatory interleukins such as IL1B and IL6 do not appear to influence the inflammatory stage of repair 14,20,21 .…”

“…It has been established that stress can suppress or stimulate the immune defense, depending on the stressor 14 . Moreover, stress activates the hypothalamic-pituitary-adrenal axis, which causes the release of neuroendocrine hormones, resulting in cortisol secretion by the adrenal cortex 15 , often making the individual susceptible to disease 16 .…”