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Abstract
This study aimed to examine the effect of chronic restraint stress (RS) on the severity of experimental periodontal disease in rats. A total of 32 male Sprague Dawley (SD) rats were divided into four groups: i) Rats receiving two treatment regimens, chronic stress induced by movement restriction in acrylic cylinders for 1–1.5 h daily and induction of experimental periodontal disease, using a nylon ligature which was placed around the first left mandibular molars (n=8); ii) induction of periodontal disease, without RS (n=8); iii) RS (n=8) and iv) control (n=8). After 15 days, blood samples were obtained, and blood glucose levels and the corticosterone concentration were measured as stress markers. The severity of periodontal disease was analyzed according to the level of gingival and bone inflammation, leading to compromise of the teeth involved. Chronic stress was induced with movement restriction (P≤0.05, Mann-Whitney U-test) and increased the severity (P≤0.05, Mann-Whitney U-test) of experimental perio dontal disease in rats, according to the level of gingival and bone inflammation around the first left mandibular molars. The results of the present study showed that RS modulates periodontal inflammation and that the rat model described herein is suitable for investigating the association between stress and periodontal disease.
Highlights
The development of periodontal inflammation is a complex process, animal models have been developed to assist in its understanding
Results of the Mann-Whitney U test established significant differences between the groups treated with Restraint stress (RS) (RS/PD and RS), compared with final measurements of corticosterone in the groups not treated with RS (PD and control; P≤0,05)
Results of this study have shown that RS was an effective method for causing chronic stress in rats, measured with plasma corticosterone levels
Summary
The development of periodontal inflammation is a complex process, animal models have been developed to assist in its understanding. The main etiological factor of periodontal disease is bacterial plaque, but the pathogenesis of the disease is affected by. It has been reported that stress produces neuroendocrine changes and certain adverse effects on the immune system, which affect the inflammatory response on periodontal tissues [11,12]. The restriction movement technique has become a standard procedure to study stress effects, when using rodents as study subjects [13,14]. This model has been previously used to associate chronic exposure to stress and periodontal destruction [1,2,3,15,16]
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