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Background & objectives: Epidemiological and clinical studies have shown a close relationship between asthma and obesity. The present study examined the effect of obesity on the airway response to methacholine and the number of inflammatory cells in the bronchoalveolar fluid of ovalbumin-sensitized male rats.
Methods: Twenty-four male Wistar rats were divided into 4 groups: normal diet (C+ND), OVA‐sensitized with the normal diet (S+ND), high-fat diet (C+HFD) and OVA‐sensitized with high‐fat diet (S+HFD). All animals were fed for 8 weeks with standard diet or high-fat diet, and then were sensitized with ovalbumin or normal saline for another 4 weeks while receiving the designed regimens. At the end of the study, the number of inflammatory cells in bronchoalveolar fluid (BALF) and tracheal responsiveness to methacholine were examined.
Results: In diet-induced obesity groups, weight and obesity indices increased (p<0.05 to p<0.001). The results also showed that tracheal responsiveness to methacholine in S+HFD group compared to S+ND group, was significantly increased (p<0.05). In addition, the number of inflammatory cells in the BAL, in the S+HFD group was higher than other groups (p<0.001).
Conclusion: the results of this study suggest that the response of the airways to methacholine and the number of inflammatory cells are increased in obese-asthmatic male rats.
 

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Background & objectives: There is a tendency to increase the risk of dementia in patients with periodontitis, but the opposite, the role of Alzheimer's disease on periodontal disease is still unclear, so in this study, the effect of experimental Alzheimer's disease on periodontal inflammatory cells, collagen fibers and neovascularization was investigated in male rats.
Methods: In this experimental study, 16 Wistar male rats (230-250 grams) were randomly divided into 2 groups; control (saline) and streptozotocin 3 mg/kg (bilateral ICV injection, with a volume of 10 μl, in both groups). After 4 weeks of treatment, two groups were tested with the Morris water maze. Then the rats were killed by deep anesthesia and sampling from the papilla around the two central incisor teeth was done. Samples were fixed and the paraffin block was prepared, serial 5-micron slices were made with a microtome. After hematoxylin & eosin staining, the number of inflammatory cells (PMNs, eosinophils, and mast cells), angiogenesis, and fibroblasts were counted using a microscope (400×). Data were analyzed using SPSS 21 software and an independent T-test.
Results: The results showed that Alzheimer's disease causes an increase in periodontal inflammatory cells, collagen fibers and new vessels in the gums of mice, and the difference between these changes between the experimental and control groups was significant in all parameters (p<0.00).
Conclusion: According to these findings, Alzheimer's disease causes or aggravates inflammation and increases the rate of periodontal diseases in rat and may have the same effect in humans.