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Objective: The purpose of this study was to evaluate whether local administration of TIL could influence the expression of the inflammatory mediators IL-1β, TNF-α, MMP-8 and COX-2 in rats with experimental periodontitis (EP)., Methods: Twenty-four adult male rats (Rattus norvegicus, albinus, Wistar) were assigned to groups C, EP, EP-TIL (CControl group, EP-Periodontitis groups). On EP groups, a ligature was placed around maxillary 2nd molars on day 1. On group EP-TIL, 20 μL of TIL solution (1 mg/kg body weight) was injected into the subperiosteal palatal area adjacent to the maxillary 2nd molar every other day until euthanasia (day 11). Alveolar bone loss was morphometrically analyzed. mRNA expressions of IL-1β, TNF-α, MMP-8 and COX-2 were assessed by qPCR. IL-1β, TNF-α, MMP-8 and COX-2 were immunohistochemically analyzed. Data were analyzed statistically., Results: Group EP-TIL presented reduced alveolar bone loss when compared with group EP (p < 0.05). Group EP-TIL presented decreased mRNA expressions of IL-1β, TNF-α, MMP-8 and COX-2 and reduced immunolabeling of IL-1β, TNF-α and MMP-8 when compared with group EP (p < 0.05). No differences regarding the immunolabeling of COX-2 were found when group EP-TIL was compared with the other groups (p > 0.05)., Conclusion: Within the limits of this study, it can be concluded that local administration of TIL downregulates important mediators involved in periodontal tissue destruction in ligature-induced periodontitis in rats., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Objective: To evaluate the effects of osteoporosis induced by glucocorticoid (GIOP) on bone tissue of rats with experimental periodontitis (EP)., Design: 48 male Wistar rats divided into groups: Naïve, EP, GIOP and GIOP+EP. Rats of GIOP and GIOP+EP groups received 7mg/kg of dexamethasone intramuscularly once a week for 5 weeks. Following, EP and GIOP+EP groups were subjected to ligature-induced periodontitis. Naïve group experienced no manipulation. After 11 days, the animals were euthanized and left maxillae collected for macroscopic, radiographic, micro-tomographic and microscopic analysis of alveolar bone loss (ABL). Blood samples were collected for determination of bone-specific alkaline phosphatase (BALP) levels and the right femurs were removed for radiographic and biomechanical analysis., Results: EP caused ABL and reduced BALP levels (p<0,05), but it did not change the architecture or biomechanics of femur, compared to Naïve. GIOP did not cause ABL, but it significantly decreased alveolar bone mineral density (ABMD), bone percentage and trabecular thickness (Tb.Th) and increased alveolar bone porosity (p<0.05) and significantly reduced BALP serum levels, as well as radiographic density and Young's module of femur, compared to Naïve. There was a greater ABL in group GIOP+EP when compared to EP (p<0.05). GIOP+EP caused a greater decrease on ABMD, Tb.Th, bone percentage and increased bone porosity (p<0.05) and also presented a significant reduction in BALP levels (p<0.05), in radiographic density and in Young's module of femur compared to EP (p<0.05)., Conclusions: GIOP can potentiate the destructive effects of EP on alveolar bone and alter the systemic bone loss, by promoting bone resorption and reducing osteoblast activity., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: Periodontitis is the most frequent cause of tooth loss in adults. Nitric oxide (NO) has been linked to bone resorption mechanisms during inflammation processes. The aim of this study was to investigate the effect of NOS (NO synthase) inhibitors in the alveolar bone loss in an experimental periodontitis disease (EPD) model., Methods: Wistar rats were subjected to a ligature placement around the second upper left molars and were sacrificed at 11 days. Alveolar bone loss was evaluated by the sum of distances between the cusp tips and the alveolar bone along the axis of each molar root, subtracting from the contralateral side. Histopathological analysis was based on cell influx, alveolar bone, and cementum integrity. Leukogram was performed at 6 hours and 1, 7, and 11 days after the EPD induction. Groups were treated with the NOS inhibitors, aminoguanidine (AG) (2.5 to 10 mg/kg/d), or L-arginine methyl ester (L-NAME, 5 to 20 mg/kg/d) intraperitoneally (i.p.), 1 hour before the EPD induction and daily for 11 days. Controls received only saline (EPD group). As controls for L-NAME specificity, groups were co-treated with either L-arginine (150 to 600 mg/kg/d) or D-arginine (600 mg/kg/d) and L-NAME (20 mg/kg/d). Different groups were used for morphometric and histopathological analysis., Results: Both L-NAME and AG significantly and dose-dependently inhibited the alveolar bone loss as compared to EPD group. L-NAME (20 mg/kg/d) reduced the alveolar bone loss by 50%, whereas AG (5 mg/kg/d) reduced it by 47% compared to EPD. This result was coupled to a significant reduction of cell influx to the periodontium, as well as to the preservation of alveolar bone and cementum, seen at histopathology, for both compounds. The co-administration of L-arginine, but not of D-arginine reversed L-NAME effects., Conclusion: These data provide evidence that NOS inhibitors prevent inflammatory bone resorption in experimental periodontitis.

Background: The role of nitric oxide (NO) on bone metabolism is controversial, since it can either stimulate bone formation or resorption. We investigated the effect of local administration of the NO donor isosorbide in an experimental periodontal disease model., Methods: Wistar rats were subjected to a ligature placement around the cervix of the right second upper molar and were sacrificed after 11 days. Alveolar bone loss was measured in one quadrant as the sum of the distances between the cuspid tip and the alveolar bone along the axis of each molar root, which was subtracted from the contralateral side, used as unligated control. The semiquantitative histopathological scale of the periodontium was based on cell infiltration and alveolar bone and cementum integrity. Groups were treated with a gel containing 1% or 5% isosorbide applied to the vestibular side of the molar gingiva 1 hour before the placement of the ligature and then twice daily until sacrifice. Controls included one group subjected to periodontitis and no treatment (NT) and another that received the gel containing just the vehicle (V)., Results: The application of the vehicle gel produced an increase of the alveolar bone resorption, without altering the inflammatory changes, compared to the NT group. The 5% isosorbide produced a significant reduction of the alveolar bone resorption, compared to V and NT. This reduction was confirmed by histological analysis, showing less inflammatory cell infiltration and preservation of the cementum and the alveolar process., Conclusion: Local application of isosorbide reduces alveolar bone resorption in experimental periodontal disease in rats, suggesting a local anti-inflammatory effect of isosorbide.