Search

Background and Objective: There is a close relationship between inflammation and bone remodeling in the periodontium. However, previous studies have not delineated the alterations in calcium (Ca) metabolism during periodontitis progression. The aim of this current investigation was to examine Ca dynamics in alveolar bone of rats during progression of ligature‐induced periodontal inflammation by using 45Ca, which is an index of hard tissue neogenesis. Material and Methods: To induce periodontitis, the maxillary right first molar (M1) of 8‐week‐old male rats was ligated with a silk suture for 1, 3, 7, and 28 days. The left M1 was not ligated as a control. To evaluate resultant changes in bone neogenesis, 45CaCl2 was injected intraperitoneally 24 hours before euthanasia. The left‐and‐right palatal mucosa, molar teeth (M1 and M2), and alveolar bone were harvested for evaluation of 45Ca radioactivity using a liquid scintillation counter. The distribution of 45Ca in maxillary tissues was evaluated using autoradiography (ARG). In addition, we analyzed the bone volume fraction (BV/TV) and bone mineral density (BMD) of the alveolar bone by micro‐computed tomography. To investigate the number of osteoclasts and osteoblasts, tartrate‐resistant acid phosphatase (TRAP) and bone‐specific alkaline phosphatase (BAP) were measured by an enzymatic assay and immunohistochemistry, respectively. Results: 45Ca radioactivity in the alveolar bone of the ligature side decreased by 8% compared to the unligated control‐side on day 1, whereas on day 7, it markedly increased by 33%. The 45Ca levels in the gingival tissue and molar teeth were slightly but significantly lower than the control‐side on day 1 and higher from day 3 to 28. The variation in 45Ca levels for the alveolar bone was greater and specific compared with other tissues. Furthermore, on day 7, ARG data revealed that 45Ca on the control side was primarily localized to the periodontal ligament (PDL) space and alveolar bone crest and barely detected in the gingival tissues and deeper parts of the alveolar bone. On the ligature side, 45Ca disappeared from the PDL and alveolar crest, but instead was broadly and significantly increased within the deeper zones of the alveolar bone and furcation areas and distant from the site of ligature placement and periodontal inflammation. In the shallow zone of the alveolar bone, these changes in 45Ca levels on day 7 were consistent with decreases in the bone structural parameters (BV/TV and BMD), enhanced osteoclast presence, and suppressed levels of BAP expression in osteoblasts. In contrast, the deep zone and furcation area showed that TRAP‐positive cells increased, but BAP expression was maintained in the resorption lacunae of the alveolar bone. Conclusion: During periodontitis progression in rats, 45Ca levels in the alveolar bone exhibited biphasic alterations, namely decreases and increases. These data indicate that periodontitis induces a wide range of site‐specific Ca metabolism alterations within the alveolar bone. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate temporal changes in gingival blood flow (GBF) during progression of periodontitis in rats using a laser Doppler flowmeter (LDF) approach and to characterize morphological and biochemical features in the periodontium associated with GBF. Materials and Methods: Forty‐two Wistar rats were divided into a ligature‐induced periodontitis group and a control group. To induce periodontitis, ligatures were tied around maxillary first molars bilaterally. GBF was measured in palatal gingiva at pretreatment and following ligature placement after 30 min, 1, 3, 7, 14, 21, and 28 days using LDF with a non‐contact probe. Bone loss and gene expression in gingival tissues were assessed using micro‐computed tomography (μCT) and quantitative polymerase chain reaction (PCR), respectively. Immunostaining for vascular endothelial growth factor (VEGF) in the maxilla was also histologically evaluated. Results: GBF in the ligature group increased significantly compared with the control group 30 min after ligation. However, on days 3 and 7, GBF decreased in the ligature group. Also, after day 10, there was no difference in GBF between groups. The levels of alveolar bone loss, gene expression (interleukin‐6, cluster of differentiation‐31, VEGF‐A, and lymphatic vessel endothelial hyaluronan receptor‐1), and immunostained VEGF‐positive vessels correlated well with changes in GBF. Conclusion Progression of Periodontitis: In rats was associated with a triphasic pattern of GBF, consisting of a short initial increase, followed by a rapid decrease, and then a gradual plateau phase. [ABSTRACT FROM AUTHOR]

Background and Objective: Theaflavins (TFs), the major polyphenol in black tea, have the ability to reduce inflammation and bone resorption. The aim of this study was to evaluate the effects of TFs on experimental periodontitis in rats. Material and Methods: Thirty rats were divided into five groups: Control (glycerol application without ligation), Ligature (glycerol application with ligation), TF1 (1 mg/mL TF application with ligation), TF10 (10 mg/mL TF application with ligation), and TF100 (100 mg/mL TF application with ligation). To induce experimental periodontitis, ligatures were placed around maxillary first molars bilaterally. After ligature placement, 100 μL glycerol or TFs were topically applied to the rats daily, and rats were euthanized 7 days after ligature placement. Micro‐computed tomography was used to measure bone resorption in the left side of the maxilla, and quantitative polymerase chain reaction was used to measure the expression of interleukin (IL)‐6, growth‐regulated gene product/cytokine‐induced neutrophil chemoattractant (Gro/Cinc‐1, rat equivalent of IL‐8), matrix metalloproteinase‐9 (Mmp‐9), receptor activator of nuclear factor‐kappa Β ligand (Rankl), osteoprotegerin (Opg), and the Rankl/Opg ratio in gingival tissue. With tissue from the right side of the maxilla, hematoxylin and eosin staining was used for histological analysis, immunohistochemical staining for leukocyte common antigen (CD45) was used to assess inflammation, and tartrate‐resistant acid phosphatase (TRAP) staining was used to observe the number of osteoclasts. Results: The TF10 and TF100 groups, but not the TF1 group, had significant inhibition of alveolar bone loss, reduction in inflammatory cell infiltration in the periodontium, and significantly reduced numbers of CD45‐positive cells and TRAP‐positive osteoclasts compared with the Ligature group. Correspondingly, the TF10 and TF100 groups had significantly downregulated gene expression of IL‐6, Gro/Cinc‐1(IL‐8), Mmp‐9, and Rankl, but not of Opg. Consequently, Rankl/Opg expression was significantly increased in the Ligation group but was attenuated in the TF10 and TF100 groups. Conclusion: The results of this study suggest that topical application of TFs may reduce inflammation and bone resorption in experimental periodontitis. Therefore, TFs have therapeutic potential in the treatment of periodontal disease. [ABSTRACT FROM AUTHOR]