Periodontal tissue deteriorates under persistent oxidative stress induced by inflammatory reactions in the microflora of the oral cavity. This study aimed to evaluate the cellular properties of mouse gingival fibroblasts (MGFs) in the presence of oxidative stress. MGFs from 10-, 30- and 52-week-old mice were used to evaluate the changes in the cellular properties with aging. The study investigated the effects of oxidative stress on the cellular properties of MGFs from 10-week-old mice. The expression of p53, p21 and murine double minute 2 (Mdm2) in the MGFs in response to oxidative stress was also examined. By day 8, the number of MGFs increased in culture. However, the increase was markedly lower in MGFs derived from aged mice. Oxidative stress due to hydrogen peroxide (H2O2)-induced morphological changes characterized by a round shape with enlarged nuclei and expanded cytoplasm. The cell number of MGFs was decreased subsequent to treatment with 50 μM or a higher concentration of H2O2. MGFs treated with H2O2 at 20 μM showed a similar cell growth curve as the one seen in 52-week-old mice. Phosphorylated p53 protein was increased in MGFs subsequent to treatment with 20 μM H2O2, along with an upregulated transcription of p21 and Mdm2 mRNAs. These results suggest that treatment with a lower concentration of H2O2 in MGFs induces cell cycle arrest, resulting in stress-induced premature senescence, possibly correlated with the development of periodontal diseases.
Laser-irradiated extraction wound healing showed characteristics different from those of the normal healing process, suggesting a favorable healing-promoting effect.
This study investigated the age-dependent changes in the number of BrdU- and TUNEL-positive cells in murine gingival tissue and submandibular gland, and compared the findings with those in other tissues and organs. The cell proliferative activity was decreased after 20 weeks of age in epithelial cells of the gingiva, tongue, buccal mucosa and skin. A decreased cell proliferative activity was also associated with aging in the liver and kidney parenchymal cells. Meanwhile, cell death showed peculiar changes in gingival subepithelial tissue, and mucous and serous acini of the submandibular gland. An increase of TUNEL-positive cells was demonstrated in gingival subepithelial tissue after 20-week-old of age. A significant increase of TUNEL-positive cells was also found in the mucous acinar cells in the 20-week-old mice and in the serous acini after 20 weeks. The fluctuation in the number of TUNEL-positive cells in the subepithelial tissue of the skin, and BrdU- and TUNEL-positive staining ratios in the liver was smaller than that in other tissue and organs throughout life. This study may provide useful information for better understanding the influence of aging on the functional alteration that occurs in the gingival tissue and submandibular gland of the elderly.
FThe purpose of this study is to clarify the destructive processes of periodontal tissue, especially of alveolar bone, induced by food impaction. Streptozotocin-induced diabetic rat was used, gutter percha point (GP) was inserted into interdental gingival col space between upper M1 and M2, and the change of body weight, histopathological findings and 3D SEM structure of alveolar bone were compared between diabetic (Group DM) and control (Group N) animals (Experiment 1). Large amounts of bacterial deposits and sequester were observed at the alveolar crest, and subsequently experiment 2 was carried out to explore the relationship between bacterial infection and sequester formation. The combination of mechanical compression and daily twice cleaning with 3% oxydol and Periocline were carried out. As a result of experiment 1, ulceration with partial exposure of alveolar crest, inflammatory infiltrates and hyaline degeneration occurred in the col, and bone resorption was scarcely observed at 1d in Group N. Bone resorption of alveolar bone progressed at 3d and 5d, decreasing the height of alveolar crest and the width of alveolar bone. Reepithelization of ulcer surface was observed at 7d and 14d, and concurrently bone resorption regressed and new bone formation suggested reparative changes. SEM observation confirmed these changes of alveolar bone. On the contrary, massive bacterial deposits were observed, and bone resorption was scanty in the upper region and slight in the middle to lower region of alveolar bone at 1 day of Group DM. Massive bacterial deposits with partial exposure of alveolar bone were observed at 3d and 5d, and sequester was isolated owing to intense undermining bone resorption. Regeneration of epithelium was seen beneath the sequester at 14d, showing the phenomenon of foreign body exclusion. The light microscopic changes of Group DM were consistent with SEM findings. The total number of osteoclasts was fewer at 1d and larger at 3d and 5d in Group DM. Osteoclasts at the upper region of alveolar bone increased from 1d to 5d in Group N, although the number of osteoclasts did not show a significant change in Group DM. At the middle to lower portion of alveolar bone, the number of osteoclast was significantly fewer at 1d, larger at 3d and 5d in Group DM. In experiment 2, the col with ulceration and necrosis did not show bacterial deposits or sequester, suggesting the intimate relation between bacterial infection and sequestration. The present study suggests that food impaction and subsequent mechanical compression to the col could induce various damages of periodontal tissue, including sequester formation, and elaborate plaque control at the initial stage of food impaction could prevent sequester formation and protect the height of alveolar bone.
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