• 대한치주과학회:학술대회논문집
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• 2003.05a
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• pp.14-14
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• 2003

• Journal of Periodontal and Implant Science
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• v.25 no.3
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• pp.568-586
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• 1995

542 periodontal patients having early-onset periodontitis(EOP) have been reclassified into a more homogeneous phenotypic subsets by newly revised radiographic criteria. Representative patients of each EOP subform have been examined of serum IgG subclass antibodies against periodontopathic bacteria, Porphyromonas gingivalis(Pg) 381 and of genetic markers for IgG allotypes to clarify the relationship between these parameters and phenotype expression of each subform. The early onset periodontitis could be reclassified by the radiographic parameters combining the mean interproximal alveolar bone loss(BL) and the radiographic ratio(between 1st molars and the adjacent teeth: Ratio) with statistical significance(p<0.001 by MANOVA). Moreover these EOP subforms could clearly be delineated from adult periodontitis. Of subform I and II(localized type EOP) patients with minimal mean bone loss(BL<5.0), patients demonstrating disease activities in localized areas(Ratio.>1.5) showed the elevated responses in all the IgG subclasses against Pg compared with those of patients without disease activity(Ratio <1.5). There were gradual increase in the IgG2 and IgG4 titers against Pg as the disease developed into the generalized forms suggesting the possible role of these antibodies in modulating the phenotype expression. The genetic marker study for IgG allotype revealed that mean IgG2 and IgG4 subclass titers were significantly higher(p<0.01, p<0.05, respectively) in patients who were positive for G2m(n). This indicated that IgG subclass responsiveness against the bacterial antigens are under the immnuogenetic control. The observed frequencies of G2m(n) were significantly higher (p<0.05) in subfrom IV patients who had the characteristic features of classical rapidly progressing periodontitis indicating the possible genetic predisposition in these patients.

• International Journal of Oral Biology
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• v.42 no.3
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• pp.137-142
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• 2017

To determine the effect of the tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) in odontoclast formation, we administrated a $TNF-{\alpha}$ inhibitor in rats with diabetes rats with periodontitis. The rats included in the study were divided into three groups: control rats without diabetes or periodontitis (the C group), rats with periodontitis and diabetes (the PD group), and rats with periodontitis and diabetes treated by infliximab, the TNF inhibitor (the PD+infliximab group). The PD and PD+infliximab groups received intravenous administrations of streptozotocin (STZ, 50 mg/kg) to induce diabetes. After 7 days of STZ injections, the mandibular first molars were ligatured to induce periodontitis. The PD+infliximab group was intrapenitoneally administrated by infliximab (5 mg/kg). On days 3 and 20 after the ligature administration, odontoclast formation along root surfaces was evaluated by tartrate resistant acid phosphatase (TRAP) staining and cathepsin K immunohistochemistry. On day 3, the number of TRAP- and cathepsin K-positive cells increased more so in the PD group than in the C group. The PD+infliximab group showed a lower number of positive cells than the PD group. There was no difference in all the groups on day 20. On day 3, the cathepsin-K positive multinucleated and mononucleated cells were higher in the PD group than in the C group. The number of cathepsin-K positive multinucleated cells was lower in the PD+infliximab group than in the PD group. The PD group showed more cathepsin K-positive cells in the furcation and distal surfaces than the c group. The Cathepsin K-positive cells of the PD+infliximab group were lower than that of the PD group in furcation. These results suggest that $TNF-{\alpha}$ stimulates odontoclast formation in diabetes with periodontitis.