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Ishikawa I, Kawashima Y, Oda S, Iwata T, Arakawa S. Three case reports of aggressive periodontitis associated with Porphyromonas gingivalis in younger patients. J Periodont Res 2002; 37; 324–332. © Blackwell Munksgaard, 2002 --> The terms 'early onset periodontitis' (EOP) and 'juvenile periodontitis' (JP) were replaced by that of 'aggressive periodontitis' in a recent international workshop for the classification of periodontal diseases and conditions. The chief etiologic agent for aggressive periodontitis is considered to be Actinobacillus actinomycetemcomitans in localized juvenile periodontitis. Porphyromonas gingivalis is also mentioned as the etiologic agent of the aggressive periodontitis, although to date its role remains questionable. This communication describes three cases of aggressive periodontitis found to be associated with P. gingivalis but not A. actinomycetemcomitans by polymerase chain reaction (PCR) and enzyme‐linked immunosorbent assay (ELISA). Our findings clarify the role of P. gingivalis as an etiologic agent in this type of periodontitis and confirm its inclusion in the current definition of aggressive periodontitis. [ABSTRACT FROM AUTHOR]

Prostaglandin E2 (PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(1L-6) production in human gingival fibroblasts (HGF) stimulated with 1L-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced 1L-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA, of EP1, EP2, and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1m, a selective EP2, EP3/EP4 agonist, abd butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, and EP1 agonist, enhanced IK-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory periodontal conditions. [ABSTRACT FROM AUTHOR]

Prostaglandin F2α (PGF2α) is a bioactive lipid mediator which has been suggested to be involved in the pathogenesis of periodontal disease. However, the roles of PGF2α in periodontal lesions are poorly understood. In the present study, we investigated the effect of PGF2α on interleukin (IL)-6 production in human gingival fibroblasts(HGF). PGF2α-stimulated IL-6 production in a time- and concentration-dependent fashion. IL-1β and tumor necrosis factor α (TNFα), proinflammatory cytokines, induced IL-6 production in a time-dependent manner, and PGF2α synergistically enhanced IL-6 production induced by IL-1β and TNFα. IL-6 mRNA was expressed in PGF2α-stimulated HGF, and PGF2α increased IL-6 mRNA levels induced by IL-1β and TNFα. Fluprostenol, a selective FP receptor agonist, could mimic PGF2α-induced IL-6 production. Since FP receptors are coupled to elevation of intracellular calcium and activation of protein kinase C (PKC), the mechanism of IL-6 production by PGF2α was investigated using TMB-8, an inhibitor of Ca2+ mobilization from intracellular stores, and calphostin C, an inhibitor of PKC. TMB-8 significantly suppressed PGF2α-induced IL-6 production, whereas calphostin C showed a stimulatory effect on PGF2α-induced IL-6 production. From these data, we suggest that PGF2α upregulates IL-6 production through FP receptors in HGF, that PGF2α synergistically enhances IL-6 production in IL-1β- and TNFα-stimulated HGF, and that PGF2α-induced IL-6 production may be dependent on intracellular Ca2+ mobilization and be downregulated by PKC activation. PGF2α may be involved in the pathogenesis of periodontal disease by enhancing IL-6 levels in periodontal lesions. [ABSTRACT FROM AUTHOR]

Prostaglandin E2 (PGE2) exerts its biological actions via EP receptors, which are divided into 4 subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated intercellular adhesion molecule-1 (ICAM-1) expression in human gingival fibroblasts (HGF) stimulated with tumor necrosis factor-α (TNFα) and if so, which subtype(s) of PGE2 receptors was involved. Exogenous addition of PGE2 to HGF inhibited ICAM-1 expression elicited by TNFα in a concentration-dependent manner. Treatment of HGF with indomethacin, a cyclo-oxygenase inhibitor, had no effect on TNFα-elicited ICAM-1 expression, although indomethacin completely inhibited PGE2 production enhanced by TNFα. Next, we examined which subtype(s) of the 4 EP receptors modulated the ICAM-1 expression elicited by TNFα, using subtype-specific agonists and antagonists. 1 l-deoxy-PGE1, a selective EP2/EP4 agonist, inhibited TNFα-elicited ICAM-1 expression as potently as PGE2, while butaprost, a selective EP2 agonist, was somewhat less effective than PGE2. AH23848B, an EP4 antagonist, antagonized the inhibitory effect of TNFα-elicited ICAM-1 expression by PGE2. Suiprostone, an EP1/EP3 agonist, and ONO-AP-324, an EP3 agonist, were inert to TNFα-elicited ICAM-1 expression. As EP2 and EP4 receptors are linked to elevation of intracellular cyclic AMP (cAMP), the effect of dibutyryl cAMP and 8-bromo--cAMP, cAMP analogs, on TNFα-elicited ICAM-1 expression was examined. Both the agents downregulated ICAM-1 expression in TNFα-stimulated HGF. From these data, we suggest that PGE2 downregulates TNFα-induced ICAM-1 expression in HGF, via EP2 and EP4 receptors by cAMP-dependent signaling pathways, which may result in control of inflammatory and immunological responses in periodontal disease. [ABSTRACT FROM AUTHOR]

Prostaglandin F2α (PGF2α) is a bioactive lipid mediator, which has been suggested to be involved in the pathogenesis of periodontal disease. However, the roles of PGF2α in the disease are not well understood. In the present study, we investigated the effect of PGF2α on intercellular adhesion molecule-1 (ICAM-1) expression in human gingival fibroblasts (HGF) and the effect of PGF2α on ICAM-1 expression elicited by proinflammatory cytokines, interferon-γ (IFN-γ) and tumour necrosis factor α (TNF α) in the cells. PGF2α-stimulated HGF expressed ICAM-1 expression in a time- and dose-dependent manner. IFN-γ-elicited ICAM-1 expression was synergistically increased by PGF2α, whereas TNF α-induced ICAM-1 expression was slightly inhibited by PGF2α. Fluprostenol, a selective FP receptor agonist, could mimic PGF2α-induced effect on ICAM-1 expression. Furthermore, signal transduction for the regulation of ICAM-1 by PGF2α was investigated using N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W-7), a calcium calmodulin antagonist, and 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C (PKC). W-7 and H-7, remarkably, suppressed PGF2α-induced ICAM-1 expression and synergistic increase of ICAM-1 expression by combination of PGF2α and IFN-γ, while IFN-γ-elicited ICAM-1 expression was only partially inhibited by W-7 and H-7. From these data, we suggest that PGF2α upregulates ICAM-1 expression in HGF and synergistically enhances IFN-γ-induced ICAM-1 expression through FP receptor by calcium calmodulin-dependent and PKC-dependent pathways. PGF2α may be involved in the pathology of periodontal disease by upregulating ICAM-1 expression in HGF. [ABSTRACT FROM AUTHOR]

The present study investigated the effect of prostaglandin (PG) &E2 and PGI2 on intercellular adhesion molecule-1 (ICAM-1) expression in interleukin-1β (IL-1β)-stimulated human gingival fibroblasts (HGF). IL-1β potently induced ICAM-1 expression in HGF and indomethacin, a cyclooxygenase inhibitor, enhanced ICAM-1 expression in the cells. These data showed that endogenous PGs generated by HGF stimulated with IL-1β downregulated ICAM-1 expression. IL-1β significantly increased the levels of PGE2 and, to a lesser extent, those of 6-keto-PGF1α (a stable metabolite of PG12) in the culture media of HGF. Indomethacin completely inhibited the production of PGE2 and 6-keto-PGF1α in IL-1β-stimulated HGF. Exogenous PGE2 and carbacyclin (a stable derivative of PGI2) in the presence of indomethacin dose-dependently suppressed ICAM-1 expression in IL-1β-challenged HGF. Since PGE2 and PGI2are known to elevate intracellular cyclic AMP (cAMP) levels, we examined the effect of dibutyryl cAMP, a cAMP analogue, and isobutylmethylxanthine, a phosphodiesterase inhibitor, on ICAM-1 expression. Both agents downregulated ICAM-1 expression in IL-1β-stimulated HGF. These results suggest that PGE2 and PG12 downregulate ICAM-1 expression in IL-1β-stimulated HGF through a cAMP-dependent mechanism and that intracellular cAMP elevation in HGF may control inflammatory and immune responses in periodontal disease. [ABSTRACT FROM AUTHOR]

Oral Actinobacillus actinomycetemcomitans strains are serologically classified into 5 distinct groups, a to e. We examined the distribution of Actinobacillus actinomycetemcomitans serotypes in apanese patients with periodontitis. A total of 157 Actinobacillus actinomycetemcomitans clinical isolates from diseased sites of 39 patients with periodontitis were serotyped by using serotype-specific rabbit antisera against Actinobacillus actinomycetemcomitans serotypes a, b, c, d and e strains. In the immunodiffusion assay, autoclaved extracts of 42, 6, 39, 9 and 41 Actinobacillus actinomycetemcomitans clinical isolates reacted with serotypes a, b, c, d and e antisera, respectively. Although 37 patients were infected with a serotype strain, 2 patients harbored 2 different serotype strains, b/e and b/untypeable. To establish a correlation between serotype and genotype of Actinobacillus actinomycetemcomitans clinical isolates from 2 patients who had different serotype strains, we used arbitararily primed polymerase chain reaction (AP-PCR) to fingerprint clinical islates of different serotypes. The AP-PCR genotypes among 4 clinical isolates (b/e and b/untypeable) were identical to that of Actinobacillus actinomycetemcomitans Y4 (serotype b), indicating the presence of multiple Actinobacillus actinomycetemcomitans serotypes which are genetically homogeneous in the periodontally diseased sites of patients with periodontitis. [ABSTRACT FROM AUTHOR]

The article presents information on rapid identification of Porphyromonas gingivalis by bisulfite-modified DNA probe methods. The purpose of the present study was to evaluate the effectiveness of the bisulfite-modified DNA probe from P. gingivalis to detect homologous bacteria when it is applied on clinical samples. The application of this labeling method could be considerably expanded if it was used in conjunction with antibodies which specifically recognized the modified bases. This probe was also applied on subgingival plaque samples collected by the paper point method.

Polymorphonuclear leukocytes (PMNs) are the most abundant emigrating cells in the dentogingival junction. PMNs are protective by their phagocytic and bacteriocidal activities against plaque bacteria, and a reduced function of the cells invites a severe condition of periodontal disease. The purpose of this experiment was to determine whether a granule extract from human PMNs can destroy rabbit gingival tissue in vivo. Changes in the rabbit gingival sulcus were observed histologically after the extract was applied to the sulcus.

The aim of this study was to detect the specific immunoglobulin G antibodies against periodontopathic bacteria by dot blotting. In the procedure used, bacterial preparations were blotted on a nitrocellulose membrane. After blocking the nonspecific binding sites, the diluted serum was blotted onto the preparations. The membrane was immersed in secondary antibodies and then in substrate buffer. The colored blots were then evaluated. To test the reliability of this procedure, 20 serum samples were examined for antibody: ten for anti-Porphyromonas gingivalis antibody, and the other ten for anti-Actinobacillus actinomycetemcomitans antibody. Five samples out of each set of ten had previously been confirmed as having high enzyme-linked immunosorbant assay (ELISA) titers to the antigen, while the other five had been confirmed as having average titer levels. Both whole-cell sonic extracts and fimbriae of P. gingivalis were used as antigens in the dot blotting, in order to compare their use as antigens in assays of the patients' sera. ELISA was also used to measure anti-P. gingivalis antibody titers. For the measurement of IgG antibodies against A. actinomycetemcomitans, formalin-killed whole cells were used. Fifty serum samples were examined for IgG antibodies against A. actinomycetemcomitans by dot blotting and ELISA. With both antigens, after 4 h, coloration of blots was more clearly visible for the high-titer sera than for the average-titer sera. The intensity of coloration of the blots for P. gingivalis and A. actinomycetemcomitans showed correlation with the ELISA titers. A particularly significant correlation was shown when P. gingivalis fimbriae were used as antigen. These results suggest that this dot blot method is a simple and rapid means of detection of serum antibodies, and that it shows promise as a chair-side assay method.

Prostaglandin E2 (PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin (IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1beta and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1beta-induced IL-6 production by HGF, although it completely inhibited IL-1beta-induced PGE2 production. Exogenous PGE2 suppressed the IL-1beta-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1beta-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1beta-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-omega-trinor PGE2, an EP1 agonist, enhanced IL-1beta-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1beta-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory periodontal conditions.