Gene/Protein Disease Symptom Drug Enzyme Compound
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The distribution of type I, III and IV collagens and their ultrastructural organization have been studied in diseased gingival connective tissue of patients with rapidly progressive periodontitis. This disease is characterized by acute destruction of the gingival collagenous components. The use of an immunofluorescent procedure has shown that the diseased connective tissue was made up of both type I and III collagens but that type III collagen was less resistant to acute inflammation. Ultrastructural immunolabelling, using the peroxidase procedure has shown that the large, dense bundles of type I collagen of PI, the main pattern of organization of the gingival connective tissue offered a better resistance to acute destruction than PII, a loose pattern of organization mainly composed of type III collagen. Type IV collagen was exclusively located in degraded lamina densa of basement membrane.
Cell Mol Biol 1989
PMID:Immunohistochemical study of types I, III and IV collagen in diseased human gingiva of patients with rapidly progressive periodontitis: a light and electron microscopic study. 261 33

Topical application of Coenzyme Q10 (CoQ10) to the periodontal pocket was evaluated with and without subgingival mechanical debridement. Ten male patients with adult periodontitis participated and 30 periodontal pockets were selected. During the first 3 weeks, the patients did not receive any periodontal therapy except the topical application of CoQ10. After the first 3-week period, root planning and subgingival scaling were performed in all sites. CoQ10 was applied in 20 of the pockets once a week for a period of 6 weeks. Soybean oil was applied to the remaining 10 sites as a control. In the first 3-week period, significant reductions in gingival crevicular fluid flow, probing depth and attachment loss were found only at experimental sites. After mechanical subgingival debridement, significant decreases in the plaque index, gingival crevicular fluid flow, probing depth and attachment loss were found both at experimental and control sites. However, significant improvements in the modified gingival index, bleeding on probing and peptidase activity derived from periodontopathic bacteria were observed only at experimental sites. These results suggest that topical application of CoQ10 improves adult periodontitis not only as a sole treatment but also in combination with traditional nonsurgical periodontal therapy.
Mol Aspects Med 1994
PMID:Effect of topical application of coenzyme Q10 on adult periodontitis. 775 36

Porphyromonas gingivalis has been implicated as an important pathogen in severe adult periodontitis. We have previously cloned a 40-kDa outer membrane protein from P. gingivalis 381 and succeeded in producing sufficient quantities of the recombinant protein (r40-kDa OMP). r40-kDa OMP has been the subject of considerable interest to us as a possible vaccine candidate. To understand the role of anti-r40-kDa OMP antibody in the host defense mechanisms against P. gingivalis, we examined the involvement of a rabbit antibody against r40-kDa OMP (r40-kDa OMP Ab) to an in vitro complement-mediated bactericidal assay for P. gingivalis 381. By measuring the absorbance values in order to assay the surviving bacteria, we found significant anti-P. gingivalis activity of r40-kDa OMP Ab when guinea pig complement was present. Using affinity-purified immunoglobulin G of r40-kDa OMP Ab (IgG-r40-kDa OMP), we demonstrated that the IgG contributed to anti-P. gingivalis activity in the antibody-complement system. This was effected by measuring the incorporation of tritiated thymidine into newly synthesized nucleic acids. Finally, we confirmed the cell lysis of P. gingivalis 381 exposed to IgG-r40-kDa OMP in the presence of complement sources in a radioactive bactericidal assay using bacteria labeled with [14C]sodium acetate. Assembling the data from experiments using component-deficient complements, we concluded that IgG-r40-kDa OMP was related to the killing of P. gingivalis 381 by mediation in the complement activated through both the classical and the alternative pathways.
Biochem Mol Med 1996 Aug
PMID:Complement-mediated killing of porphyromonas gingivalis 381 by the immunoglobulin G induced by recombinant 40-kDa outer membrane protein. 881 38

Porphyromonas gingivalis, a Gram-negative anaerobe, is known to be involved in the pathogenesis of periodontitis. P. gingivalis fimbriae, which are proteinaceous appendages extending from the cell surface, may contribute to the adherence of the organism to the host cell surface. We previously suggested that arginine-specific protease produced by P. gingivalis enhanced the adherence of purified fimbriae to fibroblasts or matrix proteins. In this study, we have revealed the mechanism of the enhanced binding of fimbriae by the protease in more detail. Arg-specific protease and fimbriae were obtained from P. gingivalis 381 cells and purified. We then analysed the interaction of fimbriae and immobilized fibronectins (intact or partially degraded fibronectin by the purified protease) by using the real-time biomolecular interaction analysis (BIAcore) system with an optical biosensor based on the principles of surface plasmon resonance. BIAcore profiles demonstrated an enhanced interaction between fimbriae and protease-degraded fibronectin. We also showed specific binding of fimbriae to the degraded fibronectin by means of BIAcore analysis. The binding of biotinylated fimbriae to immobilized fibronectin was examined by enzyme-linked biotin-avidin assay. The purified protease enhanced the fimbrial binding to the immobilized fibronectin. The enhancement was inhibited by the addition of L-Arg, or oligopeptides containing the Arg residue at the C-terminus in the fimbrial binding reaction, suggesting that the P. gingivalis fimbriae may potentially have an ability to bind tightly to the Arg residue at C-terminus. Taken together, these studies indicate that P. gingivalis arginine-specific protease can expose a cryptitope in the matrix protein molecules, i.e. the C-terminal Arg residue of the host matrix proteins, so that the organism can adhere to the surface layer in the oral cavity through fimbriae-Arg interaction (a novel host-parasite relationship).
Mol Microbiol 1997 Jun
PMID:Adherence of Porphyromonas gingivalis to matrix proteins via a fimbrial cryptic receptor exposed by its own arginine-specific protease. 921 67

Actinobacillus actinomycetemcomitans (Aa) strain ST1 carries the tetracycline (Tc) resistance transposon Tn916 and the Aa phi ST1 prophage, which is closely related to temperate bacteriophage Aa phi 23. High titre phage preparations were obtained from this strain by mitomycin C induction and were used to transduce the TcR determinant to the TcS recipient strains ZIB1001 and ZIB1015 (MIC 2 micrograms Tc/ml). TcR transductants (MIC > or = 32 micrograms Tc/ml) were detected at frequencies of 3 x 10(-6) to 5 x 10(-8) per pfu. All TcR transductants examined contained the entire Tn916 inserted at several different locations within the Aa genome. They appear to have resulted from generalized transduction. In addition both bacteriophages, Aa phi 23 and Aa phi ST1, were capable of transducing the chloramphenicol (Cm) resistance marker of plasmid pKT210 (transduction frequencies of 2 x 10(-5) to 3 x 10(-7) per pfu) to the recipient strain ZIB1001 (MIC 8 micrograms Cm/ml). Eleven CmR ZIB1001 transductants (MIC > or = 100 micrograms Cm/ml) studied carried a plasmid indistinguishable from pKT210 by restriction analyses. In view of the high prevalence of this phage family, and the increasing use of tetracycline in periodontitis therapy, these findings may have clinical importance.
Cell Mol Life Sci 1997 Dec
PMID:Transduction of antibiotic resistance markers among Actinobacillus actinomycetemcomitans strains by temperate bacteriophages Aa phi 23. 944 41

Porphyromonas gingivalis, a black-pigmented, gram-negative anaerobe, is found in periodontitis lesions, and its presence in subgingival plaque significantly increases the risk for periodontitis. In contrast to many bacterial pathogens, P. gingivalis strains display considerable variability, which is likely due to genetic exchange and intragenomic changes. To explore the latter possibility, we have studied the occurrence of insertion sequence (IS)-like elements in P. gingivalis W83 by utilizing a convenient and rapid method of capturing IS-like sequences and through analysis of the genome sequence of P. gingivalis strain W83. We adapted the method of Matsutani et al. (S. Matsutani, H. Ohtsubo, Y. Maeda, and E. Ohtsubo, J. Mol. Biol. 196:445-455, 1987) to isolate and clone rapidly annealing DNA sequences characteristic of repetitive regions within a genome. We show that in P. gingivalis strain W83, such sequences include (i) nucleotide sequence with homology to tRNA genes, (ii) a previously described IS element, and (iii) a novel IS-like element. Analysis of the P. gingivalis genome sequence for the distribution of the least used tetranucleotide, CTAG, identified regions in many of the initial 218 contigs which contained CTAG clusters. Examination of these CTAG clusters led to the discovery of 11 copies of the same novel IS-like element identified by the repeated sequence capture method of Matsutani et al. This new 1,512-bp IS-like element, designated ISPg5, has features of the IS3 family of IS elements. When a recombinant plasmid containing much of ISPg5 was used in Southern analysis of several P. gingivalis strains, including clinical isolates, diversity among strains was apparent. This suggests that ISPg5 and other IS elements may contribute to strain diversity and can be used for strain fingerprinting.
 ...
PMID:Characterization of Porphyromonas gingivalis insertion sequence-like element ISPg5. 1094 51

With the increase in the number of antibiotic resistant strains of microorganism, the search for alternative treatments of microbial infections becomes all the more important. We report a novel method for bacterial inactivation based on the optical excitation of the naturally occurring (endogenous) photosensitzing porphyrins by red light. In particular, the pathogenic Gram-positive porphyrin producing ATCC strains Propionibacterium acnes, Actinomyces odontolyticus and Porphyromonas gingivalis were investigated. Sensitive autofluorescence spectroscopy revealed that these bacteria naturally synthezise the fluorescent photosensitizer protoporphyrin IX. In addition, bacterial plaque samples of periodontitis patients were studied. Non-labeled fluorescent bacterial colonies were exposed to red light at 632.8 nm, 100 mW/cm2 light intensity and 360 J/cm2 energy density using a helium-neon laser. The survival rate after a single phototreatment with red light was found to be 0.58 +/- 0.09 in the case of Propionibacterium acnes, 0.30 +/- 0.04 in Actinomyces odontolyticus and 0.59 +/- 0.10 in Porphyrormonas gingivalis compared to non-exposed bacteria suspensions. No photoeffect was found for the bacterium Streptococcus mutans which exhibited no detectable porphyrin autofluorescence. Red-light exposed plaque samples of patients showed significant reduction of colony forming units by 50% as well as a pronounced photoeffect on the pigmented species Prevotella intermedia. Taken together, these results suggest the treatment with red light can be potentially employed as an therapeutic method to inactivate certain pathogenic strains of porphyrin producing bacteria without the use of external photosensitizers.
Cell Mol Biol (Noisy-le-grand) 2000 Nov
PMID:Red light kills bacteria via photodynamic action. 1107 59

Dental caries and periodontitis, although generally not life threatening, are nevertheless of significant importance. An understanding of the molecular nature of these diseases could aid the development of novel methods of prevention and control, and increase our knowledge of their etiology. The identification of virulence factors in oral bacteria could lead to the development of vaccines directed against these organisms, the design of inhibitors of biofilm formation, and the development of replacement therapy strategies.
Curr Issues Mol Biol 2001 Apr
PMID:Virulence properties of oral bacteria: impact of molecular biology. 1147 73

Periodontitis is a complex, multifactorial process affected by bacterial plaque-components and host defense mechanisms. Inflammation of the periodontitium may lead the destruction of the underlying ligament and alveolar bone. Receptor activator of NF-kappaB ligand (RANKL), a novel TNF receptor-related protein is an important factor for osteoclast differentiation and activation. Given osteolysis by osteoclast has been demonstrated in periodontitis, we hypothesized that RANKL expression may be associated with bone destruction in periodontitis. We used semi-quantitative RT-PCR to compare the gene expression of RANKL and osteoprogerin (OPG), a decoy receptor of RANKL, between moderate and advanced periodontitis, and healthy subjects. The level of RANKL mRNA was highest in advanced periodontitis. In contrast, the level of OPG mRNA in both advanced and moderate periodontitis was lower than that in the healthy group. It appears that the ratio of RANKL to OPG mRNA in periodontitis has increased. To determine the localization of RANKL gene transcripts in gingival tissue at the cellular level, in situ hybridization was performed using digoxigenin-labeled specific riboprobes. RANKL mRNA was expressed in inflammatory cells, mainly lymphocyte and macrophages. In addition, proliferating epithelium in the vicinity of inflammatory cells expressed high levels of RANKL mRNA. In short, our data suggest that up regulation of RANKL mRNA in both inflammatory cells and epithelium may be associated with the activation of osteoclastic bone destruction in periodontitis.
Int J Mol Med 2003 Jan
PMID:Expression of RANKL and OPG mRNA in periodontal disease: possible involvement in bone destruction. 1246 11

Host immune response has been considered as an important disease-modifying factor of periodontitis, however, which immune cell(s) or factor(s) are involved in the destruction of periodontium remains unclear. Previously, we reported that osteoclastogenesis is enhanced by activated B cells but suppressed by activated CD8+ T cells. We present new data that B cells activated in the presence of Th1 cytokines inhibit osteoclastogenesis. Purified murine B cells were activated with anti-IgD mAb, IL-4, and anti-CD40 mAb, in the absence (BTh2) or presence of Th1 cytokines, either IL-2 (BIL-2) or IFN-gamma (BIFN-gamma). Each activated B cell population was co-cultured with RAW264.7 cells in the presence of soluble receptor activator of NF-kappaB ligand (sRANKL), and the effect on osteoclastic differentiation was evaluated. While BTh2 increased osteoclastogenesis, BIL-2 and BIFN-gamma suppressed it profoundly. To verify the mediating molecule(s), we analyzed cytokine profiles of the activated B cells. Compared to BTh2, BIL-2 expressed increased amount of IFN-gamma and BIFN-gamma expressed decreased amounts of IL-4, IL-5, and IL-10. IFN-gamma was a key negative regulator of osteoclastic differentiation, and mediated the inhibition by BIL-2. These results suggest that Th1 cytokines may have new important roles in resistance to periodontitis, acting directly on osteoclasts or indirectly through B cells.
Exp Mol Med 2003 Oct 31
PMID:B cells activated in the presence of Th1 cytokines inhibit osteoclastogenesis. 1464 92


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