Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the oxidative burst (hydrogen peroxide-dependent oxidative product formation) of polymorphonuclear leukocytes (PMNL) in the peripheral blood from the patients with various types of periodontal diseases including localized juvenile (LJP), generalized juvenile (GJP) and adult periodontitis (AP). Heparinized peripheral blood was obtained from 15 LJP, 13 GJP and 52 AP patients and from 30 healthy control subjects. The oxidative product (2',7'-dichlorofluorescein; DCF) formation of PMNL by stimulation with phorbol myristate acetate myristate acetate was evaluated by a rapid quantitative assay using flow cytometry. The results indicated that all patient groups contained variable populations with normal or increased DCF formation, while the control subjects exhibited DCF formation as a single population. No significant differences in average DCF formation were found among the three patient groups. Although individual patients gave various values, the average DCF formation of the three patient groups was much higher than that of the control group. Statistical analysis revealed a significant positive correlation between DCF formation and the clinical periodontal parameters on an individual basis. Furthermore, after initial periodontal treatment, DCF formation decreased to normal levels. These results suggest that the capacity of peripheral blood PMNL to mount oxidative burst reactions might reflect the inflammatory status of periodontal disease.
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PMID:Increased oxidative product formation by peripheral blood polymorphonuclear leukocytes in human periodontal diseases. 849 83

As a diagnostic test, "Periocheck" can detect the N-carbobenzoxyglycyl-glycy-arginyl peptidase that is produced by Treponema denticola, Porphyromonas gingivalis, and Bacteroides forsythus. The aim of this study was to clarify the relationship between peptidase activity and attachment loss. After Phase 1 and surgical therapy, a total of 111 sites from 47 adult periodontitis patients were divided into four groups according to peptidase activity (trypsin unit, TU): A, < 0.1 TU; B, 0.1-0.2 TU; C and D > or = 0.2 TU. All sites in groups A, B, and C were untreated, whereas both subgingival 3% hydrogen peroxide irrigation and 2% minocycline application were undertaken every 45 days throughout the experiment in group D. All subjects were recalled at 3-month intervals. Peptidase activity and clinical assessments were measured for the 18-month period. Significant attachment loss associated with high values of the peptidase activity was found through the experimental period in groups B and C. In contrast, no obvious change of attachment loss was found in groups A and D following low peptidase activity at 6, 12, and 18 months. The mean attachment loss throughout the 18-month period was 0.22 mm in group A, 1.04 mm in group B, 1.53 mm in group C, and -0.35 mm in group D. Probing depth and percentages of bleeding on probing significantly increased in group C, whereas they decreased in group D. This peptidase test displayed a 77.8% sensitivity and 68.6% specificity regarding the detection of > or = 1 mm attachment loss with a cut-off value of 0.1 TU. Multiple linear regression analysis showed a close relationship between peptidase activity and predictable attachment loss within a 12-month period. These findings suggest that this peptidase test is useful in identifying the risk sites for predictable attachment loss.
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PMID:Relationship between peptidase activity from Treponema denticola, Porphyromonas gingivalis, and Bacteroides forsythus and attachment loss. 911 69

We have earlier reported a higher Fcgamma-receptor (FcgammaR)-mediated generation of reactive oxygen species, measured as luminol-enhanced chemiluminescence (CL) from peripheral neutrophils in adult periodontitis patients. The aims of this study were to confirm our previous results and to elucidate the mechanism of this phenomenon by measuring CL in parallel with the intracellular production of hydrogen peroxide, after stimulation with opsonized bacteria. To determine whether the higher CL was associated with altered responsiveness to priming, the cells were preincubated with tumor necrosis factor alpha (TNFalpha) and lipopolysaccharide (LPS). While CL was significantly higher in subjects with periodontitis, there was no difference in hydrogen peroxide production between the patients and the controls, indicating that the hyperreactivity is related to the generation of other oxygen species than H2O2 and/or to processes in the outer cell membrane. The responsiveness to priming with LPS on CL was slightly but not significantly higher in the periodontitis group, suggesting that priming could be of value for distinguishing subjects with periodontitis. When assaying intracellular production of H2O2, TNFalpha and LPS had both a priming and an activating effect. There were no significant differences between the two groups. In conclusion, this study shows a higher FcgammaR-mediated CL of peripheral neutrophils from adult patients with periodontitis, thus confirming our earlier results. The hyperreactivity seems to be related to the outer cell membrane or to oxygen species other than H2O2.
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PMID:Hyper-reactive peripheral neutrophils in adult periodontitis: generation of chemiluminescence and intracellular hydrogen peroxide after in vitro priming and FcgammaR-stimulation. 965 Aug 76

Actinobacillus actinomycetemcomitans is a Gram-negative bacterium which has an important role in localized juvenile and in progressive periodontitis. It is sensitive to killing by the myeloperoxidase (MP)-hydrogen peroxide (H2O2)-chloride system which is part of the innate host defense mediated by polymorphonuclear leukocytes. Since it has been recently suggested that thiocyanate, instead of chloride, could serve as a main substrate for MP as for lactoperoxidase (LP) and salivary peroxidase, we investigated in this study the effect of both LP and MP systems on A. actinomycetemcomitans with different (pseudo)halide substrates, thiocyanate, chloride and iodide. The concentrations of the substrates were physiological for oral fluids, as was the concentration range of H2O2. Both peroxidases produced end products with identical antibacterial activity with thiocyanate and iodide. The oxidation of iodide resulted in the highest antimicrobial efficiency followed by chloride and thiocyanate. Addition of thiocyanate into either MP-H2O2-chloride or MP/LP-H2O2-iodide system abolished the bactericidal activity of the oxidized halide. However, the chloride did not affect the bactericidality of the MP-H2O2-iodide system, but when all 3 (pseudo)halide substrates were present no antimicrobial effect was recorded. Our study shows that the presence of thiocyanate in physiological amounts is able to prevent the bactericidal activity of halide-peroxidase systems in low H2O2 concentrations. These results explain why thiocyanate-peroxidase systems of either innate origin (saliva, crevicular fluid) or introduced by commercial oral hygiene products are most probably ineffective against A. actinomycetemcomitans in vivo. Further studies of halide/thiocyanate ratio are needed to develop products which are also effective against oral anaerobes.
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PMID:The effects of different (pseudo)halide substrates on peroxidase-mediated killing of Actinobacillus actinomycetemcomitans. 984 7

Porphyromonas gingivalis is a gram-negative, obligate anaerobe strongly associated with chronic adult periodontitis. A previous study has demonstrated that this organism requires superoxide dismutase (SOD) for its modest aerotolerance. In this study, we have constructed a mutant deficient in SOD activity by insertional inactivation as well as a sod::lacZ reporter translational fusion construct to study the regulation of expression of this gene. We have confirmed that SOD is essential for tolerance to atmospheric oxygen but does not appear to be protective against hydrogen peroxide or exogenously generated reactive oxygen species. Furthermore, the sod mutant appeared to be no more sensitive to killing by neutrophils than the parental strain 381. SOD appears to be protective against oxygen-dependent DNA damage as measured by increased mutation to rifampin resistance by the sod mutant. Use of the sod::lacZ construct confirmed that SOD expression is maximal at mid-log phase and is influenced by oxygen, temperature, and pH. However, expression does not appear to be significantly affected by iron depletion, osmolarity, or nutrient depletion. The transcription start site of the sod gene was determined to be 315 bp upstream of the sod start codon and to be within an upstream open reading frame. Our studies demonstrate the essential role that SOD plays in aerotolerance of this organism as well as the selective induction of this enzyme by environmental stimuli.
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PMID:Role of superoxide dismutase activity in the physiology of Porphyromonas gingivalis. 1037 14

Actinobacillus actinomycetemcomitans has an important aetiological role in localized juvenile periodontitis and in progressive periodontitis in adults. A. actinomycetemcomitans is found mainly in periodontal pockets but also in whole saliva, a potential transmission medium. It is sensitive to peroxidase-halide systems, but the differences between periodontitis associated clinical isolates and type strains are unclear. The sensitivities of these 2 strain groups to lactoperoxidase (LP)-iodide (I(-))-hydrogen peroxide (H(2)O(2)) combinations were investigated, and the sensitivities were compared with the susceptibilities to four antibiotics. There was great variation between the sensitivities of different strains, but the 2 strain groups responded similarly. The LP (75 microg)-I(-) (100 nmol)-H(2)O(2) (1000 nmol) combination produced a similar degree of inhibition as 2 microg ampicillin. The LP-I(-) system might be a potential antimicrobial agent against A. actinomycetemcomitans transmission via saliva.
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PMID:Susceptibilities of different Actinobacillus actinomycetemcomitans strains to lactoperoxidase-iodide-hydrogen peroxide combination and different antibiotics. 1272 76

Cigarette smoking is still considered a common habit. Of smokers, increased plaque accumulation, higher incidence of gingivitis and periodontitis, higher rate of tooth loss, and increased resorption of the alveolar ridge have been found in the oral cavity. Cigarette smoking may adversely affect wound healing, and, thus, jeopardize the success of bone grafting and dental implantation. Bone grafts and sinus lift operations are both common and well-documented procedures before dental implant placement. Heat as well as toxic by-products of cigarette smoking, such as nicotine, carbon monoxide, and hydrogen cyanide, have been implicated as risk factors for impaired healing, and, thus, may affect the success and complications of those surgical procedures. An association among dental implants, grafting procedures (i.e., bone grafts, maxillary sinuses augmentation), and history of smoking has been reported. A higher degree of complication, or implant failure rates, were found in smokers with and without bone grafts. The relationship between cigarette smoking and implant-related surgical procedures, including the incidence of complications associated with these procedures, will be described and discussed based on relevant literature and results of our recent studies.
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PMID:The effect of cigarette smoking on dental implants and related surgery. 1636 86

Some Gram-negative anaerobic bacteria have been associated with the infection of tooth supporting tissues, i.e. periodontitis. Of these bacteria, Fusobacterium nucleatum is sensitive to lactoperoxidase/myeloperoxidase-iodide-hydrogen peroxide system in vitro, but salivary concentrations of thiocyanate abolishes the bactericidality. These bacteria are located in periodontal pockets, on oral mucosa and in saliva. Although F. nucleatum most probably does not belong to the group of main periodontal pathogens, it sustains its proportion in the periodontal flora when gingivitis progresses to periodontitis. In this study, the sensitivity of F. nucleatum to different horseradish peroxidase-iodide-hydrogen peroxide combinations was tested both in buffer and in sterilized human whole saliva. Horseradish peroxidase was chosen because it does not bind thiocyanate at pH > or = 6. After 1h incubation at 37 degrees C, the cell viability was estimated by plate count and with flow cytometer using LIVE/DEAD BacLight kit (Molecular Probes, USA). In saliva, the horseradish peroxidase (50 microg/mL)-iodide (2.5 mM)-hydrogen peroxide (2.5 mM) combination decreased the amount of viable bacteria to 37% compared to 85% in the control without any of the components when measured with flow cytometer. Replacement of buffer by saliva decreased the bactericidality of the peroxidase system. However, in buffer less iodide and hydrogen peroxide was needed to produce significant decrease in the number of viable bacteria when measured by plate count than with flow cytometer. Our study shows that horseradish peroxidase-iodide-hydrogen peroxide combination is able to kill F. nucleatum cells in saliva. Horseradish peroxidase-iodide-hydrogen peroxide combination may be useful to diminish the degree of re-colonization of periodontitis-associated bacteria after periodontal therapy and to inhibit the transmission of these bacteria via saliva.
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PMID:Susceptibility of Fusobacterium nucleatum to killing by peroxidase-iodide-hydrogen peroxide combination in buffer solution and in human whole saliva. 1688 84

Aggregatibacter actinomycetemcomitans is an oral pathogen causing localized aggressive periodontitis (LAP). Recently, we characterized for the first time a quinol peroxidase (QPO) that catalyzes peroxidase activity using quinol in the respiratory chain of A. actinomycetemcomitans for the reduction of hydrogen peroxide. In the present study, we characterized the phenotype of a QPO null mutant. The QPO null mutant shows an oxidative stress phenotype, suggesting that QPO plays a certain role in scavenging endogenously generated reactive oxygen species. Notably, we discovered that the QPO null mutant exhibits a production defect of leukotoxin (LtxA), which is a secreted bacterial toxin and is known to target human leukocytes and erythrocytes. This result suggests that QPO would be considered as a potential drug target to inhibit the expression of LtxA from A. actinomycetemcomitans for the treatment and prevention of LAP.
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PMID:Characterization of a quinol peroxidase mutant in Aggregatibacter actinomycetemcomitans. 1861 92

Porphyromonas gingivalis is a late-colonizing bacterium of the subgingival dental plaque biofilm associated with periodontitis. Two P. gingivalis genes, fimR and fimS, are predicted to encode a two-component signal transduction system comprising a response regulator (FimR) and a sensor histidine kinase (FimS). In this study, we show that fimS and fimR, although contiguous on the genome, are not part of an operon. We inactivated fimR and fimS in both the afimbriated strain W50 and the fimbriated strain ATCC 33277 and demonstrated that both mutants formed significantly less biofilm than their respective wild-type strains. Quantitative reverse transcription-real-time PCR showed that expression of fimbriation genes was reduced in both the fimS and fimR mutants of strain ATCC 33277. The mutations had no effect, in either strain, on the P. gingivalis growth rate or on the response to hydrogen peroxide or growth at pH 9, at 41 degrees C, or at low hemin availability. Transcriptome analysis using DNA microarrays revealed that inactivation of fimS resulted in the differential expression of 10% of the P. gingivalis genome (>1.5-fold; P < 0.05). Notably genes encoding seven different transcriptional regulators, including the fimR gene and three extracytoplasmic sigma factor genes, were differentially expressed in the fimS mutant.
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PMID:FimR and FimS: biofilm formation and gene expression in Porphyromonas gingivalis. 2006 84


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