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R J Genco

Publications and source records attributed to R J Genco.

At least 199 records · Page 11Linked to original sources

Generalized juvenile periodontitis, defective neutrophil chemotaxis and Bacteroides gingivalis in a 13-year-old female. A case report.

Host immune responses and the predominant subgingival microflora were evaluated in a 13-year-old female exhibiting a severe form of generalized juvenile periodontitis. The patient's neutrophils were chemotactically depressed but exhibited a normal oxidative capacity. Serum IgG antibody to Bacteroides gingivalis and to Actinobacillus actinomycetemcomitans serotype c were elevated. Significantly, B. gingivalis constituted 8 to 16% of the cultivable microflora and 13 to 20% of the total cell count in subgingival plaque samples obtained from five out of five periodontally diseased sites examined. It was not detectable in a healthy site. A. actinomycetemcomitans was recovered in small numbers from all subgingival plaque samples taken. The present study provides additional evidence for an etiologic association between B. gingivalis and generalized juvenile periodontitis.

Actinomyces↗

Lactic acid production by oral Streptococcus mitis inhibits the growth of oral Capnocytophaga.

Various relationships including inhibition or stimulation of growth have been demonstrated among the bacteria present in dental plaque, both in vitro and in vivo. A large number of these relationships involved oral Streptococci. An earlier study found that strains of Streptococcus mitis inhibited the growth of potential periodontopathic microorganisms, such as Actinobacillus actinomycetemcomitans, Capnocytophaga and species of Bacteroides and Fusobacterium. The present investigation showed that this inhibitory effect resulted primarily from lactic acid production.

Bacteroides↗

The Papillon-Lefèvre syndrome: neutrophil dysfunction with severe periodontal disease.

Two cases of Papillon-LeF evre are described. Both siblings demonstrated neutrophil dysfunction and severe precocious periodontal disease. The neutrophil locomotion defect was characterized by a decreased migration toward a chemotactic factor and decreased random migration. Binding of the chemotactic factor, FMLP, to the neutrophil surface was unchanged. Both patients harbored Actinobacillus actinomycetemcomitans and showed elevated serum IgG levels. Both patients also demonstrated salivary and serum antibody to A. actinomycetemcomitans. The Papillon-LeF evre syndrome is compared with the more common localized juvenile periodontitis.

Actinobacillus↗

Purification and characterization of the serotype c antigen from Actinobacillus actinomycetemcomitans.

The serotype c antigen from Actinobacillus actinomycetemcomitans was purified with fractional ethanol precipitation of cell-free culture supernatant, sequential ion-exchange chromatography, and gel filtration chromatography. The preparation obtained demonstrated a single precipitin line in immunodiffusion, immunoelectrophoresis, and crossed immunoelectrophoresis when rabbit antisera to serotype c whole bacterial cells were used. No immunological reaction was detected with antisera to serotype c lipopolysaccharide, indicating that lipopolysaccharide was not present in the preparation. The serotype c antigen was composed of 95% carbohydrate, 2% protein, and 3.1% phosphate. Gas chromatographic analysis of the antigen obtained from growth in either complex or chemically defined media revealed that the carbohydrate constituent was composed of 84 to 90.1% mannose, 4.8 to 16% glucose, 1.9% N-acetylglucosamine, 1.4% fucose, and 0.2% galactose. The present data suggest that A. actinomycetemcomitans serotype c antigen is predominantly a mannose-containing carbohydrate suggestive of a mannan.

Actinobacillus↗

Resistance of Actinobacillus actinomycetemcomitans and differential susceptibility of oral Haemophilus species to the bactericidal effects of hydrogen peroxide.

We compared the sensitivities of oral and nonoral isolates of Actinobacillus actinomycetemcomitans, Haemophilus segnis, H. aphrophilus, and H. paraphrophilus to the bactericidal action of reagent hydrogen peroxide (H2O2). Susceptibility to a range of H2O2 concentrations (10(-6) to 10(-3) M) was assessed by incubating bacterial suspensions for 1 h at 37 degrees C in the presence of H2O2 and plating on chocolate agar to determine the concentration of H2O2 that would produce a 50% reduction in CFU (50% lethal dose). As a group, A. actinomycetemcomitans was more resistant to H2O2 than the oral haemophili, and H. aphrophilus was much more sensitive than all other organisms tested. The range of 50% lethal dose values for A. actinomycetemcomitans was between 8.5 X 10(-5) and 10(-3) M H2O2 or above. In contrast, H. aphrophilus exhibited 50% lethal dose values from below 1 X 10(-6) to 3.4 X 10(-4) M H2O2. The resistance of A. actinomycetemcomitans to H2O2 may be sufficient to protect these organisms from direct H2O2-mediated killing by host phagocytes.

Actinobacillus↗

Host responses in periodontal diseases.

Great progress has been made in our understanding of the pathogenesis of periodontal disease, the primary role of bacteria as etiologic agents, and the critical modifying role of host responses. It is useful to consider several stages in the pathogenesis of periodontal disease - (a) colonization, (b) invasion, (c) destruction, and (d) healing - and to place into perspective the various host responses as they may affect each of these four stages (Table 5). With respect to colonization, although very little direct evidence is available, it is reasonable to suggest that antibodies, either secretory or serum-derived, acting by virtue of their ability to block attachment, could inhibit colonization by immune reduction of adherence mechanisms. With respect to invasion of the tissue, it appears that phagocytes, particularly the neutrophils, are important, acting in concert with opsonic antibody and complement in ingesting and killing the periodontal microflora before or during the early invasive process. A major advance in our understanding of the pathogenesis of periodontal diseases is the realization that the virulence of periodontopathic bacteria relates to their leukaggressive properties, allowing them to evade neutrophil protective mechanisms. Invasion of the periodontal tissues by bacterial products may be inhibited by the complexing of these products with antibody with the formation of antigen-antibody complexes that are phagocytosed and digested, particularly by scavenger phagocytes such as the macrophage. With respect to the destructive phase of periodontal disease, it is clear that the direct effect of lymphocytes mediated either through direct cytotoxic activity, or through biologically-active destructive lymphokines (such as alpha-lymphotoxin and osteoclast activating factor), can lead to tissue destruction. Macrophages, through the production of monokines, collagenase, and reactive oxygen species, can also lead to tissue destruction. The direct effects of bacterial toxins or enzymes which can lead to tissue destruction can be inhibited by complexing with antitoxic or enzyme-neutralizing antibodies. With respect to healing and fibrosis, very little direct information is available; however, it is possible that the lymphocytes and macrophages affect fibrosis by the production of chemotactic factors for fibroblasts which would be expected to bring them to the area of periodontal inflammation and also by production of fibroblast-activating factors, which then cause the fibroblasts to proliferate and produce collagen which replaces lost collagen or results in fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Aggressive Periodontitis↗

Microbiological and clinical effects of topical subgingival antimicrobial treatment on human periodontal disease.

This study was undertaken to evaluate the microbiological and clinical effects of a subgingivally applied mixture of H2O2-NaCl and NaHCO3 followed by subgingival irrigation with 1% Betadine in the treatment of periodontal disease. 20 adults with moderate to severe periodontal disease were included in a split mouth design study. All patients were given oral hygiene instruction and were subjected to supragingival scaling in all 4 quadrants, and subgingival scaling and root planing of half the dentition. 10 patients were instructed to use the chemical antimicrobial mixture twice a day instead of dentifrice, and also received professional application of the mixture once every 14 days for 3 months in connection with reinstruction in oral hygiene procedures. The remaining 10 patients received oral hygiene instructions combined with professional tooth cleaning without use of chemicals once every 14 days during a 3-month period. The effect of treatment was evaluated by monitoring the subgingival microflora, clinical periodontal parameters, and by computer assisted subtraction analysis of serial standardized radiographs to determine changes in mass of the supporting alveolar bone. The present study revealed that subgingival debridement combined with mechanical plaque control resulted in decreased numbers of subgingival microorganisms including spirochetes and motile rods, and arrested the progressive breakdown of the periodontal tissues. Topical antimicrobial agents used in combination with subgingival scaling further reduced the subgingival microflora and substantially improved early periodontal healing including gain of probing attachment level and gain in radiographic alveolar bone mass during the 12 months of observation. No clinical improvement but a tendency to further periodontal breakdown was found in the unscaled quadrants, even in those which were subjected to a personal application of the topical antimicrobial mixture. This study indicates that professional and personal subgingival application of a mixture of H2O2-NaCl and NaHCo3 will significantly enhance the microbiological and clinical effects of periodontal scaling and root planing. These agents, and the topical mode of antimicrobial therapy seem promising in the management of human periodontal diseases.

Administration, Topical↗

Minimal inhibitory concentrations of various antimicrobial agents for human oral anaerobic bacteria.

The minimal inhibitory concentrations of a series of antimicrobial agents for human oral organisms were determined under anaerobic growth conditions by an agar dilution assay. With the exception of black-pigmented Bacteroides spp., minimal inhibitory concentrations for oral isolates were similar to those for non-oral isolates of organisms of the same or closely related species.

Anti-Bacterial Agents↗

Studies of leukotoxin from Actinobacillus actinomycetemcomitans using the promyelocytic HL-60 cell line.

The promyelocytic HL-60 cell line was examined for susceptibility to leukotoxin from Actinobacillus actinomycetemcomitans. Strains of A. actinomycetemcomitans which caused lysis of human peripheral blood polymorphonuclear leukocytes also lysed HL-60 cells as determined by release of intracellular lactate dehydrogenase. The killing of HL-60 cells by A. actinomycetemcomitans was dose dependent and temperature dependent, reached maximal levels after 45 min of incubation, and was inhibited by rabbit antisera to A. actinomycetemcomitans. Of 100 oral isolates of A. actinomycetemcomitans from 55 subjects, 16% from 11 healthy subjects, 43% from 13 adult periodontitis patients, 75% from 4 insulin-dependent diabetics, 66% from 2 generalized juvenile periodontitis patients, and 55% from 25 localized juvenile periodontitis patients produced leukotoxin. The same subject could harbor both leukotoxin-producing and -nonproducing isolates. The significantly higher proportion of leukotoxin-producing isolates in the disease groups compared with the healthy group is consistent with the hypothesis that leukotoxin from A. actinomycetemcomitans is an important virulence factor in the pathogenesis of certain forms of periodontal disease.

Actinobacillus↗

Serology of oral Actinobacillus actinomycetemcomitans and serotype distribution in human periodontal disease.

Actinobacillus actinomycetemcomitans from the human oral cavity was serologically characterized with rabbit antisera to the type strain NCTC 9710; a number of reference strains, including Y4, ATCC 29522, ATCC 29523, ATCC 29524, NCTC 9709; and our own isolates representative of each of 10 biotypes. Using immunoabsorbed antisera, we identified three distinct serotypes by immunodiffusion and indirect immunofluorescence. Serotype a was represented by ATCC 29523 and SUNYaB 75; serotype b was represented by ATCC 29522 and Y4; and serotype c was represented by NCTC 9710 and SUNYaB 67. Indirect immunofluorescence revealed no reaction between the three A. actinomycetemcomitans serotype-specific antisera and 62 strains representing 23 major oral bacterial species. Distinct from the serotype antigens were at least one A. actinomycetemcomitans species common antigen and an antigen shared with other Actinobacillus species, Haemophilus aphrophilus, and Haemophilus paraphrophilus. All serotype a A. actinomycetemcomitans strains failed to ferment xylose, whereas all serotype b organisms fermented xylose. Serotype c included xylose-positive as well as xylose-negative strains. A total of 301 isolates of A. actinomycetemcomitans from the oral cavity of 74 subjects were serologically categorized by indirect immunofluorescence with serotype-specific rabbit antisera. Each patient harbored only one serotype of A. actinomycetemcomitans. Fourteen healthy subjects, five diabetics, and seventeen adult periodontitis patients exhibited serotypes a and b in approximately equal frequency, whereas serotype c was found less frequently. In contrast, in 29 localized juvenile periodontitis patients, the incidence of serotype b was approximately two times higher than that of serotypes a or c, suggesting a particularly high periodontopathic potential of A. actinomycetemcomitans serotype b strains. In subjects infected with A. actinomycetemcomitans, serum antibodies were detected to the serotype antigens, indicating that these antigens may play a role in the pathogenesis of periodontal disease.

Actinobacillus↗

Juvenile periodontitis as a model for neutrophil function: reduced binding of the complement chemotactic fragment, C5a.

The binding of the chemotactic complement fragment, C5a, to peripheral blood neutrophils of Localized Juvenile Periodontitis (LJP) patients and normal controls was quantitated using iodinated human C5a and a rapid centrifugation assay. There was a significant reduction in the number of binding sites per cell on neutrophils from the patient group, whereas the binding affinity remained the same as control values.

Binding Sites↗

Tetracycline and its derivatives strongly bind to and are released from the tooth surface in active form.

Several antibiotics were found to adsorb to saliva-coated enamel and to inhibit in vitro plaque formation by pure cultures of oral bacteria: Actinomyces viscosus, Actinomyces naeslundii and Streptococcus mutans. Tetracycline, minocycline and oxytetracycline adsorbed to the greatest degree, showing 100-fold higher adsorption than spiramycin, the test antibiotics with least adsorption. Inhibition of in vitro plaque formation was found to require both drug substantivity (capacity for adsorption) and antimicrobial activity. Inhibition of plaque formation in the in vitro assay employed correlated well with clinical efficacy.

Actinomyces↗

Suppression of penicillin-resistant oral Actinobacillus actinomycetemcomitans with tetracycline. Considerations in endocarditis prophylaxis.

Actinobacillus actinomycetemcomitans is an oral bacterium which is being encountered with increasing frequency in infective endocarditis. This organism occurs in high numbers in periodontitis lesions of patients with localized juvenile periodontitis (periodontosis). It is present infrequently, and only in low numbers in most other individuals. Its common resistance to penicillin, erythromycin and vancomycin represents a clinical problem in patients at risk of developing endocarditis after dental treatment. However, the high activity of tetracyclines against A. actinomycetemcomitans may be useful in prophylactic endocarditis considerations by allowing a suppression of the organism prior to the institution of recommended prophylactic protocols. In this study, we determined the effect of systemic tetracycline-HCl therapy (1 gm/day) on the oral A. actinomycetemcomitans population in five localized juvenile periodontitis patients who were heavily infected with the organism. A. actinomycetemcomitans could not be detected in samples of subgingival and supragingival dental plaque and cheek mucosal surfaces following 14 days of administration of systemic tetracycline. The organism was still undetectable 3 weeks after therapy but it reappeared at a few oral sites at week 8 post-treatment. On the basis of this data, it is proposed that the prophylactic endocarditis therapy of patients with high numbers of penicillin-resistant A. actinomycetemcomitans include a two-stage approach: first, the systemic administration of tetracycline for 14 days, and second, institution of a conventional prophylactic protocol during the time of dental treatment.

Actinobacillus↗

The periodontal microflora of juvenile diabetics. Culture, immunofluorescence, and serum antibody studies.

These studies demonstrate a unique constellation of organisms populating the subgingival area in periodontitis lesions of patients with juvenile or insulin-dependent diabetes mellitus (IDDM). The cultivable microflora was predominated by Capnocytophaga and anaerobic vibrios in the patients studied. In some patients, Actinobacillus actinomycetemcomitans were also found. This distinguishes the subgingival flora of IDDM patients suffering from periodontitis from that of patients with localized juvenile periodontitis (LJP), and that of adult periodontitis patients. In LJP most patients harbor both A actinomycetemcomitans and Capnocytophaga subgingivally; and in periodontitis lesions from nondiabetic adults, black-pigmented Bacteroides such as B gingivalis or B melaninogenicus subspecies intermedius are often found. Antibiotic susceptibility patterns suggest that penicillin or tetracycline or its analogs such as minocycline may be effective against the predominant cultivable microflora in periodontal lesions of IDDM patients; however, individual patients may harbor flora with significant resistance to these antibiotics.

Actinobacillus↗

Bacterial IgG and IgM antibody titers in acute necrotizing ulcerative gingivitis.

IgG AND IgM ANTIBODY TITERS to eight bacterial isolates were measured by indirect immunofluorescence and ELISA in sera from acute necrotizing ulcerative gingivitis (ANUG) patients during the acute phase, from ANUG patients during the convalescent phase, from patients with gingivitis and from subjects with normal gingiva. Subjects were matched with respect to age and sex. Compared to the gingivitis and healthy groups, the ANUG groups exhibited significantly higher IgG and IgM titers to intermediate-sized spirochetes and higher IgG titers to Bacteroides melaninogenicus subsp intermedius. The findings support recent studies showing that these organisms are major bacterial components in ANUG lesions. They also suggest that these bacteria proliferate above-normal levels several weeks or months prior to the clinical onset of ANUG.

Actinomyces↗