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J Slots

Publications and source records attributed to J Slots.

At least 181 records · Page 10Linked to original sources
PubMed1986

Antigenic characteristics and serological identification of 10 black-pigmented Bacteroides species.

Strains of 10 black-pigmented Bacteroides species were serologically characterized using absorbed and unabsorbed rabbit antisera. An agglutination test using intact cells or heated cells (100 degrees C for 60 min) from each species and unabsorbed antisera revealed only homologous reactions with little or no reactivity in heterologous assays. Immunodiffusion tests using sonicated antigen demonstrated that Bacteroides gingivalis, B. endodontalis, B. asaccharolyticus, B. macacae, and B. levii are antigenically distinct. Strains of B. gingivalis, B. endodontalis, and B. asaccharolyticus were also clearly identified by the indirect immunofluorescent antibody method. B. intermedius, B. corporis, B. loescheii, B. melaninogenicus, and B. denticola possessed common antigens; however, species-specific antigens detectable with immunoabsorbed antisera were also demonstrated. B. intermedius strains isolated from the human oral cavity included at least two serogroups. In each black-pigmented Bacteroides species, lipopolysaccharide constituted one of the species-specific antigens.

Agglutination Tests↗
PubMed1985

Susceptibility of human oral anaerobic bacteria to antibiotics suitable for topical use.

17 antibiotics, with potential for topical use, were tested for their activity against the human oral flora. Concentrations (mumol/l) required to inhibit 90% of test strains are presented and drug activities are compared. The total cultivable oral flora was susceptible to the tetracyclines including tetracycline itself, minocycline, doxycycline, and oxytetracycline and to erythromycin. On the other hand, actinobolin, kanamycin, neomycin, streptomycin, spiramycin, tyrothricin, vancomycin, clindamycin, and chloramphenicol were ineffective against many of the human oral anaerobic bacteria even at high concentration. Penicillin was effective at high concentrations but could not be recommended because organisms which are not inhibited by low concentrations are penicillinase producers. Carbenicillin was effective against all organisms except Actinobacillus actinomycetemcomitans. The gram-negative organisms involved in adult periodontitis were most susceptible to the tetracyclines, tyrothricin, carbenicillin and clindamycin, while those associated with localized juvenile periodontitis were susceptible to the tetracyclines or erythromycin. These data, combined with the previous findings that some tetracyclines exhibit marked substantivity and collagenase inhibition activity, indicate that tetracycline or minocycline are likely to be good choices in the treatment or prevention of oral diseases.

Administration, Topical↗
PubMed1985

Microbiological and clinical effects of surgical treatment of localized juvenile periodontitis.

Since Actinobacillus actinomycetemcomitans appears to be a key etiologic agent in localized juvenile periodontitis, this study determined the effectiveness of different treatment modalities in suppressing A. actinomycetemcomitans in localized juvenile periodontitis lesions. A total of 25 deep periodontal lesions from 7 patients with localized juvenile periodontitis were included in the study. The test periodontal lesions either received scaling and root planing alone, scaling and root planing together with soft tissue curettage, or modified Widman flap surgery. Subgingival A. actinomycetemcomitans were enumerated using selective culturing. Clinical measurements included changes in probing periodontal attachment level, probing periodontal pocket depth, gingival index, plaque index, and digital subtraction of standardized serial radiographs. The microbiological and clinical effects of treatment were monitored over a period of 16 weeks. All periodontal lesions studied demonstrated high numbers of A. actinomycetemcomitans prior to treatment. Scaling and root planing alone did not markedly change the subgingival A. actinomycetemcomitans counts, nor any of the clinical parameters studied. In contrast, soft tissue curettage as well as modified Widman flap surgery suppressed A. actinomycetemcomitans to undetectable levels immediately after therapy in more than 80% of the lesions studied. A total of 5 periodontal lesions exhibited gain of probing periodontal attachment after subgingival curettage or Widman flap treatment; 3 of these sites revealed no detectable A. actinomycetemcomitans, and the remaining 2 sites harbored only low levels of A. actinomycetemcomitans. 5 periodontal lesions which lost probing attachment after treatment all demonstrated high numbers of subgingival A. actinomycetemcomitans. Changes in alveolar bone, assessed by digital subtraction of serial radiographs, correlated with changes in probing periodontal attachment level, confirming the clinical results. The present study revealed a close relationship between post-treatment A. actinomycetemcomitans levels and the clinical response to treatment, which supports the concept that A. actinomycetemcomitans is an important organism in the etiology of localized juvenile periodontitis. This study also showed that a substantial suppression of subgingival A. actinomycetemcomitans cannot be achieved by periodontal scaling and root planing alone, but can be accomplished by surgical removal of periodontal tissues.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus↗
PubMed1985

Relationship between some subgingival bacteria and periodontal pocket depth and gain or loss of periodontal attachment after treatment of adult periodontitis.

We studied the association between post-treatment periodontal disease activity and subgingival Bacteroides gingivalis, Bacteroides intermedius, spirochetes and motile rods. 20 adults, 22-62 years, with moderate-to-severe periodontitis participated in a split-mouth treatment study. All individual quadrants received supragingival cleaning and in addition, subgingival scaling and a NaHCO3-NaCl-H2O2 slurry, subgingival scaling alone, slurry alone, or no subgingival treatment. Post-treatment periodontal disease status was determined over a period of 12 months by changes in probing periodontal pocket depth and probing periodontal attachment level. Subgingival specimens obtained by paper point-sampling were evaluated for B. gingivalis and B. intermedius using indirect immunofluorescence and for spirochetes and motile rods using bright light phase contrast microscopy. A total of 142 periodontitis lesions representing all 4 quadrants of the 20 subjects were studied. The relationship between clinical data and bacteria was analyzed using logistic regression. The probability of the study organisms being present in subgingival sites at 3 to 6 months after treatment increased with increased residual pocket depth. The presence of B. gingivalis showed a strong positive association (p less than 0.004) with loss of periodontal attachment. A significant association was also found for spirochetes (p less than 0.008) but not for motile rods (p greater than 0.35) or B. intermedius (p greater than 0.13). Similar results were obtained at 12 months after therapy, except that the presence of motile rods was significantly associated with loss of periodontal attachment (p less than 0.03). Caution must be exercised when using B. gingivalis or spirochetes to evaluate treatment efficacy. If the presence of these organisms was utilized to indicate progressing periodontitis, many active lesions could be identified, and only 1 to 17% and 13 to 43% of sites in remission at 3-6 months after therapy would be expected to harbor B. gingivalis and spirochetes, respectively. The consequences of treating periodontal sites in remission would mainly be limited to cost and inconvenience. However, since several active periodontitis lesions did not reveal the organisms, treatment decisions based solely on the absence of the organisms may result in the omission of needed therapy. As a practical consideration, periodontal treatment should be continued as long as B. gingivalis and maybe spirochetes are detectable in the subgingival microflora. In the absence of these organisms, and until additional periodontal pathogens have become known, the decision to continue or conclude periodontal therapy must b

Adult↗
PubMed1985

Subgingival microorganisms and bacterial virulence factors in periodontitis.

Considerable information has come forth in recent years on the pathogenic organisms in human periodontitis and the sequence of events by which they produce periodontal disease. Important periodontopathogens include Bacteroides gingivalis, Bacteroides intermedius and Actinobacillus actinomycetemcomitans. Virulence factors of B. gingivalis and B. intermedius may mainly involve enzymes with potential to interfere with host defenses and to disintegrate periodontal tissues. Pathogenic properties of A. actinomycetemcomitans appear predominantly to be exerted by leukotoxin and other noxious products.

Actinobacillus↗
PubMed1985

Antibiotic susceptibility of anaerobic bacteria from the human oral cavity.

Anaerobic, agar-dilution, minimal inhibitory concentrations (MICs) of 18 antibiotics are given for the numerically important bacterial groups from the human oral cavity. Strains are divided into susceptibility categories using the guidelines for interpretation of MICs suggested by the National Committee for Clinical Laboratory Standards. These guidelines are based on data on antibiotic concentrations attainable in serum following various dosage regimens. MICs are also compared with attainable gingival fluid levels where these are known. The highest percentages of strains were susceptible to tetracycline, with 89% of the 139 strains tested susceptible to serum levels and 97% conditionally susceptible to attainable gingival fluid levels. Ninety-eight percent of strains were conditionally susceptible to attainable gingival fluid levels of minocycline, but many strains, including Actinobacillus actinomycetemcomitans, were only moderately susceptible to attainable serum levels of this tetracycline analogue. Carbenicillin was effective against most groups of organisms, with the important exception of A. actinomycetemcomitans, at serum levels attainable with oral formulations of carbenicillin. Only 2% of the total strains tested were resistant to penicillin, while 33% of strains were categorized as moderately susceptible. Clindamycin was active against many strains of Gram-negative bacteria but was not active against A. actinomycetemcomitans, some Bacteroides, Eikenella corrodens, or the anaerobic vibrios. Metronidazole was active against A. actinomycetemcomitans, all five groups of oral Bacteroides tested, and against Capnocytophaga species. Chloramphenicol was active against A. actinomycetemcomitans, but not against most of the other groups of oral organisms. Nearly all groups contained strains non-susceptible to serum levels attainable with the usual doses of erythromycin, spiramycin, vancomycin, kanamycin, neomycin, streptomycin, doxycycline, oxytetracycline, or chlortetracycline; several strains were resistant to maximum attainable serum levels of each of these antibiotics except doxycycline.

Actinobacillus↗
PubMed1985

Transmission and colonization of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients.

Actinobacillus actinomycetemcomitans is a Gram-negative oral microorganism, which has been implicated in the etiology of localized juvenile periodontitis and in severe medical infections such as bacterial endocarditis. This study evaluated the ability of periodontal probes to transmit A actinomycetemcomitans from juvenile periodontitis lesions to healthy gingival sulci in the same patient. Localized juvenile periodontitis patients exhibiting first molar and incisor alveolar bone loss and with large numbers of A actinomycetemcomitans in deep periodontal pockets were included in this study. A periodontal probe was inserted into periodontal pockets of 6 mm or greater depth. The probe was then placed into a healthy gingival sulcus of 3 mm or less, in the same subject. Fifty-five transfers by probing were made and A actinomycetemcomitans in both the donor and recipient sites was assessed by a selective culture technique. The results indicate that periodontal probes can become contaminated with A actinomycetemcomitans from juvenile periodontitis lesions during routine dental examinations and can transfer this microorganism from infected to previously uninfected sites. However, A actinomycetemcomitans inoculated into the healthy gingival sulci did not permanently colonize these sites since the organisms were eliminated within 3 weeks.

Actinobacillus↗
PubMed1984

In situ identification of bacterial species in marine microfouling films by using an immunofluorescence technique.

An immunofluorescence technique was developed for the in situ identification of specific bacteria in marine microfouling films. Microorganisms adherent to glass plates after 30 days of immersion in a synthetic seawater system were cultured and classified by biochemical tests, flagellar arrangement, and the API 20E system. All isolates were gram-negative aerobic or facultative motile rods, predominantly Pseudomonas spp. Rabbit antisera to the five dominant organisms including Achromobacter spp., Comamonas terrigena, P. putrefaciens, a yellow-pigmented Pseudomonas sp., and Vibrio alginolyticus were prepared. These antisera were shown to be species specific in indirect immunofluorescence assays against a battery of 26 marine isolates from 14 bacterial species, with the exception of antisera to the Pseudomonas spp, which cross-reacted with each other but not with test bacteria of other genera. These immunofluorescent reagents enabled the in situ identification of all five bacterial species in microfouling films. Low-surface-energy test plates had smaller numbers of adherent bacteria in microfouling films than medium-surface-energy test plates, suggesting that the degree of microfouling may be influenced by the surface energy. In addition, the reagents could identify up to 39% of the attached bacteria in microfouling films spontaneously formed on steel plates in flow cells deployed in different areas of the Atlantic Ocean. The microbial composition of the ocean-formed films varied with the geographical area of their formation. The present results indicate that immunofluorescence techniques may provide a rapid and reliable means to identify, in situ, specific bacteria in marine microfouling films.

Animals↗
PubMed1984

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↗
PubMed1984

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↗