To test in vitro whether the seal provided by the locking taper used in the implant-abutment connection was capable of preventing the invasion of oral microorganisms.Twenty-five wide-body implants (5 x 11 mm) and 25 abutments were divided into 2 groups for a 2-phase experiment. The first phase tested the ability of the seal to shield the implant well from outside bacteria; the second phase tested the ability of the seal to prevent bacteria present in the implant well from seeping out. For phase 1, 10 implant-abutment units were immersed in a bacterial broth for 24 hours. The abutments were then separated from the implants and bacterial presence was evaluated using scanning electron microscopy. In phase 2, the tested abutments were inoculated with a droplet of soft agar bacterial gel and assembled with the implant. These units were incubated in a sterile nutrient broth for 72 hours, sampled, and plated to assess bacterial presence.In phase 1, no bacteria were detected in any of the implant wells. In phase 2, no bacteria were detected in the nutrient broth or on the agar plates at 72 hours.In implants where a microgap is present, microbial leakage could lead to inflammation and bone loss; thus, it is important to minimize bacterial presence in and around the the implant-abutment junction.The seal provided by the locking taper design has been demonstrated to be hermetic with regard to bacterial invasion in vitro.
In vitro topical application for 5 min or 6 h of 1.5 M ammonium fluoride with 1.5 M ammonium monofluorophosphate (MFP) to enamel was studied at pH 7.0 and 4.6. After 5-min treatments, fluoride penetrated over 10 μm, but less than 20 μm into the enamel. More fluoride deposition and penetration over 20 μm resulted from the 6-hour treatments. Most fluorapatite was formed after a 6-hour treatment with the neutral solution. Treated enamel surfaces were studied in the scanning electron microscope before and after KOH equilibration for removal of calcium fluoride. The electron micrographs were compared with others which were obtained from enamel treated for the same time with 1.5 M ammonium fluoride or 1.5 M ammonium MFP or 1.5 M ammonium fluoride with 1.5 M ammonium orthophosphate at pH 7.0 or 4.6. The findings indicated that the most extensive dissolution-precipitation reactions, with considerable calcium fluoride formation, occurred relative to the application of ammonium fluoride alone. Addition of ammonium MFP or orthophosphate to ammonium fluoride solutions reduced the extent of visible changes. Application of ammonium MFP alone caused very limited or no visible change.
The purpose of this investigation was to identify bacterial species present on or in crevicular epithelial cells in healthy and diseased sites using DNA probes. In order to achieve this aim, further improvements were made in the separation of unattached bacteria from those adherent to epithelial cells isolated from the human gingival crevice or periodontal pocket. Then the DNA probes were used to determine the prevalence of detectable DNA from 15 microbial species on or in crevicular epithelial cells. One sample was taken from a single subgingival site in each of 51 individuals ranging in age from 19 to 45 years. Samples were taken from 27 sites of clinically healthy subjects and 24 samples were taken from subjects having periodontally diseased sites. DNA‐DNA hybridization indicated that a majority of epithelial cells from healthy sites (63%) were in contact with or harbored Streptococcus oralis. On the other hand, species such as Bacteroides forsythus, Prevotella intermedia, Capnocytophaga ochracea and Campylobacter rectus were more frequently detected in elevated numbers in periodontally diseased sites. Cluster analysis of the microbial profiles generally aggregated subjects with and without periodontitis into separate cluster groups. The cluster patterns suggest the possibility that microbial complexes will be, in part, determined by the receptors available on the epithelial cells.
The effect of growth in the presence of sublethal concentrations of tetracycline on the extent of fimbriation and surface hydrophobicity of strains of Actinomyces viscosus and Bacteroides gingivalis , two species frequently isolated from patients with rapidly progressing periodontitis, was determined. Negatively‐stained cells of A. viscosus strains LY7 and S2 and B. gingivalis strain 381 showed a dramatic reduction in the number of fimbriae on their surface when grown in the presence of 50% of the minimum inhibitory concentration of tetracycline as compared to untreated controls. Similar observations were made with fixed, lanthanum‐stained thin sections. In addition to long fimbriae, the A. viscosus strains possessed stubby, densely staining tufts on their surface which were not affected by tetracycline. The hydrophobicity of antibiotic‐grown A. viscosus and B. gingivalis cells was also found to be significantly reduced. The decrease in fimbriation and surface hydrophobicity of A. viscosus and B. gingivalis when grown in the presence of low concentrations of tetracycline may explain their reduced ability to attach to experimental pellicles. These observations suggest that part of the efficacy of tetracycline therapy for destructive forms of periodontal diseases may be mediated by an alteration of the adhesive properties of subgingival bacteria which affected their colonization.
Treatment of hydroxyapatite (HA) with human type I or type III collagen strongly promoted adhesion of Actinomyces viscosus LY7 cells. Treatment with human type V collagen was somewhat less effective while treatment with human type IV or rat type I collagen was significantly less effective. Electron microscopic observations revealed that A. viscosus cells also attached to fibrils prepared from human type I collagen. The alpha 1 (1) polypeptide chain derived from type I collagen was ineffective in promoting binding and the alpha 2(1) polypeptide chain exhibited moderate activity. Heat‐ or urea‐denatured type I collagens were also ineffective in promoting binding. Mutants of A. viscosus that possess type 1 fimbriae, but not type 2 fimbriae or no fimbriae, also bound to collagen‐treated HA; this suggests that the adhesin responsible was associated with type 1 fimbriae. Strains of Actinomyces israelii and Actinomyces odontolyticus also exhibited strong binding to collagen‐treated HA, while Actinomyces naeslundii ATCC 12104 did not. The avidity of Actinomyces species for collagen would seem to be at least partially responsible for the high proportions of these organisms found on cemental and root tooth surfaces.
The invasion of gingival epithelial cells by certain pathogenic periodontal bacteria may account for their presence within diseased gingival tissue. To dissect the initial steps of a potential invasion pathway for the periodontal pathogen Porphyromonas gingivalis, laboratory and clinical bacterial isolates were tested for their interactions with a human oral epithelial cell line (KB). Several P. gingivalis strains immobilized on filters could bind oral epithelial cells. Quantitative adherence assays supported these results. The invasion of epithelial cells by P. gingivalis 33277 was measured by assay and confirmed by transmission electron microscopy. These preliminary results demonstrate that certain P. gingivalis strains are capable of internalization by human oral epithelial cells in vitro.
