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.
L ocalized juvenile periodontitis (LJP) is an early‐onset periodontal disease associated with a polymorphonuclear neutrophil (PMN) defective migratory response. Kinetics of actin polymerization–depolymerization determine the shape changes occurring in the plasma membrane‐associated cytoskeleton and provide the driving force for directed cell migration (chemotaxis). Therefore, we investigated the relation between an abnormality in LJP PMN chemotaxis and an altered reorganization of the actin filament network. PMNs isolated from peripheral blood of LJP patients (n= 14) and matching control subjects (n= 12) were evaluated for random and directed migration in a Boyden chamber assay, and the kinetics of actin polymerization were studied by flow cytometry. Three groups of LJP patients could be distinguished on the basis of their PMN–chemotactic response compared to their matched control: depressed (n= 6), normal (n= 4), and elevated (n=4). The abnormal (depressed or elevated) chemotaxis was generally not related to abnormal random migratory response, except for two patients. Since the kinetics of formyl–methionyl–leucyl–phenylalanine–induced F‐actin response were highly variable from one subject to another, means were calculated at each timepoint with the values obtained from each group of subjects and compared by a general factorial design analysis. No statistically significant differences were detected between the control group and the LJP patient group. Furthermore, the data did not show a correlation between the kinetics of actin polymerization–depolymerization and the abnormal chemotactic response observed in LJP PMNs. Hence, the chemotaxis defect in LJP PMN appears to be mediated by signaling events that carry their effect independently of an intact cytoskeleton. J Periodontol 1998;69:209–218 .
P re‐incubation of neutrophils from rapidly progressive periodontitis (RPP) patients with lipopolysaccharide (LPS) extracted from Porphyromonas gingivalis was found to prime the neutrophils for enhanced FMLP‐stimulated superoxide production in a dosedependent manner. The priming effect of P. gingivalis LPS on neutrophils from control subjects was scanty or without effect at all. Inclusion of human serum in the experimental priming conditions increased the control and RPP neutrophil response by 2 to 3 fold. Blocking of the CD14 receptor on the neutrophil surface with monoclonal antibody eliminated the priming effect. Furthermore, incubation of control neutrophils with P. gingivalis LPS in the presence of serum from RPP patients generated a higher response as compared to incubation with control serum. The data suggest that neutrophil priming described in RPP patients is dependent on a serum factor which alters the neutrophil response to priming agents such as LPS. J Periodontol 1994;65:129–133 .
Localized aggressive periodontitis (LAgP) is associated with neutrophil dysfunction including defective chemotaxis and reduced calcium influx factor activity. Nitric oxide (NO) and its enzyme, nitric oxide synthase (NOS), have been suggested to be involved in chemotaxis. Some reports, however, were unable to detect either NO or NOS in human neutrophils. In this study, we focused on NOS activity in LAgP neutrophils and examined the involvement of NOS in chemotaxis of normal neutrophils and NOS activity in neutrophils from normal subjects and patients with LAgP.Neutrophils from 10 normal subjects and 10 LAgP patients were isolated from peripheral venous blood. Membrane associated-NOS (MA-NOS) and soluble NOS (S-NOS) were extracted from cells with or without FMLP stimulation. NOS activity was measured using the radiolabeled L-arginine to L-citrulline conversion assay.N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, significantly inhibited FMLP-induced chemotaxis (P<0.01) and dibutyryl cGMP, an activator of cGMP-dependent protein kinase, significantly attenuated the inhibition by L-NAME (P<0.01). Unstimulated and FMLP-stimulated MA-NOS activity in LAgP neutrophils was statistically significantly higher than that in normal neutrophils (P<0.05). S-NOS activity in LAgP neutrophils was higher than that in normal neutrophils.This study suggests that NOS is present in human neutrophils and may be involved in FMLP-induced chemotaxis in normal neutrophils. NOS activity is increased in LAgP and is negatively correlated to chemotaxis response.
Background: Localized aggressive periodontitis (LAgP) is associated with neutrophil dysfunction including decreased chemotaxis and reduced calcium entry. It has been suggested that CD38 is involved in chemotaxis. Little is known, however, about the relationship of CD38 and LAgP patients. In this study, we focused on the level of CD38 expression between LAgP and normal subjects and examined the involvement of CD38 in abnormal neutrophil chemotaxis of LAgP patients. Methods: Neutrophils from 12 normal subjects and 12 LAgP patients were isolated from peripheral venous blood. Membrane associated proteins were extracted from cells with or without N ‐formylmethionine leucyl‐phenylalanine (fMLP) stimulation. CD38 expression was measured using Western blotting. Band density was measured using an imaging densitometer. Results: There was no statistical difference between normal subjects and LAgP patients in resting CD38 expression (basal level). However, the fMLP‐stimulated neutrophils exhibited a significant decrease of CD38 expression in LAgP subjects compared to normal subjects. The decrease of CD38 was positively correlated with the defect in chemotactic migration to fMLP. Conclusion: These data suggest that the lower expression of CD38 in neutrophils may be related to altered neutrophil function in LAgP.
Background: A randomized clinical trial was performed to test the efficacy of a fluoridated hydrogen peroxide–based mouthrinse on gingivitis and tooth whitening in a two‐phase study. The first phase (28 days) included the experimental gingivitis phase; the second phase (5 months) was the oral hygiene phase, which included rinsing. Methods: A total of 99 subjects were included in the study and were randomly assigned to receive either placebo or test mouthrinse. Clinical measures were chosen to reflect the gingival health and tooth whiteness in an intent‐to‐treat study design. Statistical analyses of clinical parameters related to gingival health and tooth color were conducted, using the method of generalized estimating equations (GEE), with an exchangeable working correlation to accommodate tooth‐level data. Baseline differences between the groups were adjusted. Microbial samples taken at the beginning and at the end of the study were analyzed by DNA‐DNA hybridization technique, to determine whether there was any adverse shift in supragingival flora. Results: Eastman bleeding index, modified gingival index, intensity of stain, and extent of stain were significantly reduced in the test group at 6 months compared to baseline ( P <0.05). In contrast, only the Eastman bleeding index was significantly reduced in the control group ( P <0.05). The reduction in the index of gingival inflammation for the test group was significantly greater than for the control group ( P = 0.004). Subjects using the test rinse were also six times more likely to exhibit an improvement in tooth color after 6 months than were subjects using placebo ( P = 0.002). As a result of the clinical evaluations and microbial analysis, test mouthrinse was found to be safe during a 6‐month period. Conclusion: The results of this study indicate that the fluoridated hydrogen peroxide–based mouthrinse effectively whitens teeth and significantly reduces gingivitis. J Periodontol 2004;75:57‐65 .
Abnormalities of neutrophil function have been highly correlated with severe, early onset periodontal diseases. Nonetheless, the identification of these patients and diagnosis of specific disease states, such as LJP or prepubertal periodontitis, are difficult and costly. In this report, the identification and quantification of neutrophil cell surface markers specific to LJP patients with neutrophil chemotaxis defects are described. GP110 and FMLP receptors were quantified by flow cytometry on neutrophils from LJP patients with neutrophil chemotaxis defects, LJP patients without chemotaxis defects, other patients with primary neutrophil chemotaxis defects, and controls. Results suggest that reduction of GP110 and FMLP receptor on neutrophils is specific for LJP patients who exhibit neutrophil chemotaxis abnormalities.
Protein kinase C is a key molecule in neutrophil signal transduction after receptor stimulation by soluble bioactive molecules. It has been reported that neutrophils from most patients with localized juvenile periodontitis (LJP) do not have a normal response after stimulation with a chemotactic ligand such as N-formylmethionylleucylphenylalanine (FMLP). To further clarify the mechanism of this altered response and to confirm and expand earlier observations, the calcium-dependent protein kinase C activity of neutrophils from patients with LJP was evaluated. Peripheral blood neutrophils from 12 patients and 12 healthy subjects, age, sex, and race matched, were sonicated and subsequently subfractionated by ultracentrifugation into a soluble fraction (cytosol rich) and a particulate fraction (membrane rich). The calcium-dependent protein kinase C activity was evaluated in each fraction by phosphorylation of histone with radiolabeled ATP in the presence or in the absence of phorbol 12-myristate 13-acetate stimulation. Results revealed that the total calcium-dependent protein kinase C activity of neutrophils from patients with LJP and depressed chemotactic migration to FMLP (201.0 +/- 63.6 pmol/min/10(7) cells) was lower than that of neutrophils from healthy subjects (287.6 +/- 55.7 pmol/min/10(7) cells) (P < 0.01). The calcium-dependent protein kinase C activity in neutrophils from patients with LJP exhibited a positive correlation with chemotactic migration to FMLP (P < 0.05). The low activity of calcium-dependent protein kinase C in neutrophils from the patients reflected the low activity in the soluble fraction from the neutrophils. After stimulation with phorbol 12-myristate 13-acetate, the calcium-dependent protein kinase C activity was found to be lower from patients with LJP than from healthy subjects. These results suggest that lower calcium-dependent protein kinase C in neutrophils is a predisposing factor for LJP.
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