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Notes: The work function of tetrahedral amorphous carbon (ta-C) has been measured by Kelvin probe to lie in the range 4–5 eV, irrespective of its sp3 content or nitrogen addition. This implies that the surface barrier to emission is dominant and that emission changes caused by sp3 bonding or nitrogen addition are not directly due to changes in work function. Hydrogen, oxygen, and argon plasma treatments are all found to increase the emission of a-C, but hydrogen and argon treatments are found to reduce the work function while oxygen treatment increases it. Detailed studies of the surface with varying plasma treatment conditions suggest that the changes in emission arise mainly from changes in the surface microstructure, such as the formation of sp2 regions within the sp3 bulk. The need for local field enhancement mechanisms to account for emission over the sizeable barrier is emphasized, which may arise from local chemical nonhomogeneity, or formation of nanometer-size sp2 clusters embedded in an sp3 matrix. © 2000 American Institute of Physics.

Notes: Background : Forty per cent of patients with inflammatory bowel disease fail to respond to standard dose azathioprine (2 mg/kg/day).Aims : To evaluate the efficacy and safety of increasing the azathioprine dose according to a fixed schedule and guided by clinical response and adverse effects.Methods : We reviewed the records of all patients with inflammatory bowel disease treated by a single clinician over 6 years, unresponsive to at least 3 months treatment with standard dose azathioprine, and whose dose was subsequently increased.Results : Forty patients (27 male; 24 Crohn's, 16 ulcerative colitis) with chronic active disease or recurrent flares despite standard dose azathioprine for a median 8 months (range 3–114) increased their dose from a median 2.02 (1.61–3.19) mg/kg/day to 2.72 (2.37–3.99) mg/kg/day in one to four increments of 0.5 mg/kg/day, and were followed over a median6 (0.5–54) months. Eleven of the 40 patients (seven Crohn's, four ulcerative colitis) responded or had reduced frequency of flare-ups at the end of follow-up, while 17 of the 40 patients had no benefit. Response was more likely for maximum doses ≤2.5 mg/kg/day (six of 11 patients) than for doses 〉2.5 mg/kg/day (five of 29 patients) (P = 0.042). Twelve patients (11 of whom received maximum doses 〉2.5 mg/kg/day) were unable to maintain an increased azathioprine dose because of leukopenia in eight, nausea in three, and raised liver enzymes in one (all transient and reversible).Conclusions : Increasing the azathioprine dose up to 2.5 mg/kg/day appears beneficial in patients who have not responded to 2 mg/kg/day. Further increase above 2.5 mg/kg/day is less likely to be efficacious, and is associated with a substantial risk of adverse reactions.

Notes: The gut flora is a vast interior ecosystem whose nature is only beginning to be unravelled, due to the emergence of sophisticated molecular tools. Techniques such as 16S ribosomal RNA analysis, polymerase chain reaction amplification and the use of DNA microarrays now facilitate rapid identification and characterization of species resistant to conventional culture and possibly unknown species. Life-long cross-talk between the host and the gut flora determines whether health is maintained or disease intervenes. An understanding of these bacteria–bacteria and bacteria–host immune and epithelial cell interactions is likely to lead to a greater insight into disease pathogenesis. Studies of single organism–epithelial interactions have revealed the large range of metabolic processes that gut bacteria may influence. In inflammatory bowel diseases, bacteria drive the inflammatory process, and genetic predisposition to disease identified to date, such as the recently described NOD2/CARD15 gene variants, may relate to altered bacterial recognition. Extra-intestinal disorders, such as atopy and arthritis, may also have an altered gut milieu as their basis. Clinical evidence is emerging that the modification of this internal environment, using either antibiotics or probiotic bacteria, is beneficial in preventing and treating disease. This natural and apparently safe approach holds great appeal.

Notes: Summary Background Autologous blood therapy (ABT) is used for treating atopic dermatitis (AD) in some European countries and is promoted on internet sites for this condition. However, there is little evidence from rigorous clinical trials to suggest that it is effective. Objectives To test the effectiveness of ABT for the symptomatic treatment of patients with AD. Methods Fifty subjects responded to press advertisements, and 31 were randomized within strata of severity at recruitment. Patients were included into a double-blind, placebo-controlled trial and received ABT or placebo once weekly for 5 weeks. Assessments were performed at baseline, at weekly intervals and after a 5-week follow up. The Six Area, Six Sign AD (SASSAD) severity index was predefined as the primary outcome measure. The Dermatology Life Quality Index and patient ratings of pruritus, quality of sleep and skin appearance on 100-mm visual analogue scales were defined as secondary outcome measures. Success of patient blinding and adverse events were assessed. Results Data were analysed on an intention-to-treat basis. Analysis of covariance suggested a significant differential change of the SASSAD score between baseline and the end of the follow-up period in favour of ABT. The mean reduction in SASSAD score was 13·5 points (95% confidence interval, CI 6·6–20·4, P 〈 0·001) over and above placebo; the corresponding value at the end of treatment was 9·6 (95% CI 4·2–14·9, P = 0·001). No clear significant intergroup differences in any of the secondary outcome measures were found. Six patients in the ABT group and seven in the placebo group reported minor and transient adverse events. Conclusions These data suggest that, according to the SASSAD score, ABT has beneficial effects in the treatment of AD, although this was not confirmed by the patient-rated assessments. The improvement in observer-rated skin condition suggested by this study needs confirmation in larger trials.

Notes: Inflammatory bowel disease involves an interaction between genetic susceptibility, a host mucosal immune response and the enteric flora. However, the relapsing and remitting course underlines the importance of other modifiers, such as psychological stress. Doctors and patients share the view that stress plays a role in the initiation and perpetuation of disease. Levels of chronic perceived stress have been shown to correlate with symptom relapse and mucosal appearance, and stress management therapy has been shown to be beneficial. Animal models provide further evidence that stress may play a role in disease initiation and reactivation.Elucidation of the gut–brain–immune axis has provided insight into the mechanisms by which stress may result in gut inflammation. Stress can alter intestinal physiological function. Stress can increase gut permeability, increase ion secretion by a mechanism involving neural stimulation or mast cells, increase mucin release and deplete goblet cells. Stress causes parasympathetic activation via a mechanism involving corticotropin releasing factor, ultimately affecting mucosal mast cells. Stress also results in increased bacterial adherence and decreased luminal lactobacilli. As a result of all these changes luminal antigens may gain access to the epithelium, causing inflammation.

Notes: Background: When the subgingival presence of periodontal pathogens is studied in groups of patients or populations, mostly a number of the deepest sites is sampled. The mean clinical parameters of these deep sites are also frequently used as a the descriptor of the clinical situation of these subjects. It can be questioned, whether these 4 deep sites are capable of predicting a full-mouth situation.Aim: The purpose of the present retrospective study was to investigate to what extent the experienced progression of periodontitis as measured in the deepest approximal pocket in each quadrant reflects the disease progression at the approximal sites on a full-mouth level.Methods: A data set of a 7-year longitudinal study of 158 young subjects (69 male, 89 female, 15–25 years of age at baseline) was used. Clinical assessments included plaque index (PI), pocket depth (PD) and attachment loss (AL) at baseline (1987) and follow-up (1994). Measurements were made at the approximal surfaces of all teeth. The deepest pocket in each quadrant was determined at follow-up. Changes of the clinical parameters between baseline and follow-up were calculated both as full-mouth mean scores as well as for these 4 deepest sites. A regression analysis was used to evaluate the relationship between full-mouth score and the 4 test sites.Results: For disease progression between baseline and follow-up, significant correlation coefficients were observed between the 4-site and full-mouth mean changes (PD: 0.80, AL: 0.70, PI: 0.77). Regression coefficients were 0.51 for PD, 0.35 for AL and 0.55 for PI. The precision of the estimate for the full-mouth mean, as predicted by the 4-site mean, is determined by the residual standard deviation. This was for PD 0.31 mm, for AL 0.31 mm and for PI 0.29. Compared to the between-patient standard deviation of the full-mouth means, the residual standard deviations were high.Conclusion: In the present population, a reasonable to good correlation between full-mouth and 4-sites data was observed. However, the high residual standard deviation in the regression analysis illustrates the inaccuracy for the 4-sites data when used as a descriptive for changes in the periodontal condition on a full-mouth level. Data evaluating progression of periodontitis based on a limited number of diseased sites should be interpreted cautiously.

Notes: Objectives: Current literature is ambivalent on the use of barrier membranes for regeneration of intraosseous defects. One of the reasons for unpredictable results may be related to infection before, during and after the surgical procedure. Therefore, the purpose of the present controlled study was to evaluate both the use of membranes (MEM) and antibiotics (AB), separately and in combination.Methods: In all, 25 patients with two intraosseous periodontal defects each were randomized in two groups: AB+ group receiving systemic antibiotics (n = 13) and AB– group without antibiotics (n = 12). After raising flaps and after debridement, both defects in each patient were covered by a bioresorbable membrane (MEM+). However, just before suturing the flaps in a coronal position, the membrane over one of the two defects was removed at random (MEM–). This protocol resulted in four groups of defects: (i) MEM– AB–; (ii) MEM+ AB–; (iii) MEM– AB+ ; (iv) MEM+ AB+. Patients were monitored clinically and microbiologically for 1 year. Data were analyzed in repeated measures ancova's and adjusted means for clinical variables were obtained from the final statistical model.Results:  Reduction in probing pocket depth (PPD) at 12 months postoperatively varied between 2.54 and 3.06 mm between the four treatment modalities, but overall no main effect of MEM or AB was found. Gains in probing attachment level (PAL) at 12 months postoperatively varied between 0.56 and 1.96 mm for the 4 treatments. In the overall analysis for PAL, no main effect of MEM or AB was found. Gains in probing bone level (PBL) 12 months postoperatively ranged from 1.39 to 2.09 mm between the treatment groups. Again, overall, no main effects of MEM or AB were found for PBL. Explorative statistical analyses indicated that smoking and not MEM or AB is a determining factor for gain in PBL (P = 0.0009). Nonsmokers were estimated to gain 2.04 mm PBL compared to 0.52 mm in smokers. The prevalence of several periodontal pathogens, at the day of surgery or postoperatively, and specific defect characteristics, were not determining factors for gain in PAL and PBL.Conclusions:  Neither the application of barrier membranes nor the use of systemic antibiotics showed an additional effect over control on both soft and hard tissue measurements in the treatment of intraosseous defects. In contrast, smoking was a determining factor severely limiting gain in PBL in surgical procedures aimed at regeneration of intraosseous defects.

Notes: Abstract The aim of the present study was to investigate the rate of development of experimentally-induced gingival inflammation in relation to the susceptibility to periodontal disease. By selection according to age, a younger (25–39 years) and an older (45–54 years) age group, with a comparable reduced but healthy periodontium, was selected. This equal amount of periodontal breakdown may suggest that the younger age group represented individuals with a relatively higher degree of susceptibility to periodontal disease. At the start of the experiment, each patient was instructed to abstain from oral hygiene procedures in 1 quadrant of the mouth for a period of 18 days. Results showed that all subjects developed signs of gingival inflammation. Regarding the development of redness and swelling, no differences could be assessed between the 2 age groups. However, analysis of the bleeding scores revealed that bleeding on probing developed more rapidly in the younger age group. It was concluded that those patients who have suffered from a more rapid form of periodontal disease also develop inflammation, in terms of bleeding on probing, more rapidly.

Notes: Abstract The purpose of the present investigation was to study the effect of age on the rate of development of gingival inflammation in individuals not susceptible to periodontal destruction. 7 younger (mean age 37 years) and 7 older (mean age 58 years) individuals were selected on the basis of the presence of at least 18 teeth, no evidence of extraction due to periodontal destruction, no loss of attachment, shallow pockets, gross amounts of plaque and a history of no interdental cleaning. All individuals were subjected to a carefully controlled oral hygiene program and experimental gingivitis was induced in 1 quadrant of the mouth during a period of 33 days. The amount of plaque, redness and swelling of the gingivitis, and bleeding on probing were assessed before, during and after the experiment. Al day 33, supra-gingival plaque samples were taken for bacteriological examination and gingival biopsies were taken for histopathological and immunohistochemical investigation. Results showed no differences between the 2 age groups with regard to the amount of plaque accumulation and the rate of development of gingival inflammation. Furthermore phase-contrast microscopy of plaque samples showed no differences between the 2 age groups. Neither his to-logical nor immunohistochemical investigation showed any differences between the 2 age groups. All biopsies diffusely showed presence of IgG, whereas in most biopsies, IgA plasma cells and in one biopsy IgM plasma cells were found. Neither IgD, IgE nor complement deposits were found. It was concluded that age is of minor importance in the development of experimentally-induced gingivitis in individuals not susceptible to periodontal destruction.

Notes: Abstract In a recent publication, it was hypothesized that the ratio between bleeding and plaque scores may act as a prognostic indicator for periodontal breakdown. Furthermore, it was found that the rate of development of gingival inflammation in terms of bleeding on probing during experimental gingivitis is more rapid in patients susceptible to periodontal breakdown than in subjects insusceptible to periodontal breakdown. The purpose of the present investigation was to compare the gingival reaction to dental plaque in an experimental gingivitis study in individuals without periodontal breakdown, having either a low or a high bleeding/plaque ratio. A group of 8 volunteers (18–23 years) with a low bleeding/plaque ratio and 7 volunteers (19–22 years) with a high bleeding/ plaque ratio were selected. In both groups, an experimental gingivitis study of 23 days duration was carried out. Results showed that individuals with a high bleeding/plaque ratio developed significantly more clinical inflammation in terms of bleeding and swelling of the gingiva than individuals with a low bleeding/plaque ratio. After 23 days of plaque accumulation, gingival biopsies as well as supragingival plaque samples were taken from both groups. Phase-contrast microscopy of the plaque samples showed no significant differences between the 2 groups. Low %s of spirochetes and motile rods were found. Stereologic point-counting procedures snowed equal amounts of infiltrated connective tissue in both groups. However, significant differences in composition of the infiltrate appeared to be present. The high ratio group showed more IgA producing plasma cells and complement activation than the low ratio group. The results of the present study suggest that the bleeding/plaque ratio of an individual may be regarded as a prognostic indicator for the degree of experimentally induced gingival inflammation in terms of bleeding and swelling of the gingiva as well as complement activation and IgA-plasma cell activity.