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Notes: Objectives: The purpose of this split-mouth study was to evaluate the clinical response of enamel matrix proteins (EMPs, Emdogain Gel®) in intra-osseous defects with or without a combined application of a tetracycline-coated expanded polytetrafluoroethylene barrier membrane (e-PTFE, Gore-Tex®).Methods: Twelve pairs of intra-osseous periodontal defects in 11 patients received the application of EMPs on the exposed root surface (EMP). One of the two defects received randomly, as an adjunct to EMP treatment, a tetracycline-coated e-PTFE membrane (MEMP). At baseline, 6- and 12-month probing pocket depth (PPD), clinical attachment level (CAL) and probing bone level (PBL) were measured.Results: After 12 months, the EMP defects showed a significant mean PPD reduction of 2.86±0.75 mm, a mean gain in CAL of 1.28±2.04 mm, a mean PBL gain of 1.63±1.21 mm and a mean increase of recession (REC) of 1.56±2.30 mm. The MEMP defects showed a significant mean PPD reduction of 3.02±1.55 mm, a mean gain in CAL of 1.65±1.29 mm, a mean PBL gain of 1.58±1.92 mm and a mean increase of REC of 1.38±1.63 mm. Except for significantly more post-operative discomfort at the MEMP sites, no significant differences were found between EMP and MEMP defects.Conclusion: Within the limits of this study, it is concluded that in the treatment of intra-osseous defects with EMP, the adjunctive use of a tetracycline-coated e-PTFE membrane failed to show more gain of CAL and PBL.

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 present study primarily aimed at investigating the oral microbiota in smokers and non-smokers with established gingivitis and monitoring its composition during experimental gingivitis. Secondly, it aimed at examining whether the composition of the microbiota is associated with different levels of gingival inflammation during this experimental gingivitis trial. For this purpose, 25 non-dental university students with gingivitis were recruited. 11 subjects were smokers and 14 were non-smokers. After achieving gingival health, they entered a 14-day experimental gingivitis trial. Plaque and bleeding were assessed before entering into the study (intake), at day 0. day 5 and at day 14 of the experiment. Microbiological samples from mucosal sites and dental plaque (taken at intake, day 0, and day 14) were analysed for the presence of Actinomyces species. Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros. Porphyromonas gingivalis, Prevotella intermedia and Streptococcus species. At day 14 of the experimental period, the level of plaque formation was not different between smokers and nonsmokers, but bleeding scores were lower in smokers than in non-smokers (15% and 30%) respectively, p= 0.01). The change from natural gingivitis to a state of gingival health and a subsequent change from gingival health to experimentally induced gingivitis was accompanied by quantitative alterations in the cultivable microbiota in both groups. Changes were most prominent in the transition from gingival health to experimental gingivitis and were found in dental plaque for Actinomyces species, C. rectus, F. nucleatum, and P. intermedia. Within the group of non-smokers, a distinction was made between subjects with a‘weak’or 'strong’inflammatory response. No relationship with a single bacterial species could be established which would likely explain the differences in levels of inflammation. It is concluded that differences in response to experimental gingivitis are not caused by major differences in the composition of the oral microbiota.

Notes: Abstract In this study, we investigate the prevalence of selected periodontal pathogens on the oral mucous membranes before and after full-mouth tooth extractions in patients with severe periodontitis. 8 patients were microbiologically examined 2 × before and 2 × after extraction; several locations on the oral mucous membranes, saliva, supra- and subgingival plaque, were sampled. Besides their presence in subgingival plaque, we detected before extraction on the mucous membranes Actinobacillus actinomycetemcomitans in 2 patients (mean 0.03%), Porphyromonas gingivalis in 6 patients (mean 9%), and Prevotella intermedia (mean 2%) and other Prevotella species (mean 7%) in all patients. At 1 and 3 months after extraction, A. actinomycetemcomitans and P. gingivalis could not be detected in any of these patients on the oral mucous membranes and in saliva, while from all patients still P. intermedia (mean 3%) and the other blackpigmented Prevotella species (mean 4%) could be isolated. These results indicate that the preferable habitat for A. actinomycetemcomitans and P. gingivalis is dental plaque in subgingival lesions. P. intermedia and the other blackpigmented Prevotella species can colonize the oral mucous membranes of edentulous patients irrespective of the presence of a subgingival microflora. We speculate that in periodontal patients the colonization of mucous membranes with P. gingivalis and A. actinomycetemcomitans is transient in nature and most likely the result of dissemination from the subgingival microflora. Thus it seems unlikely that edentulous patients constitute a reservoir of infection of P. gingivalis A. actinomycetemcomitans.

Notes: Background: The effect of smoking on the prevalence of periodontal pathogens after periodontal treatment is still not clear. Some studies found no effect of the smoking status on the prevalence of periodontal pathogens after therapy, whereas others did. The aim of this retrospective study was to investigate the influence of smoking on the treatment of periodontitis and the composition of the subgingival microflora.Method: The study included 59 periodontitis patients (mean age 41.5 years): 30 smokers and 29 nonsmokers. The treatment consisted of initial periodontal therapy and, if necessary, surgery and/or antibiotics. Clinical and microbiological data were obtained before and after treatment at the deepest site in each quadrant. A pooled sample was analysed for the presence of Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Prevotalla intermedia (Pi), Bacteroides forsythus (Bf), Fusobacterium nucleatum (Fn) and Peptostreptococcus micros (Pm).Results: For smokers and nonsmokers a significant improvement of the clinical condition was found after treatment. A decrease could be assessed for bleeding on probing (smokers: 0.46; nonsmokers: 0.52) and probing pocket depth (PPD) (smokers: 1.64 mm; nonsmokers: 2.09 mm). Furthermore, both groups showed gain of attachment (smokers: 0.68 mm; nonsmokers: 1.46 mm). No significant difference in bleeding on probing and PPD reduction was found between smokers and nonsmokers. In contrast, nonsmokers showed significantly more gain of attachment than smokers. The microbiological results revealed no differences in the prevalence of the various bacteria between smokers and nonsmokers before treatment. After treatment in nonsmokers, a significant decrease was found in the prevalence of Aa (11–3), Pg (17–7), Pi (27–11), Bf (27–11), Fn (28–20) and Pm (27–17). In smokers, a significant decrease could be shown only for the prevalence of Pg (15–5).Conclusions: Nonsmokers showed more gain of attachment and a greater decrease in the prevalence of periodontal bacteria as compared to smokers. The phenomenon that among smokers, more patients remain culture positive for periodontal pathogens after therapy, may contribute to the often observed unfavourable treatment results in smoker periodontitis patients.

Notes: Abstract. In a previous study, an edentulous subject showed the presence of P. gingivalis. only in saliva. The present case report is a longitudinal follow-up on this proband (female, 63 years) and her spouse with periodontitis (67 years). Samples were taken from the proband and the spouse for microbiological analysis at several occasions during a 3-year period and a 1 -year period respectively. In the edentulous proband, P. gingivalis was present in saliva only, at ail times. In the spouse, P. gingivalis was present in the periodontal pocket and on the mucous membranes, but the saliva was culture-negative for this species at both sampling times. The restriction enzyme analysis (REA) patterns of isolates (n=7) of P. gingivalis from the proband recovered over 3 years showed no differences. This indicated that the same clonal type of P. gingivalis persisted for 3 years in the proband. The P. gingivatis isolates (n=13) from the spouse showed no differences when REA patterns were compared. Comparison of REA patterns from the proband and the spouse also showed no differences. Thus the same clonal type of P. gingivalis can persist over several years in an edentulous subject and at least for 1 year in a subject with periodontal disease.

Notes: Background: Anemia of chronic disease (ACD) is defined as the anemia occurring in chronic infections and inflammatory conditions, that is not due to marrow deficiencies or other diseases and in the presence of adequate iron stores and vitamins. The purpose of the present study was to investigate whether periodontitis patients show signs of anemia.Method: 39 patients with severe periodontitis, 71 patients with moderate periodontitis and 42 controls, all with good general health, participated in this study. The mean age of all groups was 42 years. Several red blood cell parameters were determined from peripheral blood samples.Results: Overall data analysis indicated that periodontitis patients have a lower hematocrit, lower numbers of erythrocytes, lower hemoglobin levels and higher erythrocyte sedimentation rates. These results were adjusted for the following possible confounders: gender, age, smoking, ethnicity and level of education. Further, more periodontitis patients (23%) than controls (7%), had hemoglobin levels below the normal reference range.Conclusions: The present study provides further evidence that periodontitis has systemic effects and that periodontitis may tend towards anemia. This phenomenon may be explained by a depressed erythropoiesis.

Notes: Background: Recent studies show that subjects with natural gingivitis or periodontitis have elevated levels of salivary cystatins compared to periodontally healthy individuals. Increased glandular output of cystatins in inflammatory conditions suggests an active, most likely protective, rôle for these proteins in inflammatory processes. Furthermore, it has been shown that the development of gingival inflammation is suppressed in smokers during experimental gingivitis.Aims: The purpose of the present study was to investigate whether (i) the levels of salivary cystatins in natural gingivitis are related to smoking status, and (ii) to study whether experimentally induced gingivitis is associated with changes in salivary cystatin levels, in both smokers and non-smokers.Material and Methods: Whole saliva samples were taken in relation to natural gingivitis, gingival health and 14-day experimental gingivitis in 25 non-dental students (14 non-smokers and 11 smokers). The salivary flowrate was determined. Samples were analyzed for levels of protein, cystatin and cystatin-C.Results: Salivary flow and protein concentrations in cleared human whole saliva samples of non-smokers and smokers were not different from each other at any timepoint during the trial. With regard to cystatins, the results showed that in the state of natural gingivitis cystatin activity is lower in smokers as compared to non-smokers. In smokers, the resolution of natural gingivitis to the state of gingival health did not result in a change of cystatin activity and levels of cystatin C. At the end of the 14-day experimental gingivitis period, smokers showed a decrease in cystatin activity and cystatin C as well as lower outputs of cystatin activity and cystatin C.Conclusion: Smoking is associated with lower cystatin activity and output of cystatin C during gingival inflammation.

Notes: Background: A major aspect of the adaptive host response in periodontitis is the production of antibodies. Several risk and susceptibility factors for periodontitis, including smoking, age and composition of the subgingival microflora, have also been suggested to influence antibody production.Aim: The present study was conducted to investigate plasma levels of immunoglobulin (Ig) G, A and M antibodies in periodontitis patients of Caucasian European heritage in relation to disease severity, smoking, diagnosis and prevalence of periodontopathogens.Methods: In this study, 29 patients with severe periodontitis, 51 with moderate periodontitis and 55 controls without periodontal destruction were enrolled. From the total of 80 patients, 18 were diagnosed with aggressive periodontitis and 62 with chronic periodontitis. Total IgG, IgA and IgM as well as IgG isotypes were analyzed in plasma samples.Results: Levels of total IgG, IgA and IgM were not different between patients and controls; however, in periodontitis, higher levels of IgG1 and IgG2 were observed. Smoking appeared to be significantly and inversely related to antibody levels in periodontitis, in particular for total IgG and IgG2. The absence of an elevated total IgG and IgG2 in smoking patients was irrespective of severity, prevalence of periodontal pathogens and diagnosis. The elevation of total IgG and IgG1 and IgG2 in non-smoker periodontitis patients was observed in patients with moderate periodontitis and even greater in patients with severe periodontitis, but was independent whether patients were infected with Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis and independent of diagnosis. Clinically, it was observed that patients who smoked had more periodontal bone loss; the current findings on antibody levels may be one of several mechanisms related to more extensive periodontal breakdown in smoker patients.Conclusion: The current study shows that non-smoker periodontitis patients have higher levels of total IgG and IgG2 than smoker periodontitis patients.

Notes: Objectives: It has been suggested that periodontal inflammation may result in an altered immune response. The peripheral immune capacity in periodontitis patients can be investigated using lipopolysaccharide (LPS)-stimulated whole blood cell cultures (WBCC), known to reflect the behavior of monocytes in particular. A previous study in our laboratory revealed that monocytes in the stimulated cultures from periodontitis patients behaved functionally different compared with controls. The present study investigated whether this different response of periodontitis patients' monocytes is intrinsic or acquired.Material and Methods: The release of inflammatory mediators was measured in Escherichia coli LPS-stimulated WBCC from 12 periodontitis patients before and after periodontal therapy. In addition, the total leukocyte and leukocyte differentiation counts were also determined in the patients before and after therapy.Results: The levels of interleukin (IL)-12p70 in cell culture supernatants increased two times and those of prostaglandin E2 showed a trend towards reduction after therapy, whereas the levels of IL-1β, IL-6, IL-8, IL-10, IL-12p40 and tumor necrosis factor-α did not change. The total number of white blood cells was decreased after periodontal therapy.Conclusions: After periodontal therapy, the functional phenotype of the peripheral blood monocytes from patients was reconstituted, resembling that of subjects without periodontitis.