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The impact of osteoporosis on implant treatment is still a matter of debate in the scientific community, as it may possibly lead to higher failure rates. As long-term controlled trials are missing, the aim of this study was to verify the long-term outcome of implants placed in patients with systemic osteoporosis. Postmenopausal women in need of implants underwent bone mineral density measurements in hip and spine, using dual X-ray absorptiometry scans. Based on T-scores, they were divided into 2 groups: group O (osteoporosis group) with a T-score ≤-2 or group C (control group) with a T-score of ≥-1. Implants were placed in a 2-stage manner and loaded 4 to 8 wk after abutment surgery. Six months after loading and thereafter yearly, clinical and radiographical parameters were assessed. In total, 148 implants were placed in 48 patients (mean age: 67 y [range, 59-83]). Sixty-three implants were placed in 20 patients (group O) and 85 implants in 28 patients (group C). After 5 y, 117 implants (38 in group O and 79 in the group C) in 37 patients were assessed. Cumulative survival rate on an implant level was 96.5% (group O: 91.5%; group C: 100.0% [ P < 0.05]) and 95.7% (group O: 89.2%; group C: 100.0% [ P > 0.05]) on a patient level. The overall marginal bone-level alterations, after 5 y of loading, were -0.09 ± 0.78 mm (group O: -0.15 ± 0.50 mm; group C: -0.06 ± 0.89 mm) on an implant level and -0.09 ± 0.54 mm (group O: -0.18 ± 0.43 mm; group C: 0.06 ± 0.58 mm) on a patient level ( P > 0.05). Oral implant therapy in osteoporotic patients is a reliable treatment option with comparable osseointegration rates, implant survival, and marginal bone-level alterations after 5 y of functional loading (ClinicalTrials.gov NCT00745121). ispartof: JOURNAL OF DENTAL RESEARCH vol:98 issue:1 pages:84-90 ispartof: location:United States status: published

Periodontal diseases originate from a dysbiosis within the oral microbiota, which is associated with a deregulation of the host immune response. Although little is known about the initiation of dysbiosis, it has been shown that H2O2 production is one of the main mechanisms by which some commensal bacteria suppress the outgrowth of pathobionts. Current models emphasize the critical nature of complex microbial biofilms that form unique microbial ecologies and of their change during transition from health (homeostatic) to disease (dysbiotic). However, very little is known on how this alters their virulence and host responses. The objective of this study was to determine differences in virulence gene expression by pathobionts and the inflammatory host response in homeostatic and dysbiotic biofilms originating from the same ecology. Quantitative polymerase chain reaction was performed to quantify the pathobiont outgrowth. Expression analysis of bacterial virulence and cellular inflammatory genes together with cytokine enzyme-linked immunosorbent assays were used to detect differences in bacterial virulence and to analyze potential differences in inflammatory response. An increase in pathobionts in induced dysbiotic biofilms was observed compared to homeostatic biofilms. The main virulence genes of all pathobionts were upregulated in dysbiotic biofilms. Exposure of these dysbiotic biofilms to epithelial and fibroblast cultures increased the expression of interleukin (IL)-6, IL-1β, tumor necrosis factor-α, and matrix metalloprotease 8, but especially the chemokine CXCL8 (IL-8). Conversely, homeostatic and beneficial biofilms had a minor immune response at the messenger RNA and protein level. Overall, induced dysbiotic biofilms enriched in pathobionts and virulence factors significantly increased the inflammatory response compared to homeostatic and commensal biofilms.

The inflammatory response plays an important role in the tissue destruction associated with periodontitis. Bacterial species can regulate the inflammatory response of host cells, triggered by pathogens. It was hypothesized that also in the field of oral microbiology/immunology such effects of bacterial interactions on inflammatory host cell responses might be present. In this study the effect of beneficial, commensal and pathogenic species on Aggregatibacter actinomycetemcomitans-induced interleukin-8 (IL-8) production by human cells was investigated. The beneficial species, Streptococcus mitis, Streptococcus salivarius and Streptococcus sanguinis, were able to lower the IL-8 production triggered by A. actinomycetemcomitans. The inhibitory effect was also achieved by the application of streptococcal supernatants. In contrast, the commensal Streptococcus gordonii caused no reduction, and the pathogen Fusobacterium nucleatum increased the IL-8 production by the host cells. These results show that bacterial species can influence the inflammatory response of host cells triggered by infection with A. actinomycetemcomitans. ispartof: Journal of Dental Research vol:88 issue:11 pages:1026-1030 ispartof: location:United States status: published

The complexity of the periodontal microbiota resembles that of the gastro-intestinal tract, where infectious diseases are treatable via probiotics. In the oro-pharyngeal region, probiotic or replacement therapies have shown some benefit in the prevention of dental caries, otitis media, and pharyngitis, but their effectiveness in the treatment of periodontitis is unknown. Therefore, this study addressed the hypothesis that the application of selected beneficial bacteria, as an adjunct to scaling and root planing, would inhibit the periodontopathogen recolonization of periodontal pockets. Analysis of the data showed, in a beagle dog model, that when beneficial bacteria were applied in periodontal pockets adjunctively after root planing, subgingival recolonization of periodontopathogens was delayed and reduced, as was the degree of inflammation, at a clinically significant level. The study confirmed the hypothesis and provides a proof of concept for a guided pocket recolonization (GPR) approach in the treatment of periodontitis. ispartof: Journal of Dental Research vol:86 issue:11 pages:1078-1082 ispartof: location:United States status: published

Adherence of Actinobacillus actinomycetemcomitans to epithelial cells is an important step in periodontal disease pathogenesis. Recent publications describe the subgingival presence of a wide array of viruses [e.g., human cytomegalo-virus (hCMV)]. Since viruses can increase cellular susceptibility for bacterial adherence, we investigated whether hCMV renders epithelial cells more prone to adherence by Actinobacillus actinomycetemcomitans. Cultivated HeLa and primary epithelial cells were shown to be semi-permissive for hCMV infection, which resulted in increased bacterial adherence. This increase correlated with viral concentrations, was evident in all Actinobacillus actinomycetemcomitans strains examined, and increased during the first 24 hrs, followed by a slight decrease. Immediate early antigen expression was not correlated with the increased adherence of Actinobacillus actinomycetemcomitans. The results confirmed our hypothesis that the adherence of Actinobacillus actinomycetemcomitans is influenced by hCMV in vitro. ispartof: Journal of Dental Research vol:86 issue:2 pages:175-180 ispartof: location:United States status: published

The treatment of periodontitis/peri-implantitis involves the reduction/eradication of periopathogens. After therapy, beneficial and pathogenic species recolonize the subgingival area. The dynamics of recolonization and especially the role of the supragingival environment in this process are still not well-understood. This prospective, split-mouth study followed the early colonization of 'pristine' pockets created during implant surgery (16 partially edentulous patients), to record the time needed before a complex subgingival flora could be established with the supragingival area as the single source. Four subgingival plaque samples were taken from shallow and medium pockets around implants (test), and neighboring teeth (undisturbed microbiota as reference) 1, 2, and 4 wks after abutment connection. Checkerboard DNA-DNA hybridization and culture data revealed a complex microbiota (including several pathogenic species) in the pristine pockets within a wk, with a minimal increase in counts up to 4 wks. Analysis of these data demonstrated that, even with the supragingival environment as the single source for colonizing bacteria, a complex subgingival microbiota can develop within 1 wk. ispartof: Journal of Dental Research vol:84 issue:4 pages:340-4 ispartof: location:United States status: published

Escribano M, Herrera D, Morante S, Teughels W, Quirynen M, Sanz M. Efficacy of a low-concentration chlorhexidine mouthrinse in non-compliant periodontitis patients attending a supportive periodontal care programme: a randomized clinical trial. J Clin Periodontol 2010; 37: 266–275. doi: 10.1111/j.1600-051X.2009.01521.x. Abstract Objective: To assess the clinical and microbiological efficacy of a 0.05% chlorhexidine and 0.05% cetyl-pyridinium chloride mouth rinse in supportive periodontal care (SPC) in patients with inadequate plaque control. Material and Methods: The study was a randomized, double-blinded, placebo-controlled clinical trial in patients with moderate to severe chronic periodontitis under SPC with an inadequate plaque control (Turesky index >1). After supragingival prophylaxis and oral hygiene reinforcement, participants rinsed twice a day for 3 months with the test or placebo solutions, in addition to conventional hygiene. Primary clinical outcome variables included plaque and gingival indices. As secondary outcomes, periodontal and microbiological variables were studied. ancova and χ2 tests were used to compare the variables. Results: Forty-seven patients (22 placebo and 25 test group) participated. After 3 months, plaque levels increased in the placebo group, while diminished in the test group (p