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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

Previous studies have demonstrated that hydrogen sulfide and methyl mercaptan play a major role in oral malodor. In the present study, we tested the hypothesis that other compounds found in mouth air can also contribute to halitosis. Mouth air of 40 healthy volunteers and 40 persons with halitosis was analyzed and compared by gas chromatography-mass spectrometry, two sulfur monitors, and organoleptically. Nearly 700 different compounds were detected. Hydrogen sulfide, methyl mercaptan, dimethyl sulfide, di- and trisulfide were increased in persons with breath odor. These compounds were all significantly correlated with the organoleptic score. We concluded that hydrogen sulfide, methyl mercaptan and, to a much lesser extent, dimethyl sulfide, di- and trisulfide can contribute to oral malodor. The role of other compounds, such as amines and organic acids, seems insignificant.

Periodontitis is a polymicrobial infectious disease primarily associated with Gram-negative periodontopathogens. Bdellovibrio and like organisms are predatory bacteria that feed on Gram-negative bacteria. This study investigated whether predatory bacteria can attack Aggregatibacter actinomycetemcomitans. Therefore, A. actinomycetemcomitans was challenged with the predator Bdellovibrio bacteriovorus under conditions simulating the oral cavity. The reduction of planktonic A. actinomycetemcomitans was quantified via bacterial culture, and the development of predatory bacteria was monitored with quantitative real-time PCR. The destruction of A. actinomycetemcomitans biofilms by B. bacteriovorus was quantified by crystal violet staining and visualized by scanning electron microscopy. The in vitro results show that B. bacteriovorus can attack, prey on, and kill A. actinomycetemcomitans and suggest a potential for B. bacteriovorus as a living antibiotic for the prevention and treatment of periodontitis. ispartof: Journal of Dental Research vol:88 issue:2 pages:182-186 ispartof: location:United States status: published

This study examined the hypothesis of an intra-oral shift, during initial periodontal therapy, from a periopathogenic to a cariogenic flora. Seventy-one patients with periodontitis were randomly allocated to one of the following treatment strategies: (1) scaling and root planing, quadrant by quadrant, at two-week intervals (NC); (2) full-mouth scaling and root planing within 24 hrs (FRP); or (3) full-mouth disinfection within 24 hrs, including antiseptics [chlorhexidine (CHX) or amine fluoride/stannous fluoride (F) for 2 mos, or CHX for 2 mos followed by F for 6 mos (CHX+F)]. At baseline and after 2, 4, and 8 mos, bacterial samples were taken from supra- and subgingival plaque, saliva, and tongue. The detection frequencies and relative proportions of Streptococcus mutans increased in the NC and FRP groups, but decreased in the F group. In the CHX group, these species disappeared temporarily, but they disappeared for the entire 8 mos in the CHX+F group. These observations were similar for all sample locations. The periopathogens decreased in all groups. This finding confirms the abovementioned hypothesis and indicates a need for caries prophylactic regimens. ispartof: Journal of Dental Research vol:84 issue:1 pages:48-53 ispartof: location:United States status: published

In a standard periodontal treatment strategy with consecutive root planings ( per quadrant at a one- to two-week interval), re-infection of a disinfected area might occur before completion of the treatment. This study examines, both clinically and microbiologically, whether a full-mouth disinfection within 24 hours significantly improves the outcome of periodontal treatment. Ten patients with advanced chronic periodontitis were randomly allocated to a test and a control group. The patients from the control group received scalings and root planings as well as oral hygiene instructions per quadrant at two-week intervals. Full-mouth disinfection in the test group was sought by the removal of all plaque and calculus (in two visits within 24 hours). In addition, at each of these visits, the tongue was brushed with a 1 % chlorhexidine gel for one min and the mouth rinsed with a 0.2% chlorhexidine solution for two min. Furthermore, subgingival chlorhexidine (1%) irrigation was performed in all pockets. The recolonization of the pockets was retarded by oral hygiene and 0.2% chlorhexidine rinses during two weeks. The clinical parameters were recorded, and plaque samples were taken from the right upper quadrant at baseline and after one and two months. The test group patients showed a significantly higher reduction in probing depth for deep pockets at both follow-up visits (p < 0.05). At the one-month visit, differential phase-contrast microscopy revealed significantly lower proportions of spirochetes and motile rods in the test group (p = 0.01). Culturing showed that the test group harbored significantly fewer pathogenic organisms at one month (p = 0.005). At two months, the same sites harbored singificantly more "beneficial" bacteria (p = 0.02). Moreover, all sites of the test group initially harboring P. gingivalis (6/10) became negative after treatment. These findings suggest that it is possible to achieve a significant improvement of the treatment outcome (both microbiologically and clinically) with a one-stage full-mouth disinfection.

In nine patients with fixed prostheses supported by endosseous titanium implants, 2 titanium abutments (trans-mucosal part of the implant) were replaced by either an unused standard abutment or a roughened titanium abutment. After 3 months of habitual oral hygiene, plaque samples were taken for differential phase-contrast microscopy, DNA probe analysis, and culturing. Supragingivally, rough abutments harbored significantly fewer coccoid micro-organisms (64 us. 81%), which is indicative of a more mature plaque. Subgingivally, the observations depended on the sampling procedure. For plaque collected with paper points, only minor qualitative and quantitative differences between both substrata could be registered. However, when the microbiota adhering to the abutment were considered, rough surfaces harbored 25 times more bacteria, with a slightly lower density of coccoid organisms. The presence and density of periodontal pathogens subgingivally were, however, more related to the patient's dental status than to the surface characteristics of the abutments. These results justify the search for optimal surface smoothness for all intra-oral and intra-sulcular hard surfaces for reduction of bacterial colonization and of periodontal pathogens.

The purpose of this study was to examine the change in plaque area over nine days in vivo on four materials with different surface free-energies (s.f.e.). Twelve healthy dental students participated in a crossover, split-mouth, double-blind study. Supragingival plaque formation was recorded over a nine-day period, on four different materials: fluorethylenepropylene (Teflon) (FEP), parafilm (PAR), cellulose acetate (CA), and enamel (E) with s.fe. of 20, 26, 57, and 88 erg/cm2, respectively. Strips made from the first three materials were stuck to the buccal surface of an upper incisor. The remaining incisor was carefully polished and served as an enamel surface. The increase in plaque was evaluated after three, six, and nine days. A planimetrical analysis was used so that the plaque area could be expressed as a percentage of the total buccal tooth surface. This procedure was repeated on each subject, so that at the end, each pair of central or lateral incisors received the four tested materials. The results indicated that the adherence of micro-organisms on pellicle-coated substrata was influenced by the material's s.f.e.; there was an association between the s.f.e. of the substrata and the supragingival plaque extension in vivo. High surface free-energy substrata in the oral cavity attracted more micro-organisms than did low energetic materials. Additionally, the bacterial adhesion seemed very weak on surfaces with a low s.f.e.