Bacterial and inflammatory behavior of implants in the early healing phase of chronic periodontitis

To assess the pattern of early bacterial colonization at implants and teeth in patients with a history of chronic periodontitis compared with a group of healthy subjects. Furthermore, the presence of host-derived markers at teeth and implants in the two subject groups was determined.

Characterization of Aggregatibacter actinomycetemcomitans strains in periodontitis patients in Germany

Aggregatibacter actinomycetemcomitans strains of serotype b and with a deletion of 530 bp in the promoter region of the leukotoxin gene (JP2 clone) are known to be associated with severe periodontitis. Our study was aimed to detect virulence genes of A. actinomycetemcomitans strains obtained from patients living in four German cities with different proportions of immigrants.

Clinical and microbiologic results 12 months after scaling and root planing with different irrigation solutions in patients with moderate chronic periodontitis: a pilot randomized trial

The aim of this study is to determine in a randomized trial the impact on treatment outcome after 12 months of different subgingival irrigation solutions during scaling and root planing (SRP).

Immunization of Macaca fascicularis against experimental periodontitis using a vaccine containing cysteine proteases purified from Porphyromonas gingivalis

INTRODUCTION: Periodontitis is a common infectious disease to which Porphyromonas gingivalis has been closely linked, in which the attachment tissues of the teeth and their alveolar bone housing are destroyed. We conducted a study to determine if immunization using a purified antigen could alter the onset and progression of the disease. METHODS: Using the ligature-induced model of periodontitis in Macaca fascicularis, we immunized five animals with cysteine protease purified from P. gingivalis and used an additional five animals as controls. Alveolar bone loss was measured by digital subtraction radiography. RESULTS: Immunization induced high titers of specific immunoglobuin G serum antibodies that were opsonic. Total bacterial load, levels of P. gingivalis in subgingival plaque and levels of prostaglandin E(2) in gingival crevicular fluid were significantly reduced. Onset and progression of alveolar bone loss was inhibited by approximately 50%. No manifestations of toxicity were observed. CONCLUSIONS: Immunization using a purified protein antigen from P. gingivalis inhibits alveolar bone destruction in a ligature-induced periodontitis model in M. fascicularis.

The association of the composite IL-1 genotype with periodontitis progression and/or treatment outcomes: a systematic review

BACKGROUND: Genetically transmitted traits such as cytokine gene polymorphisms may accentuate the host inflammatory response to the bacterial challenge and influence susceptibility to periodontitis. OBJECTIVE: To systematically review the evidence of an association between the interleukin-1 (IL-1) composite genotype, i.e. presence of the allele 2 in the gene clusters IL-1A-889 and in IL-1B +3953, and periodontitis progression and/or treatment outcomes. Material and Methods: Based on the focused question, a search was conducted for longitudinal clinical trials comparing progression of periodontitis and/or treatment outcomes in IL-1 genotype-positive (carrying allele 2) and IL-1 genotype-negative (not carrying allele 2) subjects. A search in the National Library of Medicine computerized bibliographic database MEDLINE and a manual search were performed. Selection of publications, extraction of data and validity assessment were made independently by two reviewers. RESULTS: The search provided 122 titles of which 11 longitudinal publications were included. The heterogeneity of the data prevented the performance of a meta-analysis. While findings from some publications rejected a possible role of IL-1 composite genotype on progression of periodontitis after various therapies, other reported a prognostic value for disease progression of the positive IL-1 genotype status. When assessed on a multivariate risk assessment model, several publications concluded that the assessment of the IL-1 composite genotype in conjunction with other covariates (e.g. smoking and presence of specific bacteria) may provide additional information on disease progression. The small sample size of the available publications, however, requires caution in the interpretation of the results. CONCLUSION: Based on these findings, (i) there is insufficient evidence to establish if a positive IL-1 genotype status contributes to progression of periodontitis and/or treatment outcomes. Therefore, (ii) results obtained with commercially available tests should be interpreted with caution.

Influence of residual pockets on progression of periodontitis and tooth loss: results after 11 years of maintenance

BACKGROUND: Limited evidence exists on the significance of residual probing pocket depth (PPD) as a predictive parameter for periodontal disease progression and tooth loss. AIM: The aim of this study was to investigate the influence of residual PPD >or=5 mm and bleeding on probing (BOP) after active periodontal therapy (APT) on the progression of periodontitis and tooth loss. MATERIAL AND METHODS: In this retrospective cohort, 172 patients were examined after APT and supportive periodontal therapy (SPT) for 3-27 years (mean 11.3 years). Analyses were conducted using information at site, tooth and patient levels. The association of risk factors with tooth loss and progression of periodontitis was investigated using multilevel logistic regression analysis. RESULTS: The number of residual PPD increased during SPT. Compared with PPDor=7 mm 37.9 and 64.2, respectively. At patient level, heavy smoking, initial diagnosis, duration of SPT and PPD>or=6 mm were risk factors for disease progression, while PPD>or=6 mm and BOP>or=30% represented a risk for tooth loss. CONCLUSION: Residual PPD>or=6 mm represent an incomplete periodontal treatment outcome and require further therapy.

Similarities in the Subgingival Microbiota Assessed by a Curet Sampling Method at Sites With Chronic Periodontitis

Background: The goal of this study was to determine whether site-specific differences in the subgingival microbiota could be detected by the checkerboard method in subjects with periodontitis. Methods: Subjects with at least six periodontal pockets with a probing depth (PD) between 5 and 7 mm were enrolled in the study. Subgingival plaque samples were collected with sterile curets by a single-stroke procedure at six selected periodontal sites from 161 subjects (966 subgingival sites). Subgingival bacterial samples were assayed with the checkerboard DNA-DNA hybridization method identifying 37 species. Results: Probing depths of 5, 6, and 7 mm were found at 50% (n = 483), 34% (n = 328), and 16% (n = 155) of sites, respectively. Statistical analysis failed to demonstrate differences in the sum of bacterial counts by tooth type (P = 0.18) or specific location of the sample (P = 0.78). With the exceptions of Campylobacter gracilis (P <0.001) and Actinomyces naeslundii (P <0.001), analysis by general linear model multivariate regression failed to identify subject or sample location factors as explanatory to microbiologic results. A trend of difference in bacterial load by tooth type was found for Prevotella nigrescens (P <0.01). At a cutoff level of >/=1.0 x 10(5), Porphyromonas gingivalis and Tannerella forsythia (previously T. forsythensis) were present at 48.0% to 56.3% and 46.0% to 51.2% of sampled sites, respectively. Conclusions: Given the similarities in the clinical evidence of periodontitis, the presence and levels of 37 species commonly studied in periodontitis are similar, with no differences between molar, premolar, and incisor/cuspid subgingival sites. This may facilitate microbiologic sampling strategies in subjects during periodontal therapy.

A systematic review of the effects of full-mouth debridement with and without antiseptics in patients with chronic periodontitis

OBJECTIVES: To assess the clinical and microbiological effects of full-mouth debridement with (FMD) and without the use of antiseptics [full-mouth scaling and root planing (FMSRP)] in comparison with conventional staged debridement (CSD) in patients with chronic periodontitis after at least 6 months. MATERIAL AND METHODS: The search in MEDLINE (PubMed), covering a period of 1975 to October 2007, and hand searching yielded 207 titles. Forty-two abstracts and 17 full-text articles were screened for inclusion. RESULTS: Twelve articles allowed a direct comparison of FMD with CSD, FMSRP with CSD and FMD with FMSRP. Probing pocket depth reductions were significantly greater (0.2 mm) with FMD and FMSRP compared with CSD. Moreover, a modest reduction in BOP (9%) favoured FMD. Likewise, clinical attachment levels were improved by 0.2-0.4 mm in favour of FMD and FMSRP, respectively. In all comparisons, single-rooted teeth and deep pockets benefitted slightly from FMD and FMSRP. Limited differences in the changes of the subgingival microbiota were noted between the treatment modalities. CONCLUSIONS: Despite the significant differences of modest magnitude, FMD or FMSRP do not provide clinically relevant advantages over CSD. Hence, all three treatment modalities may be recommended for debridement in the initial treatment of patients with chronic periodontitis.

Staphylococcus aureus and other bacteria in untreated periodontitis

Whether the subgingival microbiota differ between individuals with chronic and those with aggressive periodontitis, and whether smoking influences bacterial composition, is controversial. We hypothesized that the subgingival microbiota do not differ between sites in individuals with chronic or aggressive periodontitis, or by smoking status. Bacterial counts and proportional distributions were assessed in 84 individuals with chronic periodontitis and 22 with aggressive periodontitis. No differences in probing pocket depth by periodontal status were found (mean, 0.11 mm; 95% CI, 0.6 to 0.8, p = 0.74). Including Staphylococcus aureus, Parvimonas micra, and Prevotella intermedia, 7/40 species were found at higher levels in those with aggressive periodontitis (p < 0.001). Smokers had higher counts of Tannerella forsythia (p < 0.01). The prevalence of S. aureus in non-smokers with aggressive periodontitis was 60.5%. The null hypothesis was rejected, in that P. intermedia, S. aureus, and S. mutans were robust in diagnosing sites in individuals with aggressive periodontitis. S. aureus, S. sanguinis, and T. forsythia differentiated smoking status.

Cardiovascular disease and periodontitis: an update on the associations and risk

BACKGROUND: Associations between periodontitis and cardiovascular diseases have been recognized. MATERIAL AND METHODS: New literature since the last European Workshop on Periodontology has been reviewed. RESULTS: The lack of reliable epidemiological data on disease prevalence makes an assessment of the associations and risks between periodontitis and cardiovascular diseases difficult. Two recent meta-analysis reports have identified associations between periodontitis and cardiovascular diseases (odds ratios: 1.1-2.2). Different surrogate markers for both disease entities, including serum biomarkers, have been investigated. Brachial artery flow-mediated dilatation, and carotid intima media thickness have in some studies been linked to periodontitis. Studies are needed to confirm early results of improvements of such surrogate markers following periodontal therapy. While intensive periodontal therapy may enhance inflammatory responses and impair vascular functions, studies are needed to assess the outcome of periodontal therapies in subjects with confirmed cardiovascular conditions. Tooth eradication may also reduce the systemic inflammatory burden of individuals with severe periodontitis. The role of confounders remain unclear. CONCLUSIONS: Periodontitis may contribute to cardiovascular disease and stroke in susceptible subjects. Properly powered longitudinal case-control and intervention trials are needed to identify how periodontitis and periodontal interventions may have an impact on cardiovascular diseases.

[Periodontitis and cardiovascular disease]

The prevalence of periodontitis and cardiovascular disease (CVD) is high. A mixed infectious biofilm etiology of periodontitis is known but not fully established in CVD. Cofactors; smoking habits, stress, ethnicity, genetics, socioeconomics and age contribute to both diseases. The objectives of this report are to summarize factors in regards to CVD and periodontitis that are clinically relevant. The hypothesis behind a relationship between the two conditions can be founded in (I) shared infections etiology, (II) shared inflammatory response, (III) epidemiological and case-control studies, and (IV) periodontal studies demonstrating improvements of CVD markers. Streptococcus species in the S. mitis group, and S. anginosus group have been identified in periodontitis and are known as pathogens in endocarditis possibly transported from the oral cavity to the heart through bacteremia during dental therapies, and tooth brushing. Other periodontal bacteria such as Porphyromonas gingivalis, Fusobacterium nucleatum and Parvimonas micra are beta-lactamase producing and may contribute to antibiotic resistance (extended spectrum beta-lactamases). Other bacteria in CVD and periodontitis include Staphylococcus aureus, and Pseudomonas aeruginosa. Chlamydia pneumoniae and P. gingivalis lipopolyysaccharide capsels share homology and induce heat-shock protein activity and a cascade of proinflammatory cytokines. Associations between periodontitis and CVD have been presented in many studies when controlling for confounders. Other studies have demonstrated that periodontal therapies increase brachial artery flow rate and reduce serum inflammatory cytokine levels. Thus, physicians caring for subjects at CVD risk should consult with dentists/periodontists. Dentists must improve their medical knowledge and also learn to consult with physicians when treating patients at CVD risk.

Periodontitis as a potential risk factor for peri-implantitis

OBJECTIVES: To review the literature regarding the possible association between a previous history of periodontitis and peri-implantitis. MATERIAL AND METHODS: A search of MEDLINE as well as a manual search of articles were conducted. Publications and articles accepted for publication up to January 2008 were included. RESULTS: Out of 951 papers retrieved, a total of three papers were selected for the review. Thus, the available evidence for an association between periodontitis and peri-implantitis is scarce. CONCLUSIONS: Based on three studies with a limited number of patients and considerable variations in study design, different definitions of periodontitis, and confounding variables like smoking that not been accounted for, this systematic review indicates that subjects with a history of periodontitis may be at greater risk for peri-implant infections. It should, however, be stressed that the data to support this conclusion are not very robust.

Cleavage of extracellular matrix in periodontitis: gingipains differentially affect cell adhesion activities of fibronectin and tenascin-C

Gingipains are cysteine proteases that represent major virulence factors of the periodontopathogenic bacterium Porphyromonas gingivalis. Gingipains are reported to degrade extracellular matrix (ECM) of periodontal tissues, leading to tissue destruction and apoptosis. The exact mechanism is not known, however. Fibronectin and tenascin-C are pericellular ECM glycoproteins present in periodontal tissues. Whereas fibronectin mediates fibroblast adhesion, tenascin-C binds to fibronectin and inhibits its cell-spreading activity. Using purified proteins in vitro, we asked whether fibronectin and tenascin-C are cleaved by gingipains at clinically relevant concentrations, and how fragmentation by the bacterial proteases affects their biological activity in cell adhesion. Fibronectin was cleaved into distinct fragments by all three gingipains; however, only arginine-specific HRgpA and RgpB but not lysine-specific Kgp destroyed its cell-spreading activity. This result was confirmed with recombinant cell-binding domain of fibronectin. Of the two major tenascin-C splice variants, the large but not the small was a substrate for gingipains, indicating that cleavage occurred primarily in the alternatively spliced domain. Surprisingly, cleavage of large tenascin-C variant by all three gingipains generated fragments with increased anti-adhesive activity towards intact fibronectin. Fibronectin and tenascin-C fragments were detected in gingival crevicular fluid of a subset of periodontitis patients. We conclude that cleavage by gingipains directly affects the biological activity of both fibronectin and tenascin-C in a manner that might lead to increased cell detachment and loss during periodontal disease.

Nonsurgical treatment of aggressive periodontitis with photodynamic therapy or systemic antibiotics. Three-month results of a randomized, prospective, controlled clinical study

The aim of this randomized, controlled clinical study was to compare the short-term effects of nonsurgical periodontal therapy with the additional administration of systemic antibiotics (AB) and the same therapy with additional photodynamic therapy (PDT) in the treatment of patients with aggressive periodontitis (AP). Thirty-six patients with AP received full-mouth nonsurgical periodontal treatment (SRP) and were then randomly divided into two groups of 18 subjects each. Group AB received amoxicillin and metronidazole three times a day for 7 days. Group PDT received two applications of PDT on the day of SRP as well as at follow-up after 7 days. The following clinical parameters were measured at baseline and 3 months after therapy: plaque index (PLI), bleeding on probing (BOP), probing depth (PD), gingival recession (GR), and clinical attachment level (CAL). After 3 months, PD was significantly reduced in both groups (from 5.0±0.8 mm to 3.2±0.4 mm with AB, and 5.1±0.5 mm to 4.0±0.8 mm with PDT; both p<0.001), while AB revealed significantly lower values compared to PDT (p = 0.001). In both groups, GR was not significantly changed. CAL was significantly reduced in both groups (PDT: 5.7±0.8 mm to 4.7±1.1 mm; p=0.011; AB: 5.5±1.1 mm to 3.9±1.0 mm; p<0.001) and differed significantly between the groups (p=0.025). The number of residual pockets (PD ≥4 mm) and positive BOP was reduced by AB from 961 to 377, and by PDT from 628 to 394. Pockets with PD ≥7 mm were reduced by AB from 141 to 7, and by PDT from 137 to 61. After 3 months, both treatments led to statistically significant clinical improvements. The systemic administration of antibiotics, however, resulted in significantly higher reduction of PD and a lower number of deep pockets compared to PDT.

Effect of photoactivated disinfection with a light-emitting diode on bacterial species and biofilms associated with periodontitis and peri-implantitis

BACKGROUND To determine the effect of photoactivated disinfection (PAD) using toluidine blue and a light-emitting diode (LED) in the red spectrum (wave length at 625-635 nm) on species associated with periodontitis and peri-implantitis and bacteria within a periodontopathic biofilm. METHODS Sixteen single microbial species including 2 Porphyromonas gingivalis and 2 Aggregatibacter actinomycetemcomitans and a multispecies mixture consisting of 12 species suspended in saline without and with 25% human serum were exposed to PAD. Moreover, single-species biofilms consisting of 2 P. gingivalis and 2 A. actinomycetemcomitans strains and a multi-species biofilm on 24-well-plates, grown on titanium discs and in artificial periodontal pockets were exposed to PAD with and without pretreatment with 0.25% hydrogen peroxide. Changes in the viability were determined by counting the colony forming units (cfu). RESULTS PAD reduced the cfu counts in saline by 1.42 log₁₀ after LED application for 30s and by 1.99 log₁₀ after LED application for 60s compared with negative controls (each p<0.001). Serum did not inhibit the efficacy of PAD. PAD reduced statistically significantly (p<0.05) the cfu counts of the P. gingivalis biofilms. The viability of the A. actinomycetemcomitans biofilms and the multi-species biofilms was statistically significantly decreased when PAD was applied after a pretreatment with 0.25% hydrogen peroxide. The biofilm formed in artificial pockets was more sensitive to PAD with and without pretreatment with hydrogen peroxide compared with those formed on titanium discs. CONCLUSIONS PAD using a LED was effective against periodontopathic bacterial species and reduced viability in biofilms but was not able to completely destroy complex biofilms. The use of PAD following pretreatment with hydrogen peroxide resulted in an additional increase in the antimicrobial activity which may represent a new alternative to treat periodontal and peri-implant infections thus warranting further testing in clinical studies.