Periodontal diseases in Thai schoolchildren. Clinical and microbiological observations.

The prevalence of periodontitis among Thai schoolchildren is unknown. In a cross-sectional study, the prevalence and severity of periodontal diseases, in a group of Thai schoolchildren, along with the presence and numbers of bacterial species commonly associated with periodontitis were investigated. A consent form was sent out to 192 schoolchildren in one school (Chanachanupathom School) in Chana, Southern Thailand (in the age range of 12-18 years) and 119 attended for a clinical and microbiological examination. Clinical recordings included number of teeth present, DMFT, plaque index, bleeding index, clinical attachment loss (CAL), and probing pocket depth (PPD). Pooled plaque samples were analyzed with culture and qPCR against bacteria associated with periodontitis. The children had low caries experience (DMFT = 3.2 ± 2.3), poor oral hygiene, high bleeding scores, and 67 (56.3%) had at least one interproximal site with CAL ≥ 1 mm. Thirty-seven (31.1%) of the children were diagnosed with periodontitis stage I, and sixteen (13.4%) were classified as periodontitis Stage II. Aggregatibacter actinomycetemcomitans was sparsely found in all but the healthy clinical groups (gingivitis, periodontitis Stage I and II), while the groups showed a high prevalence of Fusobacterium spp., Prevotella intermedia/nigrescens, and Campylobacter species as well as of the periodontitis-associated species Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Thai schoolchildren have poor oral hygiene with abundant amounts of plaque and high presence of bleeding. Early onset periodontitis is common but mostly in its mild form and is not associated with the presence of A. actinomycetemcomitans.

Antibacterial activity of salvia officinalis L. against periodontopathogens: An in vitro study.

Being aware of the remarkable antimicrobial potential of S. officinalis L., we aimed to evaluate the antimicrobial activity of the S. officinalis dichloromethane crude extract (SOD), dichloromethane-soluble fractions (SODH and SODD), SODD subfractions (SODD1 and SODD2), and pure substances (manool, salvigenin, and viridiflorol) against periodontopathogens. This bioassay-guided study comprises five antimicrobial tests-determination of the Minimum Inhibitory Concentration (MIC), determination of the Minimum Bactericidal Concentration (MBC), determination of the antibiofilm activity, construction of the Time-kill curve (determination of Bactericidal Kinetics), and determination of the Fractional Inhibitory Concentration Index-on six clinical bacterial isolates and three standard bacterial strains involved in periodontal disease. SOD has moderate activity against most of the tested bacteria, whereas SODD1, SODH1, SODH3, and manool afford the lowest results. The Porphyromonas gingivalis (ATTC and clinical isolate) biofilm is considerably resistant to all the samples. In association with chlorhexidine gluconate, only SODH1 exerts additive action against P. gingivalis (clinical isolate). Therefore, SODH1 and manool are promising antibacterial agents and may provide therapeutic solutions for periodontal infections.

Interleukin Gene Variability and Periodontal Bacteria in Patients with Generalized Aggressive Form of Periodontitis.

Host genetic predispositions to dysregulated immune response can influence the development of the aggressive form of periodontitis (AgP) through susceptibility to oral dysbiosis and subsequent host-microbe interaction. This case-control study aimed to perform a multilocus analysis of functional variants in selected interleukin (IL) genes in patients with the generalized form of AgP in a homogenous population. Twelve polymorphisms in IL-1 gene cluster, IL-6 and its receptor, IL-10, IL-17A, and IL-18 were determined in 91 AgP patients and 210 controls. Analysis of seven selected periodontal bacteria in subgingival sulci/pockets was performed with a commercial DNA-microarray kit in a subgroup of 76 individuals. The pilot in vitro study included stimulation of peripheral blood monocytes (PBMC) from 20 individuals with periodontal bacteria and measurement of IL-10 levels using the Luminex method. Only the unctional polymorphism IL­10-1087 A/G (rs1800896) and specific IL-10 haplotypes were associated with the development of the disease (P < 0.05, Pcorr > 0.05). Four bacterial species occurred more frequently in AgP than in controls (P < 0.01, Pcorr < 0.05). Elevated IL-10 levels were found in AgP patients, carriers of IL­10-1087GG genotype, and PBMCs stimulated by periodontal bacteria (P < 0.05, Pcorr > 0.05). We therefore conclude that a combination of genetic predisposition to the altered expression of IL-10 and the presence of specific periodontal bacteria may contribute to Th1/Th2 balance disruption and AgP development.

Effect of periodontal treatment on Aggregatibacter actinomycetemcomitans colonization and serum IgG levels against A. actinomycetemcomitans serotypes and Omp29 of aggressive periodontitis patients.

OBJECTIVE: To evaluate the effect of the periodontal treatment on Aggregatibacter actinomycetemcomitans JP2 clone, and the IgG serum levels against its outer membrane protein (Omp29) and A. actinomycetemcomitans serotypes in aggressive periodontitis (AgP). SUBJECTS AND METHODS: Seventeen patients with generalized (GAgP), 10 with localized (LAgP), and 10 healthy controls were included. AgP participants were submitted to periodontal treatment-scaling and root planing plus antibiotics (SRP+A). Periodontal parameters, for example, probing depth (PD) and clinical attachment loss (CAL), were evaluated at baseline and at 1-year. Serum IgG against Omp29 and serotypes a, b, and c were determined by ELISA. The levels of A. actinomycetemcomitans JP2 clone were determined in subgingival biofilm samples by qPCR. RESULTS: Periodontal treatment resulted in significant reductions of PD, CAL, and IgG levels against Omp29, serotypes b, and c. After therapy, IgG levels against A. actinomycetemcomitans serotypes, as well as the levels of the JP2 clone in AgP, became similar to controls. The reduction in JP2 clone count was correlated with a reduction of PD and IgG response against Omp29. CONCLUSION: Scaling and root planing plus antibiotics decreased IgG levels response against Omp29 and A. actinomycetemcomitans serotypes involved in the disease (b and c), while the serum response increased against tne commensal serotype (a), similar to what occurs in periodontally healthy individuals.

Efficacy of adjunctive photodynamic therapy in the treatment of generalized aggressive periodontitis: A randomized controlled clinical trial.

OBJECTIVES: Generalized aggressive periodontitis (GAgP) is a distinct type of periodontal disease characterized by rapid loss of attachment and alveolar bone occurring in young individuals. Photodynamic therapy (PDT) was introduced in periodontology as an adjunctive approach to non-surgical periodontal treatment (NPT) in periodontitis patients. In this trial, the aim was to evaluate the clinical and microbiological effects of adjunctive PDT to NPT in patients with GAgP. METHODS: In this prospective controlled clinical study, 24 systemically healthy, non-smoking subjects with GAgP were enrolled. Subjects were randomly assigned into a control group (n = 12) treated with NPT only or to a test group (n = 12) treated with NPT and PDT. Plaque index, sulcus bleeding index (SBI), probing depth (PD), relative attachment level, gingival recession, and tooth mobility were recorded at baseline and on day 63. Microbiological samples were obtained from the sites with PD ≥ 5 mm at both time periods and evaluated for Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, and Treponema denticola via micro-IDent® test. RESULTS: Clinical and microbial parameters declined significantly in both groups after the treatments (P < 0.01). The comparisons between the groups showed that only the full mouth SBI score of the test group was significantly lower than the control group on day 63 (P < 0.05). Although the reduction in periodontopathogens of the test group was greater than the control group, there was no significant difference between the groups (P > 0.05). CONCLUSIONS: Within the limits of this study, it can be concluded that in the treatment of GAgP, usage of PDT as an adjunct to NPT does not lead to any beneficial effects on the investigated clinical and microbiological parameters except for SBI. Nevertheless, the statistically significant difference for the SBI score demonstrates that PDT may have additional effect on the reduction in gingival bleeding. Lasers Surg. Med. 51:167-175, 2019. © 2018 Wiley Periodicals, Inc.

Wild-type isolates of Porphyromonas gingivalis derived from periodontitis patients display major variability in platelet activation.

In vitro studies revealed that Porphyromonas gingivalis (Pg), a pathogen intimately associated with the onset and progression of periodontitis, is able to activate platelets, thus linking periodontal inflammation with the endangerment of vascular health. As wild-type Pg strains are characterized by major genetic heterogeneity, the commonness of platelet-activating Pg strains in periodontitis patients is unknown as of yet. Therefore, this study evaluated the platelet activation capacity of wild-type Pg isolates sampled from patients with aggressive periodontitis. METHODS: Extent and velocity of platelet aggregation were determined by light transmission aggregometry. Platelet surface expression of P-selectin was measured by flow cytometry, activation of p38 MAP kinase, and protein kinase C by Western blot using phospho-specific antibodies. RESULTS: Pg isolates displayed high variability regarding extent and velocity of platelet activation, as well as the involved activating pathways. Corresponding results were observed for platelet P-selectin expression, activation of p38 MAP kinase, or protein kinase C. Inhibitors of platelet immune receptor FcγRIIA and protease-activated receptors revealed several, diverging pathways of activation. Some isolates induced platelet aggregation even in the presence of potent therapeutical platelet inhibitors. CONCLUSIONS: Chronic bacteremia involving specific, platelet-activating Pg strains may constitute a substantial hazard for the integrity of cardiovascular health.

Shift in the subgingival microbiome following scaling and root planing in generalized aggressive periodontitis.

AIM: To investigate the shift in the subgingival microbiota under scaling and root planing (SRP) in patients with generalized aggressive periodontitis (GAgP). MATERIALS AND METHODS: After undergoing supragingival scaling, 12 individuals with GAgP were enrolled in this longitudinal study. Full-mouth SRP was accomplished in 3 weeks and re-evaluated 6 weeks later. Pooled subgingival samples (posterior-mesial, posterior-buccal, anterior-mesial, and anterior-buccal) were obtained from each patient before SRP (pre-treatment group) and at the time of re-evaluation (post-treatment group). 16S rRNA PCR products were generated and sequenced after DNA isolation. RESULTS: Under SRP, the diversity of the subgingival community was consistent, whereas genus-level biomarkers transformed from Porphyromonas, Treponema, and Fretibacterium to Actinomyces, Streptococcus, and Haemophilus. In a network analysis, pathogen-related and non-pathogen-related components were identified in both the pre- and post-treatment groups; the pathogen component was dramatically augmented, while the non-pathogen component shrank after treatment. Hubs were also distributed in both components pre-treatment and were confined to the pathogen component post-treatment. CONCLUSIONS: Scaling and root planing decreased periodontal pathogens in the subgingival microbiota of patients with GAgP. However, the shift in the microbiota composition was characterized by the expansion of pathogen-related components and the contraction of non-pathogen-related components 6 weeks after SRP. Clinicaltrials.gov #NCT03090282.

Inflammatory serum markers up to 5 years after comprehensive periodontal therapy of aggressive and chronic periodontitis.

AIM: The aim of the study is to assess the long-term effect of active periodontal therapy on serum inflammatory parameters in patients with aggressive (AgP) and chronic (ChP) periodontitis in a non-randomised clinical study. METHODS: Twenty-five ChP and 17 AgP were examined clinically prior to (baseline), 12 weeks and 60 months after subgingival debridement of all pockets within 2 days. Systemic antibiotics were prescribed if Aggregatibacter actinomycetemcomitans was detected (10 AgP, 8 ChP), flap surgery was rendered if required. Neutrophil elastase (NE), C-reactive protein (CRP), lipopolysaccharide binding protein, interleukin 6, 8, and leukocyte counts were assessed at baseline, 12 weeks and 60 months. RESULTS: Clinical parameters improved significantly in both groups from 12 weeks to 60 months. Eleven AgP and 18 ChP patients received surgical treatment after the 12 weeks examination. Only 3 patients in each group attended ≥ 2 supportive maintenance visits per year. NE and CRP were significantly higher in AgP than ChP at baseline and 60 months (p < 0.01). For leukocyte counts in ChP, significant changes were observed (baseline: 6.11 ± 1.44 nl-1; 12 weeks: 5.34 ± 1.40 nl-1; 60 months: 7.73 ± 2.89 nl-1; p < 0.05). Multiple regression analysis identified African origin, surgical treatment and female sex to correlate with better clinical improvement. CONCLUSION: Despite comprehensive periodontal treatment, AgP patients exhibit higher NE and CRP levels than ChP patients up to 5 years after therapy. CLINICAL RELEVANCE: Systemic inflammatory burden in AgP patients is higher than in ChP patients even 5 years after periodontal treatment.

Oral pathogenesis of Aggregatibacter actinomycetemcomitans.

Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) is a Gram-negative, facultative anaerobic bacillus that causes periodontal diseases such as localized aggressive periodontitis (LAP) and. consequently. bone resorption. The potential virulence factors of this organism are powerful leukotoxin, lipopolysaccharide (LPS), cell surface-associated materials, enzymes, and less well-defined virulence factors that will modulate the activity of the host defenses. This organism can induce bone resorption by various virulence factors in periodontal disease. In this review article, we reviewed the pathogenic roles of A. actinomycetemcomitans in periodontal disease and the mechanism which can induce bone resorption. Findings from several studies indicate that the interaction between virulence factors and the host immune system's response often progress bone resorption in periodontal disease. In this organism, GroEL, DnaK, HtpG, LTX, CDT, LPS, and cell surface-associated materials produce cytokines when exposed to the immune system. The produced cytokines are the main cause of tissue destruction and bone resorption in A. actinomycetemcomitans inflammation in periodontal disease.

What exactly distinguishes aggressive from chronic periodontitis: is it mainly a difference in the degree of bacterial invasiveness?

At the International Workshop for Classification of Periodontal Diseases and Conditions in 1999, the classification of aggressive and chronic periodontitis that is presently used was introduced. A literature review of papers published in 2015 and having aggressive periodontitis in the title revealed that most studies use this terminology but it is questionable whether all established criteria were really applied correctly. Review of the literature showed no qualitative differences between aggressive and chronic periodontitis regarding bacterial and viral aspects. It is also unlikely that that there are major immunologic differences between aggressive and chronic periodontitis. Neutrophil function can be compromised in both conditions but may be more genetically related in aggressive periodontitis and be associated more with lifestyle factors in chronic periodontitis. In general, genetics plays a more important role in aggressive periodontitis than in chronic periodontitis. It is likely that periodontitis progresses by recurrent acute episodes during which invasion of bacteria into the connective tissue may occur. Two cases are presented for which invasive periodontitis is treated with systemic antibiotics, showing remarkable periodontal healing in terms of probing attachment gain, as well as radiographic bone gain. Periodontitis in an active state with bacterial invasion is probably accompanied with a significant increase in subgingival temperature. It is hypothesized that elevated subgingival temperature may help to distinguish between bacterial and nonbacterial invasive periodontitis. Scaling and root planing during a burst of disease activity may result in removal of connective tissue fiber attachment and down-growth of epithelium, thereby preventing the reattachment of connective tissue. Because the burst of disease is accompanied by an increase of temperature, assessment of the temperature may help in deciding whether or not to prescribe systemic antibiotics. When the use of systemic antibiotics is indicated, the antibiotic therapy may help to maintain the connective tissue attachment at the most possible coronal level. The above implies that the ability to diagnose bacterial invasive periodontitis is quite important, and future research is needed to determine if assessment of subgingival temperature may help in diagnosing invasive periodontitis. In addition, it is suggested that future classification systems of periodontitis include the item of bacterial invasive periodontitis.

Peri-implant and periodontal microbiome diversity in aggressive periodontitis patients: a pilot study.

AIM: To investigate the bacterial microbiome in periodontal and peri-implant biofilms deriving from aggressive periodontitis patients (AgP) in conditions of health and disease. MATERIAL AND METHODS: Ninety-one plaque samples were collected from 18 patients previously diagnosed and treated for AgP. The samples were taken from (i) 24 residual periodontal pockets (TD) (n = 6 patients), (ii) 24 healthy periodontal sites (TH) (n = 6 patients), (iii) 24 dental sites from the same implant patients (TM) (n = 6 patients), (iv) 5 peri-implantitis sites (II) (n = 2 patients), (v) 6 peri-mucositis sites (IM) (n = 2 patients) and (vi) 8 healthy implant sites (IH) (n = 2 patients). All subjects underwent periodontal clinical and radiographic assessments. Bacterial DNA was extracted, PCR amplified using 16S rRNA gene V5-V7 primers (barcoded amplicons 785F;1175R), purified, pooled at equimolar concentrations and sequenced (MiSeq, Illumina) yielding 250 bp paired-end reads. The 16S rRNA reads were filtered, assembled and analysed. RESULTS: The genera Propionibacterium, Paludibacter, Staphylococcus, Filifactor, Mogibacterium, Bradyrhizobium and Acinetobacter were unique to peri-implant sites (P = 0.05). In TM samples, different proportions and bacterial spp. were found when compared with the same patients' samples at implant sites. Specifically, Actinomyces (P = 0.013) and Corynebacterium (P = 0.030) genera showed to be significantly more abundant in the TM group when compared to the II. The highest phylogenetic diversity was observed in residual periodontal pocket sites (TD). Increased annual tooth loss rate and residual pocketing was related to high proportions of the genera Actinomyces, Porphyromonas, Prevotella, Streptococcus, Actinomycetaceae, TM7-3, Selenomonas, and Dialister, Treponema, Parvimonas and Peptostreptococcus in the TD group. CONCLUSION: Within the limitations of this pilot study, the periodontal and peri-implant microbiome presents a dissimilar taxonomic composition across different niches within AgP patients. The host response, the habitat structure and the vast coexistence of strains and species surrounding implants and teeth in health and disease are likely to be shaping the heterogeneous composition of the subgingival biofilms. The TM7 phylum was found only in TD cases. The investigation of the impact of periodontal and peri-implant keystone species on these complex ecosystems in states of health and disease seems to be essential.

High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis.

Periodontal disease (PD) is generated by microorganisms. These microbes can enter the general circulation causing a bacteraemia. The result can be adverse systemic effects, which could promote conditions such as cardiovascular disease. Level A evidence supports that PD is independently associated with arterial disease. PD is a common chronic condition affecting the majority of Americans 30 years of age and older. Atherosclerosis remains the largest cause of death and disability. Studies indicate that the adverse cardiovascular effects from PD are due to a few putative or high-risk bacteria: Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola or Fusobacterium nucleatum There are three accepted essential elements in the pathogenesis of atherosclerosis: lipoprotein serum concentration, endothelial permeability and binding of lipoproteins in the arterial intima. There is scientific evidence that PD caused by the high-risk pathogens can influence the pathogenesis triad in an adverse manner. With this appreciation, it is reasonable to state PD, due to high-risk pathogens, is a contributory cause of atherosclerosis. Distinguishing this type of PD as causal provides a significant opportunity to reduce arterial disease.

Complementary clinical effects of red complex bacteria on generalized periodontitis in a caucasian population.

OBJECTIVES: To relate five periodontopathogenic bacteria, including the red complex, to the severity, extent, and inflammation of the periodontal lesion in Caucasian patients with generalized aggressive and chronic periodontitis and to explore whether tobacco use is associated with a specific bacterial profile. MATERIALS AND METHODS: A cross-sectional and analytic study was conducted in patients with aggressive and chronic periodontitis. Data were gathered on socio-demographic and periodontal variables, and RH-PCR was used to determine subgingival bacterial profile. Linear and logistic regression analyses were performed. RESULTS: The study included 60 patients with aggressive and 123 with chronic periodontitis. Total red complex bacteria count was higher in aggressive periodontitis, mainly due to T. denticola (P = 0.015). In both periodontitis types, models showed an association between T. forsythia count and probing depth (B = 0.157, P = 0.030) and between T. denticola count and higher bleeding scores (B = 2.371, P = 0.027). Smoking did not affect the red complex bacteria count in either disease. CONCLUSIONS: The prevalence of red complex bacteria was similar between aggressive and chronic periodontitis, but their count was higher in the former. In both diseases, T. forsythia was associated with greater severity and T. denticola with more severe bleeding. Tobacco smoking was not associated with the presence of red complex bacteria in either disease.

Detection of subgingival periodontal pathogens--comparison of two sampling strategies.

OBJECTIVE: The aim of the study is to compare detection frequency of periodontal pathogens in patients with aggressive/severe chronic periodontitis using pooled plaque samples from the deepest pockets per quadrant/per sextant. METHODS: In 100 patients with aggressive/chronic periodontitis, subgingival plaque was sampled from the deepest pockets per quadrant (MT4) and per sextant (MT6). Plaque samples were taken using two sterile paper points simultaneously. One paper point from each pocket was pooled with the three other paper points of the pockets (MT4). Subsequently, the remaining four paper points were pooled with two paper points from the deepest pockets from the two remaining sextants (MT6). The content of each vial was analyzed with nucleic-acid based methods for Aggregatibacter actinomycetemcomitans, Tannerella forsythia, Porphyromonas gingivalis, Treponema denticola, Prevotella intermedia, Parvimonas micra, Fusobacterium nucleatum, Campylobacter rectus, Eubacterium nodatum, Eikenella corrodens, and Capnocytophaga sp. RESULTS: The detection frequency of A. actinomycetemcomitans (MT4/MT6) at 22/24 %, T. forsythia at 93/96 %, P. gingivalis at 78/79 %, T. denticola at 88/90 %, P. intermedia at 40/46 %, P. micra at 75/79 %, F. nucleatum at both 99 %, C. rectus at 84/89 %, E. nodatum at 62/65 %, E. corrodens at 80/87 %, and Capnocytophaga sp. at 49/58 % was higher with MT6 than with MT4. None of these differences were statistically significant. CONCLUSION: The detection frequency of the investigated periopathogens was statistically insignificant higher with the sampling method MT6 compared with MT4. CLINICAL RELEVANCE: In daily dental practice, the plaque sampling of the deepest pockets per quadrant seems to be sufficient.

Full-mouth ultrasonic debridement associated with povidone iodine rinsing in GAgP treatment: a randomised clinical trial.

OBJECTIVE: This study evaluated the clinical, immunological and microbiological results of full-mouth ultrasonic debridement (FMUD) with 10 % povidone iodine (PVPI) as the cooling liquid in the treatment of generalised aggressive periodontitis (GAgP). MATERIAL AND METHODS: Twenty-eight patients presenting GAgP were randomly assigned to one of the following groups for evaluation: FMUD + SS (n = 14)--single session of FMUD with 0.9 % saline solution as cooling agent and FMUD + PVPI (n = 14)--single session of FMUD with PVPI solution as cooling agent. Probing depth (PD), relative clinical attachment level (RCAL), relative position of gingival margin, plaque index (FMPI) and bleeding score (FMBS), immunological (interleukin-10 and interleukin-1ß concentrations in gingival crevicular fluid) and microbiological (Aa and Pg amounts) parameters were evaluated at baseline, first, third and sixth months after treatment. RESULTS: The two groups presented reduction of FMPI and FMBS and had statistically significant PD reductions, RCAL gains and gingival recession (p < 0.05). Both therapies reduced Pg levels in deep and in moderate pockets (p < 0.05). FMUD + PVPI reduced Aa levels in deep pockets. However, no inter-group differences in clinical, immunological and microbiological parameters were observed (p > 0.05). CONCLUSIONS: It could be concluded that 10 % PVPI used as an irrigant solution in FMUD decreased Aa levels in deep pockets but had no additional benefits when compared with saline solution irrigation in terms of clinical, microbiological and immunological results. CLINICAL RELEVANCE: The FMUD is a valid option for the treatment of GAgP, but the use of 10 % PVPI did not improve the results of the periodontal therapy.

Periodontal Surgery Involving Modified Widman Flap Procedure and Connective Tissue Graft for Generalized Aggressive Periodontitis: A Case Report.

We report a case of generalized aggressive periodontitis (AgP) requiring periodontal treatment including flap surgery and ridge augmentation. The patient was a 39-year-old woman who presented with the chief complaint of pus discharge from tooth #36. No other obvious signs of gingival inflammation were observed. Periodontal examination revealed multiple sites with a probing depth of ≥10 mm. Radiography showed pro-nounced bone defects in the maxillary incisors and molar region. Real-time PCR was used to detect Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythia in subgingival plaque; all 3 pathogens were found. Based on a clinical diagnosis of generalized AgP, periodontal therapy was initiated, which resulted in an improvement in clinical and microbiological parameters. A modified Widman flap procedure was then performed on sites with residual periodontal pockets. Next, a connective tissue graft was performed for ridge augmentation at #22, which had shown evidence of ridge resorption. Postoperative reevaluation revealed a reduction in probing depth and an improvement in marginal bone levels. Oral function was then restored using a fixed bridge prosthesis and maintenance therapy initiated. The periodontal condition has remained stable over a 2.5-year period. In the present case of AgP, surgical intervention reduced periodontal pockets and periodontal pathogens and improved the architecture of both the hard and soft tissues, allowing subsequent care of the periodontium to be performed efficiently by the patient.

Maresin 1 Biosynthesis and Proresolving Anti-infective Functions with Human-Localized Aggressive Periodontitis Leukocytes.

Localized aggressive periodontitis (LAP) is a distinct form of early-onset periodontitis linked to periodontal infection with uncontrolled inflammation and leukocyte-mediated tissue destruction. The resolution of inflammation is an active process orchestrated by specialized proresolving lipid mediators (SPMs). Since the level of the Maresin pathway marker 14-hydroxy-docosahexaenoic acid (14-HDHA) was lower in activated peripheral blood from LAP patients, we investigated the Maresin 1 (MaR1) biosynthetic pathway in these subjects and its role in regulating phagocyte functions. Macrophages from LAP patients had a lower level of expression of 12-lipoxygenase (∼30%) and reduced MaR1 (LAP versus healthy controls [HC], 87.8 ± 50 pg/10(6) cells versus 239.1 ± 32 pg/10(6) cells). Phagocytosis by LAP macrophages was reduced ∼40% compared to that of HC, and killing of periodontal pathogens, including Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were similarly reduced. LAP neutrophils also displayed slower kinetics (∼30%) and decreased maximal phagocytosis (∼20% lower) with these pathogens than those of HC. The administration of MaR1 at 1 nM enhanced phagocytosis (31 to 65% increase), intracellular antimicrobial reactive oxygen species production (26 to 71% increase), bacterial killing of these periodontal pathogens (22 to 38% reduction of bacterial titers), and restored impairment of LAP phagocytes. Together, these results suggest that therapeutics targeting the Maresin pathway have clinical utility in treating LAP and other oral diseases associated with infection, inflammation, and altered phagocyte functions.

Association between Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis in subgingival plaque and clinical parameters, in Argentine patients with aggressive periodontitis.

BACKGROUND: Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) have been associated with aggressive (AgP) and chronic periodontitis. OBJECTIVE: The aim of this study was to evaluate the levels of Aa and Pg in gingival crevicular fluid (GCF) of patients with AgP and its relation with clinical parameters. DESIGN: Sixteen females and fourteen males with clinical diagnosis of AgP aged 17-23 years and their match's controls, were included in this study. Clinical recording concerning probing pocket depth, clinical attachment level, plaque index and gingival bleeding index were performed at baseline, 30 and 60 days after baseline. After clinical examination GCF samples were analyzed for Aa and Pg with a real-time polymerase chain reaction technique. Patients group was treated with a combined of mechanical and oral antibiotic therapy (doxycycline 100 mg/day, during 21 days). A multivariate analysis was used to determine the relationship between Aa and Pg counts with clinical parameters. RESULTS: GCF from all subjects was positive for Aa and PG. In controls Pg concentration was higher than Aa (Pg: 42,420 ± 3,034 copies/ml; Aa: 66.6 ± 5.4 copies/ml p < 0.001) while in patients both microbes showed the same concentration (Aa: 559,878 ± 39,698 Pg: 572,321 ± 58,752). A significant and positive correlation was observed between counts of Aa and Pg (R square: 0.7965, p < 0.0001). Female showed more counts/ml. Aa might be closely associated with clinical parameters while Pg did not. At 30 and 60 days Aa counts in patients were similar to controls while Pg counts were equal to baseline. However, in spite of Pg presence a clinical improvement was observed in all patients. CONCLUSIONS: In our population the presence of Aa may be associated with AgP while Pg may be in GCF as an opportunistic pathogen which might caused disease when the ecological balance was favorable.

Periodontal microbiology in Latin America.

This review article describes the microbiota associated with periodontal disease in Latin America. This vast territory includes 22 nations, which show great ethnic diversity, with large groups of White people, Black people, Mestizo people and Native people. Widespread poverty and limited access to education and health-care services, including periodontal care, are prominent predisposing factors for destructive periodontal disease in Latin America. Black people and Mestizo people seem to have particularly severe periodontal disease and are frequently colonized by the major periodontal pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. The 'red complex' bacterial pathogens and A. actinomycetemcomitans predominate in chronic and aggressive periodontitis, but gram-negative enteric rods and herpesviruses can also play important periodontopathic roles in Latin America. The key to minimizing the risk of periodontal disease is control of the pathogens, and new low-cost periodontal treatments deserve serious consideration in Latin America.

Periodontal herpesviruses: prevalence, pathogenicity, systemic risk.

Periodontitis is an infectious/inflammatory disease characterized by the loss of periodontal ligament and alveolar bone. Herpesviruses are frequent inhabitants of periodontitis lesions, and the periodontopathogenicity of these viruses is the topic of this review. In 26 recent studies from 15 countries, subgingival cytomegalovirus, Epstein-Barr virus and herpes simplex virus type 1, respectively, yielded median prevalences of 49%, 45% and 63% in aggressive periodontitis, 40%, 32% and 45% in chronic periodontitis, and 3%, 7% and 12% in healthy periodontium. An active herpesvirus infection of the periodontium exhibits site specificity, is a potent stimulant of cellular immunity, may cause upgrowth of periodontopathic bacteria and tends to be related to disease-active periodontitis. Pro-inflammatory cytokines induced by the herpesvirus infection may activate matrix metalloproteinases and osteoclasts, leading to breakdown of the tooth-supportive tissues. The notion that a co-infection of herpesviruses and specific bacteria causes periodontitis provides a plausible etiopathogenic explanation for the disease. Moreover, herpesvirus virions from periodontal sites may dislodge into saliva or enter the systemic circulation and cause diseases beyond the periodontium. Periodontal treatment can diminish significantly the periodontal load of herpesviruses, which may lower the incidence and magnitude of herpesvirus dissemination within and between individuals, and subsequently the risk of acquiring a variety of medical diseases. Novel and more effective approaches to the prevention and treatment of periodontitis and related diseases may depend on a better understanding of the herpesvirus-bacteria-immune response axis.