Localized Aggressive Periodontitis Patients Research Articles

Treatment of localized aggressive periodontitis alters local host immunoinflammatory profiles: A long-term evaluation.

To evaluate the local immunoinflammatory profiles in localized aggressive periodontitis patients (LAP) before and after periodontal treatment and maintenance. Sixty-six African-Americans with LAP (7-21years old) were included. After periodontal examination, all patients received periodontal treatment with mechanical debridement plus systemic amoxicillin/metronidazole for 7days. Gingival crevicular fluid was collected from diseased and healthy sites at baseline and 3, 6, 12, and 24months following treatment. Levels of 16 inflammatory/bone resorption markers were determined using Milliplex® . Univariate and correlation analyses were performed among all parameters/biomarkers. Discriminant analyses (DA) evaluated profile differences between LAP diseased and healthy sites at each time point as compared to the baseline. Reductions in the clinical parameters (except for visible plaque) were observed at all time points compared to the baseline. Levels of IL-12p70, IL-2, IL-6, MIP-1α, RANKL, and OPG were reduced after treatment, and several cytokines/chemokines were correlated with clinical parameters reductions. DA showed that differences in the immunoinflammatory profiles between LAP diseased and healthy sites decreased after periodontal treatment compared to the baseline. Periodontal treatment modified the local immunoinflammatory profile of LAP sites in the long term, as suggested by changes in biomarkers from baseline, along with clinical stability of the disease. (Clinicaltrials.gov number, NCT01330719).

Dysregulation of genes and microRNAs in localized aggressive periodontitis.

Previous data from our laboratory have demonstrated that localized aggressive periodontitis (LAP) patients produce elevated levels of pro-inflammatory cytokines in response to TLR4 and TLR2 ligation compared to unrelated and periodontally healthy controls (HC). The aim of the present work is to evaluate the contribution of TLR-related gene expression and miRNA regulation in LAP disease. Peripheral blood mononuclear cells (PBMCs) from LAP and health control (HC) patients were isolated. Gene and miRNA expression involved in TLR signalling pathway and immunopathology were evaluated in unstimulated PBMCs by real-time PCR (RT-PCR). TICAM-1 (TRIF), FOS, IRAK1, TLR2 and CCL2 genes and the miRNAs miR-9-5p, miR-155-5p and 203a-3p, miR-147a, miR-182-5p and miR-183-5p were significantly up-regulated in LAP compared to HC. Most of the genes and miRNAs overexpressed here are directly or indirectly related to immune response and inflammation. This profile supports our previous findings that suggests LAP patients have a "hyper-responsive" phenotype upon activation of TLR pathway by periodontal pathogens.

Association of P2RX7 functional variants with localized aggressive periodontitis.

The purpose of this study was to investigate involvement of the P2X7 receptor in the rare condition, localized aggressive periodontitis. Peripheral blood from 220 African Americans (103 with localized aggressive periodontitis and 117 healthy unrelated controls) was stimulated with lipopolysaccharide from Ecoli and Porphyromonas gingivalis. P2RX7 single nucleotide polymorphisms rs208294 (H155Y), rs1718119 (T348A), rs2230911 (T357S) and rs3751143 (E496A) were genotyped in 103 localized aggressive periodontitis patients and 117 healthy unrelated subjects. We examined genetic association between four P2RX7 single nucleotide polymorphisms and localized aggressive periodontitis, and tested for correlations between the single nucleotide polymorphisms and inflammatory response to lipopolysaccharide in blood samples from these patients. A significant association with localized aggressive periodontitis was observed with rs1718119 A (Thr) allele (P=0.0063, odds ratio=1.904) and with a haplotype containing this allele (P=0.0075). Additionally, significant correlations with these data were found: the rs1718119 G allele correlated with greater production of IL-6, IL-2 and GM-CSF; the C (His) allele of rs208294 correlated with lower levels of IL-12p40; and the C (Thr) allele of rs2230911 correlated with greater levels of G-CSF. The data from these analyses support a possible biological relationship between P2RX7 genetic variants and inflammatory response in localized aggressive periodontitis patients.

Evaluation of topically applied probiotic treatment on localized aggressive periodontitis patients: A split mouth study

Aim: This study aims to evaluate clinically the effect of probiotic treatment on localized aggressive periodontitis patients. Subjects and methods: This study was designed as a randomized, controlled, split mouth clinical trial, carried out on localized aggressive periodontitis (LAP) which having almost two identical sites with clinical probing depth of ≥ 5 mm. Two contralateral sites were randomly divided into two groups, Group I: received conventional periodontal treatment, scaling and root planning combined with topical application of probiotic. Group II: received conventional periodontal treatment, scaling and root planning only. Patients were evaluated clinically using the following parameters: plaque index (PI), gingival index (GI), probing pocket depth (PPD) and clinical attachment level (CAL) and radiographically by radiographic bone density (pixel) at baseline, 3, 6, and 9 months. Results: Clinical and radiographic results of this study showed that: there were a significant reduction for assessed variables (Plaque Index, gingival index, probing pocket depth and clinical attachment level and significant increase in radiographic bone density in probiotic group compared to group II. Conclusion: Adjunctive use of topically applied probiotic appeared to be beneficial effect in localized aggressive periodontitis patients when compared with scaling and root planning alone.

Impact of aggressive periodontitis and chronic periodontitis on oral health-related quality of life.

The purpose of this cross-sectional study was to investigate the effect of different forms of periodontal diseases on Oral Health-Related Quality of Life (OHRQoL). Fifty-two patients with Aggressive Periodontitis (AP) or Chronic Periodontitis (CP) were included: nine patients with Localized Aggressive Periodontitis (LAP), thirty-three patients with Generalized Aggressive Periodontitis (GAP) and ten patients with Generalized Chronic Periodontitis (GCP). Oral Health Impact Profile questionnaires (OHIP-14) were distributed after a clinical examination that measured the following periodontal parameters: tooth loss, bleeding on probing (BoP), probing depth (PD), gingival recession (REC) and clinical attachment level (CAL). The global OHIP-14 score means were 10.6 for LAP, 16.5 for GAP, and 17.5 for GCP. A statistically significant difference (p < 0.01) was observed between the LAP group and the other two groups. There was significantly less bleeding and recession in the LAP group than in the patients with the generalized forms of periodontitis. LAP, GAP and GCP have an impact on patient quality of life when measured using the OHIP-14. Patients with GAP and GCP had poorer OHRQoL than LAP patients.

OCCURRENCE OF PREVOTELLA NIGRESCENS AND PREVOTELLA INTERMEDIA IN LOCALIZED AGGRESSIVE PERIODONTITIS LESIONS

Ponte Academic JournalFeb 2018, Volume 74, Issue 2 OCCURRENCE OF PREVOTELLA NIGRESCENS AND PREVOTELLA INTERMEDIA IN LOCALIZED AGGRESSIVE PERIODONTITIS LESIONSAuthor(s): Gulden EresJ. Ponte - Feb 2018 - Volume 74 - Issue 2 doi: 10.21506/j.ponte.2018.2.7 Abstract:Prevotella intermedia is a gram negative anaerobic microorganism redefined and renamed as Prevotella nigrescens (formerly Prevotella intermedia type I) and Prevotella intermedia (formerly Prevotella intermedia type II). The frequency of occurrence of P. intermedia and P. nigrescens in the oral cavity has been reported with various percentages and the pathogenity of each is suggested to be different. P. intermedia was reported to be found more frequently in periodontal pockets and P. nigrescens in other lesions such as pericoronitis and apical abcesses. The purpose of this study was to determine the detection frequencies of P. intermedia and P. nigrescens in localized aggressive periodontitis lesions. \nSubgingival plaque samples were collected from 83 lesions of 13 localized aggressive periodontitis patients with an age range of 14 to 25 were analyzed by using dot blot hybridization method. We used synthetic oligonucleotide probes complementary to the hypervariable region of 16S rRNA of P. intermedia ATCC 25611 and P. nigrescens ATCC 33563. The detection frequencies of both species increased as the attachment level increased and 45% of the samples harbored both species while 9% harbored only P. intermedia and 37% harbored only P. nigrescens. \nThe results of this study is contradictory to the previous reports regarding the lower detection frequency of P. nigrescens in periodontal pockets and suggests that the racial differences may play a role on the occurrence of certain species in periodontal pockets. Download full text:Check if you have access through your login credentials or your institution Username Password

Effect of total sonicated Aggregatibacter actinomycetemcomitans fragments on gingival stem/progenitor cells.

BackgroundAggregatibacter-actinomycetemcomitans (A.actinomycetemcomitans) are strongly associated with localized-aggressive-periodontitis (LAgP). The study’s aim was to test for the first time the effect of total sonicated A.actinomycetemcomitans-bacterial-fragments on gingival mesenchymal stem/progenitor cells’ (G-MSCs) proliferation and regenerative gene expression in-vitro.Material and MethodsG-MSCs were isolated, characterized, expanded and stimulated by total sonicated A.actinomycetemcomitans-bacterial-fragments (0 (negative-control), 15, 60, 120 and 240µg/ml; serovar-b; n=6/group). Cellular proliferation and NF-κβ (NFKB1), Alkaline Phosphatase (ALPL), Collagen-I (COL1A1), Collagen-III (COL3A1), Osteonectin (SPARC) and Osteopontin (SPP1) m-RNA expression were assessed via reverse-transcription-polymerase-chain-reaction (RT-PCR) at 24, 48 and 72 hours and CFUs-ability evaluated at twelve days.ResultsG-MSCs demonstrated stem/progenitor cells’ characteristics. A.actinomycetemcomitans-bacterial-fragments (up to 72 hours) resulted in marked G-MSCs’ proliferation over-time (p<0.001) and elevated NFKB1 (p=0.017), COL1A1 (p=0.025), SPARC (p=0.025), decreased ALPL (p=0.017), with no significant differences for COL3A1 and SPP1 expression or stimulation times (p>0.05; Friedman-test). Longer-term stimulation for twelve days reduced G-MSCs’ CFUs.ConclusionsSonicated A.actinomycetemcomitans-bacterial-fragments’ exert beneficial short-term effects on G-MSCs’ proliferative and non-mineralized tissue forming aptitude. Results shed new light on the importance of periodontal treatment for LAgP patients, using power driven sonic/ultrasonic devices, which, in addition to reducing the subgingival microbial load, produces cell-stimulatory A.actinomycetemcomitans-bacterial-fragments, with positive attributes on tissue reparative/regenerative responses of tissue resident stem/progenitor cells in their niche. Key words:Ultrasonic, Aggregatibacter actinomycetemcomitans, stem cells, gingiva, Aggressive periodontitis.

Adjunctive Effect of Autologous Platelet-Rich Fibrin in the Treatment of Intrabony Defects in Localized Aggressive Periodontitis Patients: A Randomized Controlled Split-Mouth Clinical Trial.

The aim of this study was to investigate the clinical and radiologic efficacy of autologous platelet-rich fibrin (PRF) in the treatment of intrabony defects associated with localized aggressive periodontitis (LAP). A total of 30 sites, 2 sites per individual in 15 LAP patients, were treated with modified flap operation (MFO; Kirkland flap) alone or combined with autologous PRF. The study variables included plaque index, sulcus bleeding index, probing depth (PD), clinical attachment level (CAL), and gingival marginal level at baseline and 12 months postoperatively. The radiographic bone fill (RBF) on standardized radiographs was assessed after a year using image analysis software. The improvements in PD, CAL, and RBF in test sites compared to control sites were statistically significant (P < .05). Mean CAL gain and bone fill in the test sites were 4.0 ± 0.63 mm and 3.09 mm, respectively. Almost 80% of the PRF-treated sites showed ≥ 50% bone fill with minimal marginal tissue recession. Use of PRF significantly enhances the clinical and radiographic outcomes of open flap debridement in the treatment of periodontal intraosseous defects in patients affected by LAP.

Epigenetic regulation of inflammation in localized aggressive periodontitis

BackgroundWe have previously demonstrated a Toll-like receptor (TLR)-mediated hyper-responsive phenotype in our cohort of localized aggressive periodontitis (LAP) individuals. However, mechanisms related to this phenotype are still not clear in the literature. The objective of this cross-sectional study is to examine the role of epigenetic regulation, specifically DNA methylation status of genes in the TLR pathway in this cohort. Peripheral blood was collected from 20 LAP patients and 20 healthy unrelated controls. Whole blood was stimulated with 1 μl (100 ng/μl) of purified Escherichia coli lipopolysaccharide (LPS) for 24 h and cyto/chemokines in the supernatants analyzed by Luminex multiplex assays. Genomic DNA extracted from buffy coats prepared from a second tube of whole blood was used for DNA methylation analysis by pyrosequencing of seven TLR signaling genes (FADD, MAP3K7, MYD88, IL6R, PPARA, IRAK1BP1, RIPK2).ResultsSignificant differences in the methylation status were observed at specific CpG positions in LAP patients compared to healthy controls and interestingly also between severe and moderate LAP. Specifically, subjects with moderate LAP presented hypermethylation of both the upregulating (MAP3K7, MYD88, IL6R, and RIPK2) and downregulating (FADD, IRAK, and PPARA) genes, while severe LAP presented hypomethylation of these genes. Further analysis on CpG sites with significant differences in methylation status correlates with an increased pro-inflammatory cytokine profile for LAP patients.ConclusionsOur findings suggest that epigenetic modifications of genes in the TLR pathway may orchestrate the thresholds for balancing induction and prevention of tissue destruction during the course of disease, and thus differ significantly at different stages of the disease, where moderate LAP shows hypermethylation and severe LAP shows hypomethylation of several genes.Trial registrationhttps://clinicaltrials.gov, NCT01330719

Local and Plasma Biomarker Profiles in Localized Aggressive Periodontitis.

Localized aggressive periodontitis (LAP) patients possess a systemic hyperinflammatory response after lipopolysaccharide stimulation. However, the levels of inflammatory and bone biomarkers in plasma, as well as possible associations between local and plasma biomarkers, are unknown in LAP. This cross-sectional study aimed to characterize gingival crevicular fluid (GCF) and plasma biomarker profiles in LAP patients, their healthy siblings (HS), and healthy unrelated controls (HC). Fifty-eight LAP subjects, 33 HS, and 49 HC (African Americans, aged 5 to 25 y) were included. Following collection of clinical parameters with GCF and plasma samples, levels of 16 inflammatory and bone resorption biomarkers were determined with Milliplex. Univariate and correlation analyses were performed among all clinical and laboratorial parameters. Discriminant analyses were used to investigate groups of biomarkers discriminating LAP from HS and HC in GCF and plasma. GCF levels of multiple cytokines and chemokines and RANKL:OPG ratio (receptor activator of nuclear factor kappa-B ligand:osteoprotegerin) were higher in LAP disease, most of which positively correlated with probing depth and attachment loss of sampled sites. A group of IL-12p40, IL-6, IL-12p70, IL-2, and MIP-1α discriminated LAP diseased sites from twheir healthy sites, as well as from HS and HC healthy sites. In plasma, only RANKL levels were increased in LAP versus controls, which positively correlated with the percentage of affected sites and deep/bleeding sites. A plasma inflammatory profile including MIP-1α, IL-8, IL-10, and INF-γ could significantly discriminate LAP patients from HS and HC. No correlations were found between GCF and plasma levels of biomarkers. In conclusion, an inflammatory profile including groups of specific biomarkers in GCF and plasma may significantly discriminate LAP from healthy individuals. The hyperinflammatory response previously found in the peripheral blood of LAP patients is dependent on lipopolysaccharide stimulation, apparently resulting mostly in local tissue destruction and changes in biomarker profile, with a slight influence in the systemic inflammatory profile (ClinicalTrials.gov NCT01330719). Knowledge Transfer Statement: The results of this study can be possibly used by clinicians in the future as diagnostic tools for localized aggressive periodontitis. Thus, in the future, with proper consideration of cost, patient preference, chair-side feasibility and ultimately further studies validating the role of GCF markers for disease progression and response to treatment, this information could lead to more appropriate therapeutic decisions and the development of preventive approaches for susceptible patients.

Aggregatibacter actinomycetemcomitans in African Americans with Localized Aggressive Periodontitis.

This study aims to investigate the prevalence of the highly leukotoxic JP2 sequence versus the minimally leukotoxic non-JP2 sequence of Aggregatibacter actinomycetemcomitans within a cohort of 180 young African Americans, with and without localized aggressive periodontitis (LAP), in north Florida. The study included patients aged 5 to 25 y: 60 LAP patients, 60 healthy siblings (HS), and 60 unrelated healthy controls (HC). Subgingival plaque was collected from LAP sites-diseased (PD ≥5 mm with bleeding on probing) and healthy (PD ≤3 mm with no bleeding on probing)-and from healthy sites of HS and HC. Plaque DNA was extracted and analyzed by polymerase chain reaction for the detection of the JP2 and non-JP2 sequences of A. actinomycetemcomitans. Overall, 90 (50%) subjects tested positive for the JP2 sequence. Fifty (83.33%) LAP subjects were carriers of the highly leukotoxic JP2 sequence, detected in 45 (75%) diseased sites and 34 (56.67%) healthy sites. Additionally, JP2 carriage was found in 16 HS (26.67%) and 24 HC (40%; P < 0.0001, among groups). The non-JP2 sequence was detected in 26 (14.44%) total subjects: 17 (28.33%) LAP patients detected in equal amounts of diseased and healthy sites (n = 11, 18.33%), 6 (10%) HS sites, and 3 (5%) HC sites (P < 0.05, among groups). The JP2 sequence was strongly associated with LAP-diseased sites in young African Americans, significantly more so than the non-JP2 (ClinicalTrials.gov NCT01330719). Knowledge Transfer Statement: Clinicians may use the results of this study to identify susceptible individuals to aggressive periodontitis, potentially leading to more appropriate selection of therapeutic choices.

EXPRESSION OF MMP-1 AND MMP-9 IN LOCALIZED AGGRESSIVE PERIODONTITIS PATIENTS BEFORE AND AFTER TREATMENT: A CLINICAL AND IMMUNOHISTOCHEMICAL STUDY

Aim: This study aimed to clinically investigate the efficacy of β-glucan supplementation to non-surgical periodontal therapy in localized aggressive periodontitis (LAP) patients. In parallel, immunohistochemical detection of matrix metalloproteinase-1 (MMP-1) and MMP-9 expression levels has undergone to determine the subcellular changes behind the clinical status and reliability of each antibody in predicting the periodontal condition.Method: 40 subjects suffering from LAP were randomly and equally assigned to receive scaling and root planning (SRP); either with placebo pills (Group I) or β-glucan (100 mg/ once a day) (Group II), for 40 days. Subjects were clinically monitored on day 0 and day 91. Gingival samples were harvested from hopeless teeth sites to be investigated histologically and immunohistochemically using matrix metalloproteinase (MMP)-1 and 9 antibodies form each participating patient; at the same time intervals.Results: The experimental intervention showed a greater mean of probing pocket depth reduction (p=0.1128), with significant gain in clinical attachment (p=0.0180) and reduction of gingival inflammation (p=0.0207) compared to the control group at the end of the study. Furthermore, the experimental protocol was able to achieve better modulating effects on the levels of MMP-1 and MMP-9 compared to control therapy, along with enhancing protective healing patterns. MMP-9 was more sensitive indicator of the periodontal condition compared to MMP-1.Conclusions: The curre nt study demonstrated that the non-surgical treatment of LAP is markedly improved clinically by the adjunctive use of β-glucan, accompanied by a trend for modulation of the cytokine profile in gingival tissue samples with better healing events. The results also suggest that the expression of MMP-9 may be a precise indicator of periodontal disease activity.

Long-term clinical response to treatment and maintenance of localized aggressive periodontitis: a cohort study.

To evaluate long-term clinical response to periodontal therapy and maintenance in localized aggressive periodontitis (LAP). One hundred forty-one African Americans diagnosed with LAP, aged 5-25years, were enrolled. Patients underwent periodontal mechanical debridement plus 1 week of amoxicillin/metronidazole. Mechanical therapy was repeated as needed and clinical parameters were recorded at baseline, 3, 6, 12, 18 and 24months, and two additional annual follow-up visits after treatment. Radiographs from primary dentition of patients with LAP in permanent dentition, and additional healthy siblings (HS) were analysed retrospectively. Periodontal therapy significantly improved probing depth and clinical attachment level up to 4years (mean reductions: 2.18±1.03 and 2.80±1.43mm, respectively). Percentage of affected sites was reduced at all time points and maintained up to 4years. Non-compliance with antibiotics/appointments negatively affected the treatment response. Ninety per cent of LAP patients in permanent dentition and 32% of HS presented radiographic bone loss in primary dentition. Mechanical debridement with 1 week of systemic antibiotics along with proper periodontal maintenance was effective in the treatment and successful maintenance of LAP for up to 4years. LAP in permanent dentition may be preceded in the primary dentition. Clinicaltrials.gov #NCT01330719.

A Putative Association of a Single Nucleotide Polymorphism in GPR126 with Aggressive Periodontitis in a Japanese Population.

Periodontitis is an inflammatory disease causing loss of tooth-supporting periodontal tissue. Disease susceptibility to the rapidly progressive form of periodontitis, aggressive periodontitis (AgP), appears to be influenced by genetic risk factors. To identify these in a Japanese population, we performed whole exome sequencing of 41 unrelated generalized or localized AgP patients. We found that AgP is putatively associated with single nucleotide polymorphism (SNP) rs536714306 in the G-protein coupled receptor 126 gene, GPR126 [c.3086 G>A (p.Arg1029Gln)]. Since GPR126 activates the cAMP/PKA signaling pathway, we performed cAMP ELISA analysis of cAMP concentrations, and found that rs536714306 impaired the signal transactivation of GPR126. Moreover, transfection of human periodontal ligament (HPDL) cells with wild-type or mutant GPR126 containing rs536714306 showed that wild-type GPR126 significantly increased the mRNA expression of bone sialoprotein, osteopontin, and Runx2 genes, while mutant GPR126 had no effect on the expression of these calcification-related genes. The increase in expression of these genes was through the GPR126-induced increase of bone morphogenic protein-2, inhibitor of DNA binding (ID) 2, and ID4 expression. These data indicate that GPR126 might be important in maintaining the homeostasis of periodontal ligament tissues through regulating the cytodifferentiation of HPDL cells. The GPR126 SNP rs536714306 negatively influences this homeostasis, leading to the development of AgP, suggesting that it is a candidate genetic risk factor for AgP in the Japanese population.

Association of Interleukin-17 polymorphism (-197G/A) in chronic and localized aggressive periodontitis.

Interleukin 17(IL-17) is a pro-inflammatory cytokine produced mainly by Th17 cells. The present study was undertaken to investigate a possible association between IL-17 A genetic polymorphism at (-197A/G) and susceptibility to chronic and localized aggressive periodontitis (LAgP) in an Indian population. The study was carried out on 105 subjects, which included 35 LAgP patients, 35 chronic periodontitis patients and 35 healthy controls. Blood samples were drawn from the subjects and analyzed for IL-17 genetic polymorphism at (-197A/G), by using the polymerase chain reaction-restriction fragment length polymorphism method. A statistically significant difference was seen in the genotype distribution among chronic periodontitis patients, LAgP patients and healthy subjects. There was a significant difference in the distribution of alleles among chronic periodontitis patients, LAgP patients and healthy subjects. The odds ratio for A allele versus G allele was 5.1 between chronic periodontitis patients and healthy controls, and 5.1 between LAgp patients and healthy controls. Our study concluded that IL-17 A gene polymorphism at (-197A/G) is linked to chronic periodontitis and LAgP in Indian population. The presence of allele A in the IL-17 gene polymorphism (-197A/G) can be considered a risk factor for chronic periodontitis and LAgP.

Effects of periodontal therapy on white blood cell count and levels of transforming growth factor beta in serum of subjects with severe periodontitis.

This study aimed to investigate the effects of nonsurgical periodontal therapy on white blood cell (WBC) count and levels of transforming growth factor beta (TGF&mdash;&#946;) in serum from subjects with severe periodontitis. Serum from 28 subjects with periodontitis (mean age: 34.36±6.24; 32% men) and 27 healthy controls (mean age: 33.18±6.42; 33% men) were collected prior to therapy. Blood samples were obtained from 23 subjects who completed therapy (9&mdash;12 months). A well&mdash;controlled periodontal treatment protocol was established in three stages: mechanical periodontal therapy (scaling and root planning), reinstrumentation of dental sites, and supportive periodontal therapy. Periodontal and systemic parameters such as the total number of WBCs and TGF&mdash;&#946; levels, accessed by enzyme&mdash;linked immunosorbent assay (ELISA), were included. After therapy, all clinical periodontal parameters decreased (p&lt;0.0001). There were no statistical differences in WBC count between experimental and control groups before or after therapy. However, after therapy, the mean value of lymphocytes in patients with localized aggressive periodontitis (LAgP) was statistically higher than that of patients with generalized chronic periodontitis (GCP) (p&lt;0.0357). Additionally, TGF&mdash;&#946; levels in LAgP and GCP patients were higher compared to controls before therapy (p&lt;0.05 and p&lt;0.01, respectively). In LAgP patients, periodontal therapy was associated with increased number of lymphocytes.

IgG sera levels against a subset of periodontopathogens and severity of disease in aggressive periodontitis patients: a cross-sectional study of selected pocket sites.

To evaluate the association among serum immunoglobulin G (IgG) responses to Aggregatibacter actinomycetemcomitans (Aa) serotypes a, b and c, Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf) and clinical parameters in Aggressive Periodontitis (AP) subjects. Associations between periodontal pathogens and clinical and immunological parameters were also evaluated. Thirty-eight subjects diagnosed with generalized AP (GAP) and localized AP (LAP) were included. Ten healthy controls were also evaluated. Clinical parameters were assessed and percentages of subgingival levels of Aa, Pg and Tf (beyond bacterial load), were determined by quantitative real-time polymerase chain reaction. Serum IgG antibody levels against Aa, Pg and Tf were evaluated by enzyme-linked immunosorbent assay. Percentages of Aa, Pg and Tf were significantly higher in AP than in controls. The response to Aa serotype c was higher in LAP subjects than in controls. There were no differences in microbial composition or antibodies responses between GAP and LAP, except for IgG response to Tf. Pg levels were correlated with probing depth (PD), BoP and CAL in GAP but not in LAP subjects. Tf levels correlated with PD and CAL in GAP subjects. In GAP, the infection levels of Aa and Pg correlated with the corresponding IgG levels to Aa serotype c and Pg. Given the evidences that IgG response in AP patients correlated with bacterial infection level in GAP, but not in LAP, and that LAP patients lack a response to Tf, despite harbouring this species, our data suggest a difference in host immune defence between these two forms of aggressive periodontitis.

Clinical and microbiological characterization of localized aggressive periodontitis: a cohort study.

Localized aggressive periodontitis (LAgP) is an infectious periodontal disease which generally affects young people. Recent data suggest the involvement of different bacterial species in different populations. The causative bacterial species in Israel has never been identified despite a high prevalence of LAgP in this population. The objectives of this study were to characterize the bacterial microbiota of periodontal pockets within an Israeli LAgP population who were also clinically assessed. Twenty-one LAgP patients (test) and 12 chronic periodontitis patients (control) were examined. Bacterial samples were collected from periodontal pockets and analysed by both culture and polymerase chain reaction techniques. Mann-Whitney U test and chi-square test were used to compare results between the groups. Higher levels of Parvimonas micra (>10(6) ), Aggregatibacter actinomycetemcomitans (>10(5) ), Fusobacterium nucleatum/F. periodonticum (>10(6) ), and Tannerella forsythia (levels of 10(5) to 10(6) bacteria) were detected in the LAgP group compared to the control (p < 0.05), while levels of Porphyromonas gingivalis and Prevotella intermedia were higher in the CP group. The characteristic periodontal bacterial flora of LAgP patients in Israel is mainly comprised of P. micra, A. actinomycetemcomitans, F. nucleatum/F. periodonticum and T. forsythia. Similar population based studies of each population will improve the quality of treatment of LAgP when individual sampling is not possible.

Clinical and radiographic evaluation of intra-bony defects in localized aggressive periodontitis patients with platelet rich plasma/hydroxyapatite graft: A comparative controlled clinical trial.

Background:Aggressive periodontitis is a characterized by rapid attachment loss, bone destruction and familial aggregation. Platelet-rich plasma (PRP) has been proposed to promote regeneration of the lost periodontal tissues. The aim of this study was to evaluate and compare the efficacy of PRP combined with hydroxyapatite (HA) graft in the treatment of intra-bony defects in localized aggressive periodontitis (L-AgP) patients.Materials and Methods:Ten L-AgP patients having bilateral intra-bony defect ≥2 mm and probing depth (PD) ≥6 mm were randomly treated either with the PRP/HA graft or HA graft alone. The clinical (plaque control record, bleeding on probing index, PD, and relative attachment level [RAL]), and radiographic parameters (size of the bone defect) were recorded pre- and post-operatively at 3, 6, and 12 months.Results:After 12 months, for both maxillary and mandibular arches, the mean PD decrease was significantly more (P < 0.05) for the test group than the control group (3.2 mm vs. 1.9 mm and 3.6 mm vs. 1.9 mm, respectively). Furthermore, the mean RAL decrease in both maxillary and mandibular arches was significantly more (P < 0.05) for the test group than the control group (3.0 mm vs. 1.2 mm and 3.1 mm vs. 1.4 mm, respectively). Radiographically, the test group showed significantly more defect fill as compared with the control group.Conclusion:Both treatments provided significant improvements in clinical and radiographic parameters in a 12-month postoperative period. PRP/HA group presented superior results regarding PD reduction, clinical attachment gain and radiographic bone fill than HA group.

Correlation of Aggregatibacter actinomycetemcomitans Detection with Clinical/Immunoinflammatory Profile of Localized Aggressive Periodontitis Using a 16S rRNA Microarray Method: A Cross-Sectional Study

ObjectiveThe objective of this study was to determine whether the detection of Aggregatibacter actinomycetemcomitans (Aa) correlates with the clinical and immunoinflammatory profile of Localized Aggressive Periodontitis (LAP), as determined by by 16S rRNA gene-based microarray. Subjects and MethodsSubgingival plaque samples from the deepest diseased site of 30 LAP patients [PD ≥ 5 mm, BoP and bone loss] were analyzed by 16S rRNA gene-based microarrays. Gingival crevicular fluid (GCF) samples were analyzed for 14 cyto/chemokines. Peripheral blood was obtained and stimulated in vitro with P.gingivalis and E.coli to evaluate inflammatory response profiles. Plasma lipopolysaccharide (LPS) levels were also measured. Results Aa was detected in 56% of LAP patients and was shown to be an indicator for different bacterial community structures (p<0.01). Elevated levels of pro-inflammatory cyto/chemokines were detected in LPS-stimulated blood samples in both Aa-detected and Aa-non-detected groups (p>0.05). Clinical parameters and serum LPS levels were similar between groups. However, Aa-non-detected GCF contained higher concentration of IL-8 than Aa-detected sites (p<0.05). TNFα and IL1β were elevated upon E.coli LPS stimulation of peripheral blood cells derived from patients with Aa-detected sites. ConclusionsOur findings demonstrate that the detection of Aa in LAP affected sites, did not correlate with clinical severity of the disease at the time of sampling in this cross-sectional study, although it did associate with lower local levels of IL-8, a different subgingival bacterial profile and elevated LPS-induced levels of TNFα and IL1β.