Different scaling and root planing strategies in Turkish patients with aggressive periodontitis: A randomized controlled clinical trial.

OBJECTIVES: The aim of this study was to compare clinical, cytokine and microbiological responses after quadrant-based scaling and root planing (Q-SRP), full-mouth SRP (FM-SRP) and full-mouth disinfection (FMD) in patients with generalized aggressive periodontitis (GAgP), which is currently termed as generalized stage-III and grade-C periodontitis. METHODS: Forty-two patients with GAgP were randomly assigned into groups as Q-SRP, FM-SRP or FMD with chlorhexidine. Clinical parameters were recorded, and gingival crevicular fluid (GCF) and subgingival plaque samples were collected at baseline, 3 and 6 months after treatment. GCF levels of interleukin (IL)-1ß and IL-17 were analysed using ELISA. Quantities of six bacterial species were determined using qPCR. RESULTS: Clinical parameters improved significantly in all groups at 3 and 6 months (p < 0.05). Percentage of sites with probing depth >6 mm was lower in the FMD than Q-SRP group at 3 and 6 months (p < 0.05). FMD showed significantly higher percentage of pocket closure compared with Q-SRP and FM-SRP at both 3 and 6 months after treatment (p < 0.05). The IL-1ß levels decreased only in the FMD group (p < 0.05), whereas no changes were found in IL-17 levels in any group. The levels of five out of six bacterial species decreased at 3 and/or 6 months only in the FMD group (p < 0.05). CONCLUSIONS: The FMD treatment appears to offer superior outcome than Q-SRP and could be the first choice for patients with GAgP.

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

AIM: To evaluate the local immunoinflammatory profiles in localized aggressive periodontitis patients (LAP) before and after periodontal treatment and maintenance. METHODS: Sixty-six African-Americans with LAP (7-21 years old) were included. After periodontal examination, all patients received periodontal treatment with mechanical debridement plus systemic amoxicillin/metronidazole for 7 days. Gingival crevicular fluid was collected from diseased and healthy sites at baseline and 3, 6, 12, and 24 months 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. RESULTS: 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. CONCLUSIONS: 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).

Evaluation of Systemic Markers Related to Anemia in Aggressive Periodontitis Patients before and after Phase I Periodontal Therapy: An Interventional Study.

AIM: The main aim of the study was to evaluate the systemic markers related to anemia in generalized aggressive periodontitis (GAgP) patients before and after phase I therapy. MATERIALS AND METHODS: Based on the inclusion criteria, 15 patients with GAgP were allocated to two groups, group A (before phase I periodontal therapy) and group B (after phase I periodontal therapy). After 3 months, clinical parameters and hematological parameters were reevaluated. RESULTS: The hematological parameters like hemoglobin (Hb) and red blood cell (RBC) counts were increased significantly after therapy in group B with a significant improvement in the plaque index score, gingival bleeding index score with a reduction of probing depth, and a gain in clinical attachment levels. CONCLUSION: Within the limitation of this study, it could be concluded that GAgP was associated with reduced RBC parameters suggesting that it may tend toward anemia of chronic disease (ACD). Nonsurgical periodontal therapy (NSPT) not only reverses the periodontal health by reducing the inflammation but also improves the anemic status. CLINICAL SIGNIFICANCE: Based on several studies, it was concluded that chronic periodontitis is associated with ACD. This study results indicate that like chronic periodontitis, aggressive periodontitis is also associated with reduced RBC and Hb count suggesting the risk for ACD. So when a patient is diagnosed to have any chronic infectious disease that might lead to ACD, then it is mandatory to treat that particular disease in order to reduce the infection so as to reverse the anemic status of an individual.

A Case of Orthodontic Treatment for Generalized Aggressive Periodontitis.

Aggressive periodontitis mostly affects young people, causing rapid destruction of periodontal tissue and loss of supporting alveolar bone. The destruction of periodontal tissue induces pathological tooth movement, resulting in various types of malocclusion such as crowding or spacing in the dentition. This report describes orthodontic treatment for malocclusion due to generalized aggressive periodontitis. The patient was a 31-year-old woman who presented with the chief complaint of displacement in the anterior teeth. An oral examination revealed pathological tooth mobility throughout the entire oral cavity due to severe loss of periodontal support. Many gaps in the displaced maxillary anterior teeth and crowding in the mandibular anterior teeth were also observed. The goal of subsequent treatment was to achieve ideal overjet and overbite by aligning the teeth and closing the spaces via non-extraction orthodontic treatment with stripping. The periodontal disease was managed by a periodontist who provided guidance on oral hygiene and periodontal disease control throughout the course of orthodontic treatment. Appropriate occlusion and a good oral environment were achieved. The condition of the periodontal tissue stabilized during and after orthodontic treatment, and favourable occlusal stability was observed at the 2-year follow-up examination.

IL-13 gene polymorphisms (-1112 C/T and -1512 A/C) in patients with chronic and aggressive periodontitis: Effects on GCF and outcome of periodontal therapy.

BACKGROUND: IL-13 is the key cytokine in the regulation of inflammatory with an autoimmune disease and has an anti-inflammatory effect. AIMS: This study aimed to compare IL-13 (-1112 C/T and -1512 A/C) gene polymorphisms in patients with aggressive periodontitis (AgP), chronic periodontitis (CP), and periodontally healthy group (C) and evaluate the effect of nonsurgical periodontal therapy on gingival crevicular fluid (GCF) IL-13 levels in patients. MATERIALS AND METHODS: One hundred thirty patients with AgP, 120 patients with CP, and 70 periodontally healthy subjects were included in this study. Clinical parameters were recorded (plaque and gingival index, probing pocket depth, clinical attachment level), and GCF and blood samples were taken at baseline and 6-week. Nonsurgical periodontal therapy was performed in patients with periodontitis. Gene analyses (IL-13 - 1112C/T (rs1800925) and - 1512 A/C (rs1881457) were performed with real-time polymerase chain reaction (PCR) and cytokine levels were determined by an enzyme-linked immunosorbent assay method. RESULTS: AgP and CP patients showed significant improvement in clinical parameters after periodontal therapy (P < 0.05). According to results, genotype distributions and allele frequencies in IL-13 variants - 1112C/T and - 1512 A/C were found similarly in all groups (P > 0.05). In the AgP group, GCF IL-13 cytokine level is statistically significant and increased in 6 weeks; however, in the CP group, there is no statistically significant difference between baseline and 6 week. In the AgP group, baseline GCF IL-13 cytokine level is lower than those of the CP group and C group (P < 0.05). CONCLUSION: Within the limits of this study, IL-13 -1112 and -1512 gene polymorphisms have not been associated with AgP and CP, and GCF IL-13 cytokine level is increased after treatment in the AgP group.

Differences in the periodontal microbiome of successfully treated and persistent aggressive periodontitis.

AIMS: The primary aim of this investigation was to analyse the periodontal microbiome in patients with aggressive periodontitis (AgP) following treatment. METHODS: Sixty-six AgP patients were recalled on average 7 years after completion of active periodontal treatment and had subgingival plaque samples collected and processed for 16S rRNA gene sequencing analyses. RESULTS: Of 66 participants, 52 showed persistent periodontal disease, while 13 participants were considered as "successfully treated AgP" (no probing pocket depths >4 mm) and 1 was fully edentulous. Genera associated with persistent generalized disease included Actinomyces, Alloprevotella, Capnocytophaga, Filifactor, Fretibacterium, Fusobacterium, Leptotrichia, Mogibacterium, Saccharibacteria [G-1], Selenomonas and Treponema. "Successfully treated" patients harboured higher proportions of Haemophilus, Rothia, and Lautropia and of Corynebacterium, Streptococcus and Peptidiphaga genera. Overall, patients with persistent generalized AgP (GAgP) revealed higher alpha diversity compared to persistent localized AgP (LAgP) and stable patients (p < .001). Beta diversity analyses revealed significant differences only between stable and persistent GAgP groups (p = .004). CONCLUSION: Patients with persistent AgP showed a more dysbiotic subgingival biofilm than those who have been successfully treated. It remains to be established whether such differences were predisposing to disease activity or were a result of a dysbiotic change associated with disease recurrence in the presence of sub-standard supportive periodontal therapy or other patient-related factors.

Tooth loss in aggressive periodontitis: Results 25 years after active periodontal therapy in a private practice.

AIM: To assess tooth loss in patients with aggressive periodontitis (AgP) 10-35 years after active periodontal therapy (APT) in a private practice and to detect possible factors influencing tooth loss. MATERIAL AND METHODS: In 100 patients with AgP, tooth loss was recorded over a median follow-up period of 25.5 years after APT, retrospectively. Patient- and tooth-level factors were assessed with a Cox frailty regression model. RESULTS: Of 2,380 teeth, 227 were lost during a median follow-up time of 25.5 years (2.3 ± 3.6 teeth/patient, range 0-17 teeth), resulting in a mean tooth loss rate of 0.09 teeth/patient/year. At patient-level, statistically significant factors for tooth loss were smoking (p = .039) and the baseline diagnosis generalized AgP (p < .001). Influencing factors at tooth-level were location in the maxilla (p = .003), baseline bone loss (p < .001), molars (p < .001) and premolars (p < .001) as well as abutment teeth (p = .009). CONCLUSION: Tooth loss occurred rarely in patients with AgP treated in a private practice over a long-time period. Annual tooth loss rates are comparable with those described in university settings. Smoking, generalized form of AgP, location/type of tooth, baseline bone loss and abutment status could be detected as factors impacting upon tooth loss.

Efficacy of regenerative therapy in aggressive periodontitis: a systematic review and meta-analysis of randomised controlled clinical trials.

OBJECTIVES: To analyse evidence regarding the efficacy of periodontal regenerative procedures in intrabony defects in patients treated for aggressive periodontitis (AgP). MATERIAL AND METHODS: A systematic search of the literature for randomised controlled clinical trials including patients treated for aggressive periodontitis that compared a group treated with regenerative therapy with another group treated with surgical debridement alone was conducted by two independent reviewers. RESULTS: Six studies were included in the meta-analysis of clinical and/or radiographic parameters at 6 and 12 months. Probing pocket depth was smaller at 6 months in patients treated with regenerative therapies compared with those treated with regular debridement (1.00 mm, p < 0.001, 95% CI (0.67, 1.34)). At 12 months this difference was more marked (0.41 mm, p = 0.12, 95% CI (- 0.10, 0.91)). The distance between the cemento-enamel junction and the alveolar crest at both 6 (1.36 mm, p < 0.001, 95% CI (1.03, 1.68)) and 12 months (0.90 mm, p = 0.01, 95% CI (0.24, 1.56)) was smaller in the group treated with regeneration. CONCLUSIONS: The use of biomaterials for regenerative therapy in AgP may be more effective than surgical debridement. Better outcomes were observed in terms of probing pocket depth and distance between the cemento-enamel junction and the alveolar crest at 6 months. Regeneration should be considered as a therapy to prevent tooth loss, although more studies with larger sample size and longer follow-up are needed. CLINICAL RELEVANCE: Periodontal regeneration is effective in the treatment of intrabony defects in patients with AgP, as it leads to better outcomes in clinical and radiographic parameters.

One-year follow-up of the immune profile in serum and selected sites of generalized and localized aggressive periodontitis.

BACKGROUND: The local and systemic immunological profiles of important inflammatory mediators in the localized (LAgP) and generalized (GAgP) forms of aggressive periodontitis are still unknown, as well as the effect of periodontal therapy on these parameters. The aim of this prospective study was to evaluate clinical and immune responses of patients with AgP undergoing nonsurgical treatment. MATERIAL AND METHODS: Eighteen patients with GAgP, 10 with LAgP and 10 healthy participants were included in this study. AgP participants were submitted to scaling and root planing plus systemic antibiotics (amoxicillin and metronidazole). At baseline and 1-year follow-up were measured clinical parameters, such as probing depth [PD] and clinical attachment loss [CAL], and the levels of 10 immunological mediators (GM-CSF, M-CSF, MCP-1, ICAM-1, CXCL8, IL-1ß, TNF-α, IL-17, IL-4, and IL-10) in the gingival crevicular fluid (GCF) of selected sites [AgP forms: PD ≥ 6 mm or the deepest, bleeding on probing (BoP) and bone loss measured by periapical radiography; healthy individuals: PD ≤ 3 mm, no BoP, no bone loss] and serum. RESULTS: After periodontal treatment both forms of AgP presented a significant reduction of PD and CAL, an increase of GM-CSF, ICAM-1, MCP-1, TNF-α, IL-17, IL-4, and IL-10 in the GCF, as well as of GM-CSF and IL-4 in the serum, and a reduction in the serum concentration of IL-1ß. Serum levels of M-CSF, ICAM-1, and MCP-1 remained significantly below those found in healthy individuals in both forms of AgP even after therapy. An increase in the systemic or local levels of MCP-1, ICAM-1 and the anti-inflammatory profile (IL-4, IL-10) was correlated with an improvement in clinical parameters of LAgP patients. Also, a local reduction of IL-1ß levels in both forms of AgP was correlated with an increase in the clinical attachment gain. CONCLUSION: Nonsurgical periodontal therapy was successful in improving clinical parameters and modulating the immune response in both forms of AgP. However, this therapeutic approach does not seem to affect the deficient level of important serum mediators involved in mechanisms of cell transmigration.

Local IL-10 level as a predictive factor in generalized aggressive periodontitis treatment response.

Generalized aggressive periodontitis (GAgP) presents a reduced response to non-surgical therapy. However, it is not clear if the initial clinical, microbiological or immunological characteristics are impacting the worse response to treatment. This study aimed to identify the predictive value of clinical, microbiological and immunological patterns on the clinical response to therapy in GAgP patients. Twenty-four GAgP patients were selected, and gingival crevicular fluid (GCF) and subgingival biofilm were collected. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia levels were evaluated by qPCR, and IL-1ß and IL-10 concentration by ELISA. Twelve patients were treated with SRP (scaling and root planning), and twelve with SRP plus 375 mg amoxicillin and 250 mg metronidazole (8/8 hours, 7 days) (SRP + AM). The clinical changes (Probing Pocket Depth [PPD] reduction and Clinical Attachment Level [CAL] gain) 6 months post-treatment were correlated to the initial clinical, inflammatory and microbiological variables using stepwise logistic regression (α = 5%). CAL gain at 6 months was 1.16 ± 0.77 for SRP and 1.74 ± 0.57 mm for SRP + AM (P > .05). PPD reduction was 1.96 ± 0.82 for SRP and 2.45 ± 0.77 mm for SRP + AM (P < .05). In the SRP group, IL-10 showed a predictive value for clinical response. The higher the IL-10 concentration at baseline, the higher the reduction in PPD at 6 months (P = .01, r = .68). However, when antimicrobials were administered, no significant influence was detected (P > .05). It can be concluded that the IL-10 levels in GFC act as a predictor of clinical response to GAgP. Moreover, the intake of antimicrobials appears to overlap the influence of the inflammatory response on clinical response to treatment. Clinical trial registration number: NCT03933501.

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.

Six-month clinical outcomes of non-surgical periodontal treatment with antibiotics on apoptosis markers in aggressive periodontitis.

OBJECTIVE: Extrinsic and intrinsic pathways of apoptosis are involved in generalized aggressive periodontitis (GAgP). The aim of this study was to evaluate 6-month clinical outcomes relative to apoptosis of one-stage full-mouth disinfection (OSFMD) and systemic antibiotics (SA) in the treatment of GAgP. METHODS: Twenty-six patients with GAgP were included in this prospective follow-up intervention study. Gingival crevicular fluid (GCF) was collected from patients at baseline and 3 and 6 months after periodontal therapy, which consisted of OSFMD and SA (amoxicillin and metronidazole, 500 mg each for 7 days). The levels of p53, caspase-3, TNF-α, TRAIL, IL-1ß, and IL-10 in GCF were measured via ELISA. RESULTS: Periodontal parameters were improved at 3 and 6 months compared to baseline (p < 0.05). p53 was decreased up to 6 months (p < 0.05). TRAIL, TNF-α, and IL-10 were similar at baseline and 3 and 6 months. Caspase-3 and IL-1ß were decreased at 3 months (p < 0.05), but similar at 6 months compared to baseline (p > 0.05). CONCLUSION: Although OSFMD plus SA improves clinical periodontal parameters up to 6 months, this treatment protocol differentially regulates the apoptosis markers caspase-3 at 3 months and p53 at 6 months without influencing TRAIL in GCF.

Treatment of intrabony defects with modified perforated membranes in aggressive periodontitis: subtraction radiography outcomes, prognostic variables, and patient morbidity.

OBJECTIVES: The main objectives of this study were (1) to evaluate bone/graft density alterations by digital subtraction radiography; (2) to determine factors associated with favorable clinical and radiographic outcomes, and (3) to report on patient morbidity after guided tissue regeneration (GTR) in aggressive periodontitis (AgP) patients. MATERIALS AND METHODS: Adapting a split-mouth design, 30 comparative intrabony defects in 15 patients were randomly treated with xenogenic graft plus modified perforated membranes (MPM, tests) or xenogenic graft plus standard collagen membranes (CM, controls). The time period of observation was 12 months. RESULTS: There were significant improvements in clinical and radiographic parameters within each group, without intergroup differences. However, higher PPD reduction for three-wall defects was noted in MPM sites (5.22 versus 3.62 mm; p = 0.033). Moreover, a significant gain in bone/graft density of 4.9% from 6 to 12 months post-operatively was observed in test sites. Multivariate analysis demonstrated that morphology of intrabony defects was a predictor of CAL gain (p = 0.06), while independent prognostic variables effecting changes in bone/graft density were radiographic defect depth (p = 0.025) and radiographic angle (p = 0.033). The majority of patients reported some discomfort, pain, and edema with mild intensity without any significant differences between treatment modalities. CONCLUSIONS: This study demonstrated enhanced bone/graft density gain after GTR with MPM, which may indicate greater area of new bone formation. Independent variables effecting treatment outcomes were intrabony defect morphology, radiographic defect depth, and radiographic angle. CLINICAL RELEVANCE: This study supports the regenerative treatment of intrabony defects in AgP patients and identifies some variables with prognostic value.

Moderate- to long-term therapeutic outcomes of treated aggressive periodontitis patients without regular supportive care.

BACKGROUND AND OBJECTIVE: Risk for deterioration in treated aggressive periodontitis (AgP) individuals remained unclear. This retrospective cohort study investigated 7-26 years of periodontal outcomes and oral health-related quality of life (OHRQoL) of young adults with advanced periodontitis. MATERIAL AND METHODS: Eighty-nine previously treated patients with AgP were re-examined. Clinical and radiographic parameters before treatment discontinuation and at re-examination were compared. OHRQoL at re-call was assessed with the short-form Oral Health Impact Profile (OHIP-14S). RESULTS: None of the subjects adhered to suggested periodontal therapy and maintenance after discharge. Mean percentage of sites with probing pocket depth (PPD) ≥6 mm at re-examination was 4.5 ± 5.9%. A total of 182 teeth had been lost over time. Tooth loss rate was 0.14/patient/year. From 68 subjects with documented favorable treatment outcomes, higher percentage of sites with PPD ≥6 mm at re-examination and higher radiographic proximal bone loss was associated with current smoking status. Patients with AgP with <20 teeth at re-call had worse OHRQoL than those with ≥20 teeth. Patients with higher full-mouth mean PPD also reported poorer OHRQoL. CONCLUSION: Treatment in patients with AgP who smoke and neglect proper supportive care, risk periodontal disease progression. Substantial tooth loss and higher full-mouth mean PPD led to poorer OHRQoL in this cohort.

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.

Biomarker levels in gingival crevicular fluid of generalized aggressive periodontitis patients after non-surgical periodontal treatment.

OBJECTIVES: The aim of this study was to assess the effects of non-surgical periodontal treatment on gingival crevicular fluid (GCF) cytokines in patients with generalized aggressive periodontitis (GAgP), in relation to clinical parameters. MATERIALS AND METHODS: Data were obtained from 16 GAgP patients and 15 periodontally healthy controls. Periodontal parameters and GCF biomarker levels were evaluated at baseline and repeated 3 and 6 months after treatment for GAgP subjects. Moderate and deep pocket sites were analyzed separately. The amount of interleukin (IL)-1ß, IL-9, tumor necrosis factor (TNF)-α, platelet-derived growth factor (PDGF-bb), and vascular endothelial growth factor (VEGF) were measured using a highly specific and sensitive multiplex bead immunoassay. RESULTS: At baseline, cytokine levels in the moderate and deep pocket sites of GAgP patients were higher than those of the healthy control sites. In GAgP group, periodontal treatment led to improvement in all examined clinical parameters and resulted in a statistically significant reduction in the total amounts of IL-1ß, VEGF, and TNF-α, in comparison to baseline, already 3 months after therapy in both moderate and deep pocket sites and of PDGF-bb in deep sites (p < 0.01). At the concentration level, only IL-1ß and VEGF were affected. CONCLUSION: Non-surgical treatment of GAgP provided significant clinical benefits leading to a marked decrease in the GCF levels of some pro-inflammatory and pro-angiogenic cytokines, but not of IL-9 and PDGF-bb. CLINICAL RELEVANCE: Although the periodontal therapy successfully decreased clinical signs of inflammation, the GCF levels of some inflammatory cytokines were still elevated.

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.

Association between monocyte chemoattractant protein-1 -2518 A/G gene polymorphism and the outcome of the nonsurgical periodontal treatment.

BACKGROUND/PURPOSE: Elevated monocyte chemoattractant protein-1 (MCP-1) is related to severe periodontal destruction. Furthermore, MCP-1 -2518 A/G gene polymorphism affects MCP-1 after inflammatory stimuli. This study analyzed the association between MCP-1 -2518 gene polymorphism and the outcome of nonsurgical periodontal treatment. METHODS: Forty periodontal patients were recruited and MCP-1 -2518 A/G gene polymorphisms were analyzed using polymerase chain reaction-restriction fragment length polymorphism assay. The clinical periodontal parameters, including probing depth (PD), clinical attachment level (CAL), gingival index (GI), bleeding index (BI) and plaque index (PI), were recorded before and six weeks after nonsurgical periodontal therapy. Patients were divided into chronic periodontitis (CP) or aggressive periodontitis (AP). Multiple linear regression analysis was performed to investigate certain predictors of the therapy outcome. RESULTS: The frequency of MCP-1 -2518 genotype-positive (carrying allele G) was 42.5%. Poor treatment outcome in PD, GI and BI improvement could be predicted with MCP-1 -2518 A/G genotype and aggressive periodontitis status as the predictor variables. In contrast, MCP-1 -2518 A/A genotype and aggressive periodontitis status could predict better treatment response in PD and BI improvement. However, MCP-1 -2518 genotype did not affect the treatment outcome in patients with chronic periodontitis. CONCLUSION: MCP-1 -2518 A/G genotype might be useful in predicting less favorable nonsurgical treatment outcome in patients with aggressive periodontitis. However, MCP-1 -2518 gene polymorphism may not play a role in patients with chronic periodontitis. This study suggests that MCP-1 -2518 genotype may influence the outcome of nonsurgical periodontal treatment in aggressive periodontitis patients.

Orthodontic treatment in patients with aggressive periodontitis.

INTRODUCTION: Aggressive periodontitis (AP) is a condition that promotes breakdown of the periodontal tissues in a short time. In severe cases, pathologic migration of teeth and tooth loss can occur, producing esthetic and functional problems for the patient. Orthodontic treatment may be recommended to restore esthetics and masticatory function. We assessed the effects of orthodontic movement in the periodontal tissues of treated patients with AP. METHODS: Ten subjects (ages 25.0 ± 5.22 years) with AP received periodontal treatment followed by orthodontic treatment. Maintenance sessions were performed monthly under a strict dental biofilm control. They were compared with 10 periodontally healthy subjects (ages 22.9 ± 5.23 years) who received orthodontic treatment. Probing pocket depth, clinical attachment level, bleeding on probing, and dental plaque index were measured at baseline, after orthodontic treatment, and after 4 months. RESULTS: Statistical analysis showed improvement in all clinical parameters between baseline and 4 months after orthodontic treatment: probing pocket depth (0.29 mm), clinical attachment level (0.38 mm), bleeding on probing (4.0%), and dental plaque index (11%). CONCLUSIONS: The periodontal parameters of the AP patients remained stable during orthodontic treatment under strict biofilm control.

[Clinical study of locking-taper implants in patients treated for periodontitis].

OBJECTIVE: To evaluate the survival rate and peri-implant clinical parameters of Locking-Taper implants in patients having lost their teeth due to non-periodontitis (NP) reasons, chronic periodontitis (CP) and aggressive periodontitis (AgP). METHODS: In the study, 145 subjects were installed with 315 Bicon Locking-Taper implants and followed up for 1-5 years. The subjects and implants were classified into three groups, tooth loss by NP, CP and AgP. NP included 44 subjects with 100 implants, CP 70 subjects with 132 implants and AgP 31 subjects with 83 implants. Periodontal parameters before subgingival scaling and root planning (T0), at the end of active periodontal therapy (T1) and at the time of last recall (T2) were recorded. Right after the installation of final restoration and at the time of last recall (T2), peri-implant probing parameters were recorded. RESULTS: After active periodontal therapy, mean probing depth (PD) in CP and AgP were reduced from 4.05 mm, 5.20 mm at T0 to 3.07 mm, 2.96 mm at T1 (P<0.001, P<0.001), (PD≥6 mm)% were reduced from 33.2%, 58.5% at T0 to 14.4%, 10.5% at T1 (P<0.001, P<0.001). The periodontal parameters remained stable at T2 compared with T1 (P>0.05). Cumulative survival rates of implants in NP, CP and AgP were 100%, 97.6% and 100% for 1-5 years' follow-ups with no statistical significance found. At T2, mean implant PD was 2.78 mm, 2.96 mm and 2.97 mm in NP, CP and AgP, with NP significantly lower than the other two groups (P=0.006, P=0.01). The percentage of implant sites with PD≥6 mm was 3.7% in CP and 4.8% in AgP, both significantly higher than NP (P=0.003, P<0.001). 8.4% implant sites showed at least 2 mm deeper than those at prosthesis installation were found in CP group, significantly higher than NP (4.3%, P=0.003). CONCLUSION: Periodontal conditions of patients having lost their teeth for chronic and aggressive periodontitis were significantly improved after active periodontal therapy and remained stable during 1-5 years. Short-term survival rates of Locking-Taper implants in patients treated for CP and AgP was no less than those who lost their teeth for non-periodontitis reasons. More sites with increasing peri-implant probing depth were found in CP and AgP patients, compared with NP.