Comparison of Two Risk Assessment Scores in Predicting Peri-Implantitis Occurrence during Implant Maintenance in Patients Treated for Periodontal Diseases: A Long-Term Retrospective Study.

BACKGROUND: There is a need for reliable risk assessment tools to better predict peri-implantitis occurrence. This study compared the long-term prognosis value of two models of risk assessment scoring in predicting peri-implantitis. METHODS: Seventy-three patients with treated periodontitis representing 232 implants and attending long-term implant maintenance were evaluated. The Periodontal Risk Assessment (PRA) score, which combines only periodontal risk factors/indicators, and the Implant Risk Assessment (IRA) score, which combines both periodontal and implant risk factors/indicators, were calculated during implant maintenance. Peri-implantitis was defined by the presence of probing depth ≥6 mm with bleeding on probing/suppuration and bone level ≥3 mm. Analyses were performed at the patient level. RESULTS: The mean implant follow-up was 6.5 years. Peri-implantitis incidence was 17.8%, and high-risk PRA and IRA percentages were 36.9% and 27.3%, respectively. High-risk PRA and IRA were significantly associated with peri-implantitis incidence, with hazard ratio (HR) = 4.8 and 3.65, respectively. Risk factors/indicators considered separately showed reduced associations with peri-implantitis. CONCLUSIONS: The PRA score combining periodontal parameters and IRA score combining both periodontal and implant parameters have comparable value in predicting peri-implantitis. These scores could allow practicians to intercept the risk of peri-implantitis and to manage follow-up modalities in patients with treated periodontitis.

Influence of Periodontitis, Implant, and Prosthesis Characteristics on the Peri-Implant Status: A Cross-Sectional Study.

BACKGROUND: The association between peri-implant diseases and the periodontal, implant, and prosthesis characteristics has been characterized in various ways. PURPOSE: The aim of this study was to evaluate the link between the peri-implant and periodontal status and the influence of implant and prosthesis parameters during implant follow-up. MATERIALS AND METHODS: One hundred and seven patients with a total of 310 implants that had at least one year of function who were attending periodontal and implant maintenance at a university clinic setting were included in this cross-sectional study. The demographic, periodontal, peri-implant tissue, implant, and prosthesis parameters were recorded. A pocket depth > 4 mm with bleeding on probing defined periodontal/peri-implant soft tissue diseased sites. Analyses were performed at the patient and implant levels using univariable and multivariable mixed regression analysis. RESULTS: The mean implant follow-up was 7.22 years. At the patient level, the bleeding on probing and pocket depth measurements were more pronounced around the implant than around the teeth. The opposite was observed for plaque and the clinical attachment levels. At the implant level, multivariable analysis showed that the periodontal and corresponding peri-implant tissue parameters, such as diseased sites, were closely related. The implant location, bone level, and number were selectively associated with the implant bone level, while cemented retention and emergence restoration profile influenced the implant pocket depth. CONCLUSIONS: The present study suggested that clinical peri-implant and periodontal soft tissue statuses were different, which could be a consequence of the initial implant and prosthesis healing process. However, during implant follow-up, the peri-implant parameters were predominantly associated with their corresponding periodontal parameters regardless of an association with the implant and prosthesis characteristics. This trial is registered with ClinicalTrials.gov ID: NCT03841656.

Association between periodontitis treatment outcomes and peri-implantitis: A long-term retrospective cohort study.

OBJECTIVES: Retrospectively evaluate the association of periodontal treatment outcomes and the prevalence of peri-implant diseases around tissue-level implants. MATERIALS AND METHODS: Eighty-six patients with 260 tissue-level implants attending supporting periodontal and implant therapy for more than 3 years were evaluated. Clinical and radiographic periodontal and implant data were recorded at initial examination (T0), before implant placement (T1) and at final re-examination (T2). Two definitions of peri-implantitis severity, PIBE and PIKA, were used corresponding to the presence of periodontal pocket ≥5 mm or ≥6 mm with bleeding on probing or suppuration and radiographic signs of a bone level ≥2 mm, or ≥3 mm during implant follow-up, respectively. Analyses were performed at patient level. RESULTS: The mean implant follow-up per patient was 9.4 years and 38.0% of patients had implant for at least 10 years. Two implants were lost due to peri-implantitis. The prevalence of patients with PIKA and PIBE was 15.1% and 12.8%, respectively. Residual periodontal pockets, clinical attachment loss and bone loss/age at T2 were more pronounced in patients with PIKA and PIBE. Cox regression analysis adjusted with the number of implants per patient showed that residual pockets at T1 were independently associated with PIKA and PIBE. Initial diagnosis of severe periodontitis was associated with PIBE incidence. CONCLUSIONS: The present study showed that periodontal conditions before implant placement are a risk indicator for peri-implantitis incidence. During implant follow-up, the severity of periodontal status appeared to be a reliable indicator of patient susceptibility to peri-implantitis.

Interests of Exosomes in Bone and Periodontal Regeneration: A Systematic Review.

Periodontitis is an infectious inflammatory disease characterized by clinical attachment loss and tooth supporting tissue destruction. As exosomes demonstrated pro-regenerative ability, their use in periodontal treatment has been suggested. The aim of this systematic review is to gather and summarize the most recent data regarding exosomes to determine their potential impact in bone and periodontal regeneration. Electronic databases (Pubmed, Web of Science) were searched up to February 2020. Studies assessing the impact of exosomes administration in experimental bone and periodontal defects have been identified according to PRISMA guidelines. Among the 183 identified articles, 16 met the inclusion criteria and were included in this systematic review. Experimental bone defects were mainly surgically induced with a dental bur or distraction tools. All studies considered bone healing after exosomes administration as the primary outcome. Results showed that mesenchymal stem cells derived exosomes administration promoted bone healing and neovascularization. Nevertheless, a dose-effect relationship was observed. Exosomes administration appears to promote significantly the bone healing and periodontal regeneration. However, only a limited number of studies have been carried out so far and the optimized protocols in this context need to be evaluated.

Selective Influence of Smoking on Periodontal Treatment Outcomes after 3 Years of Follow-up.

PURPOSE: The impact of smoking habits on periodontal treatment has not been clearly elucidated. This study aimed to specify the effects of cigarette consumption and nicotine addiction on periodontal therapy. MATERIALS AND METHODS: In this retrospective case-control study, 20 moderate smokers and 20 non-smokers with severe periodontitis were examined after initial diagnosis, and non-surgical active and supportive therapies for 1-6 years (mean follow-up = 3.37 years). Fagerström's test of nicotine dependence (FTND) was evaluated at re-examination. Treatment efficacy was assessed by periodontal pocket probing depth (PPD) changes and number of teeth lost per year (TL). Bayesian multilevel and regression analyses were performed at site, tooth, and patient levels. RESULTS: During the mean follow-up period of > 3 years including active and supportive periodontal therapies, mean PPD, PPD > 3 mm and PPD > 7 mm percentage reductions were 1.03, 1.48 and 2.57 times statistically significantly less pronounced, respectively, in smokers than in non-smokers. Multilevel analysis showed that the variability of PPD > 7 mm reduction was mainly associated with patient-level factors. Smokers presented a higher risk for periodontitis progression. In smokers, periodontal parameter improvement was less pronounced in the maxilla and molars. The mean TL was related to the FTND score, not to cigarette consumption. Regression analysis did not demonstrate other influences of demographic and periodontal treatment characteristics on treatment outcomes, except patient age. CONCLUSION: Smoking negatively impacted periodontal treatment outcomes at specific tooth sites (deep pockets, maxillary molars) and periodontitis progression, independent of other risk factors.

Experimental periodontitis in Msx2 mutant mice induces alveolar bone necrosis.

BACKGROUND: Msx2 homeoprotein is a key transcription factor of dental and periodontal tissue formation and is involved in many molecular pathways controlling mineralized tissue homeostasis such as Wnt/sclerostin pathway. This study evaluated the effect of Msx2-null mutation during experimental periodontitis in mice. METHODS: Experimental periodontitis was induced for 30 days in wild-type and Msx2 knock-in Swiss mice using Porphyromonas gingivalis infected ligatures. In knock-in mice, Msx2 gene was replaced by n-LacZ gene encoding ß-galactosidase. Periodontal tissue response was assessed by histomorphometry, tartrate-resistant acid phosphatase histoenzymology, ß-galactosidase, sclerostin immunochemistry, and terminal deoxynucleotidyl transferase-mediated dUTP nickend labeling assay. Expression of Msx2 gene expression was also evaluated in human gingival biopsies using RT-qPCR. RESULTS: During experimental periodontitis, osteonecrosis area and osteoclast number were significantly elevated in knock-in mice compared with wild-type mice. Epithelial downgrowth and bone loss was similar. Sclerostin expression in osteocytes appeared to be reduced during periodontitis in knock-in mice. Msx2 expression was detected in healthy and inflamed human gingival tissues. CONCLUSION: These data indicated that Msx2 pathway influenced periodontal tissue response to experimental periodontitis and appeared to be a protective factor against alveolar bone osteonecrosis. As shown in other inflammatory processes such as atherothrombosis, genes initially characterized in early development could also play an important role in human periodontal pathogenesis.

In-situ forming implants loaded with chlorhexidine and ibuprofen for periodontal treatment: Proof of concept study in vivo.

Control of infection and inflammation is crucial for the success of periodontal treatment. In this study, in-situ forming implants (ISFI) loaded with chlorhexidine dihydrochloride (CHX) and ibuprofen (IBU) were developed and tested to optimize periodontal treatment outcomes. Release profiles were promising. Exposure to 1.5% and 5.3% CHX-IBU loaded ISFI's release media decreased significantly the P. gingivalis growth up to 20-fold and 35-fold, respectively, after 48 h (p < 0.05). The metabolic activity assay of gingival epithelial cells (EC) demonstrated 1.5% CHX-IBU-loaded ISFI to be non-toxic, therefore, it was selected for further experimentation. Furthermore, significant down-regulation of TNF-α release (34% at 6 h and 43% at 24 h, p < 0.05) in P. gingivalis lipopolysaccharide (Pg-LPS) stimulated EC exposed to 1.5% CHX-IBU ISFI release medium was demonstrated by ELISA. In vivo, 1.5% CHX-IBU ISFI was injected into the periodontal pocket in an experimental periodontitis mouse model and the reduction in inflammation and improvement in periodontal wound healing was evaluated through inflammatory cell scoring and histomorphometry at 7- and 15-days post-treatment. The results indicate that CHX-IBU loaded ISFI could be efficient as adjuvant to periodontal therapy for the control of infection and inflammation. Moreover, other (e.g., pro-regenerative) drugs could be incorporated into ISFI to further improve periodontal treatment outcomes.

Risk factors associated with long-term outcomes after active and supporting periodontal treatments: impact of various compliance definitions on tooth loss.

OBJECTIVES: The aim of this retrospective study was to determine factors influencing tooth loss during a long-term follow-up, emphasizing the impact of various compliance definitions. MATERIALS AND METHODS: Patients with periodontitis who were treated and presenting for maintenance care for at least up to 6 years were included. The effects of compliance and other patient- and treatment-related factors on tooth loss were assessed. Lack of compliance was defined in three ways: (1) fewer than 1.4 visits per year (irregular compliers), (2) no maintenance visit over a 2-year period (erratic compliers), and (3) no maintenance visit over a 2- to 5-year period (partial compliers) and no maintenance visit for a period of more than 5 years (non-compliers). RESULTS: One hundred and one patients were selected. The mean follow-up was 9.72 ± 1.17 years. Tooth loss per patient-year was significantly higher in erratic compliers (0.35 ± 0.19) and non-compliers (0.40 ± 0.20) compared with compliers (0.18 ± 0.10). No significant differences were found for irregular (0.30 ± 0.17) and partial (0.25 ± 0.15) compliers. Similar results were obtained for the number of patients who lost more than three teeth. Multivariable regression analysis showed that lack of compliance and periodontitis severity (more than 3% of periodontal pockets > 7 mm at baseline) were independent risk factors for tooth loss. CONCLUSIONS: During long-term follow-up, non-compliance and initial periodontitis severity were the principal risk factors that increased tooth loss. CLINICAL RELEVANCE: Tooth loss associated with lack of compliance was essentially observed in patients with long continuous periods without maintenance visits and was less influenced by patients' attended mean visit frequency.

Management of localized aggressive periodontitis: A 30-year follow-up.

This case report describes the long-term follow-up of a patient with localized aggressive periodontitis over a 30-year period. A 16-year-old woman was referred for periodontal assessment after starting orthodontic treatment. The patient was treated initially by combined nonsurgical and antimicrobial therapy, and autotransplantation of maxillary third molars in place of maxillary first molars, followed by a regular supportive periodontal treatment program. This challenging case demonstrated that elimination of putative bacterial pathogens and long-term supportive periodontal treatments provide an effective treatment modality for localized aggressive periodontitis.

Synthesis of a Novel Electrospun Polycaprolactone Scaffold Functionalized with Ibuprofen for Periodontal Regeneration: An In Vitro andIn Vivo Study.

Ibuprofen (IBU) has been shown to improve periodontal treatment outcomes. The aim of this study was to develop a new anti-inflammatory scaffold by functionalizing an electrospun nanofibrous poly-ε-caprolactone membrane with IBU (IBU-PCL) and to evaluate its impact on periodontal inflammation, wound healing and regeneration in vitro and in vivo. IBU-PCL was synthesized through electrospinning. The effects of IBU-PCL on the proliferation and migration of epithelial cells (EC) and fibroblasts (FB) exposed to Porphyromonas gingivlais lipopolysaccharide (Pg-LPS) were evaluated through the AlamarBlue test and scratch assay, respectively. Anti-inflammatory and remodeling properties were investigated through Real time qPCR. Finally, the in vivo efficacy of the IBU-PCL membrane was assessed in an experimental periodontitis mouse model through histomorphometric analysis. The results showed that the anti-inflammatory effects of IBU on gingival cells were effectively amplified using the functionalized membrane. IBU-PCL reduced the proliferation and migration of cells challenged by Pg-LPS, as well as the expression of fibronectin-1, collagen-IV, integrin α3ß1 and laminin-5. In vivo, the membranes significantly improved the clinical attachment and IBU-PCL also reduced inflammation-induced bone destruction. These data showed that the IBU-PCL membrane could efficiently and differentially control inflammatory and migratory gingival cell responses and potentially promote periodontal regeneration.

Anti-inflammatory effect of active nanofibrous polymeric membrane bearing nanocontainers of atorvastatin complexes.

AIM: We developed polymeric membranes for local administration of nonsoluble anti-inflammatory statin, as potential wound patch in rheumatic joint or periodontal lesions. METHODS: Electrospun polycaprolactone membranes were fitted with polysaccharide-atorvastatin nanoreservoirs by using complexes with poly-aminocyclodextrin. Characterization methods are UV-Visible and X-ray photoelectron spectroscopy, molecular dynamics, scanning and transmission electron microscopy. In vitro, membranes were seeded with macrophages, and inflammatory cytokine expression were monitored. RESULTS & CONCLUSION: Stable inclusion complexes were formed in solution (1:1 stability constant 368 M-1, -117.40 kJ mol-1), with supramolecular globular organization (100 nm, substructure 30 nm). Nanoreservoir technology leads to homogeneous distribution of atorvastatin calcium trihydrate complexes in the membrane. Quantity embedded was estimated (70-90 µg in 30 µm × 6 mm membrane). Anti-inflammatory effect by cell contact-dependent release reached 60% inhibition for TNF-α and 80% for IL-6. The novelty resides in the double protection offered by the cyclodextrins as drug molecular chaperones, with further embedding into biodegradable nanoreservoirs. The strategy is versatile and can target other diseases.

Porphyromonas gingivalis and its LPS differentially regulate the expression of peptidyl arginine deiminases in human chondrocytes.

Periodontitis, an inflammatory disease initiated by Gram-negative bacteria such as Porphyromonas gingivalis ( Pg), is considered as a risk factor for rheumatoid arthritis (RA). Our study aimed to determine the effect of Pg and its LPS on the expression of peptidyl arginine deiminase isotypes (PADs) in human primary chondrocytes (HC). HCs were infected with Pg and activated by its LPS (LPS- Pg). The mRNA expression levels of human PADs (1, 2, 3, 4 and 6) and bacterial enzyme (PADPg) were quantified by RT-qPCR. Cellular extracts served to measure the enzymatic activities of PADs and PADPg and to visualize the profiles of citrullinated proteins/peptides by Western blotting. Our data showed significant inhibitions of mRNA expressions of human PAD-2, PAD-3 and PAD-4 during infection of HC with live Pg. Activation of HC by LPS- Pg increased mRNA expressions of human PAD-2 and PAD-3. The PADPg enzymatic activity was significantly increased in only infected HC. Analysis of citrullinated proteins/peptides profiles revealed the occurrence of low molecular bands only in cellular extracts from HC infected with Pg. Our data showed that Pg and its LPS differentially regulate the expression of PADs in human chondrocytes and that Pg favors the apparition of new citrullinated proteins/peptides.

Identification and Characterization of MicroRNA Differentially Expressed in Macrophages Exposed to Porphyromonas gingivalis Infection.

MicroRNAs (miRNAs) are short, noncoding RNAs involved in the regulation of several processes associated with inflammatory diseases and infection. Bacterial infection modulates miRNA expression to subvert any innate immune response. In this study we analyzed, using microarray analysis, the bacterial modulation of miRNAs in bone marrow-derived macrophages (BMMs) in which activity was induced by infection with Porphyromonas gingivalis The expression of several miRNAs was modulated 3 h postinfection (at a multiplicity of infection of 25). A bioinformatic analysis was performed to further identify pathways related to the innate immune host response under the influence of selected miRNAs. To assess the effects of the miRNAs identified on cytokine secretion (tumor necrosis factor alpha [TNF-α] and interleukin-10 [IL-10]), BMMs were transfected with selected miRNA mimics and inhibitors. Transfection with mmu-miR-155 and mmu-miR-2137 did not modify TNF-α secretion, while their inhibitors increased it. Inhibitors of mmu-miR-2137 and mmu-miR-7674 increased the secretion of the anti-inflammatory factor IL-10. In P. gingivalis-infected BMMs, mmu-miR-155-5p significantly decreased TNF-α secretion while inhibitor of mmu-miR-2137 increased IL-10 secretion. In vivo, in a mouse model of P. gingivalis-induced calvarial bone resorption, injection of mmu-miR-155-5p or anti-mmu-miR-2137 reduced the size of the lesion significantly. Furthermore, anti-mmu-miR-2137 significantly reduced inflammatory cell infiltration, osteoclast activity, and bone loss. Bioinformatic analysis demonstrated that pathways related to cytokine- and chemokine-related pathways but also osteoclast differentiation may be involved in the effects observed. This study contributes further to our understanding of P. gingivalis-induced modulation of miRNAs and their physiological effects. It highlights the potential therapeutic merits of targeting mmu-miR-155-5p and mmu-miR-2137 to control inflammation induced by P. gingivalis infection.

Long-term prospective cohort study on dental implants: clinical and microbiological parameters.

OBJECTIVE: The aim of the present prospective cohort study is to evaluate clinical and microbiological data of dental implants after at least 8 years of follow-up. MATERIAL AND METHODS: A total of 110 patients and 232 implants were included at baseline and followed during 1 year. Fifty-two patients and 108 implants could be evaluated at the final examination. Clinical and microbiological data were taken at baseline, 1 year and at least 8 years. RESULTS: The mean follow-up time was 10.8 ± 1.7 years. Plaque index was, respectively, 0.50 ± 0.50 at baseline, 0.50 ± 0.50 at 1 year and 0.33 ± 0.67 at ≥8 years. Gingival index was, respectively, 1.08 ± 0.19 at baseline, 1.01 ± 0.39 at 1 year and 0.22 ± 0.47 at ≥8 years. Sulcular bleeding index was, respectively, 0.17 ± 0.22 at baseline, 0.11 ± 0.33 at 1 year and 0.17 ± 0.22 at ≥8 years. Probing depth was, respectively, 2.67 ± 0.75 at baseline, 3.00 ± 0.83 at 1 year and 2.74 ± 1.00 at ≥8 years. Clinical attachment level was, respectively, 3.75 ± 1.17 at baseline, 4.00 ± 1.06 at 1 year and 4.00 ± 1.17 at ≥8 years. Peri-implant mucositis was detected around 60.2% of implants in 73.1% of patients, while peri-implantitis was affecting 12% of implants in 15.4% of patients. Some bacteria species were associated with worsened clinical parameters. CONCLUSIONS: About 69.4% of implants (75/108) and 67.3% of the patients (35/52) were considered as success in the present prospective cohort study after a mean follow-up of 10.8 years. Microbial follow-up may help to identify patients at risk for peri-implant disease.

Association between periodontitis and arterial hypertension: A systematic review and meta-analysis.

BACKGROUND: Several studies have shown that periodontal diseases are associated with hypertension (HT). However, heterogeneity among populations, diagnosis criteria, and shared risk factors represent some difficulties in terms of interpretation. Therefore, the aim of this study was to determine the magnitude of the association between periodontal diseases and HT. METHODS AND RESULTS: A systematic review and meta-analysis, including studies published up to June 2016, have been performed. Sixteen studies assessing the association between periodontal diseases and HT have been included. The meta-analysis considering all included studies (moderate to severe periodontitis) showed that the presence of HT was associated with the presence of periodontal diseases (OR, 1.50; 95% CI, 1.27-1.78). To reduce potential bias, a stratified analysis has been performed illustrating the impact of inclusion criteria and adjustments on the magnitude of the association. Interestingly, when only studies with secure diagnosis of severe periodontitis and HT were considered, an OR=1.64 (95% CI, 1.23-2.19) has been measured. CONCLUSIONS: Periodontal diseases are associated with a higher risk of HT especially for severe periodontitis. However, no conclusions could be made regarding the causative involvement of periodontal diseases mainly due to the reduced number of available prospective studies and remaining questions regarding underlying biological mechanisms.

Porphyromonas gingivalis Differentially Modulates Cell Death Profile in Ox-LDL and TNF-α Pre-Treated Endothelial Cells.

OBJECTIVE: Clinical studies demonstrated a potential link between atherosclerosis and periodontitis. Porphyromonas gingivalis (Pg), one of the main periodontal pathogen, has been associated to atheromatous plaque worsening. However, synergism between infection and other endothelial stressors such as oxidized-LDL or TNF-α especially on endothelial cell (EC) death has not been investigated. This study aims to assess the role of Pg on EC death in an inflammatory context and to determine potential molecular pathways involved. METHODS: Human umbilical vein ECs (HUVECs) were infected with Pg (MOI 100) or stimulated by its lipopolysaccharide (Pg-LPS) (1µg/ml) for 24 to 48 hours. Cell viability was measured with AlamarBlue test, type of cell death induced was assessed using Annexin V/propidium iodide staining. mRNA expression regarding caspase-1, -3, -9, Bcl-2, Bax-1 and Apaf-1 has been evaluated with RT-qPCR. Caspases enzymatic activity and concentration of APAF-1 protein were evaluated to confirm mRNA results. RESULTS: Pg infection and Pg-LPS stimulation induced EC death. A cumulative effect has been observed in Ox-LDL pre-treated ECs infected or stimulated. This effect was not observed in TNF-α pre-treated cells. Pg infection promotes EC necrosis, however, in infected Ox-LDL pre-treated ECs, apoptosis was promoted. This effect was not observed in TNF-α pre-treated cells highlighting specificity of molecular pathways activated. Regarding mRNA expression, Pg increased expression of pro-apoptotic genes including caspases-1,-3,-9, Bax-1 and decreased expression of anti-apoptotic Bcl-2. In Ox-LDL pre-treated ECs, Pg increased significantly the expression of Apaf-1. These results were confirmed at the protein level. CONCLUSION: This study contributes to demonstrate that Pg and its Pg-LPS could exacerbate Ox-LDL and TNF-α induced endothelial injury through increase of EC death. Interestingly, molecular pathways are differentially modulated by the infection in function of the pre-stimulation.

Clinical efficacy of probiotics as an adjunctive therapy to non-surgical periodontal treatment of chronic periodontitis: a systematic review and meta-analysis.

FOCUSED QUESTION: What is the clinical influence of probiotics as an adjunctive therapy of scaling and root planing (SRP) when compared with SRP alone or in combination with placebo in the treatment of chronic periodontitis (CP). METHODS: Electronic databases were searched up to July 2015. Randomized controlled trials (RCTs) comparing SRP + probiotic versusSRP were included. PPD reduction and CAL gain were selected as primary outcome variables. RESULTS: Independent screening resulted in four eligible publications for the systematic review and three were included in the meta-analysis. Meta-analysis showed a statistically significant CAL gain (-0.42 mm, p = 0.002) and bleeding on probing (BOP) reduction (-14.66, p = 0.003) for SRP + probiotic treatment versusSRP at short-term. Only a tendency (p = 0.06) has been observed in terms of overall PPD reduction, whereas results were significant when stratified for moderate (-0.18, p = 0.001) and deep pockets (-0.67, p < 0.001). CONCLUSION: Within the limitations of this study, the findings of this meta-analysis seem to support the adjunctive use of L. reuteri to SRP in CP treatment at short-term, especially in deep pockets. Heterogeneity and limited available data may reduce the impact of these conclusions. Future long-term RCTs evaluating the clinical efficacy of adjunctive probiotics to SRP are needed.

Long-term follow up of post-surgical tooth autotransplantation: a retrospective study.

AIM: The aim of the present retrospective study was to evaluate the long-term results of tooth autotransplantation using the survival and success rates of transplanted teeth as outcome variables. METHODS: Thirty patients received a total of 44 transplants of immature teeth from 1987 to 1997. Seventeen of those patients with 25 transplants were recalled 10-20 years after tooth transplantation for complete clinical and radiographic examinations, followed by questionnaires that examined the patients' degrees of satisfaction. The incidence of all types of complications was carefully analyzed. Success was defined as being free of all complications over the entire observation period. RESULTS: The long-term survival rate for transplants that were observed after at least 10 years was 96%. The cumulative complication rate (pulpal, periodontal, and operative complication rates) after an observation period of 10-20 years was 38.9%. Therefore, the success rate at 10 years was 61.1%. CONCLUSION: The present study confirms that transplanted teeth have a high long-term survival rate and a lower long-term success rate. This procedure should be recommended and carried out in appropriate patients when necessary because it is the most biological approach, even though it is highly sensitive to technique.

Adiposity Measurements and Non-Surgical Periodontal Therapy Outcomes.

BACKGROUND: Obesity is considered a risk factor for periodontitis. However, its influence on periodontal therapy has not been clearly determined. The aim of this case-control study is to evaluate the association between adiposity measurements, non-surgical periodontal treatment outcomes, and influencing factors in patients with chronic periodontitis. METHODS: Eighteen obese and 18 normal-weight (NW) patients are included in this study. The waist/hip ratio (WHR), plaque index, bleeding on probing, probing depth (PD), and clinical attachment level (CAL) were measured at baseline and 3 and 6 months after treatment. Univariable and multivariable analyses were used to evaluate the influence of sex, age, baseline percentage of PD >3 mm, WHR, and obesity on periodontal treatment outcomes. RESULTS: Demographic and periodontal characteristics at baseline were similar in both groups. All periodontal parameters were improved during treatment in both groups. PD reduction and CAL gain were 0.88 and 0.84 mm in NW individuals and 0.79 and 0.68 mm in obese individuals. The difference in moderate-to-deep pocket (PD >5 mm) percentages between the baseline and 6-month examinations was 9.1% in NW individuals and 6.08% for obese individuals. Multivariable analysis showed that obesity negatively influenced changes of PD >5 mm percentages. This influence was also observed at 3 months for improving sites (PD decrease >2 mm between examinations) if WHR was also considered in the analysis. CONCLUSIONS: A negative association between adiposity measurements and periodontal treatment outcomes was observed mainly for moderate-to-deep pockets. Consideration of WHR and other influencing factors amplified the negative effect of obesity on periodontal treatment outcomes.

Porphyromonas gingivalis-impaired innate immune response via NLRP3 proteolysis in endothelial cells.

Porphyromonas gingivalis (Pg) is involved in the link between periodontal diseases and atherosclerosis worsening. In periodontal cells, Pg modifies IL-1ß expression via the NLRP3 inflammasome pathway activation. Our aim was to investigate NLRP3 inflammasome activation in endothelial cells (ECs) after Pg infection and Pg-LPS stimulation. In both situations, RT-PCR experiments demonstrated an increase of the NLRP3 mRNA level that can be potentiated by pre-treatment of ECs with 5 mM ATP. However, Western blotting analysis revealed that Pg infection induced a proteolysis of NLRP3 protein and a major decrease of the native protein. After ATP pre-treatment and/or Pg-LPS stimulation, this proteolysis was not observed, while NLRP3 protein levels were increased. Proteolysis of the NLRP3 protein was not observed with heat-killed Pg and inhibition of ECs protein synthesis with cycloheximide did not abolish the NLRP3 protein degradation induced by Pg infection in ATP pre-treated cells. Additionally, significant increases of secreted IL-1ß were measured after ATP pre-treatment and/or Pg-LPS stimulation, but not after Pg infection. These data showed that Pg and Pg-LPS differentially controlled the NLRP3 inflammasome pathway in ECs, and suggested a novel potential mechanism developed by Pg to reduce IL-1ß secretion and to escape host immune response.