Critical review on bone grafting during immediate implant placement.

In the last 20 years, immediate implant placement has been proposed as a predictable protocol to replace failing teeth. The research conducted in preclinical and clinical studies have focused on soft and hard tissue changes following tooth extraction and immediate implant placement. Different approaches for hard and soft tissue grafting together with provisional restorations have been proposed to compensate tissue alterations. This review analyzed some relevant clinical and preclinical literature focusing on the impact of bone grafting procedures on immediate implant placement in terms of hard and soft tissue changes, aesthetic results, and patient-related outcomes.

Efficacy of adjunctive measures in the non-surgical treatment of peri-implantitis: A systematic review.

AIM: The aim of this systematic review was to evaluate the efficacy of patient-performed or administered adjunctive measures to non-surgical peri-implantitis therapy in terms of probing depth (PD) and/or bleeding on probing (BoP) reductions. MATERIALS AND METHODS: Randomized and controlled clinical trials with at least 6 months of follow-up were searched in three databases. Secondary outcomes included implant loss, disease resolution, recurrence of peri-implantitis, need of re-treatment, changes in marginal bone levels, patient-reported outcomes and adverse effects. RESULTS: Of 567 titles, 10 publications, reporting 9 investigations, were included. Three types of adjunctive measures were found (local/systemic antimicrobials and probiotics). Four studies evaluated the effects of local antimicrobials (i.e., minocycline microspheres, chlorhexidine chips or a metronidazole + amoxicillin gel), three studies evaluated systemic antimicrobials (either amoxicillin + metronidazole or metronidazole alone) and two studies evaluated probiotics (Lactobacillus reuteri strains). The addition of local antimicrobials led to modest improvements in PD reduction. Systemic antimicrobials showed significantly greater reductions in PD and BoP, especially at initially deep sites (PD > 6 mm). Due to the large heterogeneity among included studies, no meta-analyses were performed. CONCLUSIONS: Different adjunctive measures in the non-surgical treatment of peri-implantitis have different impact in terms of PD and BoP reductions. Improved PD reductions result after the use of systemic antimicrobials, and to a lesser extent, after the use of local antimicrobials.

Adjunctive benefits of systemic metronidazole on non-surgical treatment of peri-implantitis. A randomized placebo-controlled clinical trial.

AIM: To study clinical, radiographic, and microbiological outcomes after non-surgical therapy of peri-implantitis with or without adjunctive systemic metronidazole. MATERIALS AND METHODS: A randomized placebo-controlled clinical trial was carried out in 32 subjects (62 implants) diagnosed with peri-implantitis. Implants received a mechanical non-surgical debridement session and systemic metronidazole or placebo. Clinical, radiographic, and microbiological outcomes were evaluated at baseline, 3, 6, and 12 months. RESULTS: After 12 months, the test treatment resulted in significantly greater PPD reduction (2.53 vs. 1.02 mm) and CAL gain (2.14 vs. 0.53 mm) (p value <.05) in comparison with placebo. The test treatment also resulted in additional radiographic bone gain (2.33 vs. 1.13 mm) compared with placebo (p value <.05). There was a significantly greater decrease in Porphyromonas gingivalis, Tannerella forsythia, and Campylobacter rectus counts compared with the control group (p value <.05). At the end of follow-up, 56.3% of patients met the success criteria in the test group and 25% in the control group. CONCLUSIONS: The use of systemic metronidazole as an adjunct to non-surgical treatment of peri-implantitis resulted in significant additional improvements in clinical, radiographic, and microbiological parameters after 12 months of follow-up. This study is registered in ClinicalTrials.gov (NCT03564301).

Comparison of clinical outcomes of immediate versus delayed placement of dental implants: A systematic review and meta-analysis.

OBJECTIVE: Two focused questions were addressed: Focused question (Q1) 1) Are there any differences between immediate and delayed placement in terms of (i) survival rate, (ii) success rate, (iii) radiographic marginal bone levels, (iv) height/(v)thickness of buccal wall, (vi) peri-implant mucosal margin position, (vii) aesthetics outcomes and (viii) patient reported outcomes? Focused question 2 (Q2) What is the estimated effect size of immediate implant placement for all parameters included in Q1? MATERIALS AND METHODS: An electronic search (MEDLINE, EMBASE, The Cochrane Central Register of Controlled Trials and OpenGray) and hand search were conducted up to November 2019. Randomised controlled trials (RCT) with delayed implant placement as controls were eligible in the analysis for Q1. Immediate dental implant arms RCTs, controlled clinical trials (CCTs) and prospective case series of immediate implant placement were eligible in the analysis for Q2. RESULTS: Six papers (RCTs) were included in the analysis for Q1 and 53 papers (22 RCTs, 11 CCTs and 20 case series) for Q2. Q1: Meta-analyses did not show any significant difference in implant survival, but it did for bone levels and PES scores at 1 year post-loading, favouring the immediate group. Q2: Meta-analyses showed that immediate implants had a high survival rate (97%) and presented high PES scores (range 10.36 to 11.25). Information regarding marginal bone loss and gingival/papillary recession varied among all included studies. CONCLUSION: Similar survival rate was found between immediate and delayed implants. Immediate implants presented threefold early complications and twofold delayed complications. Success criteria should be reported more consistently, and the incidence/type of complications associated with immediate implants should be further explored.

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.

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

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

Disease Staging Index for Aggressive Periodontitis.

Major advances in the knowledge about the aetiopathogenesis of aggressive periodontitis (AgP) have been achieved. An ever increasing number of scientific articles related to AgP are published every year contributing significantly to the knowledge of this unique and complex disease. AgP has been classified into localised and generalised forms based on their extent and disease progression with distinct clinical and radiological features. A classification of AgP based on severity (mild, moderate and severe) exists; however, it is not easily applicable. Therefore, studies on AgP do not categorise the disease based on severity. A disease staging index for AgP is proposed based on clinical and radiological features, as well as risk factors. Based on the presence or absence of risk factors confirmed by longitudinal studies, cases of AgP can be divided into low risk, medium risk and high risk profiles for disease progression. Clinicians can devise a broad treatment plan for their AgP cases based on this staging. More frequent recall intervals are proposed for patients at medium and high risk for disease progression. Ten cases of AgP with 10-year follow-up were used to validate the staging index by retrospectively assigning prognosis and associating it with tooth loss. The use of this staging by researchers would increase external validity of research on AgP. Long-term analysis of AgP cases are needed to validate this staging index longitudinally.

Disease progression in aggressive periodontitis patients. A Retrospective Study.

AIM: The primary aim of this study was to retrospectively ascertain disease progression in a cohort of aggressive periodontitis patients (AgP). MATERIALS AND METHODS: Patients treated at a specialist setting and referred back to general practice for periodontal maintenance were recalled and examined in a single visit. Disease progression during follow-up was assessed and historical data collected from the patient's records. Factors that could potentially influence tooth loss rates at the patient level were explored by linear regression analysis. At the tooth level, chi-square test and OR for tooth loss were calculated. RESULTS: Sixty-six subjects completed the study. The mean follow-up was 6.97 years (95% CI 6.25-7.69). The mean annual tooth loss rate was 0.27 teeth per patient/year (95% CI 0.17-0.36). At the patient level, having received surgical treatment and the performance of interproximal cleaning were found to significantly reduce the annual tooth loss rates. At the tooth level, deep probing depths after treatment were significantly associated with increased tooth loss rates (OR 4.39 for PPD 5-6 mm and OR 11.68 for PPD >6 mm, respectively, compared with PPD <5 mm). CONCLUSIONS: In this sample of patients, the annual tooth loss rates were found to be higher than previously described.

Association between periodontitis and peripheral markers of innate immunity activation and inflammation.

BACKGROUND: Immune response leading to increased systemic inflammation is one of the mechanisms linking periodontitis to chronic inflammatory diseases. The aim of this study was to compare the expression of toll-like receptors 2 and 4 in monocytes and neutrophils (TLR2M, TLR2N, TLR4M, and TLR4N) and its endogenous ligands (cellular fibronectin [cFN] and heat shock protein 60 [HSP60]) in patients with and without periodontitis. Additionally, the relationship between cFN and HSP60 expression with innate immunity activation and systemic inflammatory response (interleukin 6 [IL-6]) was also evaluated. METHODS: A case-controlled study was designed in which 30 patients with periodontitis (cases) and 30 age- and sex-matched participants without periodontitis (controls) were included. Fasting blood samples were collected to determine: (1) expression of TLR2N, TLR2M, TLR4N, and TLR4M by flow cytometry; and (2) serum concentrations of cFN, HSP60, and IL-6 by ELISA technique. RESULTS: Expression of TLR2M (411.5 [314.2, 460.0] vs. 236.5 [204.0, 333.0] AFU), TLR2N (387.0 [332.0, 545.5] vs 230.0 [166.2, 277.7] AFU), TLR4M (2478.5 [1762.2, 2828.0] vs 1705.0 [1274.5, 1951.2] AFU), and TLR4N (2791.0 [2306.7, 3226.2] vs. 1866.0 [1547.5, 2687.2] AFU) as well as serum levels of cFN (301.1 [222.2, 410.9] vs. 156.4 [115.3, 194.0] ng/ml) and IL-6 (10.4 [6.5, 11.5] vs. 3.5 [2.6, 4.9] pg/ml) were significantly higher in periodontitis patients than those without periodontitis. A positive association was found between periodontitis and cFN (odds ratio [OR] = 1.028, p < 0.001), TLR2N (OR = 1.026, p < 0.001), TLR4M (OR = 1.001, p = 0.002), and IL-6 (OR = 1.774, p < 0.001). CONCLUSIONS: Periodontitis patients exhibited high expression of TLRs, cFN, and IL-6.