Abstract Objectives In this study, the aim was to investigate the medium‐ to long‐term impact of peri‐implantitis treatment upon clinical parameters and implant stability quotient values and to ascertain if magnetic resonance frequency analysis can be used as a diagnostic tool to demonstrate postoperative healing following treatment of peri‐implantitis. Materials and Methods A total of n = 26 patients (n = 86 implants) diagnosed with peri‐implantitis were recruited for this prospective cohort study and four different treatment modalities were used. Baseline measurements of a number of clinical parameters as well as implant stability measurements in the form of ISQ were recorded. These measurements were repeated at 6, 12, and 24–36 months following treatment. Analysis of variance was performed for all implants treated as well as separately for each treatment modality. A regression model was also used to determine factors affecting ISQ measurements over time. Results Treatment of peri‐implantitis resulted in significant improvements of both average PPDs and BOP (p < .0001 and p < .01). ISQ values marginally improved initially for all treatment modalities, but improvement was only maintained for 2–3 years in treatment modalities I (+1.28), III (+1.49), and IV (+2.92). There was a statistically significant negative linear correlation between average PPD and the ISQ values recorded both at baseline (r = −.618, p < 0.0001) and at 2/3 years (r = −.604, p < 0.0001). Conclusion Over the 2–3‐year follow‐up period, all four treatment modalities led to improved clinical and radiographic peri‐implant parameters but implant stability posttreatment, as indicated by the fact that the recorded ISQ scores remained stable. As a result, use of MRFA as an adjunct to the traditionally used periodontal and radiographic tools for the evaluation of postoperative implant stability following the treatment of peri‐implant disease cannot be recommended.
LTF SNP rs1126478 (T>C) could modulate Lactoferrin function and release and has been associated with periodontal disease in different locations before, but not in America. Thus, this study aimed to assess the association between this SNP and Grade C Periodontitis (Generalized (PerioC-G) and Molar Incisor Pattern (PerioC-MIP)) and seek a relationship between its presence and LTF gingival crevicular fluid (GCF) production. Oral cells from 361 Brazilians and 375 North Americans patients (Diseased and Health Controls (PH) from both locations) were collected. DNA was extracted, and a prefabricated probe system determined rs116478 genotyping. Immunoenzymatic analysis detected LTF levels in GCF. Higher allelic altered-C frequency was associated with PerioC. For PerioC-G, CT and CC genotypes presented a frequency of 44.7
AIM:To (i) evaluate structured postgraduate part-time programs in periodontology, including those addressing peri-implant diseases, among members of the European Federation of Periodontology (EFP), (ii) the impact of the 2018 classification scheme and EFP clinical practice guidelines and (iii) propose a framework for periodontal vocational education and training. MATERIALS AND METHODS:A summary of relevant European guidelines for vocational education and training was compiled. In a survey and in a systematic review, current part-time programs in continuing professional education in periodontology as well as in prevention and management of peri-implant diseases were examined. The implementation and dissemination of the 2018 classification scheme and the EFP clinical practice guidelines were assessed by literature analysis. Based on these findings, a framework for periodontal vocational education and training was generated. RESULTS:Part-time programs for professional development in periodontology are established in nine EFP member countries. The systematic review identified lack of knowledge in prevention and management of peri-implant diseases among dental practitioners and hygienists. Continuing professional development was found to be important for education in prevention, classification and management of periodontal as well as peri-implant diseases. The proposed European framework consists of an escalator model with three levels (certificate, diploma and master). DISCUSSION:Considering the identified variation in the national programs, there is a need to improve education in periodontal and peri-implant diseases. The proposed framework will help harmonize the national structures. CONCLUSION:The proposed framework for part-time professional development is expected to enhance professional qualification.
BACKGROUND:The aim of the present study was to evaluate the subgingival microbiome in patients with grade C molar-incisor pattern periodontitis (C-MIP) affecting the primary or permanent dentitions. METHODS:DNA was isolated from subgingival biofilm samples from diseased and healthy sites from 45 C-MIP patients and subjected to phylogenetic microarray analysis. C-MIP sites were compared between children affected in the primary to those affected in the permanent dentitions. Within-subject differences between C-MIP-affected sites and dentition-matched healthy sites were also evaluated. RESULTS:C-MIP sites of subjects affected in the primary dentition showed partially overlapping but distinct microbial communities from C-MIP permanent dentition sites (p < 0.05). Differences were due to increased levels in primary C-MIP sites of certain species of the genera Capnocytophaga and Leptotrichia, while C-MIP permanent dentition sites showed higher prevalence of Filifactor alocis. Aggregatibacter actinomycetemcomitans (Aa) was among species seen in high prevalence and levels in both primary and permanent C-MIP sites. Moreover, both permanent and primary C-MIP sites showed distinct microbial communities when compared to dentition-matched healthy sites in the same subject (p < 0.01). CONCLUSIONS:Primary and permanent teeth with C-MIP showed a dysbiotic microbiome, with children affected in the primary dentition showing a distinct profile from those affected in the permanent dentition. However, Aa was enriched in both primary and permanent diseased sites, confirming that this microorganism is implicated in C-MIP in both dentitions.
BACKGROUND The aim of this study was to determine the clinical and inflammatory response patterns for individual siblings diagnosed with grade C molar-incisor pattern periodontitis (C-MIP) and between the related siblings within families. METHODS Sixty-nine siblings within 28 families with moderate-to-severe C-MIP were included. Clinical parameters were evaluated for symmetry regarding the affected type of teeth, side and/or arch, and bone loss pattern. The protein concentrations from in vitro whole blood cultures for 14 different lipopolysaccharide-stimulated inflammatory markers were correlated with the extent and severity of disease, within an individual sibling and among siblings within a family. RESULTS A similar disease pattern was observed among all siblings and within families. The most common teeth affected were first molars and incisors or first molars only within the permanent dentition and only molars within the primary dentition (p < 0.001). Symmetry involving molars was higher than in incisors in siblings, regardless of arch or side affected (p = 0.020). Arc-shape/vertical bone defects were the most common (p = 0.006) and higher symmetry was found for these defects in the permanent dentition (p = 0.005). Positive correlations were found between age, clinical attachment loss, and percent affected sites with several inflammatory markers. The inflammatory responses for several inflammatory markers were correlated among within and among families (p < 0.050). Specifically, the intraclass correlation coefficient within families was highest (>0.5) for interleukin (IL)-8, IL-6, and IL-10. CONCLUSIONS Families with C-MIP presented similar patterns of disease. The level of an inflammatory response to bacteria seemed to play a role in the extent and severity of this disease, exemplified by the high degree of correlation in these families.
##Statement of Problem: Concerns were raised that referrals to the Dublin Dental University Hospital (DDUH) Periodontology Department often lacked sufficient information for triaging. ##Purpose of the Study: To investigate the quality of periodontal referrals when compared with a local standard and examine if the use of the existing divisional referral proforma was associated with a higher standard of referral. ##Materials and methods: Data was collected by retrospectively auditing 150 external referrals to the DDUH Periodontology Department at representative intervals over a 12-month period. Referrals were assessed to investigate if they included 22 information points as requested by our local standard (referral proforma). Data was input into a Microsoft Excel spreadsheet and analysed. Ten periodontal referrals proforma from similar Dental Institutes across Ireland and the UK were also compared to our proforma to investigate if our institution requests a similar level of information to others. ##Results: Referral analysis indicated that clinicians provided on average 12.9 out of 22 (59%) items of required information in their referral correspondence. Referrers utilised the appropriate referral proforma in 28% of cases. Use of this proforma was associated with a better standard of referral (17.9 out of 22 required information items provided, 80%) when compared with non-proforma referrals (11.2 out of 22 required information items provided, 51%). Analysis of other institutions’ proforma highlighted that DDUH requests referring practitioners to include more information than equivalent peer institutions. ##Conclusion: Periodontal referral letters to DDUH frequently fail to include sufficient information. Practitioners seldom utilise the divisional referral proforma, although its use is associated with improved referral quality. Simplification of the existing referral proforma and dissemination of referral guidelines to practitioners is recommended moving forward.
In 2020, the European Federation of Periodontology published an S3-level clinical practice guideline for the management of Stage I-III periodontitis. This guideline discusses four steps of periodontal therapy and provides 62 individual recommendations for prevention and management of disease. Supporting information about the strength of recommendation and level of consensus for each recommendation is also provided. The S3 guideline represents a major milestone in the specialty, and is likely to play a major role in enhancing and standardising the approach to periodontal care among educators and clinicians. This article provides a review of the meeting framework and a commentary on the clinical practice guideline, highlighting key recommendations of interest to the dental team in each treatment step. Corresponding
Necrotising periodontal diseases (NPDs) are a group of infectious diseases that include necrotising gingivitis (NG), necrotising periodontitis (NP) and necrotising stomatitis (NS). These three clinical presentations may represent different stages of a continuum of the same disease process, with shared aetiological factors, and broadly similar initial clinical features and treatments. The term ‘ulcerative’ is no longer used in classification as ulceration is considered secondary to the gingival necrosis present. NP may result in destruction of periodontal ligament and supporting bone, while in NS, destruction progresses to deeper tissues such as the lip, cheeks and tongue. These presentations are more frequently seen in patients with HIV/AIDS or other systemic/immune compromise and, in developing countries, among those with severe malnourishment, respectively. In an Irish context, NG will represent the most common clinical form seen in general dental practice and may present as an acute condition requiring urgent management. Consequently, the current review will focus on NG. Table 1 provides an overview of the key aspects of NG.
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).
Aim 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. Material and methods 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). Results TICAM-1(TRIF),FOS,IRAK1,TLR2andCCL2genes 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. Conclusions 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.
Aim: This study evaluated the influence of periodontal therapy on the microbiological profile of individuals with Grade C Molar-Incisor Pattern Periodontitis (C/MIP). Methods: Fifty-three African-American participants between the ages of 5–25, diagnosed with C/MIP were included. Patients underwent full mouth mechanical debridement with systemic antibiotics (metronidazole 250 mg + amoxicillin 500 mg, tid, 7 days). Subgingival samples were collected from a diseased and a healthy site from each individual prior to treatment and at 3, 6, 12, 18 and 24 months after therapy from the same sites. Samples were subjected to a 16S rRNA gene based-microarray. Results: Treatment was effective in reducing the main clinical parameters of disease. Aggregatibacter actinomycetemcomitans (A.a.) was the strongest species associated with diseased sites. Other species associated with diseased sites were Treponema lecithinolyticum and Tannerella forsythia. Species associated with healthy sites were Rothia dentocariosa/mucilaginosa, Eubacterium yurii, Parvimonas micra, Veillonella spp., Selenomonas spp., and Streptococcus spp. Overall, treatment was effective in strongly reducing A.a. and other key pathogens, as well as increasing health-associated species. These changes were maintained for at least 6 months. Conclusions:Treatment reduced putative disease-associated species, particularly A.a., and shifted the microbial profile to more closely resemble a healthy-site profile. (Clinicaltrials.gov registration #NCT01330719).
OBJECTIVE:The purpose of this study was to investigate involvement of the P2X7 receptor in the rare condition, localized aggressive periodontitis. MATERIAL AND METHODS:Peripheral blood from 220 African Americans (103 with localized aggressive periodontitis and 117 healthy unrelated controls) was stimulated with lipopolysaccharide from E coli 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. RESULTS: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. CONCLUSION:The data from these analyses support a possible biological relationship between P2RX7 genetic variants and inflammatory response in localized aggressive periodontitis patients.
Background: Previous studies have provided substantial evidence of the association of Aggregatibacter actinomyce-temcomitans, and its highly leukotoxic JP2 genotype, with localized aggressive periodontitis (LAgP). The present study aims to evaluate presence of JP2 in individuals with LAgP after periodontal treatment. Methods: Sixty African-American patients with LAgP, aged 5 to 25 years, were examined. At baseline, probing depth (PD), clinical attachment level (CAL), bleeding on probing, and plaque index were measured, and subgingival plaque was collected from LAgP diseased and healthy sites for each participant. Patients received whole-mouth ultrasonic debridement, scaling and root planing, and a 7-day prescription of amoxicillin and metronidazole. Participants were reevaluated and resampled and received regular maintenance therapy at 3, 6, and 12 months after treatment. Polymerase chain reaction was used to detect presence of the JP2 genotype before and after treatment. Results: At baseline, the JP2 sequence was identified in 75% of LAgP diseased sites and in 56.67% of healthy sites. At 3, 6, and 12 months after treatment, the number of patients was 40, 31, and 31, respectively, and JP2 detection decreased to 17.5%, 6.45%, and 3.23%, respectively, in diseased sites (P <0.001) and to 2.5%, 3.23%, and 0%, respectively, in healthy sites (P <0.001). Clinical parameters of disease were also significantly reduced after therapy (P <0.001). Additionally, significant correlations were observed between JP2 presence and mean PD (P<0.002) and CAL (P <0.001), after therapy. Conclusion: Periodontal therapy was successful in reducing clinical parameters of LAgP and subgingival presence of JP2 in diseased and healthy sites.
AIM To evaluate long-term clinical response to periodontal therapy and maintenance in localized aggressive periodontitis (LAP). MATERIALS AND METHODS One hundred forty-one African Americans diagnosed with LAP, aged 5-25 years, 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 24 months, 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. RESULTS Periodontal therapy significantly improved probing depth and clinical attachment level up to 4 years (mean reductions: 2.18 ± 1.03 and 2.80 ± 1.43 mm, respectively). Percentage of affected sites was reduced at all time points and maintained up to 4 years. 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. CONCLUSIONS 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 4 years. LAP in permanent dentition may be preceded in the primary dentition. Clinicaltrials.gov #NCT01330719.
BACKGROUND:The comparative treatment response of children and young adults with localized aggressive periodontitis treatment (LAgP) affecting primary and permanent dentition is unknown. The objective of this study is to evaluate the influence of non-surgical periodontal therapy with adjunctive systemic antibiotics on the clinical outcome of children and young adults with primary versus permanent dentition affected by LAgP. METHODS:A cohort of 97 African American participants aged 5 to 21 years (30 males and 67 females; 22 primary and 75 permanent dentitions affected) diagnosed with LAgP were included. Patients presented with no significant medical history. All patients underwent periodontal therapy, which consisted of full-mouth mechanical debridement at baseline and the 3-, 6-, and 12-month appointments. Additionally, all patients were prescribed a 1-week regimen of systemic antibiotics at the initial appointment. Clinical parameters were analyzed, including probing depth, clinical attachment level (CAL), bleeding on probing, and percentage of visible plaque. RESULTS:Overall, periodontal therapy was found to be effective in improving the clinical outcomes of both primary and permanent dentitions. Although baseline CALs were similar between the groups, the reduction in mean CAL at 3, 6, and 12 months and reduction in percentage plaque at 3 months were significantly greater in primary dentition compared with permanent dentition. CONCLUSIONS:Non-surgical therapy with systemic antibiotics is effective for LAgP in both primary and permanent dentitions. A greater reduction in CAL in LAgP of primary dentition may suggest that younger children may carry a greater propensity for positive treatment outcomes and healing potential compared with children/young adults with permanent dentition.
BACKGROUND:Matrix metalloproteinases (MMPs) are a family of host-derived proteinases reported to mediate multiple functions associated with periodontal breakdown and inflammation. High MMP levels in African-American children with localized aggressive periodontitis (LAgP) have been reported previously by the present authors. However, little is known about MMP reductions in gingival crevicular fluid (GCF) after therapy. This study aims to evaluate MMP levels in the GCF after treatment of LAgP and to correlate these levels with clinical response. METHODS:GCF samples were collected from 29 African-American individuals diagnosed with LAgP. GCF was collected from one diseased site (probing depth [PD] >4 mm, bleeding on probing [BOP], and clinical attachment level ≥ 2 mm) and one healthy site (PD ≤ 3 mm, no BOP) from each individual at baseline and 3 and 6 months after periodontal treatment, which consisted of full-mouth scaling and root planing (SRP) and systemic antibiotics. The volume of GCF was controlled using a calibrated gingival fluid meter, and levels of MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 were assessed using fluorometric kits. RESULTS:MMP-1, MMP-8, MMP-9, MMP-12, and MMP-13 levels were reduced significantly up to 6 months, comparable to healthy sites at the same point. Significant correlations were noted between MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 levels and percentage of sites with PD >4 mm. MMP-3, MMP-12, and MMP-13 levels also correlated with mean PD of affected sites. CONCLUSION:Treatment of LAgP with SRP and systemic antibiotics was effective in reducing local levels of specific MMPs in African-American individuals, which correlated positively with some clinical parameters.
The objective of this study was to characterize the subgingival microbiota of African-American children with Localized Aggressive Periodontitis (LAP). Fifty-one children were included. Subgingival plaque samples were taken from diseased (DD) and healthy sites (DH) in LAP and from healthy sites in HS and HC and analyzed by 16S rRNA-based microarrays. Aggregatibacter actinomycetemcomitans (Aa) was the only species found to be both more prevalent (OR = 8.3, p = 0.0025) and abundant (p < 0.01) in DD. Filifactor alocis (Fa) was also found to be more prevalent in DD (OR 2.31, CI 1.06-5.01, p = 0.03). Most prevalent species in healthy sites were Selenomonas spp, Veillonella spp, Streptococcus spp, Bergeyella sp, and Kingella oralis. Overall, Streptococcus spp, Campylobacter gracilis, Capnocytophaga granulosa, Haemophilus parainfluenzae, and Lautropia mirabilis were most abundant in healthy children, while Aa, Fa, Tannerella sp, Solobacterium moorei, Parvimonas micra, and Capnocytophaga sp were most abundant in LAP. Based on a comprehensive analysis with 16S rRNA-based microarrays, Aa was strongly associated and site-specific in LAP. In contrast, other species were found to be associated with healthy sites and individuals (ClinicalTrials.gov number CT01330719). Abbreviations: healthy site in healthy sibling (HS); healthy site in healthy control child (HC).