Search

In cases of aggressive periodontal bone destruction, subgingival microbial analysis should be done, tooth extractions should be planned to control disease progression if non‐surgical periodontal treatment is ineffective. [ABSTRACT FROM AUTHOR]

An efficient synthesis of pyrimidines and pyridines has been developed from readily available aromatic ketones, aldehydes and ammonium salts under transition-metal-free conditions. In this strategy, ammonium salts were used as nitrogen sources and only water was generated as a nontoxic byproduct. A catalytic amount of NaIO4 played an important role in the selectivity control, whereas substituted pyridines were dominantly formed in its absence. [ABSTRACT FROM AUTHOR]

Objectives: To compare the periodontal and peri‐implant conditions of Chinese patients with a history of moderate or severe periodontitis and periodontally healthy patients (PHP); to evaluate the influence of maintenance therapy frequency on the outcome of implant therapy. Methods: A total of 140 participants with 227 sand‐blasted acidetched (SLA) implants were divided into three groups: PHP, moderate periodontally compromised patients (PCP) and severe PCP. The three groups were further categorized into two groups based on the frequency of maintenance (MF): MF ≥ 1 per year and MF < 1 per year. The following clinical parameters of implants were assessed: implant survival/loss, peri‐implant probing depth (PDi), peri‐implant bleeding index (BIi), peri‐implant bleeding on probing (BOPi), implant bone loss (BLi). Comparisons of the peri‐implant conditions were performed between the patients with different periodontal conditions. Results: Implant survival rate was 100% for all three groups. The severe PCP group showed significantly higher deepest PDi, mean PDi, mean BIi, and PLIi compared with PHP (p < 0.05). The severe PCP group had more implants affected with PDi ≥ 5 mm and BOPi+ compared with the PHP group (Adjusted OR = 10.89, 95% CI: 2.34, 50.74). In the patients with severe PCP, the MF < 1 per year group had a greater prevalence of PDi ≥ 5 mm and BOPi+ compared with the MF ≥ 1 per year group (Adjusted OR = 8.23, 95% CI: 2.44, 27.78). Conclusions: The patients in the severe PCP group were at greater risk of peri‐implant disease than those in the PHP group. In particular, severe PCP who had poor adherence to maintenance care showed a higher incidence of biologic complications. [ABSTRACT FROM AUTHOR]

Objectives To evaluate the influence of implant-abutment interface ( IAI) placement depth on bone remodeling around implants with two different types of tapered internal IAI: screwed-in ( SI) and tapped-in ( TI) connections in dogs. Materials and methods Eight weeks post mandibular tooth extraction in six beagle dogs, two SI implants (OsseoSpeed™, Astra Tech, DENTSPLY) and two TI implants (Integra- CP™, Bicon LLC) were placed in one side of the mandible. The four experimental groups were as follows: (i) SI-placed equicrestally ( SIC); (ii) TI-placed equicrestally ( TIC); (iii) SI-placed 1.5 mm subcrestally ( SIS); and (iv) TI-placed 1.5 mm subcrestally ( TIS). Healing abutments were connected 12 weeks after implant placement. Sixteen weeks later, the dogs were sacrificed and histomorphometric analysis was performed. Histometrical outcomes were evaluated using a nonparametric Brunner-Langer model. Results Mean distance from the IAI to first bone-implant contact (IAI- fBIC) was 0.88 mm (median: 0.77; SD: 0.54) for SIC group, 1.23 mm (median: 1.22; SD: 0.66) for TIC group, 0.41 mm (median: 0.31; SD: 0.36) for SIS group, and 0.41 mm (median: 0.26; SD: 0.45) for TIS group. Subcrestal groups showed lower IAI- fBIC compared with equicrestal groups ( P < 0.001). Connective tissue presented similar measurements regardless of the IAI placement depth and IAI type ( P > 0.05), but the epithelium length and peri-implant soft tissue length in subcrestal groups were significant larger than that in the equicrestal groups ( P < 0.001 and P = 0.004, respectively). Conclusion Subcrestal implant placement with tapered internal IAI is beneficial for bone contact with the implant neck, and concurrently, it may not increase the soft tissue inflammation around IAI. [ABSTRACT FROM AUTHOR]

Periodontitis has become the leading cause of tooth loss in adults, and the host's immunologic and inflammatory response to the bacteria can lead to periodontal destruction. In patients with periodontitis, platelets possess an increased activation status compared with platelets from healthy controls. Mean platelet volume (MPV) has been considered an important index of platelet activity and an inflammatory marker in many infectious diseases. The present study investigated the relationship between MPV and disease activity in subjects with severe periodontitis. Forty-five patients with periodontitis and 45 age and sex-matched healthy subjects were enrolled into the study. All subjects received periodontal and hematological examinations. The periodontitis patients were administered active periodontal treatment (APT). At baseline, a statistically significant decrease in MPV was noted in patients with periodontitis (9.73 ± 1.06 fL) compared with healthy controls (10.24 ± 1.07 fL). At 1 month post-APT, MPV was substantially increased (10.11 ± 1.04 fL). Positive correlation was found between increase of MPV and decrease of periodontal probing depth after treatment( r = 0.377; p = 0.014). In conclusion, the decrease of MPV was related to the severe periodontal inflammation, and the value inversed shift after APT. MPV might reflect the disease activity of periodontitis. [ABSTRACT FROM AUTHOR]

The article presents a study to review researches on families with aggressive periodontitis and to determine the use of genetic analytical tools in periodontology. It says that genetic analysis methods such as pedigree analysis, linkage, and segregation analysis can be utilized to examine the modes of inheritance of aggressive periodontitis within the family. The study concludes that genetic factors are significant in the susceptibility of siblings and pedigree members to the disease by 40-50%.

Abstract: Objective: Human periodontal ligament cells (hPDLCs) may play an important role in osteoclastogenesis in alveolar bone by expressing the receptor activator of NF-KappaB ligand (RANKL) and osteoprotegerin (OPG). The present study aimed to investigate the differences between the effects of osteogenic induction and 1,25-dihydroxyvitamin D3 (VD3) on hPDLC proliferation and the expression of RANKL, osteoprotegerin, and the vitamin D receptor (VDR) in hPDLCs. Methods: Primary cultures of 11 hPDLC populations from 11 donors were obtained. Three samples of each hPDLC population from passage 3 were, respectively, treated with osteogenic induction medium, 10−8 M VD3, or vehicle as a control. Cell proliferation at days 0, 1, 3, 5, and 7 was estimated with the MTT method. At day 6, the mRNA levels of RANKL, OPG and VDR were determined with real-time RT-PCR. Results: Osteogenic induction significantly promoted hPDLC proliferation, while VD3 inhibited proliferation. Osteogenic induction significantly down-regulated the mRNA level of RANKL by 1.61-fold (P =0.033) and decreased the level of VDR by 2.13-fold (P =0.003), while there was no change in the level of OPG and OPG/RANKL ratio with osteogenic induction. On the contrary, VD3 significantly up-regulated the level of RANKL by 9.58-fold (P =0.001) and increased the level of VDR by 3.15-fold (P =0.004), while down-regulating the OPG/RANKL ratio by 7.14-fold (P =0.004). Conclusion: Osteogenic induction and VD3 exert opposite effects in regulating hPDLC proliferation and mRNA expression of RANKL and VDR. This may induce hPDLCs to play different roles in alveolar bone metabolism. [Copyright &y& Elsevier]

El artículo trata factores que determinan la susceptibilidad del hospedador en la periodontitis agresiva. Informa que se considera que varios tipos de periodontitis agresiva pueden heredarse de manera mendeliana y que esta herencia puede ocurrir mediante el cromosoma X y la autósomica. Concluye que la periodontitis es una enfermedad compleja en que se implican una combinación de factores genéticos y ambientales.

The article examines the host susceptibility factors in patients with aggressive periodontitis disease. The factors studied include single nucleotide polymorphisms, family aggregation, polymorphonuclear neutrophils, antibodies to bacteria, smoking, stress and herpesvirus infections. The article also studies the effect of genes and environmental factors in the susceptibility of aggressive periodontitis.

ABSTRACT Objectives Materials and Methods Results Conclusions Trial Registration To compare the 5‐year outcomes of collagen matrix (CM) and free gingival graft (FGG) used to augment the keratinized mucosa (KM) around posterior dental implants.Thirty patients (44 implants) with inadequate KM (< 2 mm) on posterior dental implants were randomized into two groups that received KM augmentation with CM or FGG. Clinical measurements comprising the KM width (KMW), buccal mucosal thickness (MT), and clinical parameters were examined in a 5‐year follow‐up. Marginal bone loss (MBL) was evaluated with standardized radiographs using the paralleling technique. Patient‐reported outcomes (PROs) during the first week post‐surgery and at the 5‐year follow‐up were evaluated.KMW increased significantly during the follow‐up period in both groups. The FGG group had a significantly greater KMW than the CM group at the 1, 2‐month follow‐up and after the 6‐month follow‐up. KM shrinkage was observed, and was greatest within the first 2 months post‐surgery in both groups. At the 5‐year follow‐up, the KM shrinkage was significantly different between the groups (FGG: 47%; CM: 70%) (p < 0.01). The MT increased significantly in the FGG group. The clinical parameters and MBL were similar between the groups. The bleeding score in the FGG group was higher than that in the CM group (p < 0.05) within the first 2 days post‐surgery, while other PROs scores were similar between groups in the first week post‐surgery. At 5‐year follow‐up, all patients were highly satisfied with the treatments.FGG was superior to CM in terms of the KM augmentation and MT increase. Except for a slight difference in self‐reported bleeding during the first two post‐operative days, CM didn't demonstrate other significant advantages in PROMs.ChiCTR1800018285 (date of registration: 9/9/2018, retrospectively registered. URL: https://www.chictr.org.cn/showproj.html?proj=24156) [ABSTRACT FROM AUTHOR]

The article focuses on the perspective of periodontology by researchers in the Asian region. It states the traditional approaches practiced by Indian and Chinese cultures to periodontal treatment such as the use of traditional medicines. It discusses the epidemiological data which shows that some of the adult population have periodontal destruction. Moreover, it presents the connection between periodontal disease and systemic conditions.

Aim: To develop a nomogram‐based predictive model of tooth survival by comprehensively analysing clinical and radiographic risk factors of tooth loss (TL). Materials and Methods: In this study, 3447 teeth of 131 subjects who underwent non‐surgical periodontal treatment were examined retrospectively within a mean follow‐up period of 11.6 years. The association of risk factors including clinical and radiographic parameters with TL was assessed using univariate and multivariate Cox regression analyses. A nomogram‐based predictive model was developed, and its validation and discriminatory ability were analysed. Results: In all, 313 teeth were lost in 94 patients in this study (overall tooth loss [OTL] 9.08%; 0.21 teeth/patient/year). Male, heavy smoking, molar teeth, probing depth (PD), attachment loss (AL), tooth mobility and radiographic bone loss were significantly associated with TL (p <.05). A gradient effect of tooth mobility on TL increased from degree I to III versus none (p <.0001). The area under the curve (AUC) of the model was 0.865. Calibration curve and decision curve analysis demonstrated good performance and high net benefit, respectively. Conclusions: Adopting a specific nomogram could facilitate the prediction of tooth survival and the development of tailored treatment plans in Chinese patients with advanced periodontitis. [ABSTRACT FROM AUTHOR]

Butyrate, a four‐carbon short‐chain fatty acid (SCFA), is a metabolite of anaerobic bacteria. Butyrate has primarily been described as an energy substance in the studies on the digestive tract. The multiple mechanisms of its protective function in the gut and on underlying diseases (including metabolic diseases, diseases of the nervous system, and osteoporosis) via interaction with intestinal epithelial cells and immune cells have been well documented. There are many butyrogenic bacteria in the oral cavity as well. As essential components of the oral microbiome, periodontal pathogens are also able to generate butyrate when undergoing metabolism. Considerable evidence has indicated that butyrate plays an essential role in the initiation and perpetuation of periodontitis. However, butyrate is considered to participate in the pro‐inflammatory activities in periodontal tissue and the reactivation of latent viruses. In this review, we focused on the production and biological impact of butyrate in both intestine and oral cavity and explained the possible pathway of various diseases that were engaged by butyrate. Finally, we suggested two hypotheses, which may give a better understanding of the significantly different functions of butyrate in different organs (i.e., the expanded butyrate paradox). [ABSTRACT FROM AUTHOR]

Background: The influence of vertical soft tissue thickness on health of peri‐implant tissue has been addressed in few studies; thus, further research is needed. Purpose To evaluate the influence of vertical soft tissue thickness on the risk of peri‐implantitis and peri‐implant condition in patients with a history of periodontitis. Design/Methods: A total of 92 patients with a history of periodontitis were included in this study. During the implant placement, the distance from palatal soft tissue edge to the alveolar crest, which was defined as vertical soft tissue thickness, was measured. The characteristics of patients and implants were recorded at baseline (T1). After more than 2 years follow‐up period, 65 patients with 159 implants finally came back for T2 evaluation, and parameters of peri‐implant tissue were recorded. The associations of vertical soft tissue thickness with peri‐implant parameter and occurrence of peri‐implantitis were analyzed using the generalized estimating equation accompanying linear regression and logistic regression. In addition to conventional multivariate analysis, a propensity score for adjustment was used to reduce confounding bias. Results: At follow‐up examination (T2), survival rate at implant‐level was 98.8%. The peri‐implant parameters, including peri‐implant probing depth and marginal bone loss, increased significantly with the increasing of soft tissue thickness (P < 0.05) after adjusting for a propensity score. In multivariate analysis adjusted for different confounding factors and propensity score, the odd ratios were all approximately 2.5, which meant that the risk of peri‐implantitis increased 1.5 times for 1 mm increase of soft tissue thickness. Conclusions: The excessive vertical soft tissue thickness around implants in patients with history of periodontitis has an adverse influence on health of the peri‐implant tissue. This observation raises an important question on the association between vertical soft tissue thickness during implant surgery and history of periodontitis. Effective approaches to prevent the adverse effect of excessive soft tissue thickness on peri‐implant tissue are necessary to be further investigated. [ABSTRACT FROM AUTHOR]

Aim: To identify risk variants associated with gene expression in peripheral blood and to identify genes whose expression change may contribute to the susceptibility to periodontitis. Material and Methods: We systematically integrated the genetic associations from a recent large‐scale periodontitis GWAS and blood expression quantitative trait loci (eQTL) data using Sherlock, a Bayesian statistical framework. We then validated the potential causal genes in independent gene expression data sets. Gene co‐expression analysis was used to explore the functional relationship for the identified causal genes. Results: Sherlock analysis identified 10 genes (rs7403881 for MT1L, rs12459542 for SIGLEC5, rs12459542 for SIGLEC14, rs6680386 for S100A12, rs10489524 for TRIM33, rs11962642 for HIST1H3E, rs2814770 for AIM2, rs7593959 for FASTKD2, rs10416904 for PKN1, and rs10508204 for WDR37) whose expression may influence periodontitis. Among these genes, AIM2 was consistent significantly upregulated in periodontium of periodontitis patients across four data sets. The cis‐eQTL (rs2814770, ~16 kb upstream of AIM2) showed significant association with AIM2 (p = 6.63 × 10–6) and suggestive association with periodontitis (p = 7.52 × 10–4). We also validated the significant association between rs2814770 and AIM2 expression in independent expression data set. Pathway analysis revealed that genes co‐expressed with AIM2 were significantly enriched in immune‐ and inflammation‐related pathways. Conclusion: Our findings implicate that AIM2 is a susceptibility gene, expression of which in gingiva may influence periodontitis risk. Further functional investigation of AIM2 may provide new insight for periodontitis pathogenesis. [ABSTRACT FROM AUTHOR]

Aim: To investigate the role of platelets during the development of ligature‐induced experimental periodontitis in mice. Materials and Methods: Experimental periodontitis was induced by placement of sterilized 5‐0 cotton ligatures around the maxillary and mandibular second molars of C57BL/6 wild‐type mice. Flow cytometry was used to analyse platelet activation and platelet–leucocyte aggregate formation, and histologic analysis was used to evaluate inflammation and localization of platelets and leucocytes in periodontal tissues during the development of experimental periodontitis and in experimental periodontitis with and without antiplatelet drug treatment. Results: Experimental periodontitis induced platelet activation and platelet–leucocyte interaction. Platelets and leucocytes gradually infiltrated in inflammatory gingival tissues during the development of experimental periodontitis. The inhibition of platelet activation via drug therapy led to significant inhibition of leucocyte migration and marked reduction in periodontal inflammation. Conclusion: This study revealed that platelets are critical for inflammation and tissue injury in periodontitis and serve as mediators of inflammation in periodontal tissue. [ABSTRACT FROM AUTHOR]

Aim: To investigate the effects of sodium butyrate (NaB) and lipopolysaccharide (LPS) on gingival epithelial barrier. Material and methods: We cultured human primary gingival epithelial cells and investigated the effects of NaB and LPS on gingival epithelial barrier and involved mechanisms at in vitro and in vivo levels by immunostaining, confocal microscopy, field emission scanning electron microscopy (FE‐SEM), transmission electronic microscopy (TEM), transepithelial electrical resistance (TEER), FTIC‐dextran flux, flow cytometry, real‐time PCR and Western blot assays. Results: Our results showed that NaB, rather than LPS, destroyed the epithelial barrier by breaking down cell–cell junctions and triggering gingival epithelial cell pyroptosis with characteristic morphological changes, including swollen cells, large bubbles, pore formation in the plasma membrane and subcellular organelles changes. The upregulated expression of pyroptosis‐related markers, caspase‐3 and gasdermin‐E (GSDME) contributed to this effect. Pyroptosis aroused by NaB is a pro‐inflammatory cell death. Pyroptotic cell death provoked inflammatory responses by upregulation of IL‐8 and MCP‐1, and releasing intracellular contents into the extracellular microenvironment after pyroptotic rupture of the plasma membrane. Conclusions: Our new findings indicate that butyrate is a potent destructive factor of gingival epithelial barrier and pro‐inflammatory mediator, which shed a new light on our understanding of periodontitis initiation. [ABSTRACT FROM AUTHOR]

Aim To investigate the relationship between inflammatory markers and platelet size in generalized aggressive periodontitis ( GAgP). Material and Methods Periodontal, inflammatory and platelet indices were compared between 59 GAgP patients and 59 healthy subjects. Gingival biopsies from five patients and five healthy subjects were examined by immunohistochemistry and electron microscopy. Changes in patient periodontal and platelet indices were re-evaluated at 3 months after periodontal therapy. Results Platelet size was decreased significantly in GAgP patients compared to healthy subjects ( p ≤ 0.003). Weak negative correlations between platelet size and periodontal parameters were found in GAgP patients ( p ≤ 0.025). Platelet aggregates and adhesion to the endothelium or leucocytes were found in venules and connective tissues of gingival biopsies from GAgP patients. Mean platelet volume ( MPV) and platelet large cell ratio increased after periodontal therapy in GAgP patients ( p ≤ 0.038). The increase in MPV was related to the decrease in bleeding index in GAgP patients after periodontal therapy ( p < 0.001; r = 0.357). Conclusion Platelet size was reduced in GAgP patients compared to healthy controls, possibly due to the consumption of large platelets at sites of periodontal inflammation. Platelets may be involved in host responses to periodontal infection in GAgP. [ABSTRACT FROM AUTHOR]

Aim: To develop and validate models based on logistic regression and artificial intelligence for prognostic prediction of molar survival in periodontally affected patients. Materials and Methods: Clinical and radiographic data from four different centres across four continents (two in Europe, one in the United States, and one in China) including 515 patients and 3157 molars were collected and used to train and test different types of machine‐learning algorithms for their prognostic ability of molar loss over 10 years. The following models were trained: logistic regression, support vector machine, K‐nearest neighbours, decision tree, random forest, artificial neural network, gradient boosting, and naive Bayes. In addition, different models were aggregated by means of the ensembled stacking method. The primary outcome of the study was related to the prediction of overall molar loss (MLO) in patients after active periodontal treatment. Results: The general performance in the external validation settings (aggregating three cohorts) revealed that the ensembled model, which combined neural network and logistic regression, showed the best performance among the different models for the prediction of MLO with an area under the curve (AUC) = 0.726. The neural network model showed the best AUC of 0.724 for the prediction of periodontitis‐related molar loss. In addition, the ensembled model showed the best calibration performance. Conclusions: Through a multi‐centre collaboration, both prognostic models for the prediction of molar loss were developed and externally validated. The ensembled model showed the best performance in terms of both discrimination and validation, and it is made freely available to clinicians for widespread use in clinical practice. [ABSTRACT FROM AUTHOR]

Aim: To explore the immunological defensive effects of platelets on periodontal pathogens in the gingival crevicular fluid (GCF). Materials and Methods: GCF samples were collected from 20 patients with periodontitis and 10 healthy controls. Platelets in the GCF were detected by immunocytochemistry and immunofluorescence. Isolated platelets from healthy volunteers were co‐cultured with Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn). The interactions between platelets and periodontal pathogens were observed by transmission and scanning electron microscopy. The isolated platelets plus neutrophils were co‐cultured with Pg or Fn, and the formation of neutrophil extracellular traps (NETs) was evaluated by staining with Sytox Green. Results: The platelet level in the GCF was higher in patients with periodontitis than in healthy controls. Platelets interacted with bacteria and neutrophils in the GCF. In vitro, platelets recruited and engulfed periodontal pathogens. In response to periodontal pathogens, neutrophils released web chromatin, and platelets promoted the formation of intensive NETs. Conclusions: Platelets, migrating to the gingival sulcus, may exert direct antibacterial effects or assist neutrophils. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the clinical and radiographic outcomes of 6‐mm short implants, placed in the posterior jaws and supporting splinted crowns, at 5 years after early loading. Materials and Methods: Forty‐five patients with 95 implants (diameter: 4 mm; length: 6 mm) were enrolled at three centres. Two to three implants were placed in either the maxillary or the mandibular posterior region in each patient and restored with screw‐retained splinted crowns at 6 weeks later. Clinical and radiographic outcomes were evaluated at implant placement, at loading, and at 6, 12, 24, 36, and 60 months after loading. Biological and mechanical complications were recorded. Marginal changes in bone level in relation to clinical parameters were evaluated using a generalized linear mixed model. Results: During the 5 years of follow‐up, the mean change in the marginal bone level (MBL) was 0.04 ± 0.14 mm. Four implants in four patients were lost before loading, one implant in one patient was lost at the 5‐year follow‐up, and two patients were lost to follow‐up. The survival and success rates were 88.4% (38/43) at the patient level. The incidence rates of peri‐implant mucositis and peri‐implantitis were 29.4% and 7.0%, respectively. The rate of technical complications was 14.0%. Conclusions: Over a 5‐year period, 6‐mm short implants supporting early loaded splinted crowns in maxillary or mandibular posterior regions showed stable MBLs and acceptable technical and biological complication rates. [ABSTRACT FROM AUTHOR]

Aim: To investigate the dynamic changes of peri‐implant microbiome in patients with a history of periodontitis and to construct a microbial prediction model. Materials and methods: The prospective study was performed at one month (T1), one year (T2) and two years (T3) after restoration. Clinical examinations [probing depth (PD), bleeding on probing (BOP), suppuration (SUP)], radiographic examinations and sample collection were conducted at three timepoints. Peri‐implant sulcular fluid (PISF) was collected and analysed by 16S rRNA gene sequencing. Generalized linear mixed model (GLMM) was used to identify differences. Results: Totally, 168 subjects were assessed for eligibility. Twenty‐two patients were recruited in the longitudinal study. Eventually, 67 PISF samples from 24 implants of 12 patients were collected and analysed. Peri‐implant microbiome showed increasing diversity and complexity over time. Disease‐associated genera Porphyromonas, Tannerella, Treponema and Prevotella dramatically increased from T1 to T3. The prediction model for clinical suppuration at T1 showed a high accuracy of 90%. Conclusion: The dysbiosis of peri‐implant microbiome increased with time during the two‐year observation in patients with a history of periodontitis. Genera of Porphyromonas, Tannerella, Treponema and Prevotella were biomarkers of peri‐implant mucositis. Microbiota at the early stage could predict subsequent microbial dysbiosis and clinical suppuration. [ABSTRACT FROM AUTHOR]

Aim: To evaluate periodontal conditions in adults in mainland China based on data from the 4th National Oral Health Survey. Materials and methods: Data of adult subjects (35‐ to 44‐year‐old group [N = 4409], 55‐ to 64‐year‐old group [N = 4622], and 65‐ to 74‐year‐old group [N = 4428]) were analysed. Demographic, socio‐economic, personal habit, dental history, and health attitude data were obtained using a questionnaire. Periodontal condition was assessed using the standardized case definitions of the 2018 classification scheme. A multivariate analysis was performed to investigate the relationship between periodontitis severity and age, smoking status, gender, and region using generalized additive models after adjusting for confounders. Results: The frequency of subjects with periodontitis was 52.8%, 69.3%, and 64.6% in the three age groups, respectively. The frequency of subjects with severe periodontitis (stage III or IV) was 10.6%, 37.3%, and 43.5% in the three age groups, respectively. The severity of periodontal disease was positively associated with age. Current and former smokers exhibited significantly greater disease severity than non‐smokers after adjustment for confounders. No significant difference of severity was found between males and females. Conclusion: Within the limitations of the study, the prevalence of periodontitis is very high among adults in mainland China. Periodontal status is associated with age and smoking status. [ABSTRACT FROM AUTHOR]

Aims: To develop a nomogram prediction model of mandibular molar survival by comprehensively analysing clinical and radiographic risk factors of mandibular molar loss. Materials and Methods: Four hundred and seventy‐eight mandibular molars of 139 subjects who underwent non‐surgical periodontal treatment were examined retrospectively within a mean follow‐up period of 11.1 years. The association of risk factors including clinical and radiographic parameters with mandibular molar loss was assessed using univariate and multivariate Cox regression analyses. A nomogram prediction model was developed, and the validation and discriminatory ability of it were analysed. Results: Hundred and four molars were lost in this study. Probing depth (PD), attachment loss (AL), furcation involvement (FI), bleeding on probing (BOP), tooth mobility and radiographic bone loss were significantly associated with tooth loss (p <.01). A gradient effect of degree of FI on mandibular molar loss existed increasing from degree Ⅱ (HR = 2.37, 95% CI: 1.48, 3.79) to Ⅲ (HR = 5.61, 95% CI: 3.01, 10.45) versus none & degree Ⅰ. The area under the curve (AUC) of the model was 0.891. The calibration curve and decision curve analysis demonstrated good performance and high net benefit of nomogram, respectively. Conclusions: A specific nomogram could be adopted to predict the mandibular molar survival and formulate tailored treatment plans in Chinese. [ABSTRACT FROM AUTHOR]

Background: A few evidence is available in the literature concerning the pattern of variation in the width of keratinized mucosa (KMW) around dental implants and factors that may affect the KMW. Purpose The purpose of this study is to investigate the KMW at the buccal aspect of dental implants and to analyze its influencing factors. Materials and Methods: The current study was a retrospective study conducted on 726 patients with 1252 dental implants. The following parameters were evaluated by reviewing the medical records of each patient, including the age, gender and smoking status of each patient, the reasons of teeth loss, the position of implants, the bone augmentation procedures, and the KMW. Binary logistic regression analysis with the generalized estimating equations was utilized to analyze the factors that may affect the KMW of dental implants. Results: The KMW of implants located in the maxilla was significantly higher than that of implants located in the mandible (P <.01), except for the upper and lower canines. The logistic regression analysis indicated that the risk of the implants presenting inadequate KMW (<2 mm) in the periodontitis‐caused tooth loss group was 1.91 times of the non‐periodontitis‐caused tooth loss group. The risk of implants presenting inadequate KMW after receiving simple and complex bone augmentation procedures was 1.65 and 2.62 times of the risk of implants without bone augmentation, respectively. The longer the follow‐up period, the higher the risk of implants presenting inadequate KMW will be. Conclusions: The KMW at the buccal aspect of implants is related to the position of implants. Tooth loss due to periodontitis, the bone augmentation procedures, and the process of functional period would increase the risk of implants presenting an inadequate amount of keratinized mucosa. [ABSTRACT FROM AUTHOR]

Aim: To assess the subgingival microbial shift of maintained periodontitis treated by ultrasonic scaling (US) or air polishing (AP) during a 3‐month maintenance interval. Materials and methods: We conducted a 12‐week randomized split‐mouth controlled trial with US and AP in 17 maintained subjects (bleeding on probing [BOP%] ≤25%, probing depth [PD] ≤5 mm). They were monitored at baseline, week 2, week 8 and week 12. The V3‐V4 region of the 16S rDNA from 136 subgingival plaque samples was sequenced and analysed. Results: Treatment by US or AP could effectively reduce the PD, microbial richness, diversity, periodontitis‐associated microbiota and pathogenic metabolism in maintained periodontitis. Bacteria recolonized after treatment and returned to the pre‐treatment level 12 weeks after treatment. Ultrasonic scaling group demonstrated slight advantage in reducing BOP (%), pathogenic bacteria and metabolism than AP group. Pathogenic microbiota and commensal microbiota kept a balance in subgingival community of maintained patients during the 3‐month interval. Conclusions: Treatment by US or AP effectively reduced the pathogenicity of subgingival microbiome by reducing microbial diversity, proportion of periodontitis‐associated microbiota and pathogenic metabolism. It helped to keep a balanced subgingival community and stable periodontal condition over a single maintenance interval of 3 months. [ABSTRACT FROM AUTHOR]

• The risk of T2DM was higher in moderate/severe periodontitis. • Rs1501299 GG genotype and rs1137100 GG genotype increase the risk of T2DM. • The model shows a significant interaction among periodontitis and polymorphisms. Type 2 diabetes mellitus (T2DM) is a complex disease influenced by genes and the environment. Periodontitis a demonstrated risk factor of T2DM. Previous studies related to gene-environment interactions on the risk of T2DM mainly focused on gene-obesity interactions. However, the impact of gene-periodontitis interaction on the risk of T2DM has not yet been investigated. This study aimed to investigate gene-environment interactions among moderate/severe periodontitis, polymorphisms of adiponectin (ADIPOQ)-rs1501299, and leptin receptor (LEPR)-rs1137100 on T2DM risk in Chinese subjects. A case-control study was conducted in 239 Chinese participants from Beijing Hypertension Association Institute (BHAL). After full-mouth periodontal examinations, the participants underwent bilateral buccal swabs for DNA testing. ADIPOQ-rs1501299 and LEPR-rs1137100 were used for genotyping. Generalised multifactor dimensionality reduction (GMDR) and logistic regression were used to examine the interactions among single nucleotide polymorphisms (SNPs) and moderate/severe periodontitis on the risk of T2DM. The risk of T2DM was higher in moderate/severe periodontitis [adjusted odds ratio (AOR) = 3.67, 95% confidence interval (95%CI): 1.26–10.71] in ADIPOQ-rs1501299 GG genotype (AOR = 3.42, 95%CI: 1.81–6.46) and LEPR-rs1137100 GG genotype (AOR = 3.16, 95%CI: 1.56–6.39). The GMDR model indicated that there was a significant three-factor model (p = 0.001) involving rs1501299, rs1137100, and moderate/severe periodontitis, demonstrating a potential gene-environment interaction among periodontitis, polymorphisms of rs1501299, and rs1137100 influencing the risk of T2DM. Moderate/severe periodontitis patients with rs1501299-GG and rs1137100-GG have the highest T2DM risk after adjusting for age, gender, BMI, WHR, smoking status, alcohol consumption, economic status, and hypertension (AOR = 20.39, 95%CI: 2.64–157.26). Interactions among moderate/severe periodontitis, rs1501299-GG, and rs1137100-GG were associated with an increased risk of T2DM. This study may provide a new insight into the effect of gene-environment interactions on T2DM. [ABSTRACT FROM AUTHOR]

Background: No nomogram of peri‐implantitis was reported before which is valuable for risk‐estimating, clinical decision‐making, and better‐patients‐communicating. Purpose To identify the risk indicators and develop a nomogram prediction model of peri‐implantitis in treated severe periodontitis patients. Materials and Methods: A prospective study was conducted on 100 patients with 214 implants. Periodontal and peri‐implant parameters were evaluated at implant surgery procedure (T1), and at follow‐up (T2). Risk factors were analyzed by logistic regression analyses with generalized estimating equations. Nomogram was developed and the discriminatory ability of the model was analyzed. Results: The incidence of peri‐implantitis at patient‐level and implant level were 16% and 11.2% respectively, with no implant lost. The variables associated with peri‐implantitis were the PDT1 ≥ 6 mm (%) > 10%, the implant position, length, and diameter after adjusting for covariates. A nomogram prediction model of peri‐implantitis were developed with factors of PD T1 ≥ 6 mm (%) > 10% and implant placed in posterior. The area under the ROC curves of stepwise model was 0.794. Conclusions: The residual pockets and implants position were identified as predictors for the peri‐implantitis. The nomogram can be used to estimate the risk of peri‐implantitis in treated severe periodontitis patients. [ABSTRACT FROM AUTHOR]

Objectives To investigate the effects of different decontamination treatments on microstructure of titanium (Ti) surface as well as proliferation and adhesion of human gingival fibroblasts (HGFs). Material and methods Ti discs with machined (M) and sand blasted, acid etched (SAE) surfaces were treated with five different decontamination treatments: (1) stainless steel curette (SSC), ultrasonic system with (2) straight carbon fiber tip (UCF) or (3) metal tip (UM), (4) rotating Ti brush (RTB), and (5) Er:YAG laser (30 mJ/pulse at 30 Hz). Surface roughness was analyzed under optical interferometry. HGFs were cultured on each disc. Proliferation and adhesive strength were analyzed. qRT-PCR and ELISA were performed to detect the RNA and protein expression of FAK, ITGB1, COL1A1, and FN1 respectively from different Ti surfaces. Results Surface roughness increased on M surface. Proliferation, adhesive strength and gene expression were higher on M surface than SAE surface. Decontamination treatments affected surface parameters significantly ( P <  0.001), making M surface less smooth while SAE surface became less rough. SSC, UCF, UM and RTB decreased proliferation on M surfaces significantly ( P <  0.05). UCF, RTB and laser increased proliferation on SAE surface significantly ( P <  0.05). UM decreased adhesive strength on M surface significantly and laser increased adhesive strength on SAE surface significantly ( P  < 0.05). Gene expression increased with time and was altered by decontamination treatments significantly ( P  < 0.001). Conclusions Decontamination treatments influence surface roughness and cell behavior of HGFs. Laser might be an optimal decontamination treatment which has the least negative effect on M surface and the most positive effect on SAE surface. [ABSTRACT FROM AUTHOR]

Abstract: Background: Few prospective studies about early loading of short implant have been available and very little evidence exists on the outcomes longer than 3 years. Purpose: To assess clinical and radiographic outcomes of 6 mm‐short implants placed in the posterior maxilla and mandible applying an early loading protocol. Materials and methods: Ninety‐five short implants (6 mm‐short, Ø 4 mm) were placed in 45 subjects at 3 study sites, 2 or 3 implants per subject, using a one‐stage surgical procedure and loaded with a screw‐retained splinted fixed prosthesis 6 weeks later. Follow‐up took place at 6, 12, 24, and 36 months after loading. Marginal bone level changes, implant survival, clinical variables, and adverse events were assessed. Results: The survival rate for all implants placed was 95.8%. From implant loading to 3 years follow‐up, mean marginal bone level changes were minimal (0.07 ± 0.49 mm) and the peri‐implant soft tissue status was healthy. No major technical or biological complications occurred except for the 4 early implant losses. Conclusion: Three‐year data indicates that the use of splinted 6 mm‐short implants is a viable treatment in posterior regions with low marginal bone resorption. Early loading after 6 weeks should be taken cautiously in patients with known risk factors. [ABSTRACT FROM AUTHOR]

Objective. To explore whether GC (group-specific component) rs17467825, rs4588, and rs7041 polymorphisms are associated with generalized aggressive periodontitis. Methods. This case-control study recruited 372 patients with generalized aggressive periodontitis (group AgP) and 133 periodontal healthy subjects (group HP). GC rs17467825, rs4588, and rs7041 genotypes and plasmatic vitamin D-binding protein (DBP) were measured. Analysis of single SNP and multiple SNPs was performed and relevance between plasmatic DBP and haplotypes was analyzed. Results. GC rs17467825 GG genotype was statistically associated with lower risk for generalized aggressive periodontitis under the recessive model (OR = 0.52, 95% CI: 0.30–0.92, p=0.028). GC rs17467825 and rs4588 had strong linkage disequilibrium with r2≥0.8 and D′≥0.8. Haplotype (GC rs17467825, rs4588) GC was associated with the less risk for generalized aggressive periodontitis (OR = 0.29, 95% CI: 0.09–0.96, p=0.043). In group AgP, individuals with combined genotype (GC rs17467825, rs4588) AG+CA had significantly lower plasmatic DBP level than those with the other two combined genotypes (AG+CA versus AA+CC p=0.007; AG+CA versus GG+AA p=0.026). Conclusions. GC rs17467825 genotype GG and haplotype (GC rs17467825, rs4588) GC are associated with generalized aggressive periodontitis. The association may be acquired through regulating DBP levels. The functions of GC gene and DBP in inflammatory disease need to be further studied. [ABSTRACT FROM AUTHOR]

Objective The aim of this multicenter study was to prospectively assess clinical and radiographic outcomes of short implants (length 6 mm) in the posterior region and early-loading with splinted-fixed dental prostheses. Materials and methods A total of 45 subjects (77.8% with chronic periodontitis) were enrolled at three study sites. In total, 95 implants (diameter 4 mm, length 6 mm; OsseoSpeed™ 4.0 S; DENTSPLY Implants; Mölndal, Sweden) were placed, two or three implants per subject, using one-stage surgery and loaded with a screw-retained splinted ceramic-fixed prosthesis 6 weeks later. Clinical and radiographic examinations were performed preoperatively, post-surgery, at loading, and 6 and 12 months after prosthesis placement. Results Four implants failed before loading; all other implants showed favorable clinical and radiographic findings throughout the observation period (1-year survival and success rate: 95.8%). Postoperative pain and swelling were negligible. Mean changes in marginal bone levels measured from loading were minimal (0.01 ± 0.37 and −0.13 ± 0.46 mm after 6 months and 1 year, respectively). Bone loss less than 1.00 mm was found in 77.5% implants, and bone gain was found in 15.5% implants. Probing depth change less than 2 mm was found in 98.7% of the implants between loading and 1-year follow-up. Prosthetic complications included one ceramic veneer chipping. Conclusion One-year data indicate that the use of 6-mm-long implants is a predictable treatment. This provides a good treatment option in situations with limited bone height in posterior regions. [ABSTRACT FROM AUTHOR]

Aim: To investigate the microbiome composition in Chinese patients with aggressive periodontitis (AgP), and to compare the similarity of bacterial profiles between AgP patients and their family members. Material and Methods: Pooled subgingival plaque and saliva samples were collected from 10 AgP patients and 10 of their first-degree blood relatives with chronic periodontitis. DNA amplicons of the V1-V3 hypervariable region of the bacterial 16S rRNA gene were generated, and were subjected to 454-pyrosequencing. Results: In subgingival plaque, the unweighted UniFrac distances between family members were significantly lower than those in unrelated participants (p = 0.039). Compared with the relatives, the microbiota of subgingival plaque and saliva from AgP patients revealed significantly lower taxonomic diversity. High relative abundance of Porphyromonas gingivalis (about 35.88%) was detected in subgingival plaque from AgP patients. The relative abundance of P. gingivalis and Red complex pathogens (P. gingivalis, Treponema denticola and Tannerella forsythia) in the subgingival plaque and saliva samples from the same individual were significantly correlated in AgP patients (q= 0.687 and 0.678, respectively). Conclusions: There is a kinship in the phylogenetic architecture of microbiota among Chinese AgP patients and their family members. P. gingivalis might be a predominant pathogen in these Chinese AgP patients. [ABSTRACT FROM AUTHOR]

S100A8, S100A9, and calprotectin (the S100A8/S100A9 complex) are calcium-binding proteins that promote extracellular pro-inflammatory functions and may play an important role in periodontal disease. Both toll-like receptor 4 (TLR4) and the receptor for advanced glycation end-products (RAGE) are thought to be important receptors for S100A8, S100A9, and calprotectin, but the specific pathways in periodontal ligament (PDL) cells are not yet clear. Our study was designed to identify the specific receptors for S100A9 in human PDL cells. Additionally, we investigated the specific pathways that activate the secretion of pro-inflammatory cytokines interleukins (IL)-6 and IL-8 in PDL cells. The role of nuclear factor (NF)-κB, mitogen-activated protein kinase (MAPK) and reactive oxygen species (ROS) in S100A9-induced pro-inflammatory cytokines were investigated through western blot analysis, dichlorodihydrofluorescein diacetate (H 2 DCFDA) probe and the application of specific pathway inhibitors. Our results suggest that the S100A9-induced release of IL-6 and IL-8 from human PDL cells is dependent on TLR4, but not RAGE. We provide evidence that S100A9 promotes the secretion of IL-6 and IL-8 through different pathways. Specifically, S100A9 up-regulates the secretion of IL-6 from human PDL cells through NF-κB and p38 pathways and up-regulates the release of IL-8 from human PDL cells through the NF-κB, extracellular-regulated kinase (ERK) 1/2, c-Jun amino-terminal kinase (JNK) 1/2, and p38 signaling pathways. In addition, the release of both cytokines depends on ROS production. The release of both cytokines depends on ROS production. These results suggest that S100A9 promotes pro-inflammatory responses in PDL cells through the TLR4-mediated NF-κB and MAPK signaling pathways. [ABSTRACT FROM AUTHOR]

Objective To date, no information on the distribution of periodontal microorganisms among family members of Chinese patients with aggressive peridontitis (AgP) is available. The aim of the present study was to investigate the probability of transmission of eight periodontal microorganisms between patients with aggressive periodontitis and their family members. Design Saliva and pooled subgingival plaque samples were collected from 103 participants from 41 nuclear families (including 41 AgP probands, 19 mothers, 22 fathers, 21 siblings). Eight periodontal microorganisms, including Aggregatibacter actinomycetemcomitans , Porphyromonas gingivalis , Tannerella forsythia , Treponema denticola , Campylobacter rectus , Prevotella intermedia , Prevotella nigrescens and Fusobacterium nucleatum were detected in these samples by the polymerase chain reaction (PCR). In addition, the distribution of fimA genotypes was assessed in P. gingivalis -positive individuals by PCR. Results P. gingivalis , T. forsythia , T. denticola , C. rectus and F. nucleatum were the most frequently detected species both in AgP probands and in their relatives. Kappa statistical analysis revealed that the detection of A. actinomycetemcomitans (Kappa = 0.503) and F. nucleatum (Kappa = 0.565) in probands was highly consistent with that in their relatives. Most probands shared the identical fimA genotype of P. gingivalis with their relatives. Conclusions Our results suggested that the intrafamilial transmission of periodontal microorganisms may occur between Chinese patients with aggressive periodontitis and their relatives. [ABSTRACT FROM AUTHOR]

Calprotectin, a heterodimer of S100A8 and S100A9 subunits, is associated with inflammatory disorders such as rheumatoid arthritis and cystic fibrosis. Although calprotectin levels are increased significantly in the gingival crevicular fluid (GCF) of periodontitis patients, its effects on periodontal ligament cells (PDLCs) remain largely unknown. The aim of this study was to evaluate calprotectin levels in the GCF of generalized aggressive periodontitis (AgP) patients and to investigate the effects of recombinant human calprotectin (rhS100A8/A9) and its subunits (rhS100A8 and rhS100A9) in PDLCs. Both the concentration and amount of crevicular calprotectin were significantly higher in the AgP group compared with healthy controls. In addition, the GCF calprotectin levels were correlated positively with clinical periodontal parameters including bleeding index, probing depth, and clinical attachment loss. rhS100A8/A9 promoted cell apoptosis, whereas rhS100A8 and rhS100A9 individually exerted little effect on apoptosis in PDLCs. rhS100A9 and rhS100A8/A9 increased the activation of nuclear factor-κB (NF-κB) by promoting the nuclear translocation of p65 in PDLCs, subsequently inducing expression of the pro-inflammatory cytokines IL-6, IL-8, TNFα, and COX2. Treatment with an NF-κB inhibitor partially reversed the rhS100A9- and rhS100A8/A9-induced upregulation of the pro-inflammatory cytokines. rhS100A9, and not rhS100A8, was mainly responsible for the pro-inflammatory role of calprotectin. Collectively, our results suggest that calprotectin promotes apoptosis and the inflammatory response in PDLCs via rhS100A9. These findings might help identify novel treatments for periodontitis. [ABSTRACT FROM AUTHOR]

Leptin and its receptor (OBR) have attracted much attention since their discovery. They have been reported to play central roles in energy balance, the immune-inflammatory response and bone metabolism. Evidence indicates that leptin and OBR are associated with inflammatory diseases of dental and periodontal tissues. The first step for establishing this is to determine the expression of leptin and OBR in these tissues. Our study is the first to examine systematically the expression of leptin and OBR in dental and periodontal tissues of monkeys ( Macaca fascicularis) by immunohistochemistry and in primary cultured cells, isolated from human dental and periodontal tissues, by reverse transcription plus the polymerase chain reaction and immunocytochemistry. Our results show that leptin and OBR are constitutively expressed and widely distributed in dental and periodontal tissues of primates. Their immunoreaction is especially strong in junctional epithelium, a unique front-line defense around teeth and in mineralizing areas of the dental pulp and periodontal ligament. The expression of the long and also functional form of OBR (OBRb) indicates that leptin has a direct effect on these cells. Thus, we can reasonably infer that leptin and OBR exert effects on defense, mineralization and angiogenesis in dental and periodontal tissues of primates. [ABSTRACT FROM AUTHOR]