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Background: Periodontitis is characterized by local inflammatory conditions in the periodontium, its severe form has been associated with elevated systemic inflammatory markers. However, the long‐term effects of periodontal inflammation control on systemic inflammatory markers are unclear. Objective: This study aimed to investigate the long‐term effects of periodontal therapy on the levels of peripheral venous blood inflammatory markers in patients with generalized aggressive periodontitis (GAgP), all of whom were now diagnosed as Stage III or IV Grade C periodontitis. Methods: Patients with GAgP were consecutively recruited from April 2013 to August 2014 (T0). Active periodontal treatment (APT) was provided, and follow‐ups were conducted over a 3‐ to 5‐year period (T1). Clinical parameters were assessed and fasting venous blood was collected at T0 and T1. Complete blood cell counts were obtained, and biochemical analyses were performed to evaluate the levels of serum components. The correlations between probing depth (PD) and hematological parameters were analyzed. Results: A total of 49 patients with GAgP completed APT and follow‐ups. Probing depth (PD) reduced from 5.10 ± 1.07 mm at T0 to 3.15 ± 0.65 mm at T1. For every 1‐mm reduction in PD after treatment, the neutrophil count, neutrophil‐lymphocyte ratio, and total protein concentration were reduced by 0.33 × 109/L, 0.26, and 1.18 g/L, respectively. In contrast, the albumin/globulin ratio increased by 0.10. Conclusion: This study indicated that periodontal therapy may have beneficial effects on peripheral venous blood inflammatory markers in patients with GAgP during long‐term observation. [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]

Background: Host inflammatory mediators are associated with tissue destruction in patients suffering from generalized aggressive periodontitis (GAgP). However, the correlations between neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) with GAgP remain unknown.Methods: Periodontal clinical parameters, including probing depth (PD), bleeding index (BI) and attachment loss (AL) were collected from patients with GAgP and healthy controls. Complete blood cells analyses were obtained; further, NLR and PLR were calculated using neutrophil, platelet, and lymphocyte counts. Smooth curve fitting and segmented regression models were used to analyze the roles and predictive value of NLR with GAgP.Results: In total, 505 participants from a Chinese population were recruited, including 133 healthy controls and 372 patients with GAgP. Periodontal clinical parameters, NLR, and neutrophil counts were significantly higher in patients with GAgP than the control group. Moreover, NLR was positively correlated with the risk and clinical parameters of GAgP. When NLR < 3, the risk of GAgP increased by 20.6% for each 0.1 increase in NLR, reaching saturation when NLR > 3. An increase in NLR equivalent to 1 was associated with an increase in PD, BI, and AL by 0.41 mm, 0.26, and 0.57 mm, respectively. Notably, PLR did not show obvious correlations with GAgP.Conclusions: NLR but not PLR may be a potential marker to identify GAgP in healthy individuals, particularly in a Chinese population. [ABSTRACT FROM AUTHOR]

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]

Background: Each genetic variant individually explains only a tiny proportion of the genetic variation with insignificant predictive power. The tool of multi-locus genetic risk score (GRS), which aggregates information from multiple genetic variants, has been widely used in many complex diseases but not yet applied to generalized aggressive periodontitis (GAgP).Methods: A total of 335 GAgP patients and 114 healthy controls were enrolled in the case-control study. The unweighted GRS (uGRS) and weighted GRS (wGRS) were calculated based on significant variants. Logistic regression models were conducted for the GRS-based association analyses on the risk of GAgP. Receiver operating characteristic analysis was performed to compare the discriminatory ability of predictors of GAgP risk.Results: Four loci were found to be significantly associated with GAgP. They were matrix metalloproteinase 8 rs11225395 (odds ratio [OR] = 1.40, 95% CI: 1.03 to 1.91), epidermal growth factor rs2237051 (OR = 1.41, 95% CI: 1.03 to 1.93), PPAR-a rs4253623 (OR = 1.53, 95% CI: 1.03 to 2.26), and apolipoprotein E rs429358 (OR = 1.79, 95% CI: 1.08 to 2.97). Each additional point of the uGRS/wGRS was associated with a 50%/31% increased risk of developing GAgP (OR = 1.50, 95% CI: 1.21 to 1.85 or OR = 1.31, 95% CI: 1.14 to 1.51, respectively) after adjusting for age, sex, and body mass index (BMI). Participants in the high group of uGRS/wGRS (OR = 2.87, 95% CI: 1.59 to 5.17 or OR = 2.67, 95% CI: 1.46 to 4.88, respectively) and the middle group of uGRS/wGRS (OR = 2.21, 95% CI: 1.29 to 3.78 or OR = 1.88, 95% CI: 1.09 to 3.08, respectively) had an increased risk of GAgP compared with those in the low group of score after adjustment for age, sex, and BMI. The addition of GRS to a model of conventional risk factors improved discrimination by 4.5% (from 0.695 to 0.740, P = 0.048).Conclusions: We demonstrated that the multi-locus GRS based on four significant single nucleotide polymorphisms might be useful to assess genetic predisposition to GAgP. The GRS in combination with conventional risk factors significantly improved the power of identifying subgroups of Chinese population with a particularly high risk for GAgP. [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]

Background and objective: CYP1A1 rs1048943 polymorphism was reported to be correlated with periodontitis; however, its association with aggressive periodontitis (AgP) has not yet been investigated. The aim of the study was to investigate the association between the CYP1A1 gene rs1048943 variant with generalized aggressive periodontitis (GAgP) and platelet activation and analyse whether its interaction with hyperlipidemia affects periodontal status in a Chinese population. Methods: A case‐control study of 224 GAgP patients and 139 healthy controls was conducted. The clinical parameters of probing depth (PD), attachment loss (AL) and bleeding index (BI) were recorded. Platelet count (PLT), platelet distribution width (PDW), platelet large cell ratio (PLCR), mean platelet volume (MPV), serum total cholesterol (TC), triacylglycerol (TG), high and low‐density lipoprotein (HDL and LDL) were also measured. The CYP1A1 rs1048943 SNP was genotyped by time‐of‐flight mass spectrometry. Logistic and linear regression models were used to measure correlation. Results: The CYP1A1 rs1048943 AG/GG genotype was associated with GAgP (OR = 1.56, 95%CI: 1.01, 2.42), PD, AL and decreased PDW, PLCR and MPV after adjustment for covariates. Gene‐lipid interactions were found between CYP1A1 rs1048943 and HDL for PD (Pinteraction = 0.0033), BI (Pinteraction = 0.0311) and AL (Pinteraction = 0.0141) and between CYP1A1 rs1048943 and LDL for PD (Pinteraction = 0.013) among patients with GAgP. Conclusion: The G allele of the CYP1A1 rs1048943 gene was associated with GAgP, periodontal status and platelet‐related inflammation status in a Chinese population. Hyperlipidemia could modulate the effect of CYP1A1 rs1048943 on the periodontal status of GAgP. [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]

Background: The study was designed to compare peri-implant microbial colonization of inflamed implants placed at different levels in dogs.Methods: Two screwed-in (SI) and two tapped-in (TI) conical connection implants were placed on each side of mandibles in six dogs respectively. Four experimental groups were constituted according to implant types and placement depth in one side: SI crestally (SIC), SI 1.5 mm subcrestally (SIS), TI crestally (TIC), and TI 1.5 mm subcrestally (TIS). Plaque accumulation of implants was promoted by cotton ligatures at either side randomly selected in each dog four weeks after abutment connection. Peri-implant sulcular fluid (PISF) samples were collected at 4 weeks, 10 weeks, and 16 weeks after abutment connection. Common periodontal pathogens in PISF were analyzed by PCR and realtime-PCR to investigate the influence of placement depth on microbial accumulation. The microbial results were further correlated with clinical parameters.Results: At ligatured sides, detection rates of T. forsythia and P. gingivalis increased significantly in four groups. T. forsythia levels increased significantly from baseline in four groups at ligatured sides at 16 weeks (p < 0.05). TIS group harbored significantly more T. forsythia than TIC at ligatured sides at 16 weeks (p < 0.05). At ligatured sides, probing depth was correlated to T. forsythia level in four groups as well as in total.Conclusions: Subcrestal placement could increase the peri-implant T. forsythia level at the early stage of peri-implantitis. The T. forsythia level in the peri-implant sulcus is associated with probing depth. [ABSTRACT FROM AUTHOR]

Background: Association between BMI and periodontitis were controversial. A study indicated that not only overweight or obesity but also underweight was correlated with generalized aggressive periodontitis (GAgP). However, the exact relationship between BMI and GAgP and the optimal BMI value for the lowest risk of GAgP remain unknown.Objective: To explore the exact relationship between BMI and GAgP risk, periodontal status and WBC (white blood cell) count and find the optimal BMI value associated with the lowest risk, periodontal status and lowest WBC of GAgP in Chinese.Methods: 300 GAgP patients and 133 healthy controls were recruited. Height and weight of participants were accurately measured to calculate BMI value. Clinical periodontal parameters, including probing depth (PD), attachment loss (AL), and bleeding index (BI) were recorded. WBC was obtained from routine blood examination. Smooth curve fitting and segmented regression model were used to analyze the threshold effect between BMI and variables. The shape of the curve was used to describe the relationships between BMI and GAgP.Results: U-shaped relationships between BMI and risk of GAgP, AL, and WBC count in GAgP patients were observed. The optimal value of BMI for the lowest risk of GAgP and lowest WBC count was 22 kg/m2 . The risk of GAgP increased by 39% in patients per unit increase of BMI when BMI ranged from 22 to 28 kg/m2 (adjusted OR = 1.39, 95% CI: 1.17, 1.67) and increased by 18% per unit decrease of BMI when BMI ranged from 22 to 18 kg/m2 (adjusted OR = 0.82, 95% CI: 0.69, 0.97). The count of WBC increased by 1.12 × 109 /L in patients per unit increase of BMI when BMI ranged from 22 to 28 kg/m2 (adjusted β = 0.12, 95% CI: 0.01, 0.23) and increased by 0.2 × 109 /L per unit decrease of BMI when BMI ranged from 22 to18 kg/m2 (adjusted β = -0.2, 95% CI: -0.35, -0.04).Conclusion: U-shaped relationships exist between BMI and risk of GAgP, AL, and WBC count in patients with GAgP among Chinese aged below 36 years old with their BMI range from 18 to 28 kg/m2 ; the optimal BMI value for lowest odds ratio and lowest WBC count of GAgP was 22 kg/m2 . [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 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]

Background: The microbiologic feature of aggressive periodontitis (AgP) in Chinese patients has not yet been determined. This study aims to investigate the prevalence of eight periodontal microorganisms and the distribution of the Porphyromonas gingivatis fimA genotype in a cohort of Chinese patients with AgP. Methods: Saliva and pooled subgingival plaque samples were collected from 81 patients with AgP (25 with incisor-first molar type and 56 with generalized type [GAgP]) and 34 periodontally healthy controls. Eight periodontal microorganisms, including Aggregatibacter actinomycetem-comitans, P. gingivalis, Tannereita forsythia, Treponema denticola, Campylobacter rectus, Prevoteila intermedia, Pre-votella 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: The prevalence of P. gingivalis, T. forsythia, T. denticola, C. rectus, P. intermedia, F. nucleatum, and A. actinomycetemcomitans in patients with AgP was significantly higher than that in healthy controls. The prevalence of A. actinomycetemcomitans in patients with GAgP was relatively low (30.4%) compared with other pathogens. Results of logistic regression analysis showed that younger patients were more likely to harbor A. actinomycetemcomitans (odds ratio = 2.85). Type II was the most prevalent fimA genotype of P. gingivalis in patients with AgP. Conclusions: P. gingivalis, T. forsythia, T. denticola, C. rectus, P. intermedia, and F. nucleatum were the predominant periodontal pathogens of patients with GAgP in China. Type II of fimA was the most prevalent genotype of P. gingivalis in patients with AgP. The prevalence of A. actinomycetemcomitans in patients with GAgP was relatively low. [ABSTRACT FROM AUTHOR]

Background: Periodontal risk assessment (PRA) model was designed for risk evaluation of treated patients with periodontal disease. However, its use on generalized aggressive periodontitis (GAgP) had been scarcely reported. This study aims to investigate the association of original PRA/modified PRA (MPRA) and compliance of periodontal maintenance with long-term treatment outcomes of Chinese patients with GAgP. Methods: Eighty-eight patients from a GAgP cohort, who completed active periodontal treatment (APT) and accepted reevaluation 3 to 11 years (mean of 5.5 years) afterward, were enrolled. PRA was modified (three strategies involving replacement of bleeding on probing with bleeding index >2, counting sites with probing depth ≥6 mm and changing method of bone loss [BL] calculation) to classify patients into different risk groups based on data at the first recall after APT. PRA and three MPRA models were investigated regarding long-term association with tooth loss (TL) and alteration of bone level (ABL). Results: Based on original PRA, 87 patients (98.8%) had a high-risk profile. According to three MPRA models, annual TL per patient values were greater in high-risk groups than in low-to-moderate risk groups (MPRA-1, 0.20 ± 0.33 versus 0.04 ± 0.14; MPRA-2, 0.18 ± 0.32 versus 0.05 ± 0.14; MPRA-3, 0.17 ± 0.32 versus 0.05 ± 0.15; P <0.05). By MPRA-1, irregular compliers with low-to-moderate risk profile had greater ABL (0.027 ± 0.031, indicating bone increment) than those with high risk (-0.012 ± 0.064, tendency for BL). For regular compliers, no significant differences of annual TL or ABL were found between risk groups. Conclusions: MPRA models could be used for evaluating the long-term outcomes of Chinese patients with severe GAgP, especially irregular compliers. High-risk patients of MPRAs exhibited more TL and less bone fill than low-to-moderate risk ones. [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%.