Periodontal conditions of teeth adjacent to dental implants with or without peri-implantitis after non-surgical therapy in patients treated for periodontitis: A retrospective study.

OBJECTIVES: To retrospectively assess the periodontal conditions of teeth adjacent to and contralateral to implants presenting with or without peri-implantitis, following non-surgical periodontal and peri-implant mechanical therapy. MATERIALS AND METHODS: One hundred and one patients with existing dental implants and chronic periodontitis, who underwent non-surgical periodontal and peri-implant mechanical therapy, were included. The periodontal clinical probing depth (PPD), gingival recession (GR), and bleeding on probing (BOP) were recorded at six sites around the adjacent (Adj-) teeth and the contralateral (CL-) teeth relative to the implant. The potential factors influencing the periodontal conditions of 316 teeth were analyzed by multivariate linear regression models with generalized estimating equation methods and α = .05. RESULTS: The PPD of Adj-teeth was significantly different from that of CL-teeth before and after non-surgical therapy when the implant was diagnosed with peri-implantitis (PI) (p < .05). The PPD of teeth was shown to be affected by neighboring implants diagnosed with peri-implantitis (ß = .825 mm, p < .001), teeth adjacent to implants (ß = .245 mm, p = .004), a molar tooth type (ß = .435 mm, p = .019), and non-surgical therapy (ß = -.522 mm, p < .001). CONCLUSIONS: Relatively compromised periodontal conditions at Adj-teeth after non-surgical PI therapy were detected. Therefore, clinicians should be aware that non-surgical therapy may be less successful at teeth adjacent to implants with PI.

A bispecific antibody AP203 targeting PD-L1 and CD137 exerts potent antitumor activity without toxicity.

BACKGROUND: Bispecific antibody has garnered considerable attention in the recent years due to its impressive preliminary efficacy in hematological malignancies. For solid tumors, however, the main hindrance is the suppressive tumor microenvironment, which effectively impedes the activation of infiltrating T cells. Herein, we designed a bispecific antibody AP203 with high binding affinity to PD-L1 and CD137 and assessed its safety and anti-tumor efficacy, as well as explored the mechanism of action. METHODS: The optimal antibody binders against PD-L1 and CD137 were screened from the OmniMab phagemid library. The binding affinity of the constructed AP203 were evaluated using enzyme-linked immunosorbent assay (ELISA) and biolayer interferometry (BLI). T-cell stimulatory capacity was assessed using the allogeneic mixed lymphocyte reaction (MLR), antigen-specific recall response, and coculture with PD-L1-expressing cells. In vivo antitumor efficacy was evaluated using two models of tumor-xenografted humanized mice with profiling of tumor infiltrating lymphocytes (TILs). The possible toxicity of AP203 was examined using in vitro cytokine release assay by human PBMCs. RESULTS: AP203, which simultaneously targeted PD-L1 and costimulatory CD137, elicit superior agonistic effects over parental antibodies alone or in combination in terms of T cell activation, enhanced memory recall responses, and overcoming Treg-mediated immunosuppression (P < 0.05). The agonistic activity of AP203 was further demonstrated PD-L1-dependent by coculturing T cells with PD-L1-expressing cells. In vivo animal studies using immunodeficient or immunocompetent mice both showed a dose-related antitumor efficacy superior to parental antibodies in combination (P < 0.05). Correspondingly, AP203 significantly increased tumor infiltrating CD8 + T cells, while decreased CD4 + T cells, as well as Treg cells (P < 0.05), resulting in a dose-dependent increase in the CD8 + /CD4 + ratio. Moreover, either soluble or immobilized AP203 did not induce the production of inflammatory cytokines by human PBMCs. CONCLUSIONS: AP203 exerts potent antitumor activity not only by blocking PD-1/PD-L1 inhibitory signaling, but also by activating CD137 costimulatory signaling in effector T cells that consequently counteracts Treg-mediated immunosuppression. Based on promising preclinical results, AP203 should be a suitable candidate for clinical treatment of solid tumors.

Complement components C3b and C4b as potential reliable site-specific diagnostic biomarkers for periodontitis.

OBJECTIVE: This study aimed to investigate the correlation between the expression levels of C3b and C4b in human gingival tissue (GT) and gingival crevicular fluid (GCF) and disease severity in human periodontitis and to determine whether C3b and C4b are significant site-specific complementary diagnostic markers for periodontitis. BACKGROUND: A variety of biomarkers that have potential for informing diagnoses of periodontitis have been proposed. The complement components C3b and C4b were found to be positively correlated with disease severity. The therapeutic effect of targeting C3b and C4b on inflammatory bone loss in experimental periodontitis models has been studied. However, studies on the diagnostic potential of the gingival C3b and C4b expression levels for periodontitis are scarce. METHODS: The expression levels of C3b and C4b in the GT and GCF were investigated via immunohistochemistry and enzyme-linked immunosorbent assay, respectively. The correlation between the expression levels of C3b and C4b and disease severity with probing depth as well as the clinical attachment level were determined. To evaluate the diagnostic accuracy of the C3b and C4b expression levels at the periodontitis sites, the receiver operating characteristic (ROC) curve, cut-off point, area under the ROC curve, sensitivity, and specificity were analyzed. RESULTS: The expression levels of C3b and C4b in human GT and GCF were significantly positively correlated with periodontitis severity. The expression levels of combined C3b + C4b in the GT can significantly differentiate the disease status at the tissue level (p < .0001). Similarly, the expression levels of C3b + C4b in GCF can statistically distinguish periodontitis sites from healthy ones (p < .0001). CONCLUSIONS: Locally deposited C3b and C4b were positively correlated with periodontitis severity and recognized as site-specific diagnostic biomarkers for clinicopathological features in periodontitis. The association between the C3b and C4b network and periodontitis may be further understood and provide a basis for the development of novel screening as well as diagnostic and therapeutic strategies for periodontitis.

Targeting therapeutic agent against C3b/C4b, SB002, on the inflammation-induced bone loss in experimental periodontitis.

AIMS: To use experimental periodontitis models in rats to investigate the correlation between local expression of the complement components C3b and C4b in periodontal tissues and disease severity, and to assess the therapeutic effects of targeting C3b/C4b on inflammatory bone loss. MATERIALS AND METHODS: The gingival expression of C3, C3b, and C4b in animal experimental periodontitis models were analysed immunohistochemically. The therapeutic effects of the C3b/C4b inhibitor (SB002) on ligation-induced experimental periodontitis was examined using biochemical, histological, and immunohistochemical analyses. RESULTS: The gingival expression levels of C3, C3b, and C4b were positively correlated with the severity of periodontitis. Moreover, both single and multiple injections of the C3b/C4b inhibitor had preventive and therapeutic effects on alveolar bone loss in ligation-induced experimental periodontitis with no associated adverse consequences. CONCLUSIONS: The association between C3b/C4b and periodontitis may provide a basis for the development of novel therapeutic strategies for periodontitis and other inflammatory diseases.

Chlorhexidine gel topical application ameliorates inflammatory bone loss in experimental periodontitis.

OBJECTIVES: This study aimed to evaluate the impact of chlorhexidine (CHX) gel on inflammation-induced periodontal tissue destruction, osteoclastogenesis, subgingival microbiota, and on the modulation of the RANKL/OPG as well as inflammatory mediators during bone remodeling in vivo. MATERIALS AND METHODS: Ligation- and LPS injection-induced experimental periodontitis were created to investigate the effect of topical application of CHX gel in vivo. Alveolar bone loss, osteoclast number and gingival inflammation was evaluated by micro-CT, histological, immunohistochemistry and biochemical analysis. The composition of the subgingival microbiota was characterized by 16S rRNA gene sequencing. RESULTS: Data shows significant decreases in the alveolar bone destruction in rats from ligation-plus-CHX gel group compared to ligation group. In addition, significant decreases in the number of osteoclasts on bone surface and the protein level of receptor activator of nuclear factor κB ligand (RANKL) in gingival tissue were observed in rats from ligation-plus-CHX gel group. Moreover, data shows significantly decreased inflammatory cell infiltration and decreased expression of cyclooxygenase (COX-2) and inducible NO synthase (iNOS) in gingival tissue from ligation-plus-CHX gel group versus ligation group. Assessment of the subgingival microbiota revealed changes in rats with CHX gel application treatment. CONCLUSION: HX gel presents protective effect on gingival tissue inflammation, osteoclastogenesis, RANKL/OPG expression, inflammatory mediators, and alveolar bone loss in vivo, which may have a translational impact on the adjunctive use in the management of inflammation-induced alveolar bone loss.

The referral pattern and treatment modality for peri-implant disease between periodontists and non-periodontist dentists.

OBJECTIVES: This study is to investigate the referral pattern and treatment modality of dentists in the management of peri-implant diseases between periodontists and non-periodontist dentists (NPDs). MATERIALS AND METHODS: A total of 167 validated questionnaires were obtained from periodontists and NPDs, who had experience of placing implants for at least one year. Question I to IV asked how the dentist would respond if a patient came for treatment of their peri-implant diseases with four different scenarios according to resource of patient and disease severity. For each Scenario, dentists also replied which treatment procedures they would use if they decide to treat the patient. RESULTS: Periodontal training, resource of patient, and disease severity were shown to significantly influence the referral pattern and treatment modality in the management of peri-implant disease (p < 0.05). Periodontists were more likely to use variable treatment procedures, including occlusal adjustment (OR = 2.283, p < 0.01), oral hygiene instruction (OR = 3.751, p < 0.001), topical antiseptic agent (OR = 2.491, p < 0.005), non-surgical mechanical therapy (OR = 2.689, p < 0.001), surgical therapy (OR = 2.009, p < 0.01), and remove implant (OR = 3.486, p < 0.001) to treat peri-implant diseases, compared to NPDs. CONCLUSION: The periodontal specialty training, resource of patient, and disease severity significantly influenced the referral pattern and treatment modality of dentist treating an implant diagnosed with peri-implant disease. This study also highlighted the importance of educating basic periodontal and peri-implant disease-related knowledge to all dentists regularly performing dental implant treatments. CLINICAL RELEVANCE: Peri-implant diseases are highly prevalent among patients with dental implants. Periodontal specialty training could enhance using variable treatment procedures to treat peri-implant diseases for dentists.

Association of hepatic and systemic inflammation with localized stage II/III periodontitis in young males: The CHIEF oral health study.

AIM: To clarify the association between systemic and hepatic inflammation and localized periodontitis which has been reported to vary among races. MATERIALS AND METHODS: The study included 1112 military males, aged 18-40 years, in Taiwan. Participants were classified as periodontally healthy/stage I (n = 796) or stage II/III periodontitis (n = 316), according to the 2017 world workshop criteria. Systemic and hepatic inflammation were defined by the highest tertiles of blood leukocyte counts (7.51 × 103 /µl) and alanine aminotransferase (30 U/L), respectively. Multiple logistic regression analysis with adjustments for age, metabolic syndrome, betel nut consumption and smoking was carried out. RESULTS: There was a significant association between high systemic inflammation, irrespective of hepatic inflammation severity, and localized stage II/III periodontitis (odds ratio [OR], 1.62 [1.09-2.42] and 1.47 [1.00-2.15], respectively, in the presence of high or no hepatic inflammation. However, no significant association was found among participants with low systemic inflammation, irrespective of the severity of hepatic inflammation (OR, 1.31 [0.91-1.91]). CONCLUSIONS: An association between hepatic inflammation and localized periodontitis in Taiwanese was observed only if systemic inflammation coexisted, possibly accounting for the reported differences in the association between Japanese and non-Asian populations in prior studies.

Periodontitis, Helicobacter pylori infection, and gastrointestinal tract cancer mortality.

AIM: Periodontitis has been proposed to lead to Helicobacter pylori infection, which could cause many gastrointestinal tract cancers. This study aimed to determine the association or otherwise between periodontitis and survival outcomes in individuals with respect to H. pylori infection. MATERIALS AND METHODS: The study population comprised 4955 subjects aged 20-90 who had received both periodontal examination and H. pylori serum test in the Third National Health and Nutrition Examination Survey (NHANES III) database. Logistic regression models were used to analyse the association between periodontitis and H. pylori seropositivity (H. pylori infection). Survival analysis was performed using the NHANES III linked to mortality data. Cox proportional hazard regression was carried out to investigate the association between periodontitis and gastrointestinal tract cancer mortality in individuals with/without H. pylori infection. RESULTS: Compared to periodontal health, periodontitis was significantly associated with increased odds of H. pylori infection (OR = 1.271, 95% CI = 1.177-1.372). Periodontitis significantly increased the mortality risk from all causes (HR = 1.574, 95% CI = 1.327-1.866) and all cancers (HR = 1.948, 95% CI = 1.701-2.232), including gastrointestinal (GI) tract cancer (HR = 4.140, 95% CI = 3.656-4.687), gastric cancer (HR = 4.288, 95% CI = 3.969-4.632), and colorectal cancer (HR = 4.814, 95% CI = 3.849-6.020) in subjects with H. pylori infection after adjusting for health-related factors. Periodontitis was significantly related to the decreased survival time in subjects with GI tract (p = .001) or colorectal cancer (p = .002) and H. pylori infection. CONCLUSION: Our study demonstrated that periodontitis was significantly associated with higher mortality risk of GI tract, gastric, and colorectal cancer in subjects with H. pylori infection. Owing to an interactive effect between periodontitis and H. pylori infection on cancer mortality, H. pylori infection has a significant moderating effect in regulating the association between periodontitis and mortality due to all cancers, including GI tract cancer and colorectal cancer.

Dysregulation of the miR-30a/BiP axis by cigarette smoking accelerates oral cancer progression.

BACKGROUND: Cigarette smoking is the most significant cause of oral cancer progression. Cigarette smoke condensate (CSC) has been shown to induce endoplasmic reticulum (ER) stress. Binding immunoglobulin protein (BiP) being as an ER stress regulator, has been reported to be implicated in malignant behaviors. Therefore, the aim of this study was to investigate the role of the ER stress-responsive protein, BiP, in CSC-induced oral squamous cell carcinoma (OSCC) malignancy. METHODS: The biological role of BiP in CSC-induced tumor progression was investigated in OSCC cells (YD38 and SCC25) and in a tumor xenograft mouse model. The expressions of related genes were investigated using quantitative RT-PCR and Western blot analysis. Cell migration and invasion were assessed using scratch wound healing and Transwell invasion assays. The effects of conditioned media from OSCC cells on the angiogenic activities of endothelial cells were analyzed using a tube formation assay. The interaction between miR-30a and BiP mRNA was detected using a luciferase reporter assay. RESULTS: Our results demonstrated that CSC increased the expression of BiP in time- and dose-dependent manners in YD38 and SCC25 cells, and that silencing BiP abrogated CSC-induced cell invasion and tumor-associated angiogenesis. Notably, the putative miR-30a binding site was observed in the 3'untranslated region (UTR) of BiP mRNA, and miR-30a suppressed BiP expression by targeting 3'UTR of BiP transcript. In addition, CSC increased the expression of BiP in OSCC cells by downregulating miR-30a. We also showed that BiP promoted invasion and tumor-associated angiogenesis by increasing the production and secretion of vascular endothelial growth factor in CSC-exposed OSCC cells. Moreover, BiP inhibition suppressed OSCC growth and reduced tumor vessel density in tumor-bearing mice administered with CSC. CONCLUSIONS: These observations suggest that epigenetic regulation of BiP via miR-30a downregulation is involved in CSC-induced OSCC progression.

Associations between metabolic biomarkers and localized stage II/III periodontitis in young adults: The CHIEF Oral Health study.

AIM: To investigate the associations between metabolic risk factors and periodontitis in young adults. MATERIALS AND METHODS: The study included 1123 participants, aged 19-40 years, in Taiwan. Metabolic syndrome components were defined by the International Diabetes Federation criteria. Localized periodontitis was graded to healthy (n = 828) and stage II/III (n = 295) according to the 2017 criteria of the World Workshop. Multiple logistic regression analysis with adjustment for sex, age, betel nut consumption, and smoking were used to determine the associations. RESULTS: Greater waist circumference, serum triglycerides, and serum uric acid were associated with higher localized stage II/III periodontitis risk [odds ratio (OR) and 95% confidence interval (CI): 1.04 (1.02-1.05), 1.004 (1.002-1.006), and 1.10 (1.00-1.21), respectively]. There were no associations for total cholesterol, high-density lipoprotein, and blood pressure. There was a non-linear association between fasting glucose and localized stage II/III periodontitis, where the turning point was 105 mg/dl [OR: 0.97 (0.95-0.99) and 1.06 (1.00-1.13) when the levels were <105 and ≥105 mg/dl, respectively]. CONCLUSIONS: The risks of localized stage II/III periodontitis vary with metabolic components, in which waist circumference, serum triglycerides, and serum uric acid are the risk factors, whereas plasma glucose shows a non-linear relationship in young adults.

Association between periodontitis and pulmonary function based on the Third National Health and Nutrition Examination Survey (NHANES III).

OBJECTIVES: The purpose of this study was to investigate the association between impaired pulmonary function and periodontitis. MATERIALS AND METHODS: From the Third National Health and Nutrition Examination Survey data, we examined the association between pulmonary function and severity of periodontitis using the univariate and multivariate regression models. Moreover, the association between obstructive or restrictive spirometry patterns and periodontitis status was also determined by multivariable logistic regression analysis. RESULTS: A total of 10,645 participants were included in our study. The values of predicted FEV1%, predicted FVC%, and FEV1/FVC were found to gradually decline with increasing severity of periodontitis (p < .001). Obstructive and restrictive pulmonary functions were significantly associated with severity of periodontitis. CONCLUSION: Individuals with a greater degree of periodontitis had poor pulmonary function. However, further long-term cohort studies are required for a comprehensive evaluation.

Synthesis and Characterization of Melatonin-Loaded Chitosan Microparticles Promote Differentiation and Mineralization in Preosteoblastic Cells.

In terms of a novel scaffold with well good osteoinductive and osteoconductive capacity, melatonin (Mel) possesses positive effects on chemical linkage in scaffold structures, which may allow osteogenic differentiation. The aim of this study is to fabricate Mel-loaded chitosan (CS) microparticles (MPs) as a novel bone substitute through generating a Mel sustained release system from Mel-loaded CS MPs and evaluating its effect on the osteogenic capacity of MC3T3-E1 in vitro. The physical-chemical characteristics of the prepared CS MPs were examined by both Fourier transform infrared spectroscopy and scanning electron microscopy. The released profile and kinetics of Mel from MPs were quantified, and the bioactivity of the released Mel on preosteoblastic MC3T3-E1 cells was characterized in vitro. An in vitro drug release assay has shown high encapsulation efficiency and sustained release of Mel over the investigation period. In an osteogenesis assay, Mel-loaded CS MPs have significantly enhanced alkaline phosphatase (ALP) mRNA expression and ALP activity compared with the control group. Meanwhile, the osteoblast-specific differentiation genes, including runt related transcription factor 2 (Runx2), bone morphogentic protein-2 (Bmp2), collagen I (Col I), and osteocalcin (Ocn), were also significantly upregulated. Furthermore, quantificational alizarin red-based assay demonstrated that Mel-loaded CS MPs notably enhanced the calcium deposit of MC3T3-E1 compared with controls. In essence, Mel-loaded CS MPs can control the release of Mel for a period of time to accelerate osteogenic differentiation of preosteoblast cells in vitro.

Association between periodontitis and cognitive impairment: Analysis of national health and nutrition examination survey (NHANES) III.

OBJECTIVES: Periodontitis has been hypothesized as being one of the most common potential risk factors for the development of dementia and cognitive impairment. In order to investigate the relationship between periodontitis and cognition impairment, the National Health and Nutrition Examination Survey (NHANES) database was analysed after adjusting for potential confounding factors, including age and other systemic co-morbidities. MATERIALS AND METHODS: In total, 4,663 participants aged 20-59 years who had received full-mouth periodontal examination and undergone the cognitive functional test were enrolled. The grade of periodontal disease was categorized into severe, moderate, and mild. Cognitive function examinations, including the simple reaction time test (SRTT), symbol digit substitution test (SDST), and serial digit learning test (SDLT), were adopted for the evaluation of cognitive impairment. RESULTS: The subjects with mild and moderate to severe periodontitis had higher SDLT and SDST scores, which indicated decreased cognitive function, compared with the healthy group. After adjusting for demographic factors, education, smoking, cardiovascular diseases, and laboratory data, periodontitis was significantly correlated with elevated SDST and SDLT scores (p values for trend = 0.014 and 0.038, respectively) by generalized linear regression models. CONCLUSION: Our study highlighted that periodontal status was associated with cognitive impairment in a nationally representative sample of US adults.

Periodontitis-associated pathogens P. gingivalis and A. actinomycetemcomitans activate human CD14(+) monocytes leading to enhanced Th17/IL-17 responses.

The Th17/IL-17 pathway is implicated in the pathogenesis of periodontitis (PD), however the mechanisms are not fully understood. We investigated the mechanism by which the periodontal pathogens Porphyromonas gingivalis (Pg) and Aggregatibacter actinomycetemcomitans (Aa) promote a Th17/IL-17 response in vitro, and studied IL-17(+) CD4(+) T-cell frequencies in gingival tissue and peripheral blood from patients with PD versus periodontally healthy controls. Addition of Pg or Aa to monocyte/CD4(+) T-cell co-cultures promoted a Th17/IL-17 response in vitro in a dose- and time-dependent manner. Pg or Aa stimulation of monocytes resulted in increased CD40, CD54 and HLA-DR expression, and enhanced TNF-α, IL-1ß, IL-6 and IL-23 production. Mechanistically, IL-17 production in Pg-stimulated co-cultures was partially dependent on IL-1ß, IL-23 and TLR2/TLR4 signalling. Increased frequencies of IL-17(+) cells were observed in gingival tissue from patients with PD compared to healthy subjects. No differences were observed in IL-17(+) CD4(+) T-cell frequencies in peripheral blood. In vitro, Pg induced significantly higher IL-17 production in anti-CD3 mAb-stimulated monocyte/CD4(+) T-cell co-cultures from patients with PD compared to healthy controls. Our data suggest that periodontal pathogens can activate monocytes, resulting in increased IL-17 production by human CD4(+) T cells, a process that appears enhanced in patients with PD.

The association between temporomandibular disorders and joint hypermobility syndrome: a nationwide population-based study.

OBJECTIVES: This study aims to investigate the risk factors of temporomandibular disorders (TMDs), including disc or non-disc-related disorders, and joint hypermobility syndrome (JHS) retrospectively and to analyze the factors by estimating the magnitude of the association between the two conditions using a nationwide population-based dataset. MATERIALS AND METHODS: A total of 975,788 eligible patients' de-identified data were obtained from a representative database composed of one million of Taiwan's population since 2004 to 2008. All associated factors, such as gender, age, facial trauma, and psychosis, which correlated with TMDs and JHS were examined. Multiple logistic regression modeling adjusted for confounding variables to determine the odds ratio of variables that made an important contribution to TMDs and JHS. RESULTS: For all TMDs patients, only 1.47% patients had disc-related disorders. For all JHS patients, only 3.85% patients are diagnosed with concomitant TMDs. Statistically significant association was observed between joint hypermobility and TMDs. Furthermore, the prevalence of JHS patients shows significant difference within TMD subgroups, in which 9.52% of JHS patients have disc disorders and 90.48% of JHS patients do not. All associated factors, such as gender, age, JHS, facial trauma, and psychosis, had a significant impact on the TMDs. Interestingly, patients with TMJ articular disc disorders are 6.7 times more likely to be diagnosed with JHS compared to patients without disc-related disorders. CONCLUSIONS: Our results confirm that there is a significant positive association between TMDs and JHS, highlighting that patients with disc-related TMDs are more likely to experience JHS than patients with TMDs without disc disorders. CLINICAL RELEVANCE: Individuals with TMD associated with JHS should be carefully evaluated by inter-disciplinary specialists as these factors may eventually have impact on the prognosis of TMDs and JHS.

The presence, function and regulation of IL-17 and Th17 cells in periodontitis.

Periodontitis (PD) is a chronic inflammatory disease characterised by tissue inflammation and destruction of the associated alveolar bone. It is caused by the colonisation of the bacterial plaque biofilm and the resultant host immune responses in the surrounding periodontal tissues. The pro-inflammatory cytokine IL-17, and IL-17 producing CD4+ T cells (also called Th17 cells) have been shown to play an important role in many inflammatory diseases. There is increasing evidence of the presence of IL-17 and Th17 cells in human PD lesions and this may be associated with disease severity. Moreover, several animal studies indicate the potential role of IL-17 and Th17 cells in gingival inflammation and the resultant bone destruction in PD. Here we review recent findings regarding the presence, function and regulation of IL-17 and Th17 cells in PD, and we highlight potential areas of future research interest.

Obesity Phenotypes and Dental Calculus in Young Adults: CHIEF Oral Health Study.

AIM: The study aimed to examine the association of obesity phenotypes with dental calculus. BACKGROUND: Obesity has been recognized as a risk factor for kidney and gallbladder stones formation and periodontitis. OBJECTIVE: We have investigated the association between obesity, metabolic risk factors, and dental calculus, which is a sequela following periodontitis. METHODS: This study included 5,281 military members, aged 19-45 years, without antihypertensive medications in Taiwan. Obesity was defined as body mass index ≥27.5 kg/m2, and metabolic syndrome (MetS) was defined according to the modified ATP III criteria. Supragingival calculus in any teeth, except for impacted teeth and the third molar, was the outcome of interest. Multiple linear regression analysis with adjustments for age, sex, toxic substance use, brushing teeth frequency, and blood leukocyte counts, was used to determine the association of obesity with dental calculus numbers. Multiple logistic regression analysis was used to assess the association between obesity with or without MetS and the presence of any dental calculus. RESULTS: BMI was positively correlated to dental calculus numbers [ß and confidence intervals (CI) = 0.023 (0.014, 0.032)]. Compared to the obesity(-)/MetS(-) group, there were dosedependent associations for the obesity(-)/MetS(+), obesity(+)/MetS(-), and obesity(+)/MetS(+) groups with the presence of any dental calculus [odds ratios (ORs): 1.08 (0.76, 1.53), 1.31 (1.08, 1.58), and 1.51 (1.20, 1.90), respectively]. Of the metabolic risk factors, abdominal obesity and hypertension were independently associated with dental calculus [ORs: 1.33 (1.13, 1.55) and 1.30 (1.11, 1.52), respectively]. CONCLUSION: This study suggests general obesity as an independent risk factor for dental calculus formation, and MetS, particularly the components of abdominal obesity, and hypertension may also increase the prevalence of dental calculus. Diet control and regular exercise might be preventive measures for the development of both obesity and dental calculus.

MyD88 exacerbates inflammation-induced bone loss by modulating dynamic equilibrium between Th17/Treg cells and subgingival microbiota dysbiosis.

BACKGROUND: This study aimed to investigate the contribution of myeloid differentiation primary-response gene 88 (MyD88) on the differentiation of T helper type 17 (Th17) and regulatory T (Treg) cells and the emerging subgingival microbiota dysbiosis in Porphyromonas gingivalis-induced experimental periodontitis. METHODS: Alveolar bone loss, infiltrated inflammatory cells, immunostained cells for tartrate-resistant acid phosphatase (TRAP), the receptor activator of nuclear factor-kB ligand (RANKL), and osteoprotegerin (OPG) were quantified by microcomputerized tomography and histological staining between age- and sex-matched homozygous littermates (wild-type [WT, Myd88+/+] and Myd88-/- on C57BL/6 background). The frequencies of Th17 and Treg cells in cervical lymph nodes (CLNs) and spleen were determined by flow cytometry. Cytokine expression in gingival tissues, CLNs, and spleens were studied by quantitative polymerase chain reaction (qPCR). Analysis of the composition of the subgingival microbiome and functional annotation of prokaryotic taxa (FAPROTAX) analysis were performed. RESULTS: P. gingivalis-infected Myd88-/- mice showed alleviated bone loss, TRAP+ osteoclasts, and RANKL/OPG ratio compared to WT mice. A significantly higher percentage of Foxp3+CD4+ T cells in infected Myd88-/- CLNs and a higher frequency of RORγt+CD4+ T cells in infected WT mice was noted. Increased IL-10 and IL-17a expressions in gingival tissue at D14-D28 then declined in WT mice, whereas an opposite pattern was observed in Myd88-/- mice. The Myd88-/- mice exhibited characteristic increases in gram-positive species and species having probiotic properties, while gram-negative, anaerobic species were noted in WT mice. FAPROTAX analysis revealed increased aerobic chemoheterotrophy in Myd88-/- mice, whereas anaerobic chemoheterotrophy was noted in WT mice after P. gingivalis infection. CONCLUSIONS: MyD88 plays an important role in inflammation-induced bone loss by modulating the dynamic equilibrium between Th17/Treg cells and dysbiosis in P. gingivalis-induced experimental periodontitis.

Association Between Dental Calculus and Hypertension Phenotypes in Highly Fit Adults: CHIEF Oral Health Study.

BACKGROUND: Poor oral health evaluated by presence of dental calculus has been associated with hypertension (HTN) among middle- and old-aged adults. However, it is unclear for the association of HTN phenotypes with dental calculus in young adults. METHODS: This study examined the association between dental calculus and HTN in 5,345 military personnel, aged 19-45 years, without antihypertensive medications therapy in Taiwan from 2018 to 2021. Dental calculus was defined as presence of supragingival calculus in any teeth, except impacted teeth, and third molar. Combined HTN (CHTN) was diagnosed as systolic blood pressure (SBP) ≥130 mm Hg and diastolic blood pressure (DBP) ≥80 mm Hg. Isolated systolic and diastolic HTN were, respectively, defined as SBP ≥130 mm Hg only (ISHTN) and DBP ≥80 mm Hg only (IDHTN). Multiple logistic regression with adjustments for sex, age, toxic substance use, anthropometrics, lipid profiles, fasting glucose, and blood leukocyte counts were used to determine the association between dental calculus and HTN phenotypes in young adults. RESULTS: The prevalence of those with dental calculus, CHTN, ISHTN, and IDHTN was 20.8%, 10.8%, 10.2%, and 7.0%, respectively. The dental calculus was associated a greater possibility with CHTN [odds ratio (OR) and 95% confidence interval: 1.60 (1.31-1.95)]. However, the associations of dental calculus with ISHTN and IDHTN were null [OR: 1.05 (0.81-1.27) and 1.12 (0.86-1.46), respectively]. CONCLUSIONS: Our findings suggest that among young adults, poor oral health manifested by presence of dental calculus was associated with a greater possibility of CHTN, while not for ISHTN and IDHTN.