[Show abstract][Hide abstract] ABSTRACT: Previous studies have proposed a relationship between bone mineral density (BMD) and oral health. However, the relationship between BMD and tooth loss in female individuals is not yet well understood. Therefore, the aim of this study was to assess the association between BMD, including its related physiological factors, and tooth loss among postmenopausal women in Korea.
A total of 3,992 postmenopausal women aged 50 years or above were selected from the Fourth and Fifth Korea National Health and Nutrition Examination Surveys, which were cross-sectional in design and conducted from 2008 to 2011. The participants' BMD and number of teeth were assessed by radiologists and dentists. Socioeconomic characteristics and female-related physiological factors, including menarche age, duration of menopause, number of pregnancies, age at first child's birth, and duration of oral contraceptive or female hormone use, were surveyed.
Participants who had lower BMD had significantly fewer teeth (p < 0.001). Female-related physiological factors, including the duration of menopause, number of pregnancies, age at first child's birth, duration of oral contraceptive or female hormone use, and calcium intake level, showed a significant relationship with the number of teeth. Using multiple regression analysis, BMD, duration of menopause, age at first child's birth, and duration of female hormone use significantly influenced the number of teeth.
BMD and its related physiological factors in female individuals showed a significant relationship with the number of teeth in postmenopausal Korean women, implicating osteoporosis as a risk factor for tooth loss in postmenopausal women.
BMC Women's Health 08/2015; 15(1):65. DOI:10.1186/s12905-015-0218-x · 1.50 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Mitogen-activated protein kinases (MAPKs) are key signal transducers involved in various cellular events such as growth, proliferation, and differentiation. Previous studies have reported that H2O2 leads to phosphorylation of extracellular signal-regulated kinase (ERK), one of the MAPKs in endothelial cells. The current study shows that H2O2 suppressed ERK1/2 activation and phosphorylation at specific concentrations and times in human umbilical vein endothelial cells but not in immortalized mouse aortic endothelial cells or human astrocytoma cell line CRT-MG. Phosphorylation of other MAPK family members (i.e., p38 and JNK) was not suppressed by H2O2. The decrease in ERK1/2 phosphorylation induced by H2O2 was inversely correlated with the level of phosphorylation of Src tyrosine 530. Using siRNA, it was found that H2O2-induced suppression of ERK1/2 was dependent on Csk. Physiological laminar flow abrogated, but oscillatory flow did not affect, the H2O2-induced suppression of ERK1/2 phosphorylation. In conclusion, H2O2-induced Csk translocation to the plasma membrane leads to phosphorylation of Src at the tyrosine 530 residue resulting in a reduction of ERK1/2 phosphorylation. Physiological laminar flow abrogates this effect of H2O2 by inducing phosphorylation of Src tyrosine 419. These findings broaden our understanding of signal transduction mechanisms in the endothelial cells against oxidative stress.
[Show abstract][Hide abstract] ABSTRACT: Src homology 2-containing protein tyrosine phosphatase 2 (SHP-2) is known to protect neurons from neurodegeneration during ischemia/reperfusion injury. We have recently reported that ROS-mediated oxidative stress promotes phosphorylation of endogenous SHP-2 in astrocytes and complex formation between caveolin-1 and SHP-2 in response to oxidative stress. To elucidate the region of SHP-2 participating in the complex formation with caveolin-1, we generated three deletion mutant constructs and six point mutation constructs of SHP-2. Compared to wild-type SHP-2, the binding of N-SH2 domain deletion mutant of SHP-2 to p-caveolin-1 was largely reduced using flow cytometric competitive binding assay and surface plasmon resonance (SPR). Moreover, deletion of N-SH2 domain of SHP-2 affected H2O2-mediated ERK phosphorylation and Src phosphorylation at Tyr 419 in primary astrocytes, suggesting that N-SH2 domain of SHP-2 is responsible for the binding of caveolin-1 and contributes to the regulation of Src phosphorylation and activation following ROS-induced oxidative stress in brain astrocytes.
[Show abstract][Hide abstract] ABSTRACT: The quest for a happy life is accompanied by an increase in social activities, living standards, and socioeconomic development, with individuals showing increased interest in health and esthetics. In the field of dentistry, not only prevention and treatment but also esthetics is gaining popularity. The aim of this study was to identify tooth color reduction and consequent patient satisfaction over a period of 6 months after office and home bleaching.
[Show abstract][Hide abstract] ABSTRACT: The present study aimed to evaluate the validity of a set of self-reported questionnaires for periodontitis for estimating the prevalence of chronic adult periodontitis in the Korean population.
[Show abstract][Hide abstract] ABSTRACT: The prevalence of metabolic syndrome (MetS) increases even in adolescents. The evidence that MetS is associated with the periodontal diseases in adolescent has been understudied. Therefore, our aim was to assess the association between MetS parameters and gingivitis in adolescents.
A total of 941 participants (590 boys, 351 girls), aged 12-18 years was selected from the Fourth Korea National Health and Nutrition Examination Survey, a cross-sectional and nationally representative survey, who have had information on waist circumference, blood pressure, serum triglyceride, high-density lipoprotein (HDL) cholesterol, and the fasting blood sugar and community periodontal Index (CPI).
The number of positive parameters of MetS showed significant positive correlation with gingivitis; adjusted and crude ORs with one positive parameters of MetS were 1.92(95% CI: 1.21-3.04) and 1.88(95% CI: 1.28-2.76), respectively. And adjusted OR with three or more positive parameters of MetS was 3.29 (95% CI: 1.24-8.71). Among five parameters of MetS, Low HDL-cholesterol showed significant association with gingivitis (crude OR 2.12, 95% CI 1.20-3.73; adjusted OR 1.96, 95% CI 1.24-3.12).
Having more positive parameters of MetS and positive HDL-cholesterol parameter had an independent relationship with the prevalence of gingivitis, which may be determinants for the future periodontal diseases even in adolescents This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
[Show abstract][Hide abstract] ABSTRACT: Background:
Periodontitis is a result of a complex biologic alteration of the periodontal microenvironment and a distributional shift of key periodontal pathogens. Metabolic syndrome (MetS), a complex cluster of cardiovascular risk factors, has been linked to periodontal diseases; however, the contribution of periodontal bacteria to systemic conditions remains unclear.
The study population comprised 7,848 United States adults who participated in an interview, underwent a clinical oral-health examination, and had serum immunoglobulin G titers measured against 19 periodontal bacteria as part of the third National Health and Nutritional Examination Survey. The z-score antibody titers were clustered into four mutually exclusive groups and named after Socransky's classification of periodontal bacteria (Orange-Red, Red-Green, Yellow-Orange, and Orange-Blue). Survey logistic regression was used to investigate the independent associations between the cluster scores, and MetS and each component, including hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol, central obesity, and elevated fasting glucose.
The Orange-Red cluster score (that included Porphyromonas gingivalis and Prevotella spp.) was positively associated (odds ratio [OR] = 1.067, 95% confidence interval [CI] = 1.02 to 1.12) and the Orange-Blue cluster score (which included Actinomyces naeslundii and Eubacterium nodatum) was inversely associated (OR = 0.93, 95% CI = 0.88 to 0.97) with elevated fasting glucose (≥ 110 mg/dL) after adjustment for clusters and potential confounders. Neither MetS nor its other remaining MetS components were associated with a particular cluster score.
The associations between specific antibody clusters (Orange-Red and Orange-Blue) against periodontal bacteria and elevated plasma glucose were in qualitatively opposite directions after multivariable adjustment in a large, adult population. The periodontal bacterial profile was not found to be associated with metabolic control other than a very moderate association with elevated plasma glucose.
Journal of Periodontology 11/2014; 86(3):1-17. DOI:10.1902/jop.2014.140408 · 2.71 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Purpose:
The aim of this study was to determine the effect of hyaluronic acid (HA) on cyclooxygenase (COX)-2 expression in orbital fibroblasts from patients with thyroid-associated ophthalmopathy (TAO).
Primary cultured orbital fibroblasts were obtained from patients with TAO and non-TAO subjects. Dermal and conjunctival fibroblasts were cultured from the eyelid skin of subjects undergoing cosmetic lid surgery or cataract surgery, respectively. The cells were treated with HA and the transcriptional and translational levels of COX-2 were measured. The expression of CD44 on each type of cells was determined, and the involvement of CD44 in the HA-induced COX-2 increase in orbital fibroblasts from patients with TAO was evaluated by using CD44 knockdown cells and by pretreatment with neutralizing antibody. The relevance of the mitogen-activated protein kinase (MAPK) or nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-mediated signaling pathway was assessed by immunoblotting for the phosphorylated form of each MAPK or IκB and by using specific inhibitors to these pathways.
Hyaluronic acid increased COX-2 expression in orbital fibroblasts from patients with TAO, which was not observed in the cells from non-TAO subjects and conjunctival or dermal fibroblasts. Orbital fibroblasts from patients with TAO expressed significantly higher level of CD44 than non-TAO cells, and the increased COX-2 expression by HA in these cells was attenuated by knockdown or neutralizing of CD44. Hyaluronic acid induced MAPK and IκB phosphorylation; and cotreatment with specific MAPK or NF-κB inhibitors halted HA-induced transcription of COX-2, suggesting the involvement of these signaling pathways.
Hyaluronic acid induced COX-2 expression in orbital fibroblasts from patients with TAO via CD44 through the MAPK and NF-κB-mediated signaling pathways. These results suggest that HA may have a proinflammatory role in the pathogenesis of TAO by inducing COX-2.
[Show abstract][Hide abstract] ABSTRACT: Adrenomedullin (ADM), a secretory peptide with multiple functions in physiological to pathological conditions, is upregulated in several human cancers, including brain, breast, colon, prostate, and lung cancer. However, the molecular mechanisms underlying the regulation of ADM expression in cancerous cells are not fully understood. Here, we report that oncostatin M (OSM), a cytokine belonging to the interleukin-6 family, induces ADM expression in astroglioma cells through induction of signal transducer and activator of transcription-3 (STAT-3) phosphorylation, nuclear translocation, and subsequent DNA binding to the ADM promoter. STAT-3 knockdown decreased OSM-mediated expression of ADM, indicating that ADM expression is regulated by STAT-3 in astroglioma cells. Lastly, scratch wound healing assay showed that astroglioma cell migration was significantly enhanced by ADM peptides. These data suggest that aberrant activation of STAT-3, which is observed in malignant brain tumors, may function as one of the key regulators for ADM expression and glioma invasion.
[Show abstract][Hide abstract] ABSTRACT: The aim of the present study was to identify a new candidate anti-inflammatory compound for use in the active stage of thyroid-associated ophthalmopathy (TAO). Benzylideneacetophenone compound JC3 [(2E)-3-(4-hydroxy-3-methoxyphenyl)phenylpro-2-en-l-one] was synthesized based on a structural modification of yakuchinone B, a constituent of the seeds of Alpinia oxyphylla, which belongs to the ginger family (Zingiberaceae), has been widely used in folk medicine as an anti-inflammatory phytochemical. Orbital fibroblasts were primarily cultured from patients with TAO, and the potential of JC3 to suppress the interferon (IFN)-γ-induced protein (IP)-10/CXCL10 production in these cells was determined. IFN-γ strongly increased the level of IP-10/CXCL10 in orbital fibroblasts from patients with TAO. JC3 exerted a significant inhibitory effect on the IFN-γ-induced increase in IP-10/CXCL10 in a dose-dependent manner; its potency was greater than that of an identical concentration of yakuchinone B with no toxicity to cells at the concentration range used. Moreover, the constructed dimer and trimer polystructures of JC3, showed greater potency than JC3 in suppressing the IFN-γ-induced production of IP-10/CXCL10. JC3 significantly attenuated the IP-10/CXCL10 mRNA expression induced by IFN-γ, and a gel-shift assay showed that JC3 suppressed IFN-γ-induced DNA binding of signal transducer and activator of transcription-1 (STAT-1) in TAO orbital fibroblasts. Our results provide initial evidence that the JC3 compound reduces the levels of IP-10/CXCL10 protein and mRNA induced by IFN-γ in orbital fibroblasts of TAO patients. Therefore, JC3 might be considered as a future candidate for therapeutic application in TAO that exerts its effects by modulating the pathogenic mechanisms in orbital fibroblasts.
Experimental and Molecular Medicine 06/2014; 46(6):e100. DOI:10.1038/emm.2014.26 · 3.45 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Recognition of apoptotic cells by macrophages is crucial for resolution of inflammation, immune tolerance, and tissue repair. Cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) and hepatocyte growth factor (HGF) play important roles in the tissue repair process. We investigated the characteristics of macrophage COX-2 and PGE2 expression mediated by apoptotic cells and then determined how macrophages exposed to apoptotic cells in vitro and in vivo orchestrate the interaction between COX-2/PGE2 and HGF signaling pathways. Exposure of RAW 264.7 cells and primary peritoneal macrophages to apoptotic cells resulted in induction of COX-2 and PGE2. The COX-2 inhibitor NS-398 suppressed apoptotic cell-induced PGE2 production. Both NS-398 and COX-2-siRNA, as well as the PGE2 receptor EP2 antagonist, blocked HGF expression in response to apoptotic cells. In addition, the HGF receptor antagonist suppressed increases in COX-2 and PGE2 induction. The in vivo relevance of the interaction between the COX-2/PGE2 and HGF pathways through a positive feedback loop was shown in cultured alveolar macrophages following in vivo exposure of bleomycin-stimulated lungs to apoptotic cells. Our results demonstrate that upregulation of the COX-2/PGE2 and HGF in macrophages following exposure to apoptotic cells represents a mechanism for mediating the anti-inflammatory and antifibrotic consequences of apoptotic cell recognition.
Mediators of Inflammation 05/2014; 2014(4):463524. DOI:10.1155/2014/463524 · 3.24 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Reactive oxygen species (ROS) regulate diverse cellular functions by triggering signal transduction events, such as Src and mitogen-activated protein (MAP) kinases. Here, we report the role of caveolin-1 and Src homology 2 domain-containing protein tyrosine phosphatase 2 (SHP-2) in H2O2-induced signaling pathway in brain astrocytes. H2O2-mediated oxidative stress induced phosphorylation of caveolin-1 and association between p-caveolin-1 and SHP-2. SHP-2 specifically bound to wild-type caveolin-1 similarly to c-Src tyrosine kinase (CSK), but not to phosphorylation-deficient mutant of caveolin-1 (Y14A), and interfered with complex formation between caveolin-1 and CSK. In the presence of CSK siRNA, binding between caveolin-1 and SHP-2 was enhanced by H2O2 treatment, which led to reduced Src phosphorylation at tyrosine (Tyr) 530 and enhanced Src phosphorylation at Tyr 419. In contrast, siRNA targeting of SHP-2 facilitated H2O2-mediated interaction between caveolin-1 and CSK and enhanced Src phosphorylation at Tyr 530, leading to subsequent decrease in Src downstream signaling, such as focal adhesion kinase (FAK) and extracellular signal-related kinase (ERK). Our results collectively indicate that SHP-2 alters Src kinase activity by interfering with the complex formation between CSK and phosphotyrosine caveolin-1 in the presence of H2O2, thus functions as a positive regulator in Src signaling under oxidative stress in brain astrocytes.
PLoS ONE 03/2014; 9(3):e91582. DOI:10.1371/journal.pone.0091582 · 3.23 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Purpose:
This study aimed to investigate the effect of pirfenidone on the IL-1β-induced hyaluronic acid (HA) increase in orbital fibroblasts from patients with thyroid-associated ophthalmopathy (TAO).
Primary cultured orbital fibroblasts were obtained from patients with TAO, and the excreted levels of HA from IL-1β-treated cells with or without pirfenidone were measured. The effect of pirfenidone on IL-1β-induced hyaluronic acid synthase (HAS) expression was evaluated. The relevance of the mitogen-activated protein kinase (MAPK)-mediated signaling pathway in IL-1β-induced HAS expression was assessed using specific inhibitors to p38, extracellular signal-regulated kinase (ERK), or c-Jun N-terminal kinase (JNK). The phosphorylation level of each MAPK in IL-1β-treated cells with or without pirfenidone and the level of AP-1 DNA binding were measured. The inhibitory potency of pirfenidone on HA production was evaluated using dexamethasone as a reference agent.
Pirfenidone strongly attenuated the IL-1β-induced HA release in a dose-dependent manner. The IL-1β-induced HAS expression was decreased significantly following cotreatment with pirfenidone at the mRNA and protein levels. The production of mRNAs was halted by cotreatment with inhibitors of ERK and p38, but not by inhibitors of JNK. The IL-1β-induced ERK and p38 phosphorylation, and AP-1 DNA binding were attenuated in the presence of pirfenidone. Pirfenidone showed greater potency than dexamethasone in inhibiting increases in IL-1β-induced HA.
Pirfenidone attenuates the IL-1β-induced HA production in orbital fibroblasts from patients with TAO, at least in part, through suppression of the MAPK-mediated HAS expression. These results support the potential use of pirfenidone for treatment of patients with TAO.
[Show abstract][Hide abstract] ABSTRACT: Background:
Serum C-reactive protein (CRP) is elevated in both periodontitis and type 2 diabetes mellitus through inflammation. Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis have been found in periodontal pockets in patients with diabetes. This study examines effect modification by examining the extent to which the associations between periodontitis and hyperglycemia were different by levels of serum CRP and periodontal pathogens.
Blood samples with plasma were evaluated for immunoglobulin G antibodies, CRP, and fasting glucose from 5,731 participants ≥ 20 years old receiving oral examinations and providing other health-related data from the National Health and Nutrition Examination Survey III. The study participants were classified into quartiles of probing depth (PD) and clinical attachment level (CAL). The first quartile was the reference. Logistic regression models with survey procedures were used to explore the roles of inflammation levels from serum CRP and periodontal pathogens on the relations with periodontitis, including PD, CAL, and hyperglycemia, and their joint associations with interaction terms.
Stronger associations between PD and diabetes existed in people having elevated CRP and titers for P. gingivalis; odds ratios comparing extreme quartiles of PD were 1.31 and 3.40 in the groups with low and high CRP, respectively, and 1.28 and 2.96 in groups with low and high titers for P. gingivalis, respectively. The joint association patterns were similar for CAL and diabetes.
The strengths of association between periodontitis and diabetes were stronger in people having elevated serum CRP and P. gingivalis titers. This may suggest that chronic inflammatory conditions could increase the impact of periodontitis on hyperglycemic status.
Journal of Periodontology 01/2014; 85(9). DOI:10.1902/jop.2014.130658 · 2.71 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Rheumatoid arthritis (RA) has been associated with systemic diseases, such as periodontal diseases. Periodontal diseases and RA appear to share many pathologic features. The etiology of the two diseases may differ, but they share similar pathological characteristics. Therefore, the aim of this study was to evaluate the correlation between RA and periodontal diseases.
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to develop a self-administered questionnaire survey to determine its validity and reliability as well as to improve the instructions for measurement of periodontal disease during oral examination for reliably calculating the prevalence of periodontal disease.