Natural 4-year periodontal progression of mandibular first molars in Chinese villagers based on radiographic records.

BACKGROUND: To report 4-year natural periodontal progression of mandibular first molars based on radiographic records in 15 to 44-year-old Chinese villagers. METHODS: In 1992 (N = 486) and 1996 (N = 413), panoramic radiographs were recorded. Tooth loss of mandibular first molars was calculated. Relative bone height (RBH), intrabony defect (IBD) depth, and furcation involvement (FI) were measured on 918 and 755 mandibular first molars in 1992 and 1996, respectively. The progression of the three parameters and their relationship with widened periodontal ligament space (WPDL) were analyzed. RESULTS: In 1992, of 31 lost mandibular first molars, 29 belonged to the 35- to 44-year age group. At 4-year follow-up, five of eight lost teeth belonged to the 35- to 44-year age group. RBH decreased from 83% in 1992 to 77% in 1996. RBH progression was significantly faster in the 25- to 34- and 35- to 44-year age groups than in the 15- to 24-year age group. The mean IBD depth was 2.81 ± 0.55 mm (n = 32) in 1992 and 3.70 ± 0.73 mm (n = 33) in 1996. Prevalence of FI increased from 20.8% to 27.4%. Teeth with WPDL showed greater RBH and IBD progression than those without WPDL (RBH: 12% ± 1% versus 6% ± 0.01%, P < 0.001; IBD depth: 0.31 ± 0.08 versus 0.01 ± 0.00 mm, P <0.001). FI-area progression in teeth with WPDL showed a trend of greater expansion than in those without WPDL (0.92 ± 0.18 versus 0.56 ± 0.11 mm2 , P = 0.051). CONCLUSIONS: Tooth loss mainly occurred in the 35- to 44-year age group. RBH progression was faster in the 25- to 44-year age group. WPDL was associated with progression of RBH, IBDs, and FI.

Useful immunochromatographic assay of calprotectin in gingival crevicular fluid for diagnosis of diseased sites in patients with periodontal diseases.

BACKGROUND: Calprotectin, an inflammation-related protein, is present in gingival crevicular fluid (GCF), and the determination of calprotectin is useful for diagnosing periodontal diseases. The authors have recently developed a novel immunochromatographic (IC) chip system to determine calprotectin levels in GCF. In the present study, the usefulness of this diagnostic system is investigated in patients with periodontal diseases. METHODS: Thirty-six patients with periodontal diseases participated in this clinical test at multiple centers. Periodontitis sites (n = 118) and non-periodontitis (healthy) sites (n = 120) were selected after periodontal examination. GCF collection and periodontal examination were performed at baseline, after supragingival and subgingival scaling and root planing. Calprotectin levels in GCF were determined using a novel IC chip system and evaluated as a visual score and an IC reader value. Correlations between GCF calprotectin levels, clinical indicators, and changes in calprotectin levels by periodontal treatments were investigated. Receiver operating characteristic (ROC) analysis of IC reader value for GCF calprotectin was performed to predict periodontal diseases. RESULTS: The visual score of GCF calprotectin was highly correlated with the IC reader value. IC reader values of GCF calprotectin in the periodontitis group were higher than those of the healthy group at three dental examination stages, and they significantly decreased with periodontal treatments. Visual scores and IC reader values of GCF calprotectin were correlated to levels of clinical indicators. ROC analysis for GCF calprotectin showed an optimal cutoff value to predict periodontal diseases. CONCLUSION: Determination of GCF calprotectin using a novel IC chip system is useful for diagnosis of periodontal diseases.

A 4-year prospective study of the progression of periodontal disease in a rural Chinese population.

OBJECTIVES: The natural progression of periodontitis in the Chinese population is not well researched. We investigated the progression of periodontal disease over 4 years in 15-44-year-old Chinese villagers with no access to regular dental care. METHODS: In 1992, 486 villagers were enrolled, and in 1996, 413 villagers were re-examined. Probing depth (PD) and clinical attachment level (CAL) were examined at six sites per tooth. Sites with ΔCAL ≥3 mm were defined as active sites. Cross-sectional and longitudinal analyses were performed using means and percentile plots. RESULTS: The mean CAL increased by 0.26 mm over 4 years. The incidence of periodontitis (at least one site with CAL ≥3 mm) was 8%. The incidence of periodontitis among those with no periodontal disease at baseline was 44.9%. Seventy-eight percent of the subjects had at least one active site. In the 15-24-year group, 244 of 401 active sites had gingival recession, while only 51 active sites had both gingival recession and deeper pockets. In the 25-34-year and 35-44-year groups, almost one-third of the active sites (329/1087) and more than one-third of the active sites (580/1312) respectively had a combination of gingival recession and deeper pockets. CONCLUSIONS: In this study, we demonstrated that in Chinese population without regular dental care, both the initiation of periodontitis and progression of previously existed periodontitis contributed to the natural progression of periodontitis and periodontal pocketing played a greater role with age increasing. CLINICAL SIGNIFICANCE: This rare study reports the natural progression of periodontal disease in a group of Chinese villagers (15-44 years) with virtually no access to regular dental care.

Heterologous down-regulation of angiotensin type 1 receptors by purinergic P2Y2 receptor stimulation through S-nitrosylation of NF-kappaB.

Cross-talk between G protein-coupled receptor (GPCR) signaling pathways serves to fine tune cellular responsiveness by neurohumoral factors. Accumulating evidence has implicated nitric oxide (NO)-based signaling downstream of GPCRs, but the molecular details are unknown. Here, we show that adenosine triphosphate (ATP) decreases angiotensin type 1 receptor (AT(1)R) density through NO-mediated S-nitrosylation of nuclear factor κB (NF-κB) in rat cardiac fibroblasts. Stimulation of purinergic P2Y(2) receptor by ATP increased expression of inducible NO synthase (iNOS) through activation of nuclear factor of activated T cells, NFATc1 and NFATc3. The ATP-induced iNOS interacted with p65 subunit of NF-κB in the cytosol through flavin-binding domain, which was indispensable for the locally generated NO-mediated S-nitrosylation of p65 at Cys38. ß-Arrestins anchored the formation of p65/IκBα/ß-arrestins/iNOS quaternary complex. The S-nitrosylated p65 resulted in decreases in NF-κB transcriptional activity and AT(1)R density. In pressure-overloaded mouse hearts, ATP released from cardiomyocytes led to decrease in AT(1)R density through iNOS-mediated S-nitrosylation of p65. These results show a unique regulatory mechanism of heterologous regulation of GPCRs in which cysteine modification of transcriptional factor rather than protein phosphorylation plays essential roles.

Pertussis toxin up-regulates angiotensin type 1 receptors through Toll-like receptor 4-mediated Rac activation.

Pertussis toxin (PTX) is recognized as a specific tool that uncouples receptors from G(i) and G(o) through ADP-ribosylation. During the study analyzing the effects of PTX on Ang II type 1 receptor (AT1R) function in cardiac fibroblasts, we found that PTX increases the number of AT1Rs and enhances AT1R-mediated response. Microarray analysis revealed that PTX increases the induction of interleukin (IL)-1beta among cytokines. Inhibition of IL-1beta suppressed the enhancement of AT1R-mediated response by PTX. PTX increased the expression of IL-1beta and AT1R through NF-kappaB, and a small GTP-binding protein, Rac, mediated PTX-induced NF-kappaB activation through NADPH oxidase-dependent production of reactive oxygen species. PTX induced biphasic increases in Rac activity, and the Rac activation in a late but not an early phase was suppressed by IL-1beta siRNA, suggesting that IL-1beta-induced Rac activation contributes to the amplification of Rac-dependent signaling induced by PTX. Furthermore, inhibition of TLR4 (Toll-like receptor 4) abolished PTX-induced Rac activation and enhancement of AT1R function. However, ADP-ribosylation of G(i)/G(o) by PTX was not affected by inhibition of TLR4. Thus, PTX binds to two receptors; one is TLR4, which activates Rac, and another is the binding site that is required for ADP-ribosylation of G(i)/G(o).

Galpha12/13-mediated up-regulation of TRPC6 negatively regulates endothelin-1-induced cardiac myofibroblast formation and collagen synthesis through nuclear factor of activated T cells activation.

Sustained elevation of [Ca(2+)](i) has been implicated in many cellular events. We previously reported that alpha subunits of G(12) family G proteins (Galpha(12/13)) participate in sustained Ca(2+) influx required for the activation of nuclear factor of activated T cells (NFAT), a Ca(2+)-responsive transcriptional factor, in rat neonatal cardiac fibroblasts. Here, we demonstrate that Galpha(12/13)-mediated up-regulation of canonical transient receptor potential 6 (TRPC6) channels participates in sustained Ca(2+) influx and NFAT activation by endothelin (ET)-1 treatment. Expression of constitutively active Galpha(12) or Galpha(13) increased the expression of TRPC6 proteins and basal Ca(2+) influx activity. The treatment with ET-1 increased TRPC6 protein levels through Galpha(12/13), reactive oxygen species, and c-Jun N-terminal kinase (JNK)-dependent pathways. NFAT is activated by sustained increase in [Ca(2+)](i) through up-regulated TRPC6. A Galpha(12/13)-inhibitory polypeptide derived from the regulator of the G-protein signaling domain of p115-Rho guanine nucleotide exchange factor and a JNK inhibitor, SP600125, suppressed the ET-1-induced increase in expression of marker proteins of myofibroblast formation through a Galpha(12/13)-reactive oxygen species-JNK pathway. The ET-1-induced myofibroblast formation was suppressed by overexpression of TRPC6 and CA NFAT, whereas it was enhanced by TRPC6 small interfering RNAs and cyclosporine A. These results suggest two opposite roles of Galpha(12/13) in cardiac fibroblasts. First, Galpha(12/13) mediate ET-1-induced myofibroblast formation. Second, Galpha(12/13) mediate TRPC6 up-regulation and NFAT activation that negatively regulates ET-1-induced myofibroblast formation. Furthermore, TRPC6 mediates hypertrophic responses in cardiac myocytes but suppresses fibrotic responses in cardiac fibroblasts. Thus, TRPC6 mediates opposite responses in cardiac myocytes and fibroblasts.

Possible periodontal pathogens associated with clinical symptoms of periodontal disease in Japanese high school students.

BACKGROUND: The purpose of this study is to investigate how the components of biofilm and clinical oral status change in adolescents and to identify specific periodontal pathogens as risk markers for the onset of periodontitis. METHODS: One hundred seven high school students (72 boys and 35 girls, all 15 years old) were recruited. The mesio-lingual site of the left lower first molar was selected as the examined site. Probing depth (PD), bleeding on probing (BOP), the presence of subgingival calculus, and Community Periodontal Index (CPI) were determined by examination with a WHO probe. The prevalence and proportion of seven selected periodontal pathogens (Porphyromonas gingivalis, Tannerella forsythensis, Prevotella intermedia, Campylobacter rectus, Eikenella corrodens, and Actinobacillus actinomycetemcomitans serotypes b and c) were determined by indirect immunofluorescent technique, and the prevalence and proportion of spirochetes were determined by their morphology under dark-field microscopy. The relationship between the periodontal status and the bacterial condition was statistically analyzed. RESULTS: The mean proportion of T. forsythensis was significantly higher in BOP (+) sites compared with BOP (-) sites (3.47% +/- 5.35% versus 0.83% +/- 1.95%) and in CPI 3 sites compared with CPI 0 sites (3.29% +/- 5.28% versus 0.68% +/- 1.37%). The mean proportion of C. rectus was significantly increased in BOP (+) compared with BOP (-) (2.01% +/- 2.48% versus 0.79% +/- 0.91%) and in CPI 3 sites compared with CPI 0 sites (2.04% +/- 2.64% versus 0.80% +/- 0.79%). CONCLUSION: The results indicated that T. forsythensis and C. rectus might be able to be used as risk markers for the onset of periodontitis.

Determination of eight selected periodontal pathogens in the subgingival plaque of maxillary first molars in Japanese school children aged 8-11 years.

To prevent the onset or progression of periodontitis, we must understand when periodontal pathogens are first harbored and how they develop the biofilm that causes periodontal disease. The purpose of this study was to determine the relationship between clinical status and selected periodontal pathogens in subgingival plaque in school children. This study was conducted with 95 school children, 8-11 years old. The presence and distribution of eight selected periodontal pathogens sampled from the maxillary right first molar were determined by an indirect immunofluorescent technique and compared with clinical parameters. Of the 95 sites sampled, only one site had all eight pathogens and five sites did not have any of the eight pathogens. The mean number of positive pathogens per site was 3.5 +/- 1.8 and mean percentage of positive pathogens was 3.82 +/- 4.22%. The number and total percentage of positive pathogens were strongly correlated with the Plaque Index (PI). In addition, the number of positive pathogens was correlated to the presence of subgingival calculus. The most frequently found pathogens were Campylobacter rectus (84.2%) and Eikenella corrodens (83.2%), and the least, Actinobacillus actinomycetemcomitans serotype c (7.4%). Of the eight pathogens, the frequency and distribution of Porphyromonas gingivalis were significantly correlated with PI and the presence of calculus. In addition, seven sites with both P. gingivalis and Bacteroides forsythus showed a correlation with gingival inflammation. In conclusion, the presence of P. gingivalis or P. gingivalis and B. forsythus may be a risk marker to be sought in screening for the onset of periodontal disease.

Eikenella corrodens in subgingival plaque: relationship to age and periodontal condition.

BACKGROUND: The purpose of this study was to determine the prevalence and distribution of Eikenella corrodens (E. corrodens) in subgingival plaque in different age and periodontitis groups and to examine whether its presence is related to periodontal diseases. METHODS: A total of 273 subgingival plaque samples from 213 periodontitis patients and 60 healthy subjects were assessed. Smears from each plaque sample were made and E. corrodens was detected by means of indirect immunofluorescent technique. Mean percentage of E. corrodens per total bacteria (distribution) was calculated in each sample. The prevalence (% of positive samples) and distribution of E. corrodens were statistically analyzed based on age or diagnosis by means of Fisher's exact test and analysis of variance (ANOVA). RESULTS: Prevalence of E. corrodens decreased by age in the healthy control group; however, prevalence did not change in periodontitis groups. Distribution of E. corrodens was highest in juvenile periodontitis (JP) (2.3 +/- 1.5%) followed by post-JP (1.7 +/- 2.1%), prepubertal periodontitis (1.4 +/- 1.1%), rapidly progressive periodontitis (0.8 +/- 0.7%), adult periodontitis (0.7 +/- 0.6%), and healthy subjects (0.3 +/- 0.3%) (ANOVA, P<0.0001). The <20-year-old age group with periodontitis showed the highest distribution of E. corrodens (2.2 +/- 1.6%) compared to the older age groups who were either healthy or had periodontitis (ANOVA, P<0.0001). CONCLUSIONS: Since the distribution of E. corrodens is significantly higher in JP, post-JP, and PP, E. corrodens might play an important role in the occurrence or progression of periodontitis in young patients.