A large-scale observational study to investigate the current status of diabetic complications and their prevention in Japan (JDCP study 6): baseline dental and oral findings.

Japan Diabetes Complication and Prevention prospective (JDCP) study was conducted to examine the association between glycemic control and oral conditions in a large database of Japanese patients with diabetes. It included a total of 6099 patients with diabetes (range, 40-75 years) who had been treated as outpatients between 2007 and 2009. The mean number of present teeth at baseline was 19.8 and women with type 2 diabetes had fewer teeth than men with type 2 diabetes. Within the previous year, 17% of all patients had lost teeth. At baseline, 32% had experienced gingival swelling, 69% had brushed more than twice a day, 37% had used interdental cleaning aids, and 43% had undergone regular dental checkups. Multiple logistic regression analysis indicated that type 1 patients with HbA1c ≥ 7.0% were at higher risk of having fewer than 20 teeth (odds ratio [OR] 2.38; 95% confidence interval [CI] 1.25-4.78), and type 2 patients with HbA1c ≥ 8.0% also were at high risk of having fewer than 20 teeth (OR 1.16; 95% CI 1.00-1.34), after adjustment for nine possible confounding factors. In conclusion, patients with diabetes were found to be at high risk of tooth loss, and the poorer the glycemic control, the higher the risk of tooth loss in these patients.

Therapeutic potential for insulin on type 1 diabetes-associated periodontitis: Analysis of experimental periodontitis in streptozotocin-induced diabetic rats.

AIMS/INTRODUCTION: The association between diabetes and periodontal disease is considered to be bidirectional. However, there is still controversy surrounding the relationship between periodontal disease and type 1 diabetes. We investigated whether insulin improves periodontitis without any local treatments for periodontitis under type 1 diabetes conditions using the ligature-induced experimental periodontitis model. MATERIALS AND METHODS: Type 1 diabetic rats were induced by streptozotocin injection. Experimental periodontitis was induced by ligature in normal and diabetic rats. Half of the diabetic rats were treated with insulin. Two weeks after the ligature, periodontitis was evaluated. RESULTS: Insulin treatment significantly improved inflammatory cell infiltration and inflammatory cytokine gene expression, leading to suppression of alveolar bone loss, in the periodontitis of diabetic rats. Insulin also suppressed the periodontitis-increased nitric oxide synthase-positive cells in periodontal tissue of the diabetic rats. Even without induction of periodontitis, diabetic rats showed decreased gingival blood flow and an increased number of nitric oxide synthase-positive cells in the gingiva and alveolar bone loss compared with normal rats, all of which were ameliorated by insulin treatment. We further confirmed that insulin directly suppressed lipopolysaccharide-induced inflammatory cytokine expressions in THP-1 cells. CONCLUSIONS: There were abnormalities of periodontal tissue even without the induction of periodontitis in streptozotocin-induced diabetic rats. Insulin treatment significantly ameliorated periodontitis without local periodontitis treatment in diabetic rats. These data suggest the therapeutic impacts of insulin on periodontitis in type 1 diabetes.

Correction: Interleukin-1 Receptor Antagonist Has a Novel Function in the Regulation of Matrix Metalloproteinase-13 Expression.

[This corrects the article DOI: 10.1371/journal.pone.0140942.].

Site-level progression of periodontal disease during a follow-up period.

Periodontal disease is assessed and its progression is determined via observations on a site-by-site basis. Periodontal data are complex and structured in multiple levels; thus, applying a summary statistical approach (i.e., the mean) for site-level evaluations results in loss of information. Previous studies have shown the availability of mixed effects modeling. However, clinically beneficial information on the progression of periodontal disease during the follow-up period is not available. We conducted a multicenter prospective cohort study. Using mixed effects modeling, we analyzed 18,834 sites distributed on 3,139 teeth in 124 patients, and data were collected 5 times over a 24-month follow-up period. The change in the clinical attachment level (CAL) was used as the outcome variable. The CAL at baseline was an important determinant of the CAL changes, which varied widely according to the tooth surface. The salivary levels of periodontal pathogens, such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were affected by CAL progression. "Linear"- and "burst"-type patterns of CAL progression occurred simultaneously within the same patient. More than half of the teeth that presented burst-type progression sites also presented linear-type progression sites, and most of the progressions were of the linear type. Maxillary premolars and anterior teeth tended to show burst-type progression. The parameters identified in this study may guide practitioners in determining the type and extent of treatment needed at the site and patient levels. In addition, these results show that prior hypotheses concerning "burst" and "linear" theories are not valid.

Optimizing the reconstruction filter in cone-beam CT to improve periodontal ligament space visualization: An in vitro study.

PURPOSE: Evaluation of alveolar bone is important in the diagnosis of dental diseases. The periodontal ligament space is difficult to clearly depict in cone-beam computed tomography images because the reconstruction filter conditions during image processing cause image blurring, resulting in decreased spatial resolution. We examined different reconstruction filters to assess their ability to improve spatial resolution and allow for a clearer visualization of the periodontal ligament space. MATERIALS AND METHODS: Cone-beam computed tomography projections of 2 skull phantoms were reconstructed using 6 reconstruction conditions and then compared using the Thurstone paired comparison method. Physical evaluations, including the modulation transfer function and the Wiener spectrum, as well as an assessment of space visibility, were undertaken using experimental phantoms. RESULTS: Image reconstruction using a modified Shepp-Logan filter resulted in better sensory, physical, and quantitative evaluations. The reconstruction conditions substantially improved the spatial resolution and visualization of the periodontal ligament space. The difference in sensitivity was obtained by altering the reconstruction filter. CONCLUSION: Modifying the characteristics of a reconstruction filter can generate significant improvement in assessments of the periodontal ligament space. A high-frequency enhancement filter improves the visualization of thin structures and will be useful when accurate assessment of the periodontal ligament space is necessary.

Role of poly(ADP-ribose) polymerase activation in the pathogenesis of periodontitis in diabetes.

AIM: The aetiology of progressive periodontitis in diabetes has not yet been elucidated. We previously demonstrated that nitrosative stress is increased in diabetic rats with periodontitis. Nitrosative stress induces poly(ADP-ribose) polymerase (PARP) activation. Here, we demonstrated the involvement of PARP activation in diabetic periodontitis and detailed the therapeutic effects of PARP inhibitor. MATERIALS AND METHODS: Experimental periodontitis was induced by placing a nylon thread ligature. Half of the normal and diabetic rats received the PARP inhibitor, 1,5-isoquinolinediol, for 2 weeks. Gingival PARP activation was detected by immunostaining for poly(ADP-ribose). Periodontitis was evaluated by gingival inflammatory cell infiltration, inflammatory gene expressions and micro-CT analyses. RESULTS: Although both periodontitis and the presence of diabetes increased PARP activation in the gingiva, diabetic rats with periodontitis had the highest activation of PARP. Diabetic rats with periodontitis also showed significant increases in monocyte/macrophage invasion into the gingiva, inflammatory gene expressions, nitrotyrosine-positive cells in the gingiva and alveolar bone loss, all of which were suppressed by treatment with the PARP inhibitor. CONCLUSIONS: These results indicate the involvement of PARP activation in the pathogenesis and aggravation of periodontal disease in diabetes and suggest the therapeutic potential of PARP inhibition for treating periodontal disease, especially in patients with diabetes.

IL-15 and RANKL Play a Synergistically Important Role in Osteoclastogenesis.

Interleukin-15 (IL-15), a cytokine secreted by several cell types, has important physiological roles in the activity, proliferation, and viability of immune cells. It has both chemoattractant and proinflammatory properties, and may promote bone destruction. A previous study has shown that IL-15 alone exerts no effect on osteoclastogenesis. Therefore, the current study addressed the synergistic effect of IL-15 on osteoclast formation using RAW264.7 (RAW) cells by co-stimulation with receptor activator of nuclear factor (NF)-κB ligand (RANKL) that has a major role in osteoclastogenesis involving the pathogenesis of rheumatoid arthritis and periodontal disease. Co-stimulation of RAW cells by IL-15 and RANKL significantly increased the gene expression of osteoclast differentiation and osteoclastogenesis markers compared with stimulation by RANKL or IL-15 independently as evaluated by tartrate-resistant acid phosphate-positive cell numbers, the fusion index, a pit formation assay with Alizarin red staining (calcification estimation), and quantitative polymerase chain reaction. Phosphorylation of extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase, p38 mitogen-activated protein kinase, and NF-κB was significantly increased by RANKL and IL-15 (P < 0.05) compared with RANKL alone. In addition, these differentiation activities induced by RANKL and IL-15 were comparatively suppressed by inhibition of ERK, suggesting that this synergistic effect on osteoclastogenesis is mainly mediated by ERK. Taken together, our results demonstrate that IL-15 and RANKL induce osteoclastogenesis synergistically, and IL-15 might play a novel and major role in destructive inflammatory bone diseases. J. Cell. Biochem. 118: 739-747, 2017. © 2016 Wiley Periodicals, Inc.

Anti-inflammatory role of glucose-dependent insulinotropic polypeptide in periodontitis.

AIMS/INTRODUCTION: The involvement of glucose-dependent insulinotropic polypeptide (GIP) on inflammation was explored in atherosclerosis and adipose tissue. Periodontal disease is a chronic inflammatory disease, and is considered one of the diabetic complications. In the present study, to examine the effect of GIP on periodontitis, we induced experimental periodontitis in glucose-dependent insulinotropic polypeptide receptor-knockout mice (GIPRKO). We also investigated the anti-inflammatory effect of GIP in a culture system. MATERIALS AND METHODS: Experimental periodontitis was induced by ligature wire in GIPRKO and C57BL/C mice. Two weeks after the ligature, immunohistological evaluation and inflammatory messenger ribonucleic acid expression in the gingiva was examined. To elucidate the role of GIP in inflammation, the effects of GIP on lipopolysaccharide-induced gene expressions in THP-1 cells were evaluated. RESULTS: Periodontitis increased inflammatory cell infiltration, macrophage accumulation and tumor necrosis factor-α and nitric oxide synthase gene expressions in the gingiva. Periodontitis in GIPRKO showed a marked increase of inflammatory cells in the gingivomucosal tissue. Mac-1-positive macrophages and the inflammatory gene expressions were significantly increased in periodontitis in GIPRKO compared with C57BL/C mice periodontitis. Immunohistochemical staining confirmed that GIP receptors were expressed in residual and infiltrated Mac-1-positive macrophages. The in vitro study showed that GIP suppressed lipopolysaccharide-induced tumor necrosis factor-α and nitric oxide synthase gene expression in a dose-dependent manner. Furthermore, the inhibitory effect of GIP on lipopolysaccharide-induced inflammatory gene expressions was at least partially through cyclic adenosine monophosphate/protein kinase A pathway. CONCLUSIONS: These results suggest the beneficial effects of GIP on periodontal disease. In diabetic patients, GIP is expected to have a direct anti-inflammatory effect on periodontitis in addition to its glucose-lowering effect.

Assessment of oral malodor and tonsillar microbiota after gargling with benzethonium chloride.

The oropharyngeal area can be a source of halitosis. However, the relationship between healthy tonsillar microbiota and halitosis is poorly understood. We conducted a pilot clinical study to clarify the effect of gargling with an antiseptic agent on tonsillar microbiota in patients with halitosis. Twenty-nine halitosis patients who did not have otolaryngologic disease or periodontitis were assigned randomly to one of three groups: benzethonium chloride (BZC) gargle; placebo gargle; no gargle. Concentrations of volatile sulfur compounds (VSCs) in mouth air, the organoleptic score (ORS) and tongue-coating score (TCS) were measured before and after testing. Tonsillar microbiota were assessed by detection of periodontal pathogens, and profiling with terminal-restriction fragment length polymorphism (T-RFLP) analysis and sequencing of 16SrRNA clone libraries for taxonomic assignment. Gargling with BZC reduced the concentrations of methyl mercaptan and hydrogen sulfide and the ORS, but did not affect the TCS or prevalence of periodontal pathogens. T-RFLP analyses and 16SrRNA clone sequencing showed a tendency for some candidate species to decrease in the test group. Although gargling of the oropharyngeal area with an antiseptic agent can reduce oral malodor, it appears that tonsillar microbiota are not influenced greatly. (J Oral Sci 58, 83-91, 2016).

Adhesion Properties of Human Oral Epithelial-Derived Cells to Zirconia.

BACKGROUND: Few studies have examined epithelial attachment to zirconia and the proliferative ability of epithelial cells on zirconia surfaces. PURPOSE: To evaluate the adhesion properties of zirconia materials for epithelial cell attachment and compare this with titanium and alumina. MATERIALS AND METHODS: Human oral epithelial cells were cultured on smooth-surfaced specimens of commercially pure titanium (cpTi), ceria-stabilized zirconia/alumina nano-composite (P-NANOZR), yttria-stabilized zirconia (Cercon), and alumina oxide (inCoris AL). The cell morphology, the cell viability and mRNA of integrin ß4 , laminin γ2 , catenin δ2 , and E-cadherin were evaluated by SEM, Cell-Counting Kit-8, and real-time PCR, respectively. RESULTS: Morphology of cells attached to specimens was similar among all groups. The viable cell numbers on Cercon and inCoris AL after 24 hours culture were significantly higher than for cpTi. Integrin ß4 , laminin γ2 , and catenin δ2 mRNA expression was not different among all groups. However, at 3 and 24 hours after incubation, E-cadherin mRNA expression in the P-NANOZR group was significantly higher than for cpTi. CONCLUSION: Zirconia may support binding of epithelial cells through hemidesmosomes comparable with titanium. Furthermore, P-NANOZR may impart resistance to exogenous stimuli through strong intercellular contacts with peri-implant mucosal cells when used as an abutment and implant superstructure.

Randomized Placebo-Controlled and Controlled Non-Inferiority Phase III Trials Comparing Trafermin, a Recombinant Human Fibroblast Growth Factor 2, and Enamel Matrix Derivative in Periodontal Regeneration in Intrabony Defects.

We investigated the efficacy, safety, and clinical significance of trafermin, a recombinant human fibroblast growth factor (rhFGF)-2, for periodontal regeneration in intrabony defects in Phase III trials. Study A, a multicenter, randomized, double-blind, placebo-controlled study, was conducted at 24 centers. Patients with periodontitis with 4-mm and 3-mm or deeper probing pocket depth and intrabony defects, respectively, were included. A total of 328 patients were randomly assigned (2:1) to receive 0.3% rhFGF-2 or placebo, and 323 patients received the assigned investigational drug during flap surgery. One of the co-primary endpoints, the percentage of bone fill at 36 weeks after drug administration, was significantly greater in the rhFGF-2 group at 37.131% (95% confidence interval [CI], 32.7502 to 41.5123; n = 208) than it was in the placebo group at 21.579% (95% CI, 16.3571 to 26.8011; n = 100; p < 0.001). The other endpoint, the clinical attachment level regained at 36 weeks, was not significantly different between groups. Study B, a multicenter, randomized, blinded (patients and evaluators of radiographs), and active-controlled study was conducted at 15 centers to clarify the clinical significance of rhFGF-2. Patients with 6-mm and 4-mm or deeper probing pocket depth and intrabony defects, respectively, were included. A total of 274 patients were randomly assigned (5:5:2) to receive rhFGF-2, enamel matrix derivative (EMD), or flap surgery alone. A total of 267 patients received the assigned treatment during flap surgery. The primary endpoint, the linear alveolar bone growth at 36 weeks, was 1.927 mm (95% CI, 1.6615 to 2.1920; n = 108) in the rhFGF-2 group and 1.359 mm (95% CI, 1.0683 to 1.6495; n = 109) in the EMD group, showing non-inferiority (a prespecified margin of 0.3 mm) and superiority of rhFGF-2 to EMD. Safety problems were not identified in either study. Therefore, trafermin is an effective and safe treatment for periodontal regeneration in intrabony defect, and its efficacy was superior in rhFGF-2 compared to EMD treatments.

Interleukin-1 Receptor Antagonist Has a Novel Function in the Regulation of Matrix Metalloproteinase-13 Expression.

Interleukin-1 receptor antagonist (IL-1Ra) is an IL-1 family member, which binds to IL-1 receptors but does not induce any intracellular signaling. We addressed whether IL-1Ra has a novel function in regulation of the extracellular matrix or adhesion molecules. Polymerase chain reaction array analysis demonstrated a ~5-fold increase in matrix metalloproteinase 13 (MMP-13) mRNA expression of IL-1Ra siRNA-transfected Ca9-22 human oral squamous epithelial carcinoma cells compared with the control. In fact, MMP-13 mRNA and protein expression as well as its activity in IL-1Ra siRNA-transfected Ca9-22 cell lines were significantly higher than those in the control. IL-1Ra siRNA treatment resulted in strong elevation of MMP-13 expression, whereas addition of rhIL-1Ra (40 ng/ml) suppressed MMP-13 expression, suggesting that IL-1Ra had a specific effect on MMP-13 induction. IL-1Ra siRNA could potently suppress IL-1α. No significant difference was found between the MMP-13 mRNA expression of IL-1Ra siRNA-transfected cells and those treated with anti-IL-1α or anti-IL-1ß antibodies. These results suggested that continuous supply of IL-1 had no effect on the induction of MMP-13 by IL-1Ra siRNA. Histopathological investigation of MMP-13 in periodontal tissue showed specific localization in the junctional epithelial cells of IL-1Ra knockout (KO) mice. Furthermore, infection with Aggregatibacter actinomycetemcomitans to establish an experimental periodontitis model resulted in predominant localization of MMP-13 along apical junctional epithelial cells. Laminin-5, which is degraded by MMP-13, was found in the internal basal lamina of wild-type mice, whereas the internal basal lamina of IL-1Ra KO mice did not show obvious laminin-5 localization. In particular, laminin-5 localization almost disappeared in the internal basal lamina of IL-1Ra KO mice infected with A. actinomycetemcomitans, suggesting that the suppression of IL-1Ra resulted in strong induction of MMP-13 that degraded laminin-5. In conclusion, IL-1Ra is associated with MMP-13 expression and has a novel function in such regulation without interference of the IL-1 signaling cascade.

Increased expression of interleukin (IL)-35 and IL-17, but not IL-27, in gingival tissues with chronic periodontitis.

BACKGROUND: Interleukin (IL)-35 plays an important role in immune regulation through the suppression of effector T-cell populations, including T-helper 17 (Th17) cells. Although Th17 cells and IL-17 are involved in the pathogenesis of periodontitis, the level of IL-35 in inflamed periodontal tissues is unclear. Here, IL-35, IL-17, and IL-27 production/expression in gingival crevicular fluid (GCF) and human gingival tissue were investigated. METHODS: GCF samples were collected from buccal (mesial, center, and distal) sites of teeth from patients with chronic periodontitis (CP) and healthy controls and were analyzed by enzyme-linked immunosorbent assay for IL-35 (periodontitis, n = 36; healthy, n = 30) and IL-17 (periodontitis, n = 16; healthy, n = 13). Gingival tissue, including sulcus/pocket epithelium and underlying connective tissue, was collected from an additional 10 healthy participants and 10 patients with CP and were analyzed by quantitative polymerase chain reaction (qPCR) for Epstein Barr virus-induced gene 3 (EBI3), IL12A, and IL17A. IL27p28 was also tested by qPCR. RESULTS: IL-35 and IL-17 were significantly higher in GCF from patients with periodontitis than healthy participants (P <0.01, P <0.05, respectively). In both healthy participants and those with periodontitis, positive correlations were found among IL-35 and probing depth and clinical attachment level (CAL) as well as between IL-17 and CAL. EBI3, IL12A (components of IL-35), and IL17A messenger RNA expression levels were significantly higher in inflamed gingival tissue than in healthy control tissues (P <0.05). IL27p28 was not detected in any sample, suggesting that IL-27 is not produced in large quantities in periodontal tissue. CONCLUSION: IL-35 and IL-17, but not IL-27, may play important roles in the pathogenesis of periodontitis.

Morphological alterations of periodontal pocket epithelium following Nd:YAG laser irradiation.

OBJECTIVE: The purpose of this in vivo study was to examine morphologic alterations in the periodontal pocket epithelium with presence or absence of clinical inflammation following the use of the Neodymium: Yttrium-Aluminum-Garnet (Nd:YAG) laser irradiation. BACKGROUND DATA: Subgingival Nd:YAG laser irradiation has been proposed as an alternative technique for treatment of chronic periodontitis. Several published studies have reported the clinical outcomes of such treatment. METHODS: Twenty patients, diagnosed with moderate chronic periodontitis, were selected for the study. A total of 32 sites was identified and divided into a control (n=18) and laser-treated test groups (n=14). Probing depth (PD) and bleeding on probing (BOP) were recorded for all sites. Test sites were irradiated with an Nd:YAG laser using parameters of 2 W, 200 mJ pulse energy, and 10 pps delivered through a 320 µm diameter tip. Total laser treatment time ranged from 1 to 2 min. Following treatment, all specimens were harvested via biopsy and processed for scanning electron microscopy (SEM) and histologic examination. RESULTS: Control group specimens, depending upon initial PD, exhibited either a relatively smooth and intact epithelium with little desquamation (PD≤3 mm), or increasing degrees of epithelial desquamation and leukocytic infiltration at a PD of ≥4 mm. In the laser-treated test group, the specimens with PD≤3 mm that were BOP negative (-) exhibited a thin layer of epithelium that was disrupted. In the specimens with initial PD of ≥4 mm, complete removal of the epithelium whose extent and degree were increasing, was observed in the inflamed portion, while epithelium remained in the uninflamed portion. CONCLUSIONS: The SEM and histologic findings demonstrated the feasibility of ablating pocket epithelium with an Nd:YAG laser irradiation using parameters of 2 W of power (200 mJ, 10 pps). Furthermore, the presence or absence of clinical inflammation appeared to have an impact on the degree of laser-mediated epithelial ablation.

Isolation and characterization of the human immature osteoblast culture system from the alveolar bones of aged donors for bone regeneration therapy.

BACKGROUND: Establishment of human osteoblast cultures that retain bone-forming capacity is one of the prerequisites for successful bone regeneration therapy. Because osteoblasts harvested from adults exhibit limited growth, the use of immature osteoblasts that can expand ex vivo should greatly facilitate bone regeneration therapy. In this study, we developed immature human osteoblasts isolated from aged alveolar bone (HAOBs). METHODS: HAOBs obtained after the collagenase digestion of alveolar bones from elderly donors. Then, we assessed osteogenic ability of HAOB after treatment with recombinant human bone morphogenic protein-2 or transplantation into immunodeficient mice. In addition, we performed global gene expression analysis to identify functional marker for HAOB. RESULTS: HAOBs, which can differentiate into osteoblasts and have a robust bone-forming ability, were successfully extracted from donors who were > 60 years of age. We found that the HAOBs exhibited a higher osteogenic ability compared with those of human mesenchymal stem cells and highly expressed NEBULETTE (NEBL) with osteogenic abilities. CONCLUSIONS: HAOBs have properties similar to those of human immature osteoblasts and appear to be a novel material for cell-based bone regeneration therapy. Additionally, the expression level of NEBL may serve as a marker for the osteogenic ability of these cells.

TNF-α augmented Porphyromonas gingivalis invasion in human gingival epithelial cells through Rab5 and ICAM-1.

BACKGROUND: Tumor necrosis factor alpha (TNF-α) plays a central role in the initiation and maintenance of immune responses to periodontopathic bacteria. However, excess TNF-α leads to dysregulated immune responses and progression of periodontitis. Porphyromonas gingivalis (P. gingivalis) invades gingival epithelial cells and then multiplies and survives for a long period. Additionally, increment of TNF-α in periodontal sites is associated with a high prevalence of gram-negative anaerobes such as P. gingivalis. However, it has not been determined whether TNF-α affects invasion of P. gingivalis in periodontal tissues. RESULTS: We examined the effect of TNF-α on invasion of P. gingivalis in gingival epithelial cells and clarified the mechanism by which TNF-α augments invasion of P. gingivalis. Invasion of P. gingivalis into Ca9-22 cells was augmented by stimulation with TNF-α and it was inhibited by treatment with an antibody to TNF receptor-1. TNF-α increased production of ICAM-1, and P. gingivalis invasion was inhibited by an antibody to ICAM-1 in Ca9-22 cells. Silencing of Rab5 mRNA inhibited P. gingivalis invasion. Furthermore, the JNK inhibitor SP600125 inhibited invasion of P. gingivalis and also decreased the active form of Rab5 in Ca9-22 cells. CONCLUSION: TNF-α augments invasion of P. gingivalis in human gingival epithelial cells through increment of ICAM-1 and activation of Rab5. These phenomena may contribute to persistent infection of P. ginigvalis and prolongation of immune responses in periodontal tissues.

Management of traumatic dental injury after periodontal surgery in patient with hereditary gingival fibromatosis: case report.

Traumatic Dental Injury (TDI) is often caused by a bruise from a sports-related incident or fall. In individuals with maxillary protrusion, the risk for TDI may be higher. We treated a patient with Hereditary Gingival Fibromatosis (HGF), a rare genetic disorder characterized by proliferative fibrous overgrowth of gingival tissue, who subsequently received a TDI after periodontal surgery. A 13-year-old Japanese boy was referred to the Division of Periodontics at Aichi Gakuin University Dental Hospital in March 2005 with the chief complaint of generalized severe gingival overgrowth involving the maxillary and mandibular arches covering nearly all teeth. Prior to orthodontic treatment, periodontal surgery was performed under general anesthesia in consideration of mastication, dental esthetics, and development. However, soon thereafter in August 2007, the protruded maxillary anterior teeth received an injury while he was playing basketball and the maxillary central incisors showed extrusive luxation. Two weeks after being reset, the maxillary anterior teeth were splinted with wire and adhesive resin cement, and then the splint was removed following evaluations of clinical and radiographic showing signs of normal periodontium. The marginal bone height corresponded to that seen in radiographic findings after the reset and orthodontic treatment was started 1 year later. At the 6-year follow-up examination, the teeth remained asymptomatic, pulpal response to sensitivity tests was normal, and healing was shown in radiographic images. In the present HGF case, we speculated that removal of thick gingiva around the teeth, which might have functioned as a mouth guard, increased the risk for TDI while playing sports. TDI is more likely to occur in patients with exposed protruded misaligned teeth after periodontal surgery. Therefore, it is important for HGF patients with such protruded maxillary anterior teeth to use a mouth guard when participating in sports following periodontal surgery to prevent TDI.

Enhanced bioactivity of polyvinylidene chloride films using argon ion bombardment for guided bone regeneration.

Polyvinylidene chloride (PVDC) is a long chain carbon synthetic polymer. The objective of this study was to improve the bioactivity of PVDC films through surface modification using argon (Ar) ion bombardment to create Ar-modified PVDC films (Ar-PVDC) to address the clinical problems of guided bone regeneration (GBR), which is technique-sensitive, and low bone regenerative ability. First, the effects of Ar ion bombardment, a low temperature plasma etching technique widely used in industry, on PVDC film wettability, surface chemistry, and morphology were confirmed. Next, fibroblast-like and osteoblast-like cell attachment and proliferation on Ar-PVDC were assessed. As a preclinical in vivo study, Ar-PVDC was used to cover a critical-sized bone defect on rat calvaria and osteoconductivity was evaluated by micro-computed tomography analysis and histological examinations. We found that the contact angle of PVDC film decreased by 50° because of the production of -OH groups on the PVDC film surface, though surface morphological was unchanged at 30 min after Ar ion bombardment. We demonstrated that cell attachment increased by about 40% and proliferation by more than 140% because of increased wettability, and 2.4 times greater bone regeneration was observed at week 3 with Ar-PVDC compared with untreated PVDC films. These results suggest that Ar ion bombardment modification of PVDC surfaces improves osteoconductivity, indicating its potential to increase bone deposition during GBR.

Periodontitis-activated monocytes/macrophages cause aortic inflammation.

A relationship between periodontal disease and atherosclerosis has been suggested by epidemiological studies. Ligature-induced experimental periodontitis is an adequate model for clinical periodontitis, which starts from plaque accumulation, followed by inflammation in the periodontal tissue. Here we have demonstrated using a ligature-induced periodontitis model that periodontitis activates monocytes/macrophages, which subsequently circulate in the blood and adhere to vascular endothelial cells without altering the serum TNF-α concentration. Adherent monocytes/macrophages induced NF-κB activation and VCAM-1 expression in the endothelium and increased the expression of the TNF-α signaling cascade in the aorta. Peripheral blood-derived mononuclear cells from rats with experimental periodontitis showed enhanced adhesion and increased NF-κB/VCAM-1 in cultured vascular endothelial cells. Our results suggest that periodontitis triggers the initial pathogenesis of atherosclerosis, inflammation of the vasculature, through activating monocytes/macrophages.

Interleukin-1 receptor gene variants are associated with aggressive periodontitis in the Japanese.

OBJECTIVE: Previous studies have indicated that type-1 and type-2 interleukin-1 (IL-1) receptors (IL-1R1 and IL-1R2) play important roles in periodontitis progression. We investigated the association between periodontitis and polymorphisms in the IL-1R1 and IL-1R2 genes (IL1R1 and IL1R2). DESIGN: We searched for genetic variants in IL1R1 and IL1R2 in 24 Japanese patients with aggressive periodontitis (AgP) and 24 periodontally healthy controls. Thirty-eight single nucleotide polymorphisms (SNPs) were identified within genomic regions containing all exons and relevant exon-intron boundaries in IL1R1 and IL1R2. Possible associations of each gene locus with AgP were investigated in 119 AgP patients and 102 periodontally healthy controls using allelotypes, genotypes, and haplotypes. RESULTS: Significant differences were noted in the frequencies of 3 SNPs in IL1R2 (rs3819370, rs3218974 and rs3218977) for AgPs and controls (p=0.012, p=0.008, and p=0.038, respectively), after adjustment for gender and smoking status in the additive model (p=0.016, p=0.007, and p=0.027, respectively) and 2 haplotypes (p=0.010 and p=0.011, respectively) constructed from 2 SNPs (rs3819370 and rs3218974) that showed the lowest p-values after adjustment of covariates in additive models. CONCLUSION: A genetic susceptibility locus for AgP may lie within or close to the IL1R2 locus. Further studies in other populations are necessary to confirm these results.