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.

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.

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.

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.

Irradiation with a low-level diode laser induces the developmental endothelial locus-1 gene and reduces proinflammatory cytokines in epithelial cells.

We demonstrated previously that low-level diode laser irradiation with an indocyanine green-loaded nanosphere coated with chitosan (ICG-Nano/c) had an antimicrobial effect, and thus could be used for periodontal antimicrobial photodynamic therapy (aPDT). Since little is known about the effects of aPDT on periodontal tissue, we here investigated the effect of low-level laser irradiation, with and without ICG-Nano/c, on cultured epithelial cells. Human oral epithelial cells were irradiated in a repeated pulse mode (duty cycle, 10 %; pulse width, 100 ms; peak power output, 5 W). The expression of the developmental endothelial locus 1 (Del-1), interleukin-6 (IL-6), IL-8, and the intercellular adhesion molecule-1 (ICAM-1) were evaluated in Ca9-22 cells stimulated by laser irradiation and Escherichia coli-derived lipopolysaccharide (LPS). A wound healing assay was carried out on SCC-25 cells irradiated by diode laser with or without ICG-Nano/c. The mRNA expression of Del-1, which is known to have anti-inflammatory activity, was significantly upregulated by laser irradiation (p < 0.01). Concurrently, LPS-induced IL-6 and IL-8 expression was significantly suppressed in the LPS + laser group (p < 0.01). ICAM-1 expression was significantly higher in the LPS + laser group than in the LPS only or control groups. Finally, compared with the control, the migration of epithelial cells was significantly increased by diode laser irradiation with or without ICG-Nano/c. These results suggest that, in addition to its antimicrobial effect, low-level diode laser irradiation, with or without ICG-Nano/c, can suppress excessive inflammatory responses via a mechanism involving Del-1, and assists in wound healing.

ADAMTSL6ß protein rescues fibrillin-1 microfibril disorder in a Marfan syndrome mouse model through the promotion of fibrillin-1 assembly.

Marfan syndrome (MFS) is a systemic disorder of the connective tissues caused by insufficient fibrillin-1 microfibril formation and can cause cardiac complications, emphysema, ocular lens dislocation, and severe periodontal disease. ADAMTSL6ß (A disintegrin-like metalloprotease domain with thrombospondin type I motifs-like 6ß) is a microfibril-associated extracellular matrix protein expressed in various connective tissues that has been implicated in fibrillin-1 microfibril assembly. We here report that ADAMTSL6ß plays an essential role in the development and regeneration of connective tissues. ADAMTSL6ß expression rescues microfibril disorder after periodontal ligament injury in an MFS mouse model through the promotion of fibrillin-1 microfibril assembly. In addition, improved fibrillin-1 assembly in MFS mice following the administration of ADAMTSL6ß attenuates the overactivation of TGF-ß signals associated with the increased release of active TGF-ß from disrupted fibrillin-1 microfibrils within periodontal ligaments. Our current data thus demonstrate the essential contribution of ADAMTSL6ß to fibrillin-1 microfibril formation. These findings also suggest a new therapeutic strategy for the treatment of MFS through ADAMTSL6ß-mediated fibrillin-1 microfibril assembly.

Involvement of nitrosative stress in experimental periodontitis in diabetic rats.

AIM: Periodontal disease is highly prevalent and severe in diabetic patients, and is considered one of the diabetic complications. To elucidate how periodontitis progresses in diabetes, we examined an animal model of periodontitis in diabetic rats. MATERIALS AND METHODS: Two weeks after the induction of diabetes by streptozotocin, surgical nylon thread was ligated around the cervical portion of the unilateral maxillary second molar to induce periodontitis. Periodontitis was evaluated 2 weeks after the ligation by gingival blood flow, mRNA expressions, Western blot analysis, histological examination and micro CT. RESULTS: Ligation-induced severe periodontitis in the diabetic rats, which was apparently shown by the increase of TNF-α and iNOS mRNA expressions and inflammatory cell infiltration in the gingiva and alveolar bone loss. The number of nitrotyrosine, a footprint of nitrosative stress, -positive cells was significantly higher in the periodontitis of the diabetic rats compared with that in the normal rats. Western blot analysis confirmed that the nitrotyrosine was increased in the periodontitis of the diabetic rats. CONCLUSIONS: This is the first study to confirm increased nitrosative stress due to periodontitis in diabetic rats. Nitrosative stress may play a crucial role in the exacerbation of periodontitis in diabetic patients.

Social nicotine dependence in Australian dental undergraduate students.

OBJECTIVES: This study aimed to investigate dental undergraduate students' tobacco usage and social nicotine dependence in Australia. A special interest was to identify the role of factors such as age, gender, year of dental education and cohabitants' smoking status for social nicotine dependence. MATERIALS AND METHODS: A sample of 252, first-to-fifth year undergraduate students in an Australian dental school was used. Each completed a self-administered questionnaire. RESULTS: The smoking rate was 4.8%. Current smokers displayed higher social nicotine dependence than those that had never smoked (t=3.1, df=244, P=0.002). Dental undergraduate students that showed higher social nicotine dependence (P=0.001, OR=1.3, 95% CI: 1.1-1.6), or that had smoking cohabitants (P=0.016, OR=4.8, 95% CI: 1.3-17.0), were more likely to smoke. Students' social nicotine dependence increased with year of dental study (P=0.043, ß=0.4, t=2.0). Social nicotine dependence enhanced tobacco usage among Year-1-to-4 students (P=0.005, OR=1.4, 95% CI: 1.1-1.7) but not Year-5 undergraduates (P=0.432). CONCLUSIONS: Social nicotine dependence has become a developing issue in dental education. Tobacco control should be highlighted in the dental curriculum. Future investigations into the effects of dental education on social nocotine dependence and tobacco usage are indicated.

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.

MyD88 but not TRIF is essential for osteoclastogenesis induced by lipopolysaccharide, diacyl lipopeptide, and IL-1alpha.

Myeloid differentiation factor 88 (MyD88) plays essential roles in the signaling of the Toll/interleukin (IL)-1 receptor family. Toll-IL-1 receptor domain-containing adaptor inducing interferon-beta (TRIF)-mediated signals are involved in lipopolysaccharide (LPS)-induced MyD88-independent pathways. Using MyD88-deficient (MyD88-/-) mice and TRIF-deficient (TRIF-/-) mice, we examined roles of MyD88 and TRIF in osteoclast differentiation and function. LPS, diacyl lipopeptide, and IL-1alpha stimulated osteoclastogenesis in cocultures of osteoblasts and hemopoietic cells obtained from TRIF-/- mice, but not MyD88-/- mice. These factors stimulated receptor activator of nuclear factor-kappaB ligand mRNA expression in TRIF-/- osteoblasts, but not MyD88-/- osteoblasts. LPS stimulated IL-6 production in TRIF-/- osteoblasts, but not TRIF-/- macrophages. LPS and IL-1alpha enhanced the survival of TRIF-/- osteoclasts, but not MyD88-/- osteoclasts. Diacyl lipopeptide did not support the survival of osteoclasts because of the lack of Toll-like receptor (TLR)6 in osteoclasts. Macrophages expressed both TRIF and TRIF-related adaptor molecule (TRAM) mRNA, whereas osteoblasts and osteoclasts expressed only TRIF mRNA. Bone histomorphometry showed that MyD88-/- mice exhibited osteopenia with reduced bone resorption and formation. These results suggest that the MyD88-mediated signal is essential for the osteoclastogenesis and function induced by IL-1 and TLR ligands, and that MyD88 is physiologically involved in bone turnover.

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.].

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.

Degradation of vascular endothelial thrombomodulin by arginine- and lysine-specific cysteine proteases from Porphyromonas gingivalis.

BACKGROUND: The endothelial cell surface glycoprotein thrombomodulin (TM) inhibits vascular coagulation and inflammation via regulation of thrombin-mediated activation of protein C. Porphyromonas gingivalis is the major periodontopathic bacterium and has been found in vessel walls and atherosclerotic lesions in humans. P. gingivalis-derived cysteine proteases (gingipains) are known to enhance inflammatory and coagulant responses of vascular endothelial cells. However, it has not been elucidated whether gingipains affect vascular endothelial TM. METHODS: Purified arginine-specific gingipains (Rgps) and lysine-specific gingipain (Kgp) from P. gingivalis were used to investigate the effects of gingipains on recombinant human TM by immunoblot analyses. Flow cytometry and activated protein C assay were carried out to examine the effects of gingipains on vascular endothelial cell surface TM. Immunohistochemistry was performed to investigate TM expression in microvascular endothelia in gingival tissues taken from patients with periodontitis. RESULTS: Rgps and Kgp cleaved TM in vitro. Endothelial cell surface TM was also degraded by Rgps. Thrombin-mediated activation of protein C was reduced by Rgps through TM inactivation. Gingival microvascular endothelial TM was reduced in patients with periodontitis. CONCLUSIONS: P. gingivalis gingipains induced the degradation and inactivation of endothelial TM, which may promote vascular coagulation and inflammation. In addition, in vivo relevance was demonstrated by reduced expression of TM in gingival microvascular endothelia in patients with periodontitis, which may be involved in the pathogenesis of periodontitis.

Assessment of chromosome 19 for genetic association in severe chronic periodontitis.

BACKGROUND: A genome-association study is a powerful tool for analyzing small gene effects in complex diseases such as chronic periodontitis (CP), although the cost of analysis is prohibitive. We designed a study using the DNA pooling method, which could be a breakthrough in lowering such costs. This study was conducted to assess the genetic association in severe CP in a Japanese population. METHODS: We adopted a DNA pooling method by genotyping 454 densely spaced microsatellite (MS) markers in chromosome 19 as a pilot study, with the possibility of future use in a whole-genome study. This can reduce the high cost and technical burden, which is generally unavoidable in a genomic association study. Pooled DNA samples from 300 case subjects, 300 control subjects, and 200 systemically healthy subjects were screened by genotyping MS markers. The case-control association in the candidate region was analyzed by individual typing of MS and single nucleotide polymorphisms (SNPs). RESULTS: The single MS marker allele 17 of 1902G31 was isolated in association with severe CP (P = 0.0012 for 2 x 2; P <0.046 for 2 x m, where m refers to the number of polymorphic alleles observed in a population). No other SNP or MS polymorphism hypothesized to affect biologic functions in the critical region was found in the linkage disequilibrium block analysis. CONCLUSIONS: We efficiently isolated the susceptible locus for severe CP in chromosome 19 and identified a useful marker to evaluate the risk for disease. This approach can be applied to a whole-genome study in severe CP.

Lipopolysaccharide-mediated enhancement of bone metabolism in estrogen-deficient mice.

BACKGROUND: Osteoporosis may be a risk factor in periodontal disease. However, biologic mechanisms explaining the apparent interaction between these two diseases have not been defined. It is well known that lipopolysaccharide (LPS) increases the resorption of alveolar bone. We hypothesized that LPS and estrogen deficiency have synergistic effects on bone metabolism and may lead to enhanced bone resorption. METHODS: Eighty 8-week-old female ddY mice were divided into two groups and underwent a sham operation or bilateral ovariectomy. They were maintained for 4 weeks to assess estrogen-deficient bone loss. Osteoblasts and bone marrow cells (BMCs) were collected from ovariectomized (OVX) and sham-operated mice. Osteoclast differentiation in a coculture of osteoblasts and BMCs was investigated by tartrate-resistant acid phosphatase staining. Receptor activator of nuclear factor-kappa B ligand (RANKL) mRNA expression in LPS-treated osteoblasts was investigated using real-time polymerase chain reaction. Interferon-gamma (IFN-gamma) and interleukin (IL)-6 and -10 levels in the culture supernatants were evaluated by enzyme-linked immunosorbent assay. Group means were compared by analysis of variance followed by Tukey's honestly significant difference. RESULTS: There was a significant increase in the number of osteoclasts in LPS-treated cocultures from OVX mice compared to sham controls (P <0.05). RANKL mRNA expression in LPS-treated osteoblasts from OVX mice was greater than in sham mice (P <0.05). In contrast, the production of IFN-gamma in LPS-treated coculture from OVX mice was significantly lower than in sham mice (P <0.05). CONCLUSION: LPS-bearing Gram-negative organisms are abundant in periodontal disease, and the results supported the hypothesis that bone resorption is increased in estrogen-deficient patients.

Transcriptome database KK-Periome for periodontal ligament development: expression profiles of the extracellular matrix genes.

Specialized connective tissues such as tendon/ligament develop through a series of events that require temporal and spatial expression of numerous genes in mesenchymal progenitors. However, the genes required for tendon/ligament development have not been identified yet. To solve this problem, we made a cDNA library from periodontal ligament and sequenced 11,520 cDNA clones, as a model for investigating tendon/ligament development. The resulting sequence data was assembled to 617 expressed sequence tag (EST) clusters, and an EST database for human periodontal ligament (PDL) was constructed (designated as the KK-Periome database). In the KK-Periome database, the top 13 EST clusters were related to extracellular matrix (ECM) genes. The temporal and spatial expression patterns of these genes during mouse PDL development were examined by in situ hybridization. Among these genes, F-spondin was expressed specifically in dental follicle (DF) cells during tooth germ development, whereas tenascin-N was strongly expressed in the terminally differentiated PDL. This characteristic expression profile was confirmed by in vivo differentiation assay of human PDL (hPDL) cells in the mouse transplant. Thus, the KK-Periome database was proven to be a useful resource for PDL-derived ESTs (transcriptome), and in fact, initial evidence indicated that F-spondin and tenascin-N might serve as markers for DF and PDL, respectively.

Arginine-specific gingipain A from Porphyromonas gingivalis induces Weibel-Palade body exocytosis and enhanced activation of vascular endothelial cells through protease-activated receptors.

Gingipains, cysteine proteases derived from Porphyromonas gingivalis, are important virulence factors in periodontal diseases. We found that arginine-specific gingipain A (RgpA) increased the responsiveness of vascular endothelial cells to P. gingivalis lipopolysaccharides (LPS) and P. gingivalis whole cells to induce enhanced IL-8 production through protease-activated receptors (PARs) and phospholipase C (PLC) gamma. We therefore investigated whether RgpA-induced enhanced cell activation is mediated through exocytosis of Weibel-Palade bodies (WPBs) because they store vasoactive substances. RgpA rapidly activated PAR- and PLCgamma-dependent WPB exocytosis. In addition, angiopoietin (Ang)-2, a substance of WPB, enhanced IL-8 production by P. gingivalis LPS, suggesting that Ang-2 mediates the RgpA-induced enhanced cell responses. Thus, we propose a novel role for RgpA in induction of a proinflammatory event through PAR-mediated WPB exocytosis, which may be an important step for enhanced endothelial responses to P. gingivalis.

Interaction of obesity and skeletal bone mineral density in tooth retention in Japanese postmenopausal women.

OBJECTIVE: To investigate whether being overweight is associated with increased or decreased risk of tooth loss in Japanese postmenopausal women. DESIGN: The number of remaining teeth (total, anterior, and posterior teeth), mandibular bone height, and mandibular cortical mass were evaluated on the dental panoramic radiographs of 450 Japanese postmenopausal women. The bone mineral densities (BMDs) at the lumbar spine and femoral neck were measured by dual-energy x-ray absorptiometry. These measurements were compared among participants in three body mass index (BMI) categories (underweight, normal BMI, and overweight). RESULTS: Analysis of covariance adjusted for confounding variables revealed that participants who were overweight had a significantly lower number of total (P = 0.019) and anterior (P = 0.012) remaining teeth than did those with normal BMI, although the former had significantly higher skeletal BMD values than the latter. No significant difference was observed in mandibular bone height between the overweight participants and those with normal BMI. There were no significant differences in the number of remaining teeth between the under- and overweight participants. Overweight participants had significantly higher skeletal BMDs (P < 0.001) and tended to have larger mandibular cortical masses than those who were underweight. CONCLUSIONS: Despite their higher skeletal BMD, postmenopausal women who are overweight may have an increased risk of tooth loss, especially of the anterior teeth, compared with women who have normal BMI. This risk appears to be similar to that for underweight women.

Effects of Er,Cr:YSGG laser irradiation on the root surface: morphologic analysis and efficiency of calculus removal.

BACKGROUND: This in vitro study was performed to determine the appropriate power output setting for an erbium, chromium-doped:yttrium, scandium, gallium, and garnet (Er,Cr:YSGG) laser used in periodontal pocket irradiation by examining the morphologic alterations of the root surfaces and the efficiency of calculus removal. METHODS: Sixty-five non-carious extracted human teeth were used in this study. For morphologic analysis of the root surface, the clean, single roots of 22 teeth were separated into 91 pieces, and these pieces were immersed in acrylic resin. The specimens with root-surface exposure were prepared and divided randomly into three groups: a control group (N=8), an irradiation without water group (no water [NW] group; N=39), and an irradiation in water to simulate the conditions in a periodontal pocket group (in water [IW] group; N=44). The power output settings for laser irradiation were 0.5, 1.0, 1.5, and 2.0 W for each group. The roughness (Ra), depth (Z), and width (X) of the disk specimens were determined after laser irradiation. Eight other single-rooted teeth were examined by scanning electron microscopy (SEM) after laser irradiation under the same conditions. Thirty-five single- or multirooted teeth with heavy subgingival calculus were used to test the efficiency of laser scaling. The efficiency of calculus removal was quantified by measuring the time needed to remove the calculus completely using the laser. RESULTS: The mean Ra and Z values in the IW group were significantly higher than in the NW group with the same power output. In addition, these values with 0.5- and 1.0-W power output settings were significantly lower than with 1.5- and 2.0-W settings in the NW and IW groups. No obvious morphologic differences could be found between the 0.5- and 1.0-W power output specimens under SEM. Additionally, thermal alterations, i.e., carbonization or melting, were completely absent in the IW group. Regarding the efficiency of calculus removal, the 0.5-W setting (0.11+/-0.036 mm2/second) was significantly inferior to the 1.0-W setting (0.27+/-0.043 mm2/second). However, there was no significant difference between 1.0- and 1.5-W (0.36+/-0.11 mm2/second). The 2.0-W setting (0.63+/-0.272 mm2/second) was much more efficient but resulted in significant morphologic alterations. CONCLUSIONS: Based on these findings, it is appropriate to use a 1.0-W power output setting with an Er,Cr:YSGG laser for root scaling. This may be done without any conspicuous morphologic alterations to the root surface and with acceptably efficient removal of calculus.

[Oral osteoporosis: a review and its dental implications].

In post-menopausal osteoporosis, lack of estrogen will affect the remodeling of the bone tissue in such a way that, in most patients with periodontitis, the amount of bone resorbed exceeds that being formed, resulting in net bone loss. Osteoporosis can be treated by a variety of methods, the hormone replacement therapy (HRT), the selective estrogen receptor modulators (SERM) and the bisphosphonates. The HRT or bisphosphonates treatments improve the clinical outcome of periodontal disease and may be an adjunctive treatment to preserve periodontal bone mass. This paper reviews the current evidence on the mechanism of periodontal breakdown after menopause and the benefit to oral health by treatments for osteoporosis.