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Aims/introduction: To explore the relationships between periodontitis and microvascular complications as well as glycemic control in type 2 diabetes patients., Materials and Methods: This multicenter, hospital-based, cross-sectional study included 620 patients with type 2 diabetes. We compared the prevalence and severity of periodontitis between patients with ≥1 microvascular complication and those without microvascular complications. We also compared the prevalence and severity of periodontitis among patients with different degrees of glycemic control., Results: After adjusting for confounding factors, multiple logistic regression analysis showed that the severity of periodontitis was significantly associated with the number of microvascular complications (odds ratio 1.3, 95% confidence interval 1.1-1.6), glycated hemoglobin ≥8.0% (64 mmol/mol; odds ratio 1.6; 95% confidence interval 1.1-2.3), and older age (≥50 years; odds ratio 1.7; 95% confidence interval 1.1-2.6). However, the prevalence of periodontitis was not significantly associated with the number of microvascular complications, but was associated with male sex, high glycated hemoglobin (≥8.0% [64 mmol/mol]), older age (≥40 years), longer duration of diabetes (≥15 years) and fewer teeth (≤25). Furthermore, propensity score matching for age, sex, diabetes duration and glycated hemoglobin showed that the incidence of severe periodontitis was significantly higher among patients with microvascular complications than among those without microvascular complications (P < 0.05)., Conclusions: The number of microvascular complications is a risk factor for more severe periodontitis in patients with type 2 diabetes, whereas poor glycemic control is a risk factor for increased prevalence and severity of periodontitis., (© 2017 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)

Objectives: We investigated incidence and risk factors for postextraction bleeding in patients receiving warfarin and those not receiving anticoagulation therapy., Design: Cross-sectional, multicentre, observational study., Setting: 26 hospitals where an oral surgeon is available., Participants: Data on 2817 teeth (from 496 patients receiving warfarin, 2321 patients not receiving warfarin; mean age (SD): 62.2 (17.6)) extracted between 1 November 2008 and 31 March 2010, were collected. Warfarin-receiving patients were eligible when prothrombin time-international normalised ratio (PT-INR) measured within 7 days prior to the extraction was less than 3.0., Interventions: Simple dental extraction was performed, and incidence of postextraction bleeding and comorbidities were recorded., Primary and Secondary Outcome Measures: Postextraction bleeding not controlled by basic haemostasis procedure was clinically significant., Results: Bleeding events were reported for 35 (7.1%) and 49 (2.1%) teeth, of which 18 (3.6%) and 9 (0.4%) teeth were considered clinically significant, in warfarin and non-warfarin groups, respectively, the difference between which was 3.24% (CI 1.58% to 4.90%). The incidence rates by patients were 2.77% and 0.39%, in warfarin and non-warfarin groups, respectively (incidence difference 2.38%, CI 0.65% to 4/10%). Univariate analyses showed that age (OR 0.197, p=0.001), PT-INR (OR 3.635, p=0.003), mandibular foramen conduction anaesthesia (OR 4.854, p=0.050) and formation of abnormal granulation tissue in extraction socket (OR 2.900, p=0.031) significantly correlate with bleeding incidence. Multivariate analysis revealed that age (OR 0.126, p=0.001), antiplatelet drugs (OR 0.100, p=0.049), PT-INR (OR 7.797, p=0.001) and history of acute inflammation at extraction site (OR 3.722, p=0.037) were significant risk factors for postextraction bleeding., Conclusions: Our results suggest that there is slight but significant increase in the incidences of postextraction bleeding in patients receiving warfarin. Although absolute incidence was low in both groups, the bleeding risk is not negligible., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

The surgical strategy for tumors located in or extending from the intracranial space to the infratemporal fossa was analyzed in 12 cases with various pathologies. A case of mandibular nerve schwannoma, which extended 1 cm below the external orifice of the foramen ovale, was completely removed via the epidural subtemporal approach without zygomatic osteotomy with partial removal of the middle cranial base. The inferior margin of infratemporal tumor could be accessed via the transcranial route with zygomatic or orbitozygomatic osteotomy without complications including facial nerve injury in nine cases, and the lowest level of the infratemporal tumors was approximately 4.5 cm below the outer surface of the middle cranial base. In five of these 9 cases (2 schwannomas, 1 myxoma, 1 chondrosarcoma, and 1 malignant peripheral nerve sheath tumor), the tumors were localized in the infratemporal fossa, and in the other 4 cases (2 meningiomas, 1 glioblastoma, and 1 ameloblastoma), the tumors extended to both the intracranial space and the infratemporal fossa. In two cases (recurrent jugular schwannoma and mandibular osteosarcoma), a combined transcranial and transcervical approach (mandibular swing approach) was essential, because the resection line of the lower margin was too far from the middle cranial base. These results indicate that the transcranial approach, with or without zygomatic or orbitozygomatic osteotomy (zygomatic infratemporal fossa approach), is safe and effective for removal of some infratemporal tumors, and that a combined transcranial and transcervical approach is useful for removing infratemporal tumors with extensive downward extension.

Species-level differences in response to micronucleus induction with haloperidol, a drug that can induce hypothermia, were investigated. Haloperidol was intraperitoneally (i.p.) administered to mice (12.5-50 mg/kg) and rats (25-100 mg/kg), and the rectal temperature was then measured. At every investigated dose, haloperidol transiently decreased the rectal temperature in mice to less than 30 degrees C. However, the rectal temperature decreased to approximately 34 degrees C in rats. For micronucleus induction, haloperidol at doses of 25 and 50 mg/kg resulted in a statistically significant increase in micronucleated polychromatic erythrocyte frequency in the 48 h sampling group of mice, but not in rats. In addition, relatively large micronuclei (diameter of micronucleus > one-fourth the diameter of the cytoplasm) accounted for 46-47% of the induced micronuclei in mice, suggesting that hypothermia affected the mitotic apparatus. Thus, hypothermia can induce micronuclei in vivo as a secondary effect, and the hypothermic response to haloperidol in mice was stronger than that of rats. Micronuclei could only be induced in mice during this study. Therefore, species-level differences may exist in regards to micronucleus induction by hypothermia-inducing drugs.

Objective: Laugier-Hunziker-Baran syndrome represents a rare acquired pigmentary disorder which has no relevance to internal disorders and has no familial association. There are few reports on histopathologic studies of this syndrome concerning Japanese individuals. The differential diagnosis of oral and pigmented lesions between Laugier-Hunziker-Baran syndrome and other disorders, Peutz-Jeghers syndrome in particular, requires our utmost consideration., Study Design: Biopsy specimens of 2 cases were taken from pigmented maculae on the lower lips, buccal mucosa, tongue, and palate., Results: Similar histopathologic findings were observed for all locations. The histopathologic examination showed that there was an accumulation of melanin in the basal layer as well as an increase in the number of melanophages in the subepithelial area., Conclusions: Oral scientists and clinicians must be familiar with Laugier-Hunziker-Baran syndrome, because this syndrome is probably more common than is generally recognized.

The use of mandibular subperiosteal implants was first reported by Dahl in the 1940s. It was followed by a more comprehensive report by Goldberg and Gershkoff, who published the first case series in the United States. We describe a case of an orocutaneous fistula that developed secondary to a chronic infection attributed to a failing subperiosteal implant. Elemental analysis of the metal framework revealed an implant composed of mainly a cobalt-chromium alloy. Cobalt, which was frequently used in subperiosteal implant manufacturing, is associated with a higher corrosion rate than other metals and is no longer used to fabricate subperiosteal implants. The strength of subperiosteal implants is their ability to be used in a mandible with an atrophic alveolar ridge. Unfortunately, this feature of the hardware is also its weakness in that reconstructive procedures after their removal are difficult. The failing subperiosteal implant in our patient was subsequently removed, and primary closure of the intraoral wound and extraoral fistula as well as resolution of the patient's symptoms was obtained with no lasting complications.

We previously reported that both hyperthermia and hypothermia induced micronuclei in mouse bone marrow cells (Asanami and Shimono, 1997a, 1997b, 1999). To investigate the effects of temperature on chromosome aberration in vitro, we conducted chromosome aberration and micronucleus tests under hyper- and hypothermic conditions using Chinese hamster lung (CHL) cells. In the chromosome aberration test, we observed positive responses at 40 degrees C and 41 degrees C for 24 hr, and at 42 degrees C for 6 hr and over. In the micronucleus test, we observed positive responses at 31 degrees C, 33 degrees C, and 40 degrees C for 24 hr, and at 42 degrees C for 2 hr. The results suggest that in CHL cells, hypothermic conditions can induce micronuclei while hyperthermic conditions can induce both chromosome aberrations and micronuclei.

We recently experienced a case of mandibular gingival cancer T4N0M0 which markedly responded to a combination therapy of nedaplatin (254-S) with 5-fluorouracil (5-FU). The patient was a 68-year-old male who visited our department with the main complaint of ulceration in the left mandibular gingiva. Biopsy revealed a moderately differentiated squamous cell carcinoma which extended to the mandible, mandibular gingiva, buccal mucosa, half tongue and oral floor on the left side of the face. As a neoadjuvant chemotherapy (NAC), 254-S at a dose of 100 mg/m2 was intravenously administered on day 1, while 5-FU at a dose of 700 mg/m2/day was intravenously administered from day 1 to 5 in succession. Hydration (2,000 ml/day) was performed from day 1 to 3. Adverse reactions observed included thrombocytopenia, anorexia, nausea, vomiting, stomatitis and SIADH, but no sign of renal dysfunction was observed. The clinical outcome was evaluated as CR. Surgery was performed later. Pathological examination of the extracted tissues showed tumor cells in the tongue only, indicating an excellent effect of this combination therapy of 254-S and 5-FU.

To examine whether micronucleus tests can be incorporated into general toxicology assays, we performed micronucleus tests applying the treatment protocols typically used in such assays. In this 13th Collaborative Study of the CSGMT, both rats and mice were tested, although rats were used in the majority of the studies. Fifteen mutagens were tested in rats, mainly by oral (p.o.) administration. Micronucleus induction was evaluated 2, 3, and 4 days, and 1, 2, 3, and 28 days after the beginning of the treatment in the peripheral blood, and at 28 days in the bone marrow. Of the 15 chemicals that induced micronuclei in rats in short-term assays, two chemicals (1,2-dimethylhydrazine.2HCl and mitomycin C) were negative in all our experiments, possibly because of insufficient dose levels. The remaining 13 were positive within the estimated dose range of a general toxicology assay, suggesting the possibility of integrating the micronucleus assay into general toxicology assays. Three patterns were observed in micronucleus induction during the period of repeated treatment: (1) gradual increases in micronucleus frequency with sequential doses, (2) a peak at 3-5 days followed by gradual decreases in micronucleus frequency with sequential doses, and (3) a rapid increase in micronucleus frequency followed by a plateau. We evaluated factors that might have been involved in those patterns, such as the spleen function, target organ exposure, extramedullary hematopoiesis, hypothermia, and hypoxia. Another factor we considered was dosage. Because the dosages employed in a general toxicity assay are usually lower than those used in short-term micronucleus assays, this discrepancy was considered the greatest potential problem for integrating the micronucleus assay into general toxicology assays. Our results indicate that the integration of the micronucleus assay into a 28-day toxicological assay is feasible. To serve this purpose, blood samples collected 4 days after the beginning of treatment and blood and bone marrow samples collected at autopsy should be examined. Furthermore, although it is recognized that mice may be suitable for performing independent micronucleus assays, we propose that rats can provide biologically important and relevant information regarding potential chemical mutagens that can be evaluated under conditions used in the conduct of general toxicology studies., (Copyright 2001 Wiley-Liss, Inc.)

We investigated micronucleus induction in rats treated with chlorpromazine and reserpine, drugs that induce hypothermia. We administered chlorpromazine (31.3--250mg/kg) or reserpine (500--2000 mg/kg) intraperitoneally and measured temperature rectally. Chlorpromazine at 62.5-250mg/kg and reserpine at all doses significantly decreased rectal temperature, although the hypothermic response was weaker than previously reported in mice. Only chlorpromazine at 250mg/kg decreased rectal temperature transiently to <33 degrees C for 20h and induced a statistically significant increase in micronucleated polychromatic erythrocyte frequency. When rats treated with reserpine at 500mg/kg were exposed to an environmental temperature of 16 degrees C for 6, 12, or 24h to keep their body temperature under 33 degrees C, only the 24h treatment group significantly induced micronuclei. In addition, relatively large micronuclei (diameter of micronucleus> or = 1/4 diameter of cytoplasm) accounted for 33.0% of the induced micronuclei, suggesting that hypothermia affected the mitotic apparatus. The hypothermic response to chlorpromazine and reserpine was weaker in rats than in mice, and it was correspondingly more difficult to induce micronuclei in rats with those drugs.

This study aims to determine the pH that peripheral veins can tolerate. Intravenous nutrient solutions with different pHs (from 4.52 to 6.71) were infused into rabbit ear veins, and the veins were examined histopathologically. After 6-hr infusion at 10 mL/kg/hr, a commercial 2.72% amino acid/7.5% glucose solution with electrolytes (AG) caused obvious phlebitic changes, such as loss of venous endothelial cells, inflammatory cell infiltration, and perivascular edema, in all 6 rabbits because of its low pH (4.52) and high titratable acidity (22 mEq/L). The phlebitis was reduced when the solution was neutralized with NaOH to pH 5.93, and was almost eliminated when the pH was neutralized to 6.49. After 8-hr infusion at 15 mL/kg/hr, AG-adjusted pH to 6.30 caused slight phlebitic changes, but AG-adjusted pH to 6.71 scarcely caused any change. Furthermore, 24-hr infusion of the pH 6.49 solution caused no histopathological changes in 3 rabbits. These results suggest that the tolerance pH for the peripheral vein is about 6.5, and that an infusion solution does not cause phlebitis due to acidity if the pH is not lower than the tolerance pH.

This study aimed to determine the osmolality that peripheral venous endothelial cells can tolerate and to clarify the relationship between tolerance osmolality and duration of infusion. Nutrient solutions of 539-917 mOsm/kg, prepared to have no acidic effect, were infused into rabbit ear veins, and the veins were examined histopathologically. In each experiment of 8-, 12-, or 24-h infusion, the higher osmolality solutions caused some phlebitic changes, such as loss of venous endothelial cells, inflammatory cell infiltration, and edema; however, the lowest osmolality solution caused few changes. Infusion of 120 mL/kg of 814 mOsm/kg solution caused phlebitis at 5 or 10 mL.kg-1.h-1, however, the same volume of the same solution scarcely caused phlebitis at 15 mL.kg-1.h-1 because of the shortened infusion duration. These results suggest that the tolerance osmolality of peripheral venous endothelial cells with poor blood flow is about 820 mOsm/kg for 8 h, 690 mOsm/kg for 12 h, and 550 mOsm/kg for 24 h, and that the tolerance osmolality falls as the duration of infusion increases. In conclusion, hypertonic solutions should be infused at as high a rate as is clinically acceptable and compatible with nutrient bioavailability because increasing the infusion rate reduces the duration of infusion and phlebitis.

We investigated the effect of hypothermia on micronucleus induction in mouse bone marrow cells. To induce hypothermia, we administered chlorpromazine, which was negative in an in vitro chromosome aberration test, at 3.13, 6.25, 12.5, 25, 50, and 100 mg/kg intraperitoneally. Doses of 12.5-100 mg/kg decreased rectal temperature transiently to less than 33 degrees C. The temperature depression following 25-100 mg/kg lasted for 11 h before returning to normal 24 h later except for the 100 mg/kg treatment group. Doses of 25-100 mg/kg produced a statistically significant (p < 0.01) increase in micronucleated polychromatic erythrocyte frequencies 48 h after dosing. When mice that were administered chlorpromazine at 25, 50, and 100 mg/kg were exposed to an environmental temperature of 30 degrees C for 46 h to keep their body temperature within normal range, the frequency of micronucleated erythrocytes did not increase. In addition, relatively large micronuclei (diameter of micronucleus > or = 1/4 diameter of cytoplasm) accounted for 53-58% of the induced micronuclei. The results suggest that the transient hypothermia of less than 33 degrees C for 11 h induced micronuclei in bone marrow cells, and one possible mechanism was disturbance of the mitotic apparatus.

To clarify conflicting clinical results that had been reported as to whether dilution is effective or not in reducing infusion phlebitis, this study was undertaken. We undertook two experiments with the different infusion conditions in rabbits to confirm the generality and the reproducibility of the results. To test the effect of dilution, 120 mL/kg of solution A (784 mOsm/kg) was infused into rabbit ear veins at 10 mL.kg-1.h-1 for 12 h, and 144 mL/kg of 1.2-fold-diluted solution A (648 mOsm/kg) was infused at 12 mL.kg-1.h-1 for 12 h. Similarly, 120 mL/kg of solution B (718 mOsm/kg) was infused at 5 mL.kg-1.h-1 for 24 h, and 168 mL/kg of 1.4-fold-diluted solution B (514 mOsm/kg) was infused at 7 mL.kg-1.h-1 for 24 h. The infused veins were sampled 24 h after the end of the infusion and examined histopathologically. After the 12-h infusion, phlebitic changes were observed in six of eight rabbits given solution A but in only one of eight rabbits given diluted solution A, although the same quantities of the same nutrients were infused. Also, after the 24-h infusion, phlebitic changes were observed in six of eight rabbits given solution B but in no animals given diluted solution B. The same result that dilution reduced or eliminated phlebitic changes was confirmed in the different conditions. These results suggest that osmolality of the infusion solution is an important factor in the development of phlebitis regardless of infusion volume or infusion rate and that dilution is effective in reducing the phlebitic potential of infusion solutions.