Journal of oral biology (Northborough, Mass.)最新文献

{"title":"Dental Calculus Arrest of Dental Caries.","authors":"Paul H Keyes, Thomas E Rams","doi":"10.13188/2377-987x.1000017","DOIUrl":"10.13188/2377-987x.1000017","url":null,"abstract":"<p><strong>Background: </strong>An inverse relationship between dental calculus mineralization and dental caries demineralization on teeth has been noted in some studies. Dental calculus may even form superficial layers over existing dental caries and arrest their progression, but this phenomenon has been only rarely documented and infrequently considered in the field of Cariology. To further assess the occurrence of dental calculus arrest of dental caries, this study evaluated a large number of extracted human teeth for the presence and location of dental caries, dental calculus, and dental plaque biofilms.</p><p><strong>Materials and methods: </strong>A total of 1,200 teeth were preserved in 10% buffered formal saline, and viewed while moist by a single experienced examiner using a research stereomicroscope at 15-25× magnification. Representative teeth were sectioned and photographed, and their dental plaque biofilms subjected to gram-stain examination with light microscopy at 100× magnification.</p><p><strong>Results: </strong>Dental calculus was observed on 1,140 (95%) of the extracted human teeth, and no dental carious lesions were found underlying dental calculus-covered surfaces on 1,139 of these teeth. However, dental calculus arrest of dental caries was found on one (0.54%) of 187 evaluated teeth that presented with unrestored proximal enamel caries. On the distal surface of a maxillary premolar tooth, dental calculus mineralization filled the outer surface cavitation of an incipient dental caries lesion. The dental calculus-covered carious lesion extended only slightly into enamel, and exhibited a brown pigmentation characteristic of inactive or arrested dental caries. In contrast, the tooth's mesial surface, without a superficial layer of dental calculus, had a large carious lesion going through enamel and deep into dentin.</p><p><strong>Conclusions: </strong>These observations further document the potential protective effects of dental calculus mineralization against dental caries.</p>","PeriodicalId":91029,"journal":{"name":"Journal of oral biology (Northborough, Mass.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34596073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serpine1 Mediates <i>Porphyromonas gingivalis</i> Induced Insulin Secretion in the Pancreatic Beta Cell Line MIN6.","authors":"Uppoor G Bhat,&nbsp;Keiko Watanabe","doi":"10.13188/2377-987X.1000008","DOIUrl":"https://doi.org/10.13188/2377-987X.1000008","url":null,"abstract":"<p><p>Periodontitis is an inflammatory disease resulting in destruction of gingiva and alveolar bone caused by an exuberant host immunological response to periodontal pathogens. Results from a number of epidemiological studies indicate a close association between diabetes and periodontitis. Results from cross-sectional studies indicate that subjects with periodontitis have a higher odds ratio of developing insulin resistance (IR). However, the mechanisms by which periodontitis influences the development of diabetes are not known. Results from our previous studies using an animal model of periodontitis suggest that periodontitis accelerates the onset of hyperinsulinemia and IR. In addition, LPS from a periodontal pathogen, <i>Porphyromonas gingivalis (Pg)</i>, stimulates Serpine1 expression in the pancreatic beta cell line MIN6. Based on these observations, we hypothesized that a periodontal pathogen induces hyperinsulinemia and Serpine1 may be involved in this process. To test this hypothesis, we co-incubated Pg with the pancreatic beta cell line MIN6 and measured the effect on insulin secretion by MIN6 cells. We further determined the involvement of Serpine1 in insulin secretion by downregulating Serpine1 expression. Our results indicated that Pg stimulated insulin secretion by approximately 3.0 fold under normoglycemic conditions. In a hyperglycemic state, Pg increased insulin secretion by 1.5 fold. Pg significantly upregulated expression of the Serpine1 gene and this was associated with increased secretion of insulin by MIN6 cells. However, cells with downregulated Serpine1 expression were resistant to Pg stimulated insulin secretion under normoglycemic conditions. We conclude that the periodontal pathogen, Pg, induced insulin secretion by MIN6 cells and this induction was, in part, Serpine1 dependent. Thus, Serpine1 may play a pivotal role in insulin secretion during the accelerated development of hyperinsulinemia and the resulting IR in the setting of periodontitis.</p>","PeriodicalId":91029,"journal":{"name":"Journal of oral biology (Northborough, Mass.)","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511159/pdf/nihms681036.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33938117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Colonization and Persistence of Labeled and \"Foreign\" Strains of <i>Aggregatibacter actinomycetemcomitans</i> Inoculated into the Mouths of Rhesus Monkeys.","authors":"Daniel H Fine,&nbsp;Maribasappa Karched,&nbsp;David Furgang,&nbsp;Vandana Sampathkumar,&nbsp;Senthil Velusamy,&nbsp;Dipti Godboley","doi":"10.13188/2377-987X.1000005","DOIUrl":"https://doi.org/10.13188/2377-987X.1000005","url":null,"abstract":"<p><p><i>Aggregatibacter actinomycetemcomitans</i> (<i>Aa</i>) is a pathobiont and part of a consortium of bacteria that can lead to periodontitis in humans. Our aim was to develop a model for oral inoculation of labeled <i>Aa</i> into a suitable host in order to study <i>Aa</i> traits and ecological factors that either enhance or repress its persistence. Primate species were screened for <i>Aa</i> to select a host for colonization studies. Macaca mulatta (Rhesus/Rh) was selected. Rh <i>Aa</i> strains were isolated, subjected to sequencing and functional analysis for comparison to human strains. \"Best\" methods for microbial decontamination prior to inoculation were assessed. Three groups were studied; Group 1 (N=5) was inoculated with <i>Aa</i> Spectinomycin resistant (SpecR) Rh strain 4.35, Group 2 (N=5) inoculated with <i>Aa</i> SpecR human strain IDH 781, and Group 3 (N=5) the un-inoculated control. Repeated feeding with pancakes spiked with SpecRAa followed high dose oral inoculation. Cheek, tongue, and plaque samples collected at baseline 1, 2, 3, and 4 weeks after inoculation were plated on agar; 1) selective for <i>Aa</i>, 2) enriched for total counts, and 3) containing 50 µg/ml of Spec. <i>Aa</i> was identified by colonial morphology and DNA analysis. Rh and human <i>Aa</i> had > 93-98 % genome identity. Rh <i>Aa</i> attached to tissues better than IDH 781 <i>in vitro</i> (p < 0.05). SpecR IDH 781 was not recovered from any tissue at any time; whereas, RhSpecR 4.35 was detected in plaque, but never tongue or cheek, in all monkeys at all times (> 1 × 10⁵ colonies/ml; p < 0.001). In conclusion, the primate model provides a useful platform for studying integration of <i>Aa</i> strains into a reduced but established oral habitat. Primate derived SpecR<i>Aa</i> was consistently detected in plaque at all collection periods; however, human derived <i>Aa</i> was never detected. The model demonstrated both microbial as well as tissue specificity.</p>","PeriodicalId":91029,"journal":{"name":"Journal of oral biology (Northborough, Mass.)","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.13188/2377-987X.1000005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33938116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetic Lactoferrin Deficient Mice Demonstrates Greater Susceptibility to Experimental Periodontal Disease.","authors":"Waad Alabdulmohsen, S. Rozario, K. Markowitz, D. Fine, K. Velliyagounder","doi":"10.13188/2377-987X.1000012","DOIUrl":"https://doi.org/10.13188/2377-987X.1000012","url":null,"abstract":"The objective of this study is to detrmine whether alloxan-induced diabetic Lactoferrin knockout (LFKO-/-) mice are more susceptible to periodontal disease caused by Aggregatibacter actinomycetemcomitans compared to the diabetic wild-type (WT) mice. Diabetes was induced in mice by a single dose of alloxan (60 mg/kg) injected intravenously. Mice were categorized as diabetic when blood glucose levels >250 mg/dL were measured on the 7th day after the injection. Periodontal disease was experimentally induced by A. actinomycetemcomitans infection in alloxan induced diabetic WT and LFKO-/- mice. Fasting blood glucose levels and body weight were monitored throughout the study. At the end of the 12th week of infection, mice were sacrificed and bone loss among the groups was estimated by measuring the distance between cemento-enamel junction (CEJ) to the alveolar bone crest (ABC) at 12 sites on the molars. A. actinomycetemcomitans infected mice groups developed more alveolar bone loss than sham-infected animals. Diabetic LFKO-/- infected mice exhibited significant bone loss (P<0.01) and a higher mean fasting blood glucose level (P<0.05) when compared to diabetic WT infected mice. No statistically significant difference in fasting blood glucose level was found between the infected and sham-infected groups. Peripheral blood analysis at the end of the 12th week revealed a significant reduction in the platelet counts in LFKO-/- mice when compared to WT mice. Furthermore, diabetic LFKO-/- presented with lower counts than non-diabetic LFKO-/- mice (P<0.01). In conclusion, diabetic lactoferrin deficient mice are at a higher risk of developing periodontal infection induced by A. actinomycetemcomitans when compared to diabetic WTI mice.","PeriodicalId":91029,"journal":{"name":"Journal of oral biology (Northborough, Mass.)","volume":"2 2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66211780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}