D Saito, T L Marsh, F de Souza Cannavan, J F Höfling, R B Gonçalves
{"title":"Assessment of intraradicular bacterial composition by terminal restriction fragment length polymorphism analysis.","authors":"D Saito, T L Marsh, F de Souza Cannavan, J F Höfling, R B Gonçalves","doi":"10.1111/j.1399-302X.2009.00525.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00525.x","url":null,"abstract":"<p><strong>Background: </strong>The aim of the study was to assess the bacterial community structures associated with endodontic infections using terminal restriction fragment length polymorphism (T-RFLP), and to investigate the correlation of whole community profiles with the manifestation of particular clinical features.</p><p><strong>Methods: </strong>Intraradicular samples were collected from 34 subjects and classified into three study groups based on the observed clinical symptoms: acute (n = 16), sub-acute (n = 8), and asymptomatic (n = 10). Genomic DNA was extracted from each sample, submitted to polymerase chain reaction using a fluorescently labeled 16S ribosomal DNA forward primer, and digested with two tetrameric endonucleases (HhaI and MspI). The terminal restriction fragments (T-RFs) were subsequently discriminated in an automated DNA sequencer, and the results were filtered using a statistics-based criterion.</p><p><strong>Results: </strong>Totals of 138 (HhaI) and 145 (MspI) unique T-RFs were detected (means 13.1 and 11.9) and there was high inter-subject variability in the bacterial assemblages. Odds-ratio analysis unveiled the existence of higher order groups of positively associated T-RFs, restating the concept that intricate ecological relationships may take place in the root canal space. A significantly greater T-RF prevalence was detected in acute cases, suggesting a straight correlation between species richness and spontaneous pain.</p><p><strong>Conclusion: </strong>Overall, no T-RFLP profile representing a specific bacterial consortium could be associated with the manifestation of symptoms of endodontic origin.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 5","pages":"369-76"},"PeriodicalIF":0.0,"publicationDate":"2009-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00525.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28358182","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}
S Joly, L M Compton, C Pujol, Z B Kurago, J M Guthmiller
{"title":"Loss of human beta-defensin 1, 2, and 3 expression in oral squamous cell carcinoma.","authors":"S Joly, L M Compton, C Pujol, Z B Kurago, J M Guthmiller","doi":"10.1111/j.1399-302X.2009.00512.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00512.x","url":null,"abstract":"<p><strong>Introduction: </strong>Human beta-defensins (HBDs) are cationic, antimicrobial peptides produced by epithelial cells and involved in various aspects of the innate and acquired immune responses. They are expressed by oral tissues as constitutive and inducible genes. Recently, single nucleotide polymorphisms (SNPs) of beta-defensins have been correlated with increased susceptibility to certain diseases. Studies have reported altered expression of beta-defensins in cancers suggesting their involvement in carcinogenesis. The purpose of this study was to evaluate the regulation of HBD-1 (also published as DEFB1), HBD-2 (DEFB4) and HBD-3 (DEFB103A) (http://www.genenames.org/index.html) and HBD-1 SNPs in oral squamous cell carcinoma cell lines (OSCC) and healthy gingival keratinocytes.</p><p><strong>Methods: </strong>beta-defensin expression was quantitatively assessed using real-time polymerase chain reactions in OSCC and control cell lines after exposure to interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma. Control data were obtained in a previous study. DNA from 19 OSCC cell lines and 44 control subjects were extracted and the HBD-1 region spanning the 5' untranslated region to the first intron was sequenced and analysed for SNP identification and distribution.</p><p><strong>Results: </strong>HBD-1 and HBD-2 basal messenger RNA expression were significantly lower in OSCC. In addition, the ability to be induced was significantly reduced in OSCC for all three beta-defensins. Four HBD-1 SNPs were differentially distributed between cancer and control populations. Genotype distribution at the HBD-1 locus also suggested loss of heterozygosity in OSCC.</p><p><strong>Conclusions: </strong>The genetic variation observed in OSCC compared with that in control cell lines may account for differences in beta-defensin expression. These results suggest a putative role for beta-defensins in carcinogenesis and indicate that beta-defensins may be useful markers of OSCC.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 5","pages":"353-60"},"PeriodicalIF":0.0,"publicationDate":"2009-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00512.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28358180","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}
I Saygun, S Sahin, U Muşabak, S Enhoş, A Kubar, O Günhan, J Slots
{"title":"Human cytomegalovirus in peripheral giant cell granuloma.","authors":"I Saygun, S Sahin, U Muşabak, S Enhoş, A Kubar, O Günhan, J Slots","doi":"10.1111/j.1399-302X.2009.00535.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00535.x","url":null,"abstract":"<p><strong>Background: </strong>The peripheral giant cell granuloma is a relatively common non-neoplastic inflammatory lesion of gingiva, but the etiopathogeny remains unknown. This study aimed to evaluate the importance of human cytomegalovirus and Epstein-Barr virus in a peripheral giant cell granuloma of a 47-year-old female.</p><p><strong>Methods: </strong>The lesion was studied clinically, histopathologically, immunologically and virologically using established procedures.</p><p><strong>Results: </strong>The gingival growth was located at the mesial surface of the maxillary left canine having a vital pulp. The mass was 12 x 21 mm in size and exhibited a smooth surface with no evidence of fluctuation on palpation. An excisional biopsy revealed giant cells in a fibrohistiocytic stroma with areas of haemorrhage. Serum protein levels and lymphocyte subsets were within normal limits, except CD3(+) and CD4(+) cells were below normal ranges. Polymorphonuclear leukocytes expressed p150,95 (CD11c/CD18) and CXCR-2 receptors within normal ranges, but the CXCR1 receptor showed decreased density, and CD15 were below normal range. A virological sample of the tooth surface adjacent to the gingival swelling yielded 7.6 x 10(3) copy-counts of cytomegalovirus and 4.3 x 10(3) copy-counts of Epstein-Barr virus.</p><p><strong>Conclusions: </strong>The clinical and histological findings were consistent with the diagnosis of peripheral giant cell granuloma. Cytomegalovirus has the potential to induce multinucleated giant cells, and the possibility that the virus contribute to the development of peripheral giant cell granuloma merits further study.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 5","pages":"408-10"},"PeriodicalIF":0.0,"publicationDate":"2009-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00535.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28359747","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}
C B Huang, K A Emerson, O A Gonzalez, J L Ebersole
{"title":"Oral bacteria induce a differential activation of human immunodeficiency virus-1 promoter in T cells, macrophages and dendritic cells.","authors":"C B Huang, K A Emerson, O A Gonzalez, J L Ebersole","doi":"10.1111/j.1399-302X.2009.00533.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00533.x","url":null,"abstract":"<p><strong>Introduction: </strong>The human immunodeficiency virus (HIV) can integrate into T cells, macrophages and dendritic cells resulting in a latent infection. Reports have also demonstrated that various microbial and host cell factors can trigger HIV reactivation leading to HIV recrudescence, potentially undermining highly active antiretroviral therapies.</p><p><strong>Methods: </strong>This study evaluated the capacity of oral bacteria associated with chronic periodontal infections to stimulate HIV promoter activation in various cell models of HIV latency.</p><p><strong>Results: </strong>T cells (1G5) challenged with oral bacteria demonstrated a dose-response of HIV promoter activation with a subset of the bacteria, as well as kinetics that were generally similar irrespective of the stimuli. Direct bacterial challenge of the T cells resulted in increased activation of approximately 1.5- to 7-fold over controls. Challenge of macrophages (BF24) indicated different kinetics for individual bacteria and resulted in consistent increases in promoter activation of five fold to six fold over basal levels for all bacteria except Streptococcus mutans. Dendritic cells showed increases in HIV reactivation of 7- to 34-fold specific for individual species of bacteria.</p><p><strong>Conclusion: </strong>These results suggested that oral bacteria have the capability to reactivate HIV from latently infected cells, showing a relationship of mature dendritic cells > immature dendritic cells > macrophages > or = T cells. Expression of various pattern recognition receptors on these various cell types may provide insight into the primary receptors/signaling pathways used for reactivation by the bacteria.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 5","pages":"401-7"},"PeriodicalIF":0.0,"publicationDate":"2009-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00533.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28359746","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}
M Matsumoto-Nakano, M Tsuji, S Inagaki, K Fujita, K Nagayama, R Nomura, T Ooshima
{"title":"Contribution of cell surface protein antigen c of Streptococcus mutans to platelet aggregation.","authors":"M Matsumoto-Nakano, M Tsuji, S Inagaki, K Fujita, K Nagayama, R Nomura, T Ooshima","doi":"10.1111/j.1399-302X.2009.00521.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00521.x","url":null,"abstract":"<p><strong>Introduction: </strong>Streptococcus mutans is considered to be one of the pathogens that cause infective endocarditis. The purpose of the present study was to examine the properties of S. mutans with regard to platelet aggregation by focusing on its high molecular protein antigen c (PAc).</p><p><strong>Methods: </strong>The platelet aggregation properties of six clinical strains and one isogenic mutant strain of S. mutans were analysed using an aggregometer and confocal microscopy, as well as with an inhibition assay of platelet aggregation using anti-PAc serum.</p><p><strong>Results: </strong>S. mutans strains with PAc expression induced platelet aggregation, while a PAc-deficient mutant and two clinical isolates with no PAc expression did not. When platelets were pretreated with higher amounts of anti-PAc serum, the platelet aggregation rate was reduced in a dose-dependent manner, indicating that PAc binds directly to platelets.</p><p><strong>Conclusion: </strong>S. mutans PAc is involved in human platelet aggregation and may be one of the virulence factors in the pathogenesis of infective endocarditis.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 5","pages":"427-30"},"PeriodicalIF":0.0,"publicationDate":"2009-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00521.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28360654","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}
{"title":"The effect of lactoferrin on oral bacterial attachment.","authors":"S Y Arslan, K P Leung, C D Wu","doi":"10.1111/j.1399-302X.2009.00537.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00537.x","url":null,"abstract":"<p><strong>Introduction: </strong>Lactoferrin (Lf), an iron-binding salivary glycoprotein, plays an important role in human innate defense against local mucosal infection. We hypothesized that Lf interferes with initial oral bacterial attachment to surfaces by iron sequestration, so inhibiting subsequent biofilm formation. The objective was to investigate the effect of Lf on the early stages of single-species and multi-species oral biofilm development.</p><p><strong>Methods: </strong>Streptococcus gordonii, Streptococcus mutans, Fusobacterium nucleatum and Porphyromonas gingivalis were used in this study. Glass disks of a two-track flow cell coated with flowing artificial saliva (0.3 ml/min) with and without Lf (100 microg/ml) were used for studying bacterial attachment (3 h, 37 degrees C). Attachment was also examined by incubating single or multiple species of test bacteria (10(7) colony-forming units/ml) with Lf-coated (20-100 microg/ml) and uncoated glass slides. The effects of beta-lactoglobulin, 2,2'-dipyridyl (25-100 microg/ml), an iron chelator, and FeCl3 on attachment were also examined.</p><p><strong>Results: </strong>Lf inhibited the initial attachment of S. gordonii (50.3%, P < 0.05) but not that of F. nucleatum and P. gingivalis. However, the attachment of a dual-species biofilm containing S. gordonii (i.e. S. gordonii/F. nucleatum or S. gordonii/P. gingivalis) was significantly reduced (48.7% or 62.1%, respectively, P < 0.05) in the presence of Lf. beta-Lactoglobulin did not affect the attachment of S. gordonii. In the presence of 100 microm 2,2'-dipyridyl, attachment of S. gordonii was reduced by 53.87%. No reduction in attachment was noted in S. gordonii pretreated with Lf (100 microg/ml) and FeCl3 (20-200 microm).</p><p><strong>Conclusion: </strong>Lf suppresses initial attachment of S. gordonii and S. gordonii coaggregates by iron sequestration. This may lead to subsequent inhibition of oral biofilm development.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 5","pages":"411-6"},"PeriodicalIF":0.0,"publicationDate":"2009-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00537.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28359748","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}
T Shimada, N Sugano, K Ikeda, K Shimada, T Iizuka, K Ito
{"title":"Protease-activated receptor 2 mediates interleukin-8 and intercellular adhesion molecule-1 expression in response to Aggregatibacter actinomycetemcomitans.","authors":"T Shimada, N Sugano, K Ikeda, K Shimada, T Iizuka, K Ito","doi":"10.1111/j.1399-302X.2009.00507.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00507.x","url":null,"abstract":"<p><strong>Introduction: </strong>We investigated the mechanisms by which extracts of Aggregatibacter actinomycetemcomitans affect the inflammatory response in gingival epithelial cells.</p><p><strong>Methods: </strong>Human gingival cells (Ca9-22) were cultured in bacterial extracts prepared from A. actinomycetemcomitans ATCC 29522. The cells were pretreated with protease inhibitors or transfected with small interfering RNA (siRNA) specific for protease-activated receptor 2 (PAR-2).</p><p><strong>Results: </strong>The pretreatment of cells with serine protease inhibitors significantly inhibited A. actinomycetemcomitans extract-induced expression of interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1) at both the messenger RNA and protein levels. In addition, A. actinomycetemcomitans extract-induced IL-8 and ICAM-1 expression was significantly decreased in PAR-2/siRNA-transfected cells.</p><p><strong>Conclusions: </strong>A. actinomycetemcomitans extract-induced IL-8 and ICAM-1 expression in gingival epithelial cells is mediated by PAR-2.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 4","pages":"285-91"},"PeriodicalIF":0.0,"publicationDate":"2009-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00507.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28282342","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}
E Igarashi, A Kamaguchi, M Fujita, H Miyakawa, F Nakazawa
{"title":"Identification of oral species of the genus Veillonella by polymerase chain reaction.","authors":"E Igarashi, A Kamaguchi, M Fujita, H Miyakawa, F Nakazawa","doi":"10.1111/j.1399-302X.2009.00513.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00513.x","url":null,"abstract":"<p><strong>Introduction: </strong>Members of the genus Veillonella cannot be reliably distinguished by their biochemical characteristics and phenotypic features. Moreover, DNA-DNA hybridization and sequence analyses of the 16S ribosomal RNA gene including random fragment length polymorphism analysis, are complex and time-consuming procedures that are not well-suited to identifying oral species of Veillonella: Veillonella atypica, Veillonella denticariosi, Veillonella dispar, Veillonella parvula, and Veillonella rogosae.</p><p><strong>Methods: </strong>In this study, five forward primers and a reverse primer were designed for polymerase chain reaction (PCR) according to the partial sequences of the rpoB genes of these oral Veillonella species.</p><p><strong>Results: </strong>The forward primers were species-specific for these five Veillonella species, and could produce specific amplicons when used together with reverse primer and individual DNA templates of these species in PCR. These primer pairs were also found to discriminate between the respective species, and the Veillonella strains isolated from human oral cavities were successfully assigned to one of the five oral species of the genus Veillonella based on their specific products by PCR.</p><p><strong>Conclusion: </strong>A simple two-step PCR procedure using the five sets of primer pairs developed in the present study is a rapid and reliable method for the identification of the recognized oral Veillonella species.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 4","pages":"310-3"},"PeriodicalIF":0.0,"publicationDate":"2009-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00513.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28282346","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}
{"title":"Transient acid-impairment of growth ability of oral Streptococcus, Actinomyces, and Lactobacillus: a possible ecological determinant in dental plaque.","authors":"M Horiuchi, J Washio, H Mayanagi, N Takahashi","doi":"10.1111/j.1399-302X.2009.00517.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00517.x","url":null,"abstract":"<p><strong>Introduction: </strong>Dental plaque pH decreases to about 4 through bacterial fermentation of carbohydrates and this low pH is maintained for from several minutes to about an hour. Repeated acidification causes demineralization of the tooth surface, resulting in caries formation. The acidification also influences plaque bacteria. Severe acidification kills bacteria efficiently, while physiological acidification, the condition occurring in plaque, kills bacteria partially and may impair growth ability. We, therefore, investigated the effects of physiological acidification on representative caries-related bacteria.</p><p><strong>Methods: </strong>Streptococcus mutans, Streptococcus sobrinus, Streptococcus sanguinis, Streptococcus oralis, Lactobacillus paracasei, and Actinomyces naeslundii were used. Effects of physiological acidification at pH 4.0 on cell viability and growth ability, as well as the growth rate of these bacteria at pH 4.0-7.0, were investigated.</p><p><strong>Results: </strong>Mutans streptococci and Lactobacillus grew at pH 4.0 but the growth of S. sanguinis and S. oralis ceased below pH 4.2 and pH 4.2-4.4, respectively. Acidification at pH 4.0 for 1 h killed 43-89%, 45% and 35-76% of S. sanguinis, S. oralis, and Actinomyces, respectively. Furthermore, assessment of bacterial growth curves revealed that the growth ability of the surviving cells of S. sanguinis, S. oralis and Actinomyces was impaired, but it was recovered within 2-5 h after the environmental pH had returned to 7.0. The acidification neither killed nor impaired the growth of mutans streptococci and Lactobacillus.</p><p><strong>Conclusions: </strong>These results indicate that physiological and transient acidification is not sufficient to kill bacteria, but it causes a temporary acid-impairment of their growth ability, which may function as an ecological determinant for microbial composition in dental plaque.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 4","pages":"319-24"},"PeriodicalIF":0.0,"publicationDate":"2009-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00517.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28282348","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}
M P Morran, L A Alexander, B D Slotterbeck, M F McInerney
{"title":"Dysfunctional innate immune responsiveness to Porphyromonas gingivalis lipopolysaccharide in diabetes.","authors":"M P Morran, L A Alexander, B D Slotterbeck, M F McInerney","doi":"10.1111/j.1399-302X.2009.00522.x","DOIUrl":"https://doi.org/10.1111/j.1399-302X.2009.00522.x","url":null,"abstract":"INTRODUCTION\u0000Type 1 diabetes is a major risk factor for the development of severe periodontal disease. As diabetes increases in severity, so does the susceptibility to and severity of periodontitis. People with diabetes who have periodontal disease have a harder time maintaining healthy blood glucose levels. Macrophages play an important role in both diabetes and periodontitis. Previous research comparing bone-marrow-derived macrophages (BM-Mvarphi) from diabetic non-obese diabetic (NOD) mice and control mice illustrates that a dysregulation in cytokine, Toll-like receptor (TLR) expression, and cell signaling occurs in the diabetic state.\u0000\u0000\u0000METHODS\u0000This study examines the effect of chronic hyperglycemia on BM-Mvarphi TLR expression and activation, cell signaling, cytokine production, and phagocytic function in the diabetic state, when challenged with the periodontal stimulus Porphyromonas gingivalis lipopolysaccharide (LPS) to further understand how diabetes and associated hyperglycemia may contribute to the increased susceptibility of people with diabetes to periodontitis.\u0000\u0000\u0000RESULTS\u0000When BM-Mvarphi, obtained from diabetic NOD mice, are stimulated with P. gingivalis LPS under hyperglycemic conditions the following changes occur: reduced messenger RNA expression and cell surface expression of TLR2, reduced messenger RNA expression and protein production of tumor necrosis factor-alpha, reduced signal transduction, and a reduction in phagocytic function. All the activity of BM-Mvarphi from diabetic NOD mice was restored when differentiation and stimulation occurred under normoglycemic conditions.\u0000\u0000\u0000DISCUSSION\u0000Diabetic patients in a hyperglycemic state may be generating macrophages that are inherently immunocompromised, contributing to an environment allowing periodontal infections to flourish. As a consequence, people with diabetes who maintain proper control of blood sugar levels may experience an increased immunological benefit when challenged with a periodontal infection.","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 4","pages":"331-9"},"PeriodicalIF":0.0,"publicationDate":"2009-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00522.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28281125","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}