Добірка наукової літератури з теми "Periodontal disease Molecular aspects"

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Статті в журналах з теми "Periodontal disease Molecular aspects":

1
Taubman, M. A., E. D. Stoufi, G. J. Seymour, D. J. Smith, and J. L. Ebersole. "Immunoregulatory Aspects of Periodontal Disease." Advances in Dental Research 2, no. 2 (November 1988): 328–33. http://dx.doi.org/10.1177/08959374880020022201.
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This manuscript reviews our studies of the composition and functional capabilities of gingival tissue lymphocytes from patients with periodontal disease. The emphasis has been on phenotyping the local lymphoid infiltration in gingival and periodontal disease. The preparation and phenotypic analyses of cells recovered from diseased and healthy human periodontal tissues indicated that T-cell subset ratios from diseased tissue were significantly decreased compared with peripheral blood or normal tissue ratios. These reductions were verified in a second study we performed using two-color immunofluorescence analyzed by flow cytofluorometry. Local variations in the CD4 + cell population were also found in diseased tissue cells when these were compared with normal tissue cells. The relative percentage of CD4+ cells labeled with anti-helper inducer (4B4) or anti-suppressor inducer (2H4) monoclonal antibodies was increased above that of normal tissue cells. Functional studies of immunoglobulin production by gingival cells from adult periodontitis tissues showed two discrete patterns of synthesis and also suppression of immunoglobulin synthesis after addition of mitogen to the cultures. Removal of macrophages also drastically reduced immunoglobulin synthesis by gingival cells. These results indicate that there is an abundance of suppressor T-cells in diseased tissue and that functional suppression is demonstrated by lymphocytes from periodontal disease tissue. The findings of these investigations have suggested potentially important roles for immune regulation in periodontal disease.
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Thomson, W. Murray, Aubrey Sheiham, and A. John Spencer. "Sociobehavioral aspects of periodontal disease." Periodontology 2000 60, no. 1 (August 2012): 54–63. http://dx.doi.org/10.1111/j.1600-0757.2011.00405.x.
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Evstropov, Vladimir, Galina Zelenkova, Sergei Tresnitskii, Anna Spirina, Pavel Bykadorov, Mikhael Yenin, Еkaterina Danileyko, and Alexey Ermakov. "Immunological aspects of inflammatory periodontal disease (analytical review)." E3S Web of Conferences 210 (2020): 06005. http://dx.doi.org/10.1051/e3sconf/202021006005.
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Clinical and immunological parallels in inflammatory periodontal diseases are considered taking into account some features of the functioning of general and local structures of the immune system in periodontitis of varying severity, chronic generalized periodontitis, aggressive periodontitis. In the analysis of immunopathogenesis of inflammatory periodontal diseases, an essential role is given to an imbalance in the immune and cytokine system.
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Kinane, Denis F., and David F. Lappin. "Clinical, pathological and immunological aspects of periodontal disease." Acta Odontologica Scandinavica 59, no. 3 (January 2001): 154–60. http://dx.doi.org/10.1080/000163501750266747.
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Velea, Oana A., Dan Onisei, Doina Onisei, Andreea Pogan, Corrado Paganelli, and Iulian P. Velea. "Microbiological Aspects In Periodontal Disease And Diabetes Mellitus." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 21, no. 2 (June 2014): 151–61. http://dx.doi.org/10.2478/rjdnmd-2014-0020.
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Abstract Background and Aims. Scientists are constantly showing a high interest for the relationship between Periodontal Disease (PD) and Diabetes Mellitus (DM). PD, “the sixth complication” of DM is recognized to be a chronic gram-negative anaerobic infectious disease. This paper is aimed at reviewing and evaluating the correlations between PD and DM from a microbiological point of view. Treatment implications of PD’s management as an important component of DM care is reviewed in the light of microbiological current knowledge. Materials and Methods. Microbiological studies and clinical trials were selected from medical and dental journals, and studied thoroughly. Results. Plaque biofilm and prolonged hyperglycemia increase the risk of PD development in DM. These two features determine inflammatory reactions that end-up in tissue destruction and impaired healing responses. Few pathogens are considered highly prevalent periodontal pathogens, with destructive actions. Studies have shown that metabolic balance or lack of balance determines bacterial variations in diabetic patients with PD. Other results demonstrate the importance of microbial tests (especially PCR techniques) as indicators for healing or disease progression. Conclusions. There aren’t many studies assessing the relationship between PD and DM from microbiological points of view. In light of increasing evidence, larger interventional studies are needed
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Puri, Komal, Nikhil Puri, Vidya Dodwad, and Sujata Surendra Masamatti. "Restorative aspects of periodontal disease: an update part 1." Dental Update 41, no. 6 (July 2014): 545–52. http://dx.doi.org/10.12968/denu.2014.41.6.545.
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Puri, Nikhil, Komal Puri, Sujata Surendra Masamatti, and Vidya Dodwad. "Restorative aspects of periodontal disease: an update part 2." Dental Update 41, no. 7 (September 2014): 638–52. http://dx.doi.org/10.12968/denu.2014.41.7.638.
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Degasperi, Giovanna R., Augusto Etchegaray, Larissa Marcelino, Ahron Sicard, Karina Villalpando, and Sérgio L. Pinheiro. "Periodontal Disease: General Aspects from Biofilm to the Immune Response Driven by Periodontal Pathogens." Advances in Microbiology 08, no. 01 (2018): 1–17. http://dx.doi.org/10.4236/aim.2018.81001.
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Voinescu, I., D. Ferechide, CM Cristache, L. Burlibasa, and M. Burlibasa. "Ethical and legal aspects in periodontal disease diagnosis and therapy." Romanian Journal of Legal Medicine 27, no. 1 (March 2019): 57–64. http://dx.doi.org/10.4323/rjlm.2019.57.
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Horne, Poppy E., Lyndie A. Foster Page, Jonathan W. Leichter, Ellie T. Knight, and W. Murray Thomson. "Psychosocial aspects of periodontal disease diagnosis and treatment: A qualitative study." Journal of Clinical Periodontology 47, no. 8 (June 2020): 941–51. http://dx.doi.org/10.1111/jcpe.13309.
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Дисертації з теми "Periodontal disease Molecular aspects":

1
Kennedy, Rebekah Storm. "Microbiological and immunological aspects of equine periodontal disease." Electronic Thesis or Dissertation, University of Glasgow, 2017. http://theses.gla.ac.uk/8064/.
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Periodontal disease is a common and painful condition in the horse. Although awareness of the condition is growing amongst the veterinary profession and horse owners, the presence of the disease is often overlooked and treatment can be difficult. Despite this, there have been few recent studies of the aetiopathogenesis of the condition. Certain species of bacteria may act as periodontal pathogens, stimulating a destructive inflammatory response in periodontal tissues and this has been well recognised as being important to the aetiopathogenesis of the disease in man. However few equine studies on this aspect of the disease have been carried out. The main aims of this study were: - 1) to identify the bacteria associated with a healthy oral cavity and periodontitis in horses using culture dependent and independent methods; 2) to assess the differences in bacterial populations between the healthy and periodontitis groups and identify putative pathogens; 3) to quantify the expression patterns of TLRs 2, 4 and 9, the pro-inflammatory cytokines IL-1β and TNFα, anti-inflammatory cytokine IL-10 and Th1/Th2/Th17 cytokines IL-4, IL-6/ IL-12, IFNɣ/ IL-17, within gingival tissue from each sample group; 4) to use matched data to establish if associations exist between the presence and quantity of bacterial species present and TLR expression and 5) to determine activation of TLRs 2, 4 and 9 by putative pathogens using specific in- vitro TLR assays. Swabs were taken from the gingival sulcus of 42 orally healthy horses and plaque samples were taken from the periodontal pockets of 61 horses with periodontal disease. The location and grade of the lesion was noted and an equine dental chart completed for each case. Bacteria were identified using high throughput 16S rRNA gene sequencing, QPCR, whole genome sequencing and conventional culture followed by 16S gene sequencing. Gingival biopsies were taken from 13 orally healthy horses and 20 horses with periodontitis and gene expression of TLR 2, TLR 4, TLR 9, IL-1β, IL-4, IL-6, IL-10, IL-12, IL-17, TNFα and IFNɣ was measured. THP-1X Blue, MyD88 THP-1X Blue, HEK hTLR 2 Blue and HEK hTLR 4 Blue human cell lines were co-cultured with putative periodontal pathogens and their response measured via level of secreted embryonic alkaline phosphatase. Clinical, microbiological and immunological data underwent cross-matching analysis. Microbial populations showed 89% dissimilarly between oral health and periodontitis with a less diverse population present in diseased equine periodontal pockets. The most discriminative bacteria between health and disease identified at genus level were Fusobacteria and Acinetobacter in health and Pseudomonas and Prevotella in periodontitis. The most abundant genera were Gemella (36.5%), Pseudomonas (14%) and Acinetobacter (8%) in orally healthy samples and Pseudomonas (25%), Prevotella (14%) and Acinetobacter (9.4%) in periodontitis samples. Whole genome sequencing revealed the presence of 75 species of Prevotella in the equine oral cavity and a significantly higher number of reads corresponding to Prevotella bivia, Prevotella dentalis, Prevotella denticola, Prevotella intermedia, Prevotella melaninogenica, Prevotella nigrescens were noted in diseased samples. Significant increases in expression of TLR 4 mRNA, TLR 9 mRNA and, in particular TLR 2, mRNA were noted in diseased equine gingival tissue in addition to increased pro-inflammatory and anti-inflammatory cytokine mRNA expression. Presence of P. intermedia was significantly positively correlated with expression of TLR 2 in equine periodontitis. In addition, the presence of Aggregatibacter actinomycetemcomitans was positively associated with disease severity and expression of TLR 4 mRNA in the horse. Co-culture of periodontal pathogens with human cell lines revealed that the innate immune response to the presence of these bacteria is mainly mediated through TLR 2 activation. The use of both culture dependent and culture independent methods to investigate the equine oral microbiome has provided significant breadth and depth of information on the microbiology of equine periodontal disease. Microbial populations are significantly different as expected and bacteria belonging to the Prevotella genus have been strongly implicated in the aetiopathogenesis of the condition. The innate immune response produced in periodontally diseased equine gingival tissue has been characterised for the first time in the horse.
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Mooney, John. "Molecular and cellular aspects of the humoral immune response in periodontal disease and other related conditions." Electronic Thesis or Dissertation, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321510.
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3
Ng, Kwai-sang Sam, and 吳桂生. "Psychological perspectives of periodontal disease." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36918210.
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4
Porter, S. R. "Immunological aspects of rapidly progressive periodontitis." Electronic Thesis or Dissertation, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377350.
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Sörgjerd, Karin. "Molecular Aspects of Transthyretin Amyloid Disease." Doctoral thesis, comprehensive summary, Linköpings universitet, Biokemi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-12566.
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This thesis was made to get a deeper understanding of how chaperones interact with unstable, aggregation prone, misfolded proteins involved in human disease. Over the last two decades, there has been much focus on misfolding diseases within the fields of biochemistry and molecular biotechnology research. It has become obvious that proteins that misfold (as a consequence of a mutation or outer factors), are the cause of many diseases. Molecular chaperones are proteins that have been defined as agents that help other proteins to fold correctly and to prevent aggregation. Their role in the misfolding disease process has been the subject for this thesis. Transthyretin (TTR) is a protein found in human plasma and in cerebrospinal fluid. It works as a transport protein, transporting thyroxin and holo-retinol binding protein. The structure of TTR consists of four identical subunits connected through hydrogen bonds and hydrophobic interactions. Over 100 point mutations in the TTR gene are associated with amyloidosis often involving peripheral neurodegeneration (familial amyloidotic polyneuropathy (FAP)). Amyloidosis represents a group of diseases leading to extra cellular deposition of fibrillar protein known as amyloid. We used human SH-SY5Y neuroblastoma cells as a model for neurodegeneration. Various conformers of TTR were incubated with the cells for different amounts of time. The experiments showed that early prefibrillar oligomers of TTR induced apoptosis when neuroblastoma cells were exposed to these species whereas mature fibrils were not cytotoxic. We also found increased expression of the molecular chaperone BiP in cells challenged with TTR oligomers. Point mutations destabilize TTR and result in monomers that are unstable and prone to aggregate. TTR D18G is naturally occurring and the most destabilized TTR mutant found to date. It leads to central nervous system (CNS) amyloidosis. The CNS phenotype is rare for TTR amyloid disease. Most proteins associated with amyloid disease are secreted proteins and secreted proteins must pass the quality control check within the endoplasmic reticulum (ER). BiP is a Hsp70 molecular chaperone situated in the ER. BiP is one of the most important components of the quality control system in the cell. We have used TTR D18G as a model for understanding how an extremely aggregation prone protein is handled by BiP. We have shown that BiP can selectively capture TTR D18G during co-expression in both E. coli and during over expression in human 293T cells and collects the mutant in oligomeric states. We have also shown that degradation of TTR D18G in human 293T cells occurs slower in presence of BiP, that BiP is present in amyloid deposition in human brain and mitigates cytotoxicity of TTR D18G oligomers.
Denna avhandling handlar om proteiner. Särskilt de som inte fungerar som de ska utan har blivit vad man kallar ”felveckade”. Anledningen till att proteiner veckas fel beror ofta (men inte alltid) på mutationer i arvsmassan. Felveckade proteiner kan leda till sjukdomar hos människor och djur (man brukar tala om amyloidsjukdomar), ofta av neurologisk karaktär. Exempel på amyloidsjukdomar är polyneuropati, där perifera nervsystemet är drabbat, vilket leder till begränsad rörelseförmåga och senare till förlamning; och Alzheimer´s sjukdom, där centrala nervsystemet är drabbat och leder till begränsad tankeförmåga och minnesförluster. Studierna som presenteras i denna avhandling har gått ut på att få en bättre förståelse för hur felveckade proteiner interagerar med det som vi har naturligt i cellerna och som fungerar som skyddande, hjälpande proteiner, så kallade chaperoner. Transtyretin (TTR) är ett protein som cirkulerar i blodet och transporterar tyroxin (som är ett hormon som bland annat har betydelse för ämnesomsättningen) samt retinol-bindande protein (vitamin A). I TTR genen har man funnit över 100 punktmutationer, vilka har kopplats samman med amyloidsjukdomar, bland annat ”Skellefteåsjukan”. Mutationer i TTR genen leder ofta till att proteinet blir instabilt vilket leder till upplösning av TTR tetrameren till monomerer. Dessa monomerer kan därefter sammanfogas på nytt men denna gång på ett sätt som är farligt för organismen. I denna avhandling har fokus legat på en mutation som kallas TTR D18G, vilken har identifierats i olika delar av världen och leder till en dödlig form av amyloidos i centrala nervsystemet. Det chaperon som vi har studerat benämns BiP och är beläget i en cellkomponent som kallas för det endoplasmatiska retiklet (ER). I ER finns cellens kontrollsystem i vilket det ses till att felveckade proteiner inte släpps ut utan istället bryts ned. Denna avhandling har visat att BiP kan fånga upp TTR D18G inuti celler och där samla mutanten i lösliga partiklar som i detta fall är ofarliga för cellen. Avhandligen har också visat att nedbrytningen av TTR D18G sker mycket långsammare när BiP finns i riklig mängd.
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Hanley, Shirley Anne. "Molecular characterisation of an immunodominant 55kDa surface antigen of Porphyromonas gingivalis W50." Electronic Thesis or Dissertation, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312824.
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Watkins, Craig Allen. "Molecular aspects of punta toro virus." Electronic Thesis or Dissertation, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239272.
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Jim, Jin-to, and 詹展韜. "Genetics and molecular characterization of degenerative disc disease." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B35720189.
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Abuaisha, Karim Belkais Faraj. "Prognostic biomarkers of periodontal disease." Electronic Thesis or Dissertation, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/prognostic-biomarkers-of-periodontal-disease(77882787-a695-42a3-b7e4-7caa8e9c4bde).html.
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Objectives: Previous studies in our laboratory have identified the antimicrobial proteins Human Neutrophil Protein 1 – 3 (HNP1-3), Myeloid Related Protein 8 (S100A8/MRP8) and LL-37 as putative periodontal salivary biomarkers. The aims of the studies reported in this thesis were to investigate the diagnostic and prognostic potential of these markers, together with Matrix Metalloproteinase- 8 (MMP-8), serum markers C - reactive protein (CRP) and Interleukin-6 (IL-6), on the initial outcome of nonsurgical periodontal treatment. Material & Methods: We carried out a cross sectional study which aimed to verify and establish a diagnostic threshold for a group of salivary biomarkers (MMP-8, HNP1-3, S100A8 and LL-37) and to test the validity of the diagnostic utility of these biomarkers. A total of 133 unstimulated saliva samples (46 with chronic periodontitis, 38 with aggressive periodontitis and 49 with gingivitis) were analysed by ELISA. In addition multiple markers were combined to give a single combined cut off point by normalising each biomarker to percentage of cut-off point value, (such that x + y = combined cut off point). These pre-determined cut-off points were applied to salivary AMPs levels in an independent cohort originally collected to investigate the effects of diabetes on periodontitis. To investigate prognostic potential a total of 66 participants were recruited to a longitudinal intervention study of patients with moderate–severe Chronic Periodontitis. 53 subjects completed the protocol and were included in the final analysis. Subjects (28 male, 25 female) age range (23-65 years) with were recruited, with 14 smokers and 3 with type II diabetes, and saliva and serum samples were collected prior to periodontal examination. Patients were then given a course of non-surgical periodontal therapy over 2 visits. 8-10 weeks post-operatively saliva/serum sampling and clinical examination were repeated. Salivary MMP-8, S100A8 and HNP1-3 concentrations were all determined by ELISAs. In addition we measured serum levels of CRP and Interleukin 6. Results: In the cross-sectional study the HNP1-3 and S100A8 could differentiate between gingivitis and chronic periodontitis with high specificity (around 90%) and around 75% sensitivity compared to MMP-8 which was able to discriminate between gingivitis and periodontitis (chronic and aggressive) with both high 3 specificity and sensitivity. LL37 showed no significant diagnostic potential. Within the independent cohort the application of pre-determined thresholds, either individual or combined cut-offs, were able to detect periodontitis with specificity of between 75 – 85 % but with very low sensitivity. In addition diabetic status was found to result in significantly increased MMP-8 and S100A8 concentrations in subjects with periodontal disease. In the intervention study, treatment resulted in reductions in the mean: a) number of deep sites (>4mm) (33.57 ± 20.75 vs 18.51 ± 13.87; mean ± SD, p<0.0001); b) probing pocket depths (5.92 ± 0.47 mm vs 4.74 ± 0.76 mm, p<0.0001); c) bleeding index (0.32 ± 0.20 vs 0.21 ± 0.16, p<0.0001); d) plaque index (0.46 ± 0.20 vs 0.37 ± 0.18, p=0.0003). Only the mean concentrations of MMP-8 and S100A8 showed significant reductions post-treatment (MMP-8: 355.4 ± 319.9 ng/ml vs 216.6 ± 217.2 ng/ml, p<0.0001), (S100A8: 1182 ± 1095 ng/ml vs 693.9 ± 719.6 ng/ml, p=0.0007). Only the change in concentrations of MMP-8 were strongly associated with magnitude of treatment response (MMP-8: r2= 0.1, p=0.02). In addition, the baseline levels of MMP-8 & S100A8 were also associated with treatment response (MMP-8: r2= 0.1, p=0.03; S100A8: r2=0.1, p=0.02). Overall, there were 13 out of 53 participants who did not respond to the treatment (24.5% of cases). MMP-8 baseline concentrations were significantly higher in responders (419.3 ± 343.1 ng/ml) than non-responders (158.8 ± 73.3 ng/ml) (p=0.009). MMP-8 concentrations at baseline that were above the cut-off (<182.8 ng/ml) predicted a good response to periodontal treatment with 77% sensitivity and 70% specificity. There was no effect of the single round of non-surgical periodontal treatment on the levels of systemic markers CRP & IL-6, and also there was no correlation between local and systemic markers. Conclusion: These results of both studies suggest that MMP-8, HNP1-3 and S100A8 may be useful to identify cases of periodontitis with good specificity and moderate sensitivity and may give superior results when combined. In addition the salivary MMP-8 and S100A8 showed promising periodontal prognostic ability to detect the likelihood of a good response to treatment, with MMP-8 showed the best results with moderate sensitivity and specificity. However, further validation studies would be useful in larger, non-diabetic cohorts.
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BrÃgido, Jandenilson Alves. "Prevalence and distribution of Aggregatibacter actinomycetemcomitans serotypes in periodontal disease Brazilian subjects." PublishedVersion, Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=9056.
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nÃo hÃ
Studies suggest that subjects with severe periodontal lesions are more likely to colonize Aggregatibacter actinomycetemcomitans. This species is genetically heterogeneous and can be grouped into six serotypes (a-f), which may differ regarding virulence characteristics. Ethnic differences and geographic population can influence the distribution and prevalence of these serotypes regarding periodontal disease. The aims of this dissertation, comprised of two manuscripts, were to review the literature concerning A. actinomycetemcomitans serotypes regarding to periodontal status and geographic origin of individuals (chapter 1); and to investigate the prevalence and distribution of A. actinomycetemcomitans serotypes in Brazilian subjects with chronic and aggressive periodontitis, identifying possible relationship of the different A. actinomycetemcomitans serotypes with periodontal disease (chapter 2). In study 1 was performed a systematic review of the pertinent literature related to the issue and in study 2, subgingival plaque sample of 71 subjects with aggressive or chronic periodontitis positive to A. actinomycetemcomitans were analysed by polymerase chain reaction (PCR). The literature analysis presented in study 1 showed that different ethnic groups are preferentially colonized by different A. actinomycetemcomitans serotypes. Serotypes a, b and c were largely found, and serotype c was the most prevalent in the majority of studies. The results of study 2 demonstrated that serotype c was detected with the highest frequency and serotypes d-f were not detected. It was also observed that individuals with aggressive periodontitis showed higher prevalence of both serotypes b and c (p<0.05), and in chronic periodontitis subjects the serotype c was significantly more prevalent (p<0.05). In conclusion, the results of these studies suggest that the relationship between the different serotypes and periodontal conditions remains unclear (chapter 1). Serotype c was dominant among Brazilian subjects with periodontal disease and aggressive periodontitis subjects were associated both serotypes b and c (chapter 2).
Estudos indicam que indivÃduos com lesÃes periodontais mais severas apresentam maior probabilidade de serem colonizados por Aggregatibacter actinomycetemcomitans. Essa espÃcie à geneticamente heterogÃnea e pode ser agrupada em seis sorotipos (a-f), que podem diferir quanto a suas caracterÃsticas de virulÃncia. As diferenÃas Ãtnicas e populaÃÃes geogrÃficas podem influenciar na distribuiÃÃo e prevalÃncia desses sorotipos em relaÃÃo ao tipo de doenÃa periodontal. Os objetivos dessa dissertaÃÃo, constituÃda por dois artigos, foram: revisar a literatura concernente aos sorotipos de A. actinomycetemcomitans em relaÃÃo à condiÃÃo periodontal e origem geogrÃfica dos indivÃduos (capÃtulo 1); e avaliar a prevalÃncia e distribuiÃÃo dos sorotipos de A. actinomycetemcomitans em pacientes brasileiros com periodontite crÃnica e agressiva, identificando a possÃvel relaÃÃo dos diferentes sorotipos de A. actinomycetemcomitans com a patologia periodontal (capÃtulo 2). No estudo 1, foi realizada uma revisÃo sistemÃtica da literatura pertinente ao assunto e no estudo 2, amostras de biofilme bacteriano subgengival de 71 pacientes com periodontite agressiva ou crÃnica positivos para A. actinomycetemcomitans foram analisadas atravÃs da reaÃÃo em cadeia da polimerase (PCR). A anÃlise da literatura apresentada no estudo 1 mostrou que diferentes grupos Ãtnicos sÃo preferencialmente colonizados por diferentes sorotipos de A. actinomycetemcomitans. Os sorotipos a, b e c foram largamente encontrados e o sorotipo c foi o mais prevalente na maioria dos estudos. Os resultados do estudo 2 demonstraram que o sorotipo c foi encontrado com maior frequÃncia e os sorotipos d-f nÃo foram detectados. Foi verificado tambÃm que indivÃduos com periodontite agressiva apresentaram maior prevalÃncia de ambos os sorotipos b e c (p<0.05), e que em pacientes com periodontite crÃnica o sorotipo c foi significativamente mais prevalente (p<0.05). Em conclusÃo, os resultados desses estudos indicam que a relaÃÃo entre os diferentes sorotipos e a condiÃÃo periodontal permanece obscura (capÃtulo 1). O sorotipo c foi dominante entre pacientes brasileiros com doenÃa periodontal e os indivÃduos com periodontite agressiva foram associados com os sorotipos b e c (capÃtulo 2).

Книги з теми "Periodontal disease Molecular aspects":

1
Bartold, P. Mark. Biology of the periodontal connective tissues. Chicago: Quintessence Pub. Co., 1998.
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2
Kinane, Denis F. Periodontal disease. Basel: Karger, 2012.
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3
European, Symposium on the Borderland Between Caries and Periodontal Disease (4th 1990 Geneva Switzerland). Application of molecular science to caries and periodontal disease: 4th European Symposium of Borderland Between Caries and Periodontal Disease, Geneva, Switzerland, 25-26 January, 1990. Oxford: Pergamon, 1990.
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4
Ekuni, Daisuke, Maurizio Battino, Takaaki Tomofuji, and Edward E. Putnins, eds. Studies on Periodontal Disease. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9557-4.
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5
Saleh, Mazen T. Molecular aspects of infectious disease. New York: Nova Science Publishers, 2011.
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6
Preber, Hans. Cigarette smoking and periodontal disease: Clinical and therapeutical aspects. [S.l: s.n.], 1986.
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7
Dumitrescu, Alexandrina L. Genetic Variants in Periodontal Health and Disease. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.
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8
Berns, Joel M. Understanding periodontal diseases. 2nd ed. Carol Stream, Ill: Quintessence Books, 1993.
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9
Yamamoto, Sho L. Periodontal disease: Symptoms, treatment, and prevention. Hauppauge, N.Y: Nova Science, 2010.
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Gokhale, David Anand. Molecular genetic aspects of Hodgkin's disease. Manchester: University of Manchester, 1996.
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Частини книг з теми "Periodontal disease Molecular aspects":

1
Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Periodontal Diseases." In Encyclopedia of Molecular Mechanisms of Disease, 1620–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1396.
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2
Dumitrescu, Alexandrina L., and Masashi Tanaka. "Particular Aspects of Periodontal Disease Pathogenesis." In Etiology and Pathogenesis of Periodontal Disease, 77–124. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_3.
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3
Taylor, Shelley Segrest. "Periodontal Disease." In Encyclopedia of Otolaryngology, Head and Neck Surgery, 2133. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23499-6_200156.
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4
Gooch, Jan W. "Periodontal Disease." In Encyclopedic Dictionary of Polymers, 913. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14452.
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Schäfer, Arne S. "Periodontal Disease." In Genomics, Personalized Medicine and Oral Disease, 145–66. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17942-1_7.
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Scarfe, William C., Bruno Azevedo, Lucas Rodrigues Pinheiro, Menik Priaminiari, and Marcelo Augusto Oliveira Sales. "Periodontal Disease." In Maxillofacial Cone Beam Computed Tomography, 923–49. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62061-9_23.
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Nemcovsky, Carlos E., José Luis Calvo Guirado, and Ofer Moses. "Endodontic-Periodontal Lesions: Periodontal Aspects." In Endodontic-Periodontal Lesions, 59–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-10725-3_5.
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8
Dumitrescu, Alexandrina L. "Aspects of the Research Methodology for Periodontal Disease Assessment in Epidemiological Surveys." In Understanding Periodontal Research, 575–643. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28923-1_19.
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9
Ivanyi, L., and H. N. Newman. "Periodontal Diseases." In Immunological Aspects of Oral Diseases, 85–100. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4167-0_4.
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Pandolfo, Ignazio, and Silvio Mazziotti. "The Periodontal Disease." In Orthopantomography, 121–38. Milano: Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5289-5_6.
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Тези доповідей конференцій з теми "Periodontal disease Molecular aspects":

1
Weersink, Robert A. "Photodynamic therapy for periodontal disease." In Opto-Canada: SPIE Regional Meeting on Optoelectronics, Photonics, and Imaging, edited by John C. Armitage. SPIE, 2017. http://dx.doi.org/10.1117/12.2283905.
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2
Colston, Jr., Bill W., Matthew J. Everett, Luiz B. Da Silva, and Linda L. Otis. "OCT for diagnosis of periodontal disease." In BiOS '98 International Biomedical Optics Symposium, edited by Valery V. Tuchin and Joseph A. Izatt. SPIE, 1998. http://dx.doi.org/10.1117/12.306070.
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Albalat, Salvador E., Mariano L. Alcaniz-Raya, M. Carmen Juan, Vincente Grau Colomer, and Carlos Monserrat. "Automated system for periodontal disease diagnosis." In Medical Imaging 1997, edited by Kenneth M. Hanson. SPIE, 1997. http://dx.doi.org/10.1117/12.274099.
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4
Joo, Jaehan, Sinjin Jeong, Heetae Jin, Uhyeon Lee, Ji Young Yoon, and Suk Chan Kim. "Periodontal Disease Detection Using Convolutional Neural Networks." In 2019 International Conference on Artificial Intelligence in Information and Communication (ICAIIC). IEEE, 2019. http://dx.doi.org/10.1109/icaiic.2019.8669021.
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5
Aberin, Shannah Therese A., and Joel C. de Goma. "Detecting Periodontal Disease Using Convolutional Neural Networks." In 2018 IEEE 10th International Conference on Humanoid, Nanotechnology, Information Technology,Communication and Control, Environment and Management (HNICEM). IEEE, 2018. http://dx.doi.org/10.1109/hnicem.2018.8666389.
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Colston, Jr., Bill W., Matthew J. Everett, Luiz B. Da Silva, Linda L. Otis, and Howard Nathel. "Optical coherence tomography for diagnosing periodontal disease." In BiOS '97, Part of Photonics West, edited by Harvey A. Wigdor, John D. B. Featherstone, and Peter Rechmann. SPIE, 1997. http://dx.doi.org/10.1117/12.273591.
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Askarian, Behnam, Fatemehsadat Tabei, Grace Anne Tipton, and Jo Woon Chong. "Smartphone-Based Method for Detecting Periodontal Disease." In 2019 IEEE Healthcare Innovations and Point of Care Technologies (HI-POCT). IEEE, 2019. http://dx.doi.org/10.1109/hi-poct45284.2019.8962844.
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Zakizade, A. E., and G. I. Gurbanalieva. "Clinical and therapeutic aspects of inflammatory periodontal diseases." In Global science. Development and novelty. НИЦ «Л-Журнал», 2019. http://dx.doi.org/10.18411/gdsn-25-12-2019-10.
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Giovani, Elcio M., Gilberto A. Noro-Filho, Bruno V. Caputo, Renato Casarin, Claudio Costa, Daniela Salgado, and Camila C. Santos. "PDT in periodontal disease of HAART resistance patients." In SPIE BiOS, edited by Michael R. Hamblin, James D. Carroll, and Praveen Arany. SPIE, 2016. http://dx.doi.org/10.1117/12.2212804.
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Colston, Jr., Bill W., Dora M. Gutierrez, Matthew J. Everett, Steve B. Brown, Kevin C. Langry, Weldon R. Cox, Paul W. Johnson, and Jeffrey N. Roe. "Intraoral fiber-optic-based diagnostic for periodontal disease." In BiOS 2000 The International Symposium on Biomedical Optics, edited by Tuan Vo-Dinh, Warren S. Grundfest, and David A. Benaron. SPIE, 2000. http://dx.doi.org/10.1117/12.384906.
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Звіти організацій з теми "Periodontal disease Molecular aspects":

1
Lattaf, Sara, Lamiaa Abdallaoui, and Amal Bouziane. Effect of periodontal disease on Alzheimer’s disease: protocol of a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0033.
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2
Yotis, William W. Chemical and Biological Attributes of Selected Periodontopathogens as Potential Indicators of Periodontal Disease. Fort Belvoir, VA: Defense Technical Information Center, November 1992. http://dx.doi.org/10.21236/ada259063.
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3
Kapellas, Kostas. The association between periodontal disease and dementia: a systematic review and meta-analysis. Science Repository, April 2019. http://dx.doi.org/10.31487/j.dobcr.2019.01.005.
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4
Yotis, William W. Chemical and Biological Attributes of Selected Periodontopathogens as Potential Indicators of Periodontal Disease. Fort Belvoir, VA: Defense Technical Information Center, August 1990. http://dx.doi.org/10.21236/ada226312.
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5
Guthrie, G., R. Raymond, U. Saffiotti, A. Aust, and B. Mossman. Mineralogical and geochemical aspects of mineral-induced disease. Office of Scientific and Technical Information (OSTI), April 1996. http://dx.doi.org/10.2172/212497.
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6
Burkes, E. J., Greco Jr., Marbry G. W., Scruggs D. L., Crawford R. R., and J. J. Periodontal Stain Test Diagnosis Program. Fort Belvoir, VA: Defense Technical Information Center, January 1989. http://dx.doi.org/10.21236/ada247284.
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7
Siedow, J. N. Molecular studies of functional aspects of plant mitochondria. Office of Scientific and Technical Information (OSTI), March 1992. http://dx.doi.org/10.2172/7194216.
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Hanker, Jacob S., Beverly L. Giammara, E. J. Burkes, and G. W. Greco. Stain Test Modules for Periodontal Diagnosis. Fort Belvoir, VA: Defense Technical Information Center, October 1989. http://dx.doi.org/10.21236/ada247283.
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9
Hartmann, Lynn C. Benign Breast Disease: Toward Molecular Prediction of Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada442889.
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10
Meredith, Gloria E. Identification of Splice Variants as Molecular Markers in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada463435.
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