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Aggressive Periodontitis
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Marcelo Faveri – One of the best experts on this subject based on the ideXlab platform.
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levels of selenomonas species in generalized Aggressive Periodontitis
Journal of Periodontal Research, 2012Co-Authors: Lucas F H Goncalves, Daiane Fermiano, Magda Feres, L C De Figueiredo, Flavia R P Teles, Marcia Pinto Alves Mayer, Marcelo FaveriAbstract:Goncalves LFH, Fermiano D, Feres M, Figueiredo LC, Teles FRP, Mayer MPA, Faveri M. Levels of Selenomonas species in generalized Aggressive Periodontitis. J Periodont Res 2012; 47: 711–718. © 2012 John Wiley & Sons A/S Background and Objective: To compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from periodontally healthy subjects and from subjects with generalized Aggressive Periodontitis. Material and Methods: Fifteen periodontally healthy subjects and 15 subjects with generalized Aggressive Periodontitis were recruited and their clinical periodontal parameters were evaluated. Nine subgingival plaque samples were collected from each subject and all were individually analyzed for the levels of 10 bacterial taxa, including cultured and uncultivated/unrecognized microorganisms, using the RNA-oligonucleotide quantification technique. Between-group differences in the levels of the test taxa were determined using the Mann–Whitney U-test. Results: Subjects with generalized Aggressive Periodontitis showed significantly higher mean counts of Porphyromonas gingivalis, S. sputigena and the Mitsuokella sp. Human Oral Taxon (HOT) 131 (previously described as Selenomonas sp. oral clone CS002), while higher mean counts of Actinomyces gerencseriae and Streptococcus sanguinis were found in periodontally healthy subjects (p < 0.01). Selenomonas sp. HOT 146 was only detected in the generalized Aggressive Periodontitis group. In the generalized Aggressive Periodontitis group, the levels of P. gingivalis and S. sputigena were higher in deep sites (probing depth ≥ 5 mm) than in shallow sites (probing depth ≤ 3 mm) (p < 0.01). Furthermore, in subjects with generalized Aggressive Periodontitis, sites with probing depth of ≤ 3 mm harbored higher levels of these two species than sites with the same probing depth in periodontally healthy subjects. There were positive correlations between probing depth and the levels of P. gingivalis (r = 0.77; p < 0.01), S. sputigena (r = 0.60; p < 0.01) and Selenomonas dianae (previously described as Selenomonas sp. oral clone EW076) (r = 0.42, p < 0.05). Conclusion: S. sputigena and Mitsuokella sp. HOT 131 may be associated with the pathogenesis of generalized Aggressive Periodontitis, and their role in the onset and progression of this infection should be investigated further.
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Levels of Selenomonas species in generalized Aggressive Periodontitis
Journal of periodontal research, 2012Co-Authors: Lucas F H Goncalves, Daiane Fermiano, Magda Feres, L C De Figueiredo, Flavia R P Teles, Marcia Pinto Alves Mayer, Marcelo FaveriAbstract:Goncalves LFH, Fermiano D, Feres M, Figueiredo LC, Teles FRP, Mayer MPA, Faveri M. Levels of Selenomonas species in generalized Aggressive Periodontitis. J Periodont Res 2012; 47: 711–718. © 2012 John Wiley & Sons A/S Background and Objective: To compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from periodontally healthy subjects and from subjects with generalized Aggressive Periodontitis. Material and Methods: Fifteen periodontally healthy subjects and 15 subjects with generalized Aggressive Periodontitis were recruited and their clinical periodontal parameters were evaluated. Nine subgingival plaque samples were collected from each subject and all were individually analyzed for the levels of 10 bacterial taxa, including cultured and uncultivated/unrecognized microorganisms, using the RNA-oligonucleotide quantification technique. Between-group differences in the levels of the test taxa were determined using the Mann–Whitney U-test. Results: Subjects with generalized Aggressive Periodontitis showed significantly higher mean counts of Porphyromonas gingivalis, S. sputigena and the Mitsuokella sp. Human Oral Taxon (HOT) 131 (previously described as Selenomonas sp. oral clone CS002), while higher mean counts of Actinomyces gerencseriae and Streptococcus sanguinis were found in periodontally healthy subjects (p
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FAM5C contributes to Aggressive Periodontitis
PloS one, 2010Co-Authors: Flavia M. De Carvalho, Marcelo Faveri, Eduardo Muniz Barretto Tinoco, Kathleen Deeley, Poliana Mendes Duarte, Marcelo Rocha Marques, Adriana Cutrim De Mendonça, Xiao Jing Wang, Karen T. Cuenco, Renato MenezesAbstract:Aggressive Periodontitis is characterized by a rapid and severe periodontal destruction in young systemically healthy subjects. A greater prevalence is reported in Africans and African descendent groups than in Caucasians and Hispanics. We first fine mapped the interval 1q24.2 to 1q31.3 suggested as containing an Aggressive Periodontitis locus. Three hundred and eighty-nine subjects from 55 pedigrees were studied. Saliva samples were collected from all subjects, and DNA was extracted. Twenty-one single nucleotide polymorphisms were selected and analyzed by standard polymerase chain reaction using TaqMan chemistry. Non-parametric linkage and transmission distortion analyses were performed. Although linkage results were negative, statistically significant association between two markers, rs1935881 and rs1342913, in the FAM5C gene and Aggressive Periodontitis (p = 0.03) was found. Haplotype analysis showed an association between Aggressive Periodontitis and the haplotype A-G (rs1935881-rs1342913; p = 0.009). Sequence analysis of FAM5C coding regions did not disclose any mutations, but two variants in conserved intronic regions of FAM5C, rs57694932 and rs10494634, were found. However, these two variants are not associated with Aggressive Periodontitis. Secondly, we investigated the pattern of FAM5C expression in Aggressive Periodontitis lesions and its possible correlations with inflammatory/immunological factors and pathogens commonly associated with periodontal diseases. FAM5C mRNA expression was significantly higher in diseased versus healthy sites, and was found to be correlated to the IL-1beta, IL-17A, IL-4 and RANKL mRNA levels. No correlations were found between FAM5C levels and the presence and load of red complex periodontopathogens or Aggregatibacter actinomycetemcomitans. This study provides evidence that FAM5C contributes to Aggressive Periodontitis.
Lucas F H Goncalves – One of the best experts on this subject based on the ideXlab platform.
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levels of selenomonas species in generalized Aggressive Periodontitis
Journal of Periodontal Research, 2012Co-Authors: Lucas F H Goncalves, Daiane Fermiano, Magda Feres, L C De Figueiredo, Flavia R P Teles, Marcia Pinto Alves Mayer, Marcelo FaveriAbstract:Goncalves LFH, Fermiano D, Feres M, Figueiredo LC, Teles FRP, Mayer MPA, Faveri M. Levels of Selenomonas species in generalized Aggressive Periodontitis. J Periodont Res 2012; 47: 711–718. © 2012 John Wiley & Sons A/S Background and Objective: To compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from periodontally healthy subjects and from subjects with generalized Aggressive Periodontitis. Material and Methods: Fifteen periodontally healthy subjects and 15 subjects with generalized Aggressive Periodontitis were recruited and their clinical periodontal parameters were evaluated. Nine subgingival plaque samples were collected from each subject and all were individually analyzed for the levels of 10 bacterial taxa, including cultured and uncultivated/unrecognized microorganisms, using the RNA-oligonucleotide quantification technique. Between-group differences in the levels of the test taxa were determined using the Mann–Whitney U-test. Results: Subjects with generalized Aggressive Periodontitis showed significantly higher mean counts of Porphyromonas gingivalis, S. sputigena and the Mitsuokella sp. Human Oral Taxon (HOT) 131 (previously described as Selenomonas sp. oral clone CS002), while higher mean counts of Actinomyces gerencseriae and Streptococcus sanguinis were found in periodontally healthy subjects (p < 0.01). Selenomonas sp. HOT 146 was only detected in the generalized Aggressive Periodontitis group. In the generalized Aggressive Periodontitis group, the levels of P. gingivalis and S. sputigena were higher in deep sites (probing depth ≥ 5 mm) than in shallow sites (probing depth ≤ 3 mm) (p < 0.01). Furthermore, in subjects with generalized Aggressive Periodontitis, sites with probing depth of ≤ 3 mm harbored higher levels of these two species than sites with the same probing depth in periodontally healthy subjects. There were positive correlations between probing depth and the levels of P. gingivalis (r = 0.77; p < 0.01), S. sputigena (r = 0.60; p < 0.01) and Selenomonas dianae (previously described as Selenomonas sp. oral clone EW076) (r = 0.42, p < 0.05). Conclusion: S. sputigena and Mitsuokella sp. HOT 131 may be associated with the pathogenesis of generalized Aggressive Periodontitis, and their role in the onset and progression of this infection should be investigated further.
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Levels of Selenomonas species in generalized Aggressive Periodontitis
Journal of periodontal research, 2012Co-Authors: Lucas F H Goncalves, Daiane Fermiano, Magda Feres, L C De Figueiredo, Flavia R P Teles, Marcia Pinto Alves Mayer, Marcelo FaveriAbstract:Goncalves LFH, Fermiano D, Feres M, Figueiredo LC, Teles FRP, Mayer MPA, Faveri M. Levels of Selenomonas species in generalized Aggressive Periodontitis. J Periodont Res 2012; 47: 711–718. © 2012 John Wiley & Sons A/S Background and Objective: To compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from periodontally healthy subjects and from subjects with generalized Aggressive Periodontitis. Material and Methods: Fifteen periodontally healthy subjects and 15 subjects with generalized Aggressive Periodontitis were recruited and their clinical periodontal parameters were evaluated. Nine subgingival plaque samples were collected from each subject and all were individually analyzed for the levels of 10 bacterial taxa, including cultured and uncultivated/unrecognized microorganisms, using the RNA-oligonucleotide quantification technique. Between-group differences in the levels of the test taxa were determined using the Mann–Whitney U-test. Results: Subjects with generalized Aggressive Periodontitis showed significantly higher mean counts of Porphyromonas gingivalis, S. sputigena and the Mitsuokella sp. Human Oral Taxon (HOT) 131 (previously described as Selenomonas sp. oral clone CS002), while higher mean counts of Actinomyces gerencseriae and Streptococcus sanguinis were found in periodontally healthy subjects (p
Feyza Otan – One of the best experts on this subject based on the ideXlab platform.
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Aggressive Periodontitis With Supernumerary Teeth: A Retrospective Study
Journal of periodontology, 2004Co-Authors: Gökhan Açikgöz, Aydan Açikgöz, Ilker Keskiner, Tamer Türk, Feyza OtanAbstract:Background: There are four key studies in the periodontology literature reporting the correlation between supernumerary teeth and Aggressive Periodontitis. The aim of this study is to detect such a relationship. Methods: Patients with supernumerary teeth were identified retrospectively from their orthopantomographs and were invited to the periodontology department for intraoral examination. They were then evaluated for Aggressive Periodontitis. The number of existing teeth, age, family histories, attachment loss, probing depths, and bleeding on probing scores were recorded. Results: Of the 5,850 subjects randomly observed among 48,000 patients, only 174 exhibited supernumerary teeth. Of these 174 subjects, only three patients were diagnosed with Aggressive Periodontitis. One of the patients was also suffering from Fanconi’s anemia. Conclusions: Despite the similarities (Aggressive Periodontitis accompanied by supernumerary teeth) in the previous reports, we do not agree with the earlier results. We rather suggest that this association might be a random occurrence, rather than a biological one, although this observation should be further investigated using genetic testing. J Periodontol 2004;75:1458-1460.
Jasim M. Albandar – One of the best experts on this subject based on the ideXlab platform.
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Epidemiology and demographics of Aggressive Periodontitis
Periodontology 2000, 2014Co-Authors: Cristiano Susin, Alex Nogueira Haas, Jasim M. AlbandarAbstract:Epidemiologic studies of Aggressive Periodontitis have used different study designs and a range of examination methods and case definitions, and this greatly complicates the study of disease prevalence in populations. The wide range of disease case definitions, in particular, profoundly impacts the reported rate of disease, and the use of a standard disease definition is strongly recommended. Surveys of Aggressive Periodontitis that use only clinical examinations, without radiographic examination to confirm the presence of a distinctive pattern of tissue loss, may overestimate the prevalence of this disease, particularly when a low threshold of attachment loss is used. The prevalence of Aggressive Periodontitis varies significantly between populations, and differences in race/ethnicities seem to be a key factor. Studies consistently show that Aggressive Periodontitis is most prevalent in Africa and in populations of African descent and is least prevalent in Caucasians in Europe and North America. Among children and young adults the prevalence of this disease is higher in older than in younger age groups. Most studies show comparable disease prevalence in male and female subjects. These findings show that Aggressive Periodontitis is a significant health problem in certain populations. This review also highlights a lack of information on the epidemiology and demographics of this disease in many parts of the world, particularly in Asia and Africa. Epidemiologic studies of Aggressive Periodontitis in high-risk populations are important and could provide vital data on the determinants of this disease, and this information is needed for the establishment of effective health-promotion measures.
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Aggressive Periodontitis: case definition and diagnostic criteria.
Periodontology 2000, 2014Co-Authors: Jasim M. AlbandarAbstract:Aggressive Periodontitis is a destructive disease characterized by the following: the involvement of multiple teeth with a distinctive pattern of periodontal tissue loss; a high rate of disease progprogression; an early age of onset; and the absence of systemic diseases. In some patients periodontal tissue loss may commence before puberty, whereas in most patients the age of onset is during or somewhat after the circumpubertal period. Besides infection with specific microorganisms, a host predisposition seems to play a key role in the pathogenesis of Aggressive Periodontitis, as evidenced by the familial aggregation of the disease. In this article we review the historical background of the diagnostic criteria of Aggressive Periodontitis, present a contemporary case definition and describe the clinical parameters of the disease. At present, the diagnosis of Aggressive Periodontitis is achieved using case history, clinical examination and radiographic evaluation. The data gathered using these methods are prone to relatively high measurement errors. Besides, this diagnostic approach measures past disease history and may not reliably measure existing disease activity or accurately predict future tissue loss. A diagnosis is often made years after the onset of the disease, partly because current assessment methods detect established disease more readily and reliably than they detect incipient or initial lesions where the tissue loss is minimal and usually below the detection threshold of present examination methods. Future advancements in understanding the pathogenesis of this disease may contribute to an earlier diagnosis. Insofar, future case definitions may involve the identification of key etiologic and risk factors, combined with high-precision methodologies that enable the early detection of initial lesions. This may significantly enhance the predictive value of these tests and detect cases of Aggressive Periodontitis before significant tissue loss develops.
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Role of genetic factors in the pathogenesis of Aggressive Periodontitis
Periodontology 2000, 2014Co-Authors: Alexandre R. Vieira, Jasim M. AlbandarAbstract:This article critically reviews the evidence for a role of genetic factors in the pathogenesis of Aggressive Periodontitis and discusses the study approaches commonly used to identify genetic riskrisk factors of this disease. Available data suggest that Aggressive Periodontitis is caused by mutations in multiple genes, combined with environmental effects. Syndromic periodontal diseases include certain monogenic disorders that express phenotypes showing Aggressive forms of Periodontitis, and the genetic triggering factors of most of these syndromes have been identified. Other periodontal disease phenotypes seem to occur through different genetic predisposition patterns. Case-control and genome-wide studies have been used to investigate the association with gene polymorphisms. Association studies and the familial aggregation of Aggressive Periodontitis suggest a significant genetic component in the increased predisposition to this disease. There is evidence to support the contribution of a few major genes or of multiple small-effects genes. In addition, there is evidence of gene-gene and gene-environment interaction effects. Early studies suggested an X-linked mode of transmission of Aggressive Periodontitis, and subsequent studies support an autosomal mode. Genetic studies have the potential to improve the screening programs of subjects at risk for developing Aggressive Periodontitis and may enhance treatment outcome through gene therapy.
Flavia R P Teles – One of the best experts on this subject based on the ideXlab platform.
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levels of selenomonas species in generalized Aggressive Periodontitis
Journal of Periodontal Research, 2012Co-Authors: Lucas F H Goncalves, Daiane Fermiano, Magda Feres, L C De Figueiredo, Flavia R P Teles, Marcia Pinto Alves Mayer, Marcelo FaveriAbstract:Goncalves LFH, Fermiano D, Feres M, Figueiredo LC, Teles FRP, Mayer MPA, Faveri M. Levels of Selenomonas species in generalized Aggressive Periodontitis. J Periodont Res 2012; 47: 711–718. © 2012 John Wiley & Sons A/S Background and Objective: To compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from periodontally healthy subjects and from subjects with generalized Aggressive Periodontitis. Material and Methods: Fifteen periodontally healthy subjects and 15 subjects with generalized Aggressive Periodontitis were recruited and their clinical periodontal parameters were evaluated. Nine subgingival plaque samples were collected from each subject and all were individually analyzed for the levels of 10 bacterial taxa, including cultured and uncultivated/unrecognized microorganisms, using the RNA-oligonucleotide quantification technique. Between-group differences in the levels of the test taxa were determined using the Mann–Whitney U-test. Results: Subjects with generalized Aggressive Periodontitis showed significantly higher mean counts of Porphyromonas gingivalis, S. sputigena and the Mitsuokella sp. Human Oral Taxon (HOT) 131 (previously described as Selenomonas sp. oral clone CS002), while higher mean counts of Actinomyces gerencseriae and Streptococcus sanguinis were found in periodontally healthy subjects (p < 0.01). Selenomonas sp. HOT 146 was only detected in the generalized Aggressive Periodontitis group. In the generalized Aggressive Periodontitis group, the levels of P. gingivalis and S. sputigena were higher in deep sites (probing depth ≥ 5 mm) than in shallow sites (probing depth ≤ 3 mm) (p < 0.01). Furthermore, in subjects with generalized Aggressive Periodontitis, sites with probing depth of ≤ 3 mm harbored higher levels of these two species than sites with the same probing depth in periodontally healthy subjects. There were positive correlations between probing depth and the levels of P. gingivalis (r = 0.77; p < 0.01), S. sputigena (r = 0.60; p < 0.01) and Selenomonas dianae (previously described as Selenomonas sp. oral clone EW076) (r = 0.42, p < 0.05). Conclusion: S. sputigena and Mitsuokella sp. HOT 131 may be associated with the pathogenesis of generalized Aggressive Periodontitis, and their role in the onset and progression of this infection should be investigated further.
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Levels of Selenomonas species in generalized Aggressive Periodontitis
Journal of periodontal research, 2012Co-Authors: Lucas F H Goncalves, Daiane Fermiano, Magda Feres, L C De Figueiredo, Flavia R P Teles, Marcia Pinto Alves Mayer, Marcelo FaveriAbstract:Goncalves LFH, Fermiano D, Feres M, Figueiredo LC, Teles FRP, Mayer MPA, Faveri M. Levels of Selenomonas species in generalized Aggressive Periodontitis. J Periodont Res 2012; 47: 711–718. © 2012 John Wiley & Sons A/S Background and Objective: To compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from periodontally healthy subjects and from subjects with generalized Aggressive Periodontitis. Material and Methods: Fifteen periodontally healthy subjects and 15 subjects with generalized Aggressive Periodontitis were recruited and their clinical periodontal parameters were evaluated. Nine subgingival plaque samples were collected from each subject and all were individually analyzed for the levels of 10 bacterial taxa, including cultured and uncultivated/unrecognized microorganisms, using the RNA-oligonucleotide quantification technique. Between-group differences in the levels of the test taxa were determined using the Mann–Whitney U-test. Results: Subjects with generalized Aggressive Periodontitis showed significantly higher mean counts of Porphyromonas gingivalis, S. sputigena and the Mitsuokella sp. Human Oral Taxon (HOT) 131 (previously described as Selenomonas sp. oral clone CS002), while higher mean counts of Actinomyces gerencseriae and Streptococcus sanguinis were found in periodontally healthy subjects (p