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Ann L. Griffen

Researcher at Ohio State University

Publications -  59
Citations -  6730

Ann L. Griffen is an academic researcher from Ohio State University. The author has contributed to research in topics: Porphyromonas gingivalis & Periodontitis. The author has an hindex of 31, co-authored 55 publications receiving 5919 citations. Previous affiliations of Ann L. Griffen include Nationwide Children's Hospital.

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Bacteria of Dental Caries in Primary and Permanent Teeth in Children and Young Adults

TL;DR: This cross-sectional preliminary study indicated that 10% of subjects with rampant caries in permanent teeth do not have detectable levels of S. mutans, and additional species, e.g., species of the genera Atopobium, Propionibacterium, and Lactobacillus, were present at significantly higher levels than those of S mutans.
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Distinct and complex bacterial profiles in human periodontitis and health revealed by 16S pyrosequencing

TL;DR: Differences between health- and periodontitis-associated bacterial communities were observed at all phylogenetic levels, and UniFrac and principal coordinates analysis showed distinct community profiles in health and disease.
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Molecular Analysis of Bacterial Species Associated with Childhood Caries

TL;DR: Comparing the bacteria found in early childhood caries (ECC) to those found in caries-free children by using molecular identification methods suggests that A. gerencseriae and other Actinomyces species may play an important role incaries initiation and that a novel Bifidobacterium may be a major pathogen in deep caries.
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New Bacterial Species Associated with Chronic Periodontitis

TL;DR: In this article, the purpose of the present investigation was to identify potential periodontal pathogens among newly identified species and phylotypes, and species-specific ribosomal 16S primers for PCR amplification were developed for detection of new species.
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Identification of Candidate Periodontal Pathogens and Beneficial Species by Quantitative 16S Clonal Analysis

TL;DR: Chronic periodontitis is the result of a global perturbation of the oral bacterial ecology rather than a disease-site specific microbial shift, and more differences were found in the bacterial profile between subjects withperiodontitis and healthy subjects than between deep and shallow sites within the same subject.