Open Access Highly Accessed Research article

The core genome of the anaerobic oral pathogenic bacterium Porphyromonas gingivalis

Jorg Brunner1, Floyd RA Wittink2, Martijs J Jonker2, Mark de Jong2, Timo M Breit2, Marja L Laine1, Johannes J de Soet1 and Wim Crielaard1*

Author Affiliations

1 Department of Oral Microbiology, Academic Centre for Dentistry Amsterdam, University of Amsterdam and Free University Amsterdam, Amsterdam, The Netherlands

2 Microarray Department and Integrative Bioinformatics Unit, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands

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BMC Microbiology 2010, 10:252  doi:10.1186/1471-2180-10-252

Published: 29 September 2010



The Gram negative anaerobic bacterium Porphyromonas gingivalis has long been recognized as a causative agent of periodontitis. Periodontitis is a chronic infectious disease of the tooth supporting tissues eventually leading to tooth-loss. Capsular polysaccharide (CPS) of P. gingivalis has been shown to be an important virulence determinant. Seven capsular serotypes have been described. Here, we used micro-array based comparative genomic hybridization analysis (CGH) to analyze a representative of each of the capsular serotypes and a non-encapsulated strain against the highly virulent and sequenced W83 strain. We defined absent calls using Arabidopsis thaliana negative control probes, with the aim to distinguish between aberrations due to mutations and gene gain/loss.


Our analyses allowed us to call aberrant genes, absent genes and divergent regions in each of the test strains. A conserved core P. gingivalis genome was described, which consists of 80% of the analyzed genes from the sequenced W83 strain. The percentage of aberrant genes between the test strains and control strain W83 was 8.2% to 13.7%. Among the aberrant genes many CPS biosynthesis genes were found. Most other virulence related genes could be found in the conserved core genome. Comparing highly virulent strains with less virulent strains indicates that hmuS, a putative CobN/Mg chelatase involved in heme uptake, may be a more relevant virulence determinant than previously expected. Furthermore, the description of the 39 W83-specific genes could give more insight in why this strain is more virulent than others.


Analyses of the genetic content of the P. gingivalis capsular serotypes allowed the description of a P. gingivalis core genome. The high resolution data from three types of analysis of triplicate hybridization experiments may explain the higher divergence between P. gingivalis strains than previously recognized.