Abstract

Porphyromonas gingivalis is an anerobic, gram negative, bacterium which is a natural inhabitant of oral microbiome. Under unhealthy oral hygiene conditions the bacterium becomes highly destructive (photobiont) and leads to periodontitis (inflammation of periodontium). Several drugs like chlorhexidine, monocycline effectively reduce the viability of biofilms formed by Porphyromonas gingivalis but, it is impossible to destroy biofilms completely. As the bacterium evolves continuously it develops drug resistance due to events like horizontal gene transfer and its biofilm mode of living. Therefore no drug is very efficient in treating Periodontitis. We have done an Insilco Synteny based comparative analysis to find a druggable target which remains unchanged in various Porphyromonas gingivalis strains. Dipeptidylaminopeptidase has been identified one such potential target which is responsible for virulence in Porphyromonas gingivalis, and is functionally and structurally conserved. Therefore, according to best knowledge of authors a drug developed against this target will be effective in treating periodontitis caused by all evolved forms of bacterium.

Highlights

  • Periodontitis is inflammatory diseases caused by peridontopathic bacteria, majorly acquires gingival crevice, often causing gums to shrink and loosening of teeth

  • The outer lining of the gingival mucosa, which function as an innate part of the innate immune system, are among the first host cells colonized by Porphyromonas gingivalis [4]

  • Porphyromonas gingivalis W83 was taken as a reference genome and was compared with the other two completely sequenced genomes of Porphyromonas gingivalis American Type Culture Collection (ATCC) 33277, and Porphyromonas gingivalis TDC60

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Summary

Introduction

Periodontitis is inflammatory diseases caused by peridontopathic bacteria, majorly acquires gingival crevice, often causing gums to shrink and loosening of teeth It is apparently caused by specific gram negative anaerobic bacteria [1], Porphyromonas gingivalis, Treponema denticola, and Tannerella (formerly Bacteroides) forsythia more commonly termed as the ‘‘red complex’’[2,3]. Treponema denticola leads to necrotizing ulcerative gingivitis after getting adhered to fibroblasts, epithelial cells, as well as to extracellular matrix components present in periodontal tissues. It posses outer-sheath-associated peptidases, chymotrypsin-like and trypsinlike proteinases, hemolytic and hemagglutinating activities, adhesins as virulence factors which aid in early periodontitis [5]. Several T.forsythia virulence factors have been identified [6], including, trypsin-like [7] and PrtH proteases [8], sialidases SiaH [9] and NanH [10], a leucine-rich repeat cell-surface-associated and secreted protein BspA [11], an apoptosisinducing activity [12], alpha-D-glucosidase and N-acetyl-beta-glucosaminidase [13], a hemagglutinin [14], components of the bacterial S-layer [15]

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