Virulence factors of Enterococcus faecalis: relationship to endodontic disease.

Creative Commons License

Kayaoglu G., Orstavik D.

Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists, cilt.15, sa.5, ss.308-20, 2004 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 15 Sayı: 5
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1177/154411130401500506
  • Dergi Adı: Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.308-20
  • Anahtar Kelimeler: Enterococcus faecalis, virulence factors, endodontic infection, apical periodontitis, EXTRACELLULAR-MATRIX PROTEINS, GINGIVAL CREVICULAR FLUID, PEPTIDE ANTIBIOTIC AS-48, MUTANS LIPOTEICHOIC ACID, URINARY-TRACT INFECTION, GRAM-POSITIVE BACTERIA, ROOT-CANAL INFECTIONS, GROUP-A STREPTOCOCCI, AGGREGATION SUBSTANCE, ORAL STREPTOCOCCI
  • Gazi Üniversitesi Adresli: Evet

Özet

Enterococcus faecalis is a micro-organism that can survive extreme challenges. Its pathogenicity ranges from life-threatening diseases in compromised individuals to less severe conditions, such as infection of obturated root canals with chronic apical periodontitis. In the latter situation, the infecting organisms are partly shielded from the defense mechanisms of the body. In this article, we review the virulence factors of E. faecalis that may be related to endodontic infection and the periradicular inflammatory response. The most-cited virulence factors are aggregation substance, surface adhesins, sex pheromones, lipoteichoic acid, extracellular superoxide production, the lytic enzymes gelatinase and hyaluronidase, and the toxin cytolysin. Each of them may be associated with various stages of an endodontic infection as well as with periapical inflammation. While some products of the bacterium may be directly linked to damage of the periradicular tissues, a large part of the tissue damage is probably mediated by the host response to the bacterium and its products.