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Enterococcus faecalis promotes osteoclastogenesis and semaphorin 4D expression.

Shuai Wang1, Zuhui Deng2, Chaminda J Seneviratne3

  • 1Endodontics, Comprehensive Dental Care, Faculty of Dentistry, The University of Hong Kong, Hong Kong SAR, China.

Innate Immunity
|July 4, 2015
PubMed
Summary
This summary is machine-generated.

Enterococcus faecalis promotes bone destruction in periapical periodontitis by driving osteoclast formation and semaphorin 4D (Sema4D) expression via MAPK pathways.

Keywords:
Enterococcus faecalisMAPK signaling pathwaysosteoclastsreceptor activator of nuclear factor-kappa B ligandtartrate-resistant acid phosphatase

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Area of Science:

  • Microbiology
  • Immunology
  • Endodontics

Background:

  • Enterococcus faecalis is a key pathogen in endodontic infections, contributing to periapical periodontitis and bone loss.
  • Understanding the mechanisms of E. faecalis-induced bone destruction is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the in vitro mechanisms by which E. faecalis causes bone destruction in periapical periodontitis.
  • To elucidate the role of E. faecalis in osteoclastogenesis and semaphorin 4D (Sema4D) expression.

Main Methods:

  • Osteoclast precursor RAW264.7 cells were treated with E. faecalis strains.
  • Receptor activator of nuclear factor-kappa B ligand (RANKL) was used to prime cells for osteoclast differentiation.
  • Expression of osteoclast-specific markers and activation of MAPK pathways were analyzed.

Main Results:

  • E. faecalis induced the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclast-like cells.
  • E. faecalis significantly upregulated osteoclast-specific markers (NFATc1, TRAP, cathepsin K) and Sema4D expression in RANKL-primed cells.
  • p38 and ERK1/2 MAPK signaling pathways were activated by E. faecalis, correlating with increased Sema4D expression.

Conclusions:

  • E. faecalis promotes bone resorption in periapical periodontitis.
  • This occurs through RANKL-dependent osteoclastogenesis and Sema4D expression, mediated by p38 and ERK1/2 MAPK activation.