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Erratum to "Porphyromonas gingivalis lipids enhance RANKL-mediated osteoclast formation" [Bone 207 (2026) 117852].

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Porphyromonas gingivalis lipids enhance RANKL-mediated osteoclast formation.

Matthew A Zambrello1, Archana Sanjay2, Amanda Rahmlow1

  • 1Department of Periodontology, United States of America.

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|March 13, 2026
PubMed
Summary
This summary is machine-generated.

Microbial lipids from Porphyromonas gingivalis (Pg) enhance osteoclast formation, a key process in periodontitis bone loss. Lipid accumulation in gingival tissues may identify sites at risk for further destruction.

Keywords:
LipidsOsteoclast formationPeriodontitis and tolerancePorphyromonas gingivalisRANKL

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Area of Science:

  • Oral microbiology
  • Immunology
  • Bone biology

Background:

  • Periodontitis involves microbial lipid accumulation in gingival tissues, particularly at sites of bone destruction.
  • Porphyromonas gingivalis (Pg) produces lipids found in diseased periodontal tissues, contributing to disease progression.
  • These lipids persist despite clearance mechanisms by gingival fibroblasts and macrophages.

Purpose of the Study:

  • To quantify the effect of microbial lipids on RANKL-mediated osteoclast formation.
  • To investigate lipid priming and concomitant exposure effects on osteoclastogenesis.
  • To determine if Pg lipids enhance osteoclast formation at concentrations found in periodontitis.

Main Methods:

  • Lipid-dependent modulation of osteoclast formation was assessed in bone marrow macrophages and RAW 264.7 cells.
  • Cells were exposed to Porphyromonas gingivalis (Pg) lipids prior to or concurrently with RANKL.
  • Osteoclast formation was quantified by counting TRAP-positive cells.

Main Results:

  • Pre-exposure (priming) of cells with Pg lipids significantly enhanced RANKL-induced osteoclast formation (2-10 fold increase).
  • Enhanced osteoclastogenesis occurred even after repeated lipid exposure, despite reduced TNF-α secretion.
  • RANKL at periodontitis-relevant concentrations promoted osteoclast formation in the presence of bacterial lipids.

Conclusions:

  • Bacterial lipids, particularly from Pg, enhance osteoclast formation in the presence of RANKL.
  • Site-specific deposition of Pg lipids may drive localized bone loss in periodontitis.
  • Lipid accumulation in gingival tissues could serve as a biomarker for identifying sites at risk for bone destruction.