Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Bacterial-responsive B lymphocytes induce periodontal bone resorption.

Xiaozhe Han1, Toshihisa Kawai, Jean W Eastcott

  • 1Department of Immunology, The Forsyth Institute, Boston, MA 02115, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 21, 2005
PubMed
Summary

B lymphocytes expressing receptor activator of NF-kappaB ligand (RANKL) contribute to periodontal bone loss. These B cells, stimulated by Actinobacillus actinomycetemcomitans, increase osteoclast differentiation and bone resorption, even without T cells.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Hyperglycemia and systemic inflammation differentially shape immune dysregulation, tissue destruction, and microbiota in experimental periodontitis and peri-implantitis in diabetic mice.

Frontiers in immunology·2026
Same author

Diabetes exacerbates experimental peri-implantitis in mice with elevated IL-17A-associated inflammation and IL-17F upregulation.

Scientific reports·2026
Same author

Exposure to Per- and Polyfluoroalkyl Substances (PFAS) Causes Dental Developmental Anomalies: Underrecognized Risk of Fluoride Bioaccumulation.

Environmental science & technology·2026
Same author

B10 Adoptive Transfer Ameliorates Inflammation and Bone Loss in Experimental Periodontitis Through Promoting Macrophage-Mediated Pro-Resolving Functions.

Inflammation·2026
Same author

Type H Vessels Are Progressively Lost in a Mouse Model of Periodontitis: A 3D Tissue-clearing Analysis of Alveolar Bone.

Operative dentistry, endodontology and periodontology·2026
Same author

Spectroscopic Analysis of the Extracellular Matrix Hierarchical Structure in Naked Mole-Rat Skin.

Gels (Basel, Switzerland)·2026

Area of Science:

  • Immunology
  • Periodontology
  • Bone Biology

Background:

  • Host immune responses are critical in periodontal diseases.
  • B lymphocytes in periodontal lesions express receptor activator of NF-kappaB ligand (RANKL), a key regulator of osteoclast differentiation.
  • The role of Actinobacillus actinomycetemcomitans-responsive B lymphocytes in periodontal bone resorption requires further investigation.

Purpose of the Study:

  • To evaluate RANKL expression in Actinobacillus actinomycetemcomitans-responsive B lymphocytes.
  • To determine the effect of these B lymphocytes on periodontal bone resorption.
  • To elucidate the mechanism by which B cells influence bone metabolism in periodontal disease.

Main Methods:

  • Congenitally athymic Rowett rats were injected with formalin-fixed Actinobacillus actinomycetemcomitans.

Related Experiment Videos

  • Donor B cells from A. actinomycetemcomitans-immunized rats were adoptively transferred.
  • Osteoclast differentiation was assessed using RAW 264.7 cells and RANKL decoy receptor osteoprotegerin fusion protein.
  • Histological analysis of gingival tissues and alveolar bone was performed.

    • Main Results:

    • B cells from A. actinomycetemcomitans-immunized rats exhibited higher RANKL expression and induced greater osteoclast differentiation compared to nonimmune B cells.
    • This osteoclastogenic activity was inhibited by osteoprotegerin fusion protein.
    • Actinobacillus actinomycetemcomitans-binding B cells (ABB) and RANKL-expressing B cells were found in gingival tissues of recipient rats, correlating with increased osteoclast formation and periodontal bone resorption.
    • Osteoprotegerin fusion protein administration antagonized these effects.

    Conclusions:

    • B lymphocytes can promote periodontal bone resorption independently of T lymphocytes.
    • Up-regulation of RANKL expression on B cells is associated with increased osteoclastogenesis and bone loss in periodontal disease.
    • Targeting RANKL may offer a therapeutic strategy for managing periodontal bone destruction.