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

Short chain carboxylic acids decrease human gingival keratinocyte proliferation and increase apoptosis and necrosis

B C Sorkin1, R Niederman

  • 1Department of Cytokine Biology, Forsyth Dental Center, Boston, MA 02115, USA.

Journal of Clinical Periodontology
|May 30, 1998
PubMed
Summary
This summary is machine-generated.

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

Pandemic Considerations on Essential Oral Health Care.

Journal of dental research·2020
Same author

Nuclear F-actin Cytology in Oral Epithelial Dysplasia and Oral Squamous Cell Carcinoma.

Journal of dental research·2020
Same author

Quality Appraisal of Child Oral Health-Related Quality of Life Measures: A Scoping Review.

JDR clinical and translational research·2019
Same author

An Economic Evaluation of a Comprehensive School-Based Caries Prevention Program.

JDR clinical and translational research·2019
Same author

Economic Evaluations of School Sealant Programs and the Consent Conundrum.

Journal of dental research·2018
Same author

School-Based Caries Prevention, Tooth Decay, and the Community Environment.

JDR clinical and translational research·2018
Same journal

Correction to ''Clinical Efficacy of Interventions Based on Professional Mechanical Plaque Removal in the Treatment of Dental Biofilm-Induced Gingivitis: A Systematic Review and Meta-Analysis''.

Journal of clinical periodontology·2026
Same journal

Extracellular Vesicles From Young Brain-Mediated Delivery of PRDX3 Ameliorates Alveolar Bone Loss in Periodontitis.

Journal of clinical periodontology·2026
Same journal

Cost Consequence Analysis of Non-Surgical Treatment Approaches for Patients With Periodontitis.

Journal of clinical periodontology·2026
Same journal

Management of Non-Plaque-Induced Gingival Conditions: A Systematic Review-Part 2: Inflammatory and Immune Conditions; Neoplasms; and Gingival Pigmentation.

Journal of clinical periodontology·2026
Same journal

Ten-Year Results of a Prospective Case Series on Immediately Provisionalized One-Piece Alumina-Toughened Zirconia (ATZ) Oral Implants for Single-Tooth Restoration and Three-Unit Fixed Dental Prostheses.

Journal of clinical periodontology·2026
Same journal

METTL14-Mediated m6A Modification of NEAT1_2 Releases YBX1 From Paraspeckles to Exacerbate Periodontitis.

Journal of clinical periodontology·2026
See all related articles

Short-chain carboxylic acids (SCCA) from bacteria reduce epithelial cell proliferation and increase cell death, potentially causing ulceration in periodontal disease. These findings highlight SCCA

Area of Science:

  • Oral biology
  • Microbiology
  • Cell biology

Background:

  • Epithelial barriers are crucial for preventing infections.
  • Periodontal disease involves ulceration of the gingival sulcular epithelium.
  • Short-chain carboxylic acids (SCCA) are bacterial byproducts found in periodontal pockets.

Purpose of the Study:

  • To investigate the effects of SCCA on keratinocyte proliferation, apoptosis, and necrosis.
  • To test the hypothesis that SCCA promote epithelial ulceration in periodontal disease.

Main Methods:

  • Assessing 3H-thymidine incorporation to measure epithelial cell proliferation.
  • Evaluating epithelial cell viability, apoptosis, and necrosis at varying SCCA concentrations.
  • Analyzing SCCA levels in relation to periodontal disease severity.

Related Experiment Videos

Main Results:

  • Neutralized SCCA decreased epithelial cell proliferation in a dose-dependent manner.
  • Epithelial cell viability decreased with increasing SCCA concentrations.
  • SCCA induced apoptosis at higher rates than necrosis, preceding cell death.

Conclusions:

  • SCCA inhibit keratinocyte proliferation and reduce cell viability, contributing to epithelial barrier dysfunction.
  • Bacterial-derived SCCA may play a role in the ulceration observed in periodontal disease.
  • Further research is needed to elucidate the molecular mechanisms underlying SCCA-induced epithelial cell damage.