Related Experiment Videos
Complex osteoclastogenic inductive effects of nicotine over hydroxyapatite.
Joao Costa-Rodrigues1,2,3, Isabel Rocha1, Maria H Fernandes1,4
1Faculdade de Medicina Dentária, U. Porto, Rua Dr. Manuel Pereira da Silva, Porto, Portugal.
Journal of Cellular Physiology
|April 14, 2017
Summary
Nicotine in cigarette smoke promotes osteoclast differentiation and bone resorption at low concentrations, potentially worsening osteoporosis and bone loss. Higher nicotine levels are cytotoxic, impacting cell density.
Area of Science:
- Bone Biology and Disease
- Cellular and Molecular Medicine
Background:
- Cigarette smoke is linked to bone tissue weakening, contributing to osteoporosis and periodontal bone loss.
- It also increases the risk of failure in bone regeneration procedures.
Purpose of the Study:
- To investigate the impact of nicotine on human osteoclastogenesis on a hydroxyapatite substrate.
- To understand nicotine's effects at concentrations found in smokers' plasma and saliva.
Main Methods:
- Human osteoclast precursors were cultured with or without M-CSF and RANKL.
- Cells were treated with varying nicotine concentrations mimicking smokers' exposure.
- Osteoclast differentiation, resorbing activity, and related molecular pathways (NFkB, TNF-α, PGE2) were analyzed.
Main Results:
- Low nicotine concentrations enhanced osteoclast differentiation, particularly in the presence of M-CSF and RANKL.
- Nicotine significantly increased osteoclast resorbing ability when combined with M-CSF and RANKL.
- Nicotine modulated the NFkB pathway and increased TNF-α and PGE2 production.
- High nicotine concentrations exhibited cytotoxic effects, reducing cell density.
Conclusions:
- Nicotine at smokers' plasma levels directly stimulates osteoclast precursor differentiation.
- The stimulatory effect depends on the precursor cell differentiation stage.
- Nicotine enhances osteoclast differentiation and resorbing capacity, potentially exacerbating bone loss conditions.