Inflammatory Mechanisms in Periodontal Stem Cell Biology

Inflammation in the periodontium profoundly influences the behaviour of resident stem cells, particularly those within the periodontal ligament. Bacterial components such as lipopolysaccharides (LPS) engage pattern recognition receptors on periodontal ligament stem cells (PDLSCs), activating signalling cascades—most notably nuclear factor-κB (NF-κB), mitogen-activated protein kinases and inflammasome pathways. These molecular events can exert dual effects, with low-grade inflammatory stimuli sometimes enhancing osteogenic differentiation via bone morphogenetic protein/Smad signalling, while sustained or high-grade challenges inhibit mineralisation and promote a senescent phenotype marked by cell-cycle arrest and pro-inflammatory secretions. Inflammatory cytokines such as interleukin-1β and interferon-γ further modulate PDLSC immunoregulatory properties, altering the balance between tissue homeostasis and destruction. Emerging evidence highlights the interplay between epigenetic modifiers—including histone deacetylases and DNA methyltransferases—and inflammatory cues in shaping stem cell fate. The plasticity of periodontal stem cells under inflammatory stress underpins both the progression of periodontitis and the potential for regenerative therapies, suggesting that precise modulation of the inflammatory microenvironment could restore stem cell function, promote tissue regeneration and mitigate systemic sequelae of chronic oral inflammation.

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Inflammatory Mechanisms in Periodontal Stem Cell Biology publication trend

The graph below shows the total number of articles in inflammatory mechanisms in periodontal stem cell biology across all publications each year (not limited to Nature Index journals).

Technical terms

Periodontal ligament stem cells (PDLSCs): Multipotent cells residing in periodontal ligament tissue that contribute to tooth support and regeneration.

Lipopolysaccharide (LPS): Bacterial endotoxin component that triggers innate immune responses via pattern recognition receptors.

Toll-like receptors (TLRs): Membrane-bound receptors that recognise pathogen-associated molecular patterns to initiate inflammatory signalling.

Nuclear factor-κB (NF-κB): A transcription factor central to the regulation of genes involved in inflammation, immunity and cell survival.

Senescence: Stable cell cycle arrest in response to stress, often accompanied by pro-inflammatory secretions.

Epigenetic regulation: Heritable changes in gene expression mediated by DNA methylation, histone modification and non-coding RNAs without altering the DNA sequence.

References

1. Dental Stem Cells and Lipopolysaccharides: A Concise Review. International Journal of Molecular Sciences (2024).
2. Senescent Markers Expressed by Periodontal Ligament-Derived Stem Cells (PDLSCs) Harvested from Patients with Periodontitis Can Be Rejuvenated by RG108. Biomedicines (2023).
3. Double-edged-sword effect of IL-1β on the osteogenesis of periodontal ligament stem cells via crosstalk between the NF-κB, MAPK and BMP/Smad signaling pathways. Cell Death & Disease (2016).
4. Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists. Scientific Reports (2017).
5. Mutual inhibition between HDAC9 and miR-17 regulates osteogenesis of human periodontal ligament stem cells in inflammatory conditions. Cell Death & Disease (2018).
6. Ascorbic Acid: A New Player of Epigenetic Regulation in LPS‐gingivalis Treated Human Periodontal Ligament Stem Cells. Oxidative Medicine and Cellular Longevity (2021).