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Targeting CTSS Rescues LPS-Induced Osteogenic Impairment in PDLSCs via Blocking NF-κB-Dependent Inflammatory
Dong Shen1, Lihua Qiu1, Jie Wang1
1Department of Stomatology, Yancheng Stomatological Hospital, Yancheng City, China.
Oral Diseases
|May 18, 2026
Summary
Cathepsin S (CTSS) drives periodontitis inflammation and hinders periodontal ligament stem cell (PDLSC) regeneration. Inhibiting CTSS promotes osteogenic differentiation and reduces inflammatory markers, suggesting CTSS as a therapeutic target.
Area of Science:
- Periodontal medicine
- Stem cell biology
- Molecular biology
Background:
- Periodontitis is a chronic inflammatory disease causing tissue destruction.
- Periodontal ligament stem cells (PDLSCs) possess regenerative potential.
- The role of Cathepsin S (CTSS) in periodontitis pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of Cathepsin S (CTSS) in periodontitis.
- To determine CTSS's impact on inflammation and PDLSC osteogenic differentiation.
Main Methods:
- Bioinformatics analysis of public datasets (GEO).
- Experimental validation using PDLSCs from healthy and periodontitis patients.
- Functional assays including CTSS manipulation, LPS stimulation, and assessment of NF-κB signaling and cytokine production.
Main Results:
- CTSS was significantly upregulated in periodontitis.
- CTSS knockdown enhanced PDLSC osteogenic differentiation and mineralization.
- CTSS inhibition reduced NF-κB activation and pro-inflammatory cytokine release (TNF-α, IL-1β, IL-6).
Conclusions:
- CTSS promotes inflammation and impairs PDLSC regenerative capacity in periodontitis.
- CTSS acts via NF-κB signaling pathway.
- CTSS represents a potential therapeutic target for periodontal regeneration.
