Stem cell‐like populations and immunoregulatory molecules in periodontal granulation tissue
Background and Objectives Determine the presence of mesenchymal stem cells (MSCs) in healthy periodontal tissue and periodontal granulation tissue (GT) and explore associations between immuno‐regulatory molecules and selected subgingival microorganisms. Material and Methods Mesenchymal stem cells we...
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Veröffentlicht in: | Journal of periodontal research 2018-08, Vol.53 (4), p.610-621 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Background and Objectives
Determine the presence of mesenchymal stem cells (MSCs) in healthy periodontal tissue and periodontal granulation tissue (GT) and explore associations between immuno‐regulatory molecules and selected subgingival microorganisms.
Material and Methods
Mesenchymal stem cells were isolated, propagated and characterised by flow cytometry from a region of healthy gingival tissue and inflamed GT of 10 systemically healthy non‐smokers with chronic periodontitis. Tissue levels of immunoregulatory molecules were determined by qPCR and Gingival Crevicular Fluid (GCF) levels by ELISA. Subgingival plaque levels of periodontal pathogens were determined by qPCR
Results
Cells with MSC‐properties were isolated from both inflamed GT and healthy gingival (G) tissue. A pro‐inflammatory process predominated in GT which was partly reflected in GCF and putative periodontal pathogens were higher at diseased sites. However, there was no significant difference in surface levels of mesenchymal (CD90, CD73, CD146, CD271, STRO‐1), endothelial (CD105, CD106), hematopoietic (CD34, CD45) and embryonic (SSEA‐4) stem cell markers between MSCs isolated from GT and G tissue.
Conclusion
Periodontal lesions, albeit inflamed, retain healing potential as inferred by the presence of MSC‐like cells with similar immunophenotypic characteristics to those found in healthy periodontal tissue. Therefore, there might be merits for healing in preserving sufficient GT in‐situ during periodontal surgery. |
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ISSN: | 0022-3484 1600-0765 |
DOI: | 10.1111/jre.12551 |