Journal of clinical periodontology · 2013
Human periodontal ligament fibroblast responses to compression in chronic periodontitis.
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El-Awady Ahmed R, Lapp Carol A, Gamal Ahmed Y, Sharawy Mohamed M, Wenger Karl H, Cutler Christopher W, Messer Regina L W
Аннотация
AIM: Test whether human periodontal ligament fibroblasts (PDLFs) retain homeostatic responses to a physiological compressive force during chronic periodontitis.
MATERIAL AND METHODS: Six cell lines were established from periodontally healthy individuals (H-PDLFs) and another six were cultured from patients diagnosed with chronic periodontitis (D-PDLFs). Compressive force at 150 psi was applied to H-and D-PDLFs for 3 h on 2 consecutive days. After compression, comparisons between H-and D-PDLFs were performed by gene expression analysis of IL-6, proteases and 84 inflammation-related targets using real-time PCR.
RESULTS: Compression of H-PDLFs resulted in a significant increase only in MMP-1 mRNA. In contrast, the same compressive force on D-PDLFs produced significant increases in the expression of MMPs-1,-7,-9 and -16. Moreover, compression of H-PDLFs resulted in down-regulation of IL-6, while IL-6 was significantly up-regulated in compressed D-PDLFs. Compression of H-PDLFs slightly up-regulated 3 and significantly down-regulated 15 inflammation-related genes, while the same treatment strongly up-regulated 21 inflammation-related genes in D-PDLFs.
CONCLUSION: These results suggest a fundamental difference in the inflammatory response of healthy versus diseased PDLFs under physiological compression. Maintenance of these characteristics in vitro suggests that these cells may be at least partly responsible for the persistence of inflammation and localized susceptibility in chronic periodontitis.
MATERIAL AND METHODS: Six cell lines were established from periodontally healthy individuals (H-PDLFs) and another six were cultured from patients diagnosed with chronic periodontitis (D-PDLFs). Compressive force at 150 psi was applied to H-and D-PDLFs for 3 h on 2 consecutive days. After compression, comparisons between H-and D-PDLFs were performed by gene expression analysis of IL-6, proteases and 84 inflammation-related targets using real-time PCR.
RESULTS: Compression of H-PDLFs resulted in a significant increase only in MMP-1 mRNA. In contrast, the same compressive force on D-PDLFs produced significant increases in the expression of MMPs-1,-7,-9 and -16. Moreover, compression of H-PDLFs resulted in down-regulation of IL-6, while IL-6 was significantly up-regulated in compressed D-PDLFs. Compression of H-PDLFs slightly up-regulated 3 and significantly down-regulated 15 inflammation-related genes, while the same treatment strongly up-regulated 21 inflammation-related genes in D-PDLFs.
CONCLUSION: These results suggest a fundamental difference in the inflammatory response of healthy versus diseased PDLFs under physiological compression. Maintenance of these characteristics in vitro suggests that these cells may be at least partly responsible for the persistence of inflammation and localized susceptibility in chronic periodontitis.
Предметные рубрики MeSH
Cell Culture TechniquesCell LineCells, CulturedChemokinesChronic PeriodontitisFibroblastsHomeostasisHumansHydrostatic PressureInflammation MediatorsInterleukin-6InterleukinsMatrix Metalloproteinase 1Matrix Metalloproteinase 16Matrix Metalloproteinase 7Matrix Metalloproteinase 9Matrix MetalloproteinasesPeriodontal LigamentTime FactorsTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-2