Abstract
Aim
Porphyromonas gingivalis (Pg) may cause an immune-inflammatory response in host cells leading to bone degradation by osteoclasts. We investigated the osteoclast-inducing capacity of periodontal ligament fibroblasts from periodontitis patients and non-periodontitis donors after a challenge with viable Pg.
Materials and methods
PDLFs from periodontitis patients (n = 8) and non-periodontitis donors (n = 7) were incubated for 6 h with or without viable Pg and subsequently co-cultured with osteoclast precursors from peripheral blood mononuclear cells (PBMCs). The number of multinucleated tartrate-resistant acid phosphatase-positive cells was determined at 21 days. Expression of osteoclastogenesis-associated genes was assessed after infection of PDLFs mono-cultures and in PDLFs-PBMCs co-cultures. Resorption activity was analysed on bone slices.
Results
Pg induced the expression of osteoclastogenesis-associated genes by PDLFs. After bacterial challenge the formation of osteoclast-like cell was decreased in co-cultures of PBMCs with non-periodontitis PDLFs, but not with PDLFs from periodontitis patients.
Conclusion
PDLFs from sites free of periodontitis respond to an infection with Pg by tempering formation of osteoclast-like cells, probably promoting clearance of the infection. PDLFs from periodontitis sites are desensitized to a Pg challenge in terms of their osteoclast-inducing capacity.
Porphyromonas gingivalis (Pg) may cause an immune-inflammatory response in host cells leading to bone degradation by osteoclasts. We investigated the osteoclast-inducing capacity of periodontal ligament fibroblasts from periodontitis patients and non-periodontitis donors after a challenge with viable Pg.
Materials and methods
PDLFs from periodontitis patients (n = 8) and non-periodontitis donors (n = 7) were incubated for 6 h with or without viable Pg and subsequently co-cultured with osteoclast precursors from peripheral blood mononuclear cells (PBMCs). The number of multinucleated tartrate-resistant acid phosphatase-positive cells was determined at 21 days. Expression of osteoclastogenesis-associated genes was assessed after infection of PDLFs mono-cultures and in PDLFs-PBMCs co-cultures. Resorption activity was analysed on bone slices.
Results
Pg induced the expression of osteoclastogenesis-associated genes by PDLFs. After bacterial challenge the formation of osteoclast-like cell was decreased in co-cultures of PBMCs with non-periodontitis PDLFs, but not with PDLFs from periodontitis patients.
Conclusion
PDLFs from sites free of periodontitis respond to an infection with Pg by tempering formation of osteoclast-like cells, probably promoting clearance of the infection. PDLFs from periodontitis sites are desensitized to a Pg challenge in terms of their osteoclast-inducing capacity.
Original language | English |
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Pages (from-to) | 95-103 |
Journal | Journal of Clinical Periodontology |
Volume | 41 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2014 |