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Inhibitory effects of advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide on the expression of osteoblastic markers of rat bone marrow cells in culture.
- Source :
-
Journal of periodontal research [J Periodontal Res] 2016 Jun; Vol. 51 (3), pp. 313-20. Date of Electronic Publication: 2015 Jul 30. - Publication Year :
- 2016
-
Abstract
- Background and Objectives: Diabetes is a major risk factor for periodontitis and there is a close relationship between the degree of hyperglycemia and the severity of periodontitis. Advanced glycation end-products (AGEs) accumulate in various tissues under diabetic conditions. AGEs in the periodontal tissues probably play a role in upregulating periodontal inflammation; however, the association of AGEs with the severity of periodontitis has not been fully clarified. Lipopolysaccharide from Porphyromonas gingivalis (P-LPS) is a potent pathogenic factor in periodontitis. Although the independent effect of AGE or P-LPS on osteoblastic cells has been reported in vitro, the effect of adding both has not been clearly elucidated. In this study, to explore factors aggravating diabetic periodontitis, we investigated the effects of AGE and P-LPS on the expression of osteoblastic markers and the expression of inflammation-related markers in vitro.<br />Material and Methods: Rat bone marrow cells were cultured, and alkaline phosphatase activity and bone nodule formation were evaluated as osteoblastic markers. Reverse transcription-polymerase chain reaction was performed to determine the mRNA expression of molecules associated with bone and inflammation. Protein levels of osteocalcin and interleukin-1β (IL-1β) were measured using enzyme-linked immunosorbent assay.<br />Results: AGEs and P-LPS independently reduced alkaline phosphatase activity and bone nodule formation. The addition of both AGE and P-LPS (AGE+P-LPS) further decreased these markers. Reverse transcription-polymerase chain reaction analysis revealed that AGE+P-LPS markedly decreased the mRNA expression of osteoblast-related molecules such as type 1 collagen, osteocalcin and Cbfa1, and markedly increased that of inflammation-related molecules such as IL1β and S100A8. AGE and P-LPS decreased the protein level of osteocalcin and increased that of IL-1β, and a further increase of IL-1β was detected for AGE+P-LPS.<br />Conclusion: AGEs and P-LPS inhibited the expression of osteoblastic markers and increased the levels of inflammatory markers in rat bone marrow cells, suggesting that both AGE and P-LPS may be important factors associated with the aggravation of diabetic periodontitis.<br /> (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
- Subjects :
- Alkaline Phosphatase analysis
Alkaline Phosphatase drug effects
Animals
Cell Survival drug effects
Diabetes Complications
Drug Combinations
Enzyme-Linked Immunosorbent Assay
Glycation End Products, Advanced administration & dosage
Interleukin-1beta metabolism
Lipopolysaccharides administration & dosage
Male
Osteoblasts drug effects
Osteoblasts metabolism
Osteocalcin metabolism
Osteogenesis drug effects
Periodontitis etiology
Periodontitis metabolism
Polymerase Chain Reaction
RNA, Messenger metabolism
Rats
Rats, Wistar
Time Factors
Bone Marrow Cells drug effects
Cells, Cultured drug effects
Glycation End Products, Advanced antagonists & inhibitors
Lipopolysaccharides antagonists & inhibitors
Porphyromonas gingivalis metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1600-0765
- Volume :
- 51
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Journal of periodontal research
- Publication Type :
- Academic Journal
- Accession number :
- 26223811
- Full Text :
- https://doi.org/10.1111/jre.12310