Transforming growth factor-beta1 promotes Geistlich Bio-Oss ® osteogenesis via inhibiting local inflammation response in vivo
Inhibiting inflammation is helpful in relieving the absorption of alveolar bone and promoting periodontal bone regeneration. In a previous study, we showed that transforming growth factor-beta1 (TGF-β1)-induced Treg cells inhibit the absorption of tissue-engineered cartilage caused by endogenous IFN...
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Published in | International journal of clinical and experimental pathology Vol. 10; no. 9; pp. 9310 - 9317 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
e-Century Publishing Corporation
01.01.2017
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Subjects | |
Online Access | Get full text |
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Summary: | Inhibiting inflammation is helpful in relieving the absorption of alveolar bone and promoting periodontal bone regeneration. In a previous study, we showed that transforming growth factor-beta1 (TGF-β1)-induced Treg cells inhibit the absorption of tissue-engineered cartilage caused by endogenous IFN-γ and TNF-α. In this study, we investigated the effect of inhibiting local inflammatory responses on Geistlich Bio-Oss
osteogenesis promotion in vivo. TGF-β1
BMMSCs (bone marrow mesenchymal stem cells) were cultured in Geistlich Bio-Oss
medium, and biocompatibility was evaluated. Alveolar bone defects in New Zealand rabbits repaired by application of Geistlich Bio-Oss
were compared to the effects of added TGF-β1
BMMSCs. There was no significant difference between the untreated Geistlich Bio-Oss
medium-control group and the group treated with the addition of TGF-β1
BMMSCs. Pro-inflammatory cytokines IFN-γ and TNF-α delayed Geistlich Bio-Oss
-induced osteogenesis, but no significant difference in osteogenesis was seen with the addition of TGF-β1
BMMSCs. Geistlich Bio-Oss
has good compatibility with TGF-β1
BMMSCs. However, the dual role of
TGF-β1
BMMSCs in regenerating periodontal bone and limiting local inflammation is not clear. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1936-2625 |