A new anabolic compound, LLP2A-Ale, reserves periodontal bone loss in mice through augmentation of bone formation

Currently, there are no effective medications to reverse periodontal disease (PD)-induced bone loss. The objective of this study was to test a new anabolic compound, LLP2A-Ale, or with the combination treatment of mesenchymal stromal cell (MSC), in the treatment of bone loss secondary to PD. PD was...

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Bibliographic Details
Published in:BMC pharmacology & toxicology 2020-11, Vol.21 (1), p.76-76, Article 76
Main Authors: Jiang, Min, Liu, Lixian, Liu, Ruiwu, Lam, Kit S, Lane, Nancy E, Yao, Wei
Format: Article
Language:English
Subjects:
Alveolar bone
Beer
Bone growth
Bone loss
Chemokines
Cytokines
Femur
Granulocyte colony-stimulating factor
Inflammation
IP-10 protein
Ligands
Macrophage inflammatory protein 1
Mesenchyme
Osteogenesis
Periodontal disease
Periodontal diseases
Software
Stem cells
Transplants & implants
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Summary:Currently, there are no effective medications to reverse periodontal disease (PD)-induced bone loss. The objective of this study was to test a new anabolic compound, LLP2A-Ale, or with the combination treatment of mesenchymal stromal cell (MSC), in the treatment of bone loss secondary to PD. PD was induced in mice by placing a ligature around the second right molar. At one week after disease induction, the mice were treated with placebo, LLP2A-Ale, MSCs, or combination of LLP2A-Ale + MSCs, and euthanized at week 4. We found that PD induced alveolar bone loss that was associated with reduced bone formation. LLP2A-Ale alone or in combination with MSCs sustained alveolar bone formation and reversed alveolar bone loss. Additionally, PD alone caused systemic inflammation and increased the circulating levels of G-CSF, IP-10, MIP-1a, and MIP2, which were suppressed by LLP2A-Ale +/- MSCs. LLP2A-Ale +/- MSCs increased bone formation at the peripheral skeletal site (distal femur), which was otherwise suppressed by PD. Our findings indicated that LLP2A-Ale treatment rescued alveolar bone loss caused by PD, primarily by increasing bone formation. LLP2A-Ale also attenuated the circulating levels of a series of inflammatory cytokines and reversed the PD-induced suppression of systemic bone formation.
ISSN:2050-6511
2050-6511
DOI:10.1186/s40360-020-00454-x