Abstract
Aim
Fas ligand (FasL) belongs to the tumor necrosis factor (TNF) superfamily regulating bone turnover, inflammation, and apoptosis. The appendicular and axial skeleton phenotype of mature Fasl gld mice was reported. The impact of FasL on the alveolar bone providing support for the teeth at mature stages under healthy and induced inflammatory conditions remains unknown.
Materials and methods
We performed a phenotypical analysis of mice carrying the homozygous Fasl gld mutation and wild-type (WT) mice (C57BL/6) under healthy conditions and upon ligature-induced periodontitis. After 12 days, μCT analysis revealed the distance between the cement enamel junction and the alveolar bone crest (CEJ-ABC). Additional structural parameters like the bone volume fraction (BV/TV) and the periodontal ligament space volume (PLS.V) were measured. Histological analyses were performed to visualize the catabolic changes at the defect site.
Results
We report that healthy Fasl gld mice have more periodontal bone than wild-type littermates. Fasl gld had no significant effect on inflammatory osteolysis compared to WT controls with ligatures. Histology revealed eroded surfaces at the root and in the interproximal bone in both strains.
Conclusions
These findings suggest that FasL is a catabolic factor in alveolar bone homeostasis, however, FasL does not affect the inflammatory osteolysis.
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