Abstract
Hyperhomocysteinemia (HHcy) affects bone remodeling since destructive process in cortical alveolar bone has been linked with it, however; the mechanism remains at large. HHcy increases pro-inflammatory cytokines viz. TNF-α, IL-1b, IL-6 and IL-8 that leads to a cascade that negatively impacts methionine-metabolism and homocysteine cycling. Further, chronic inflammation decreases vitamins B12, B6 and folic acid that are required for methionine-homocysteine homeostasis. This study aims to investigate a HHcy mouse model (cystathionine β-synthase deficient; CBS+/-) for studying the potential pathophysiological changes, if any, in the periodontium (gingiva, periodontal ligament, cement and alveolar bone). We compared periodontium, side-by-side; CBS+/- model with that of wild-type; WT (C57BL/6J) mice. Histology and histomorphometry of mandibular bone along with gene expression analyses were carried out. Also, pro-angiogenic proteins and metalloproteinases were studied. To our knowledge, this research shows, for the first time, a direct connection between periodontal disease during CBS deficiency thereby suggesting the existence of disease drivers during hyperhomocysteinemic condition. Our findings offer opportunities to develop diagnostics/therapeutics for the people who suffer from chronic metabolic disorders like HHcy.
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