Significance
Apolipoprotein E
−/−
(ApoE
−/−
) mice deficient in nucleotide binding oligomerization domain-containing protein 2 (NOD2) and subjected to an oral gavage of
Porphyromonas gingivalis
developed elevated serum inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis. Stimulation of NOD2 by Muramyl DiPeptide (MDP) in ApoE
−/−
mice reduced
P. gingivalis
-induced inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis by reducing the expression of inhibitor of NF-κB kinase-β, NF-κB, JNK mRNA, and TNF-α protein levels. A reduction in body weight gain was observed in ApoE
−/−
mice fed a high-fat diet (HFD) and injected with MDP compared to ApoE
−/−
mice fed a HFD but saline injected. MDP activation of NOD2 should be considered in the treatment of inflammatory processes affecting atherosclerosis, bone loss, and possibly, weight gain.
RANKL antagonists and Kavain effectively reduced alveolar bone loss in P. gingivalis-induced periodontitis in our mice model. Compared with RANK-Fc, Kavain-treated animals showed milder improvement of bone and connective tissue inflammation. Therapeutic implications in the prevention of periodontal bone loss are discussed.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.