PPARγ is Associated With Inflammation and Mineralization During Odontoblast Differentiation

Objectives: Peroxisome proliferator-activated receptor gama (PPARγ), one of nuclear receptors, has been reported to play roles in inflammation control and bone metabolism. This study aims to examine whether PPARγ can modulate inflammation and mineralization during Odontoblast differentiation in responding to bacterial endotoxin lipopolysaccharide (LPS) invasion in vitro.
Methods: Mouse Odontoblast-lineage Cells (OLCs) were treated with Porphyromonas gingivalis LPS (10μg/ml) to stimulate long time inflammatory condition for 15 days under mineralization inducing culture. PPARγ agonist rosiglitazone and antagonist BADGE was separately added into medium in a concentration of 20μmol/L to modulate PPARγ activity. Cells were divided into NC group (negative control), LPS group, LPS+Rosiglitazone group and LPS+BADGE group. Several odontoblastic/osteogenic molecules and inflammatory cytokines were analyzed by quantitative real-time reverse-transcription polymerase chain reaction (Q-PCR). The mineralization was determined by alizarin red stain and alkaline phosphatase (ALP) activity assay with 21-day mineralization culture. The statistical analysis for results of Q-PCR and ALP activity was performed by one-way ANOVA with a significance set at P < 0.05.
Results: Three groups with LPS showed significant elevated expression of inflammatory cytokine Cox2 on day 9, and Cox2 expression in LPS+Rosiglitazone group was obviously lower than that in LPS and LPS+BADGE groups. On day 9 and day 15, Opg, Ocn and Runx2 exhibited down-expression in all LPS treated groups, and LPS+Rosiglitazone group showed significant lower expression of them than LPS group, while LPS+BADGE group presented an elevated tendency. LPS+Rosiglitazone group presented the lowest Alp activity and the least mineralized nodules, while LPS+BADGE group exhibited mineralization promotion trend.
Conclusions: The results indicated that, during odontoblast differentiation under inflammatory condition, activation of PPARγ by agonist could attenuate inflammation and inhibit mineralization, while repression of PPARγ by antagonist could exert opposite effect.