Inhibits Alveolar Bone Destruction in a Rat Model with Lipopolysaccharide (LPS)-Induced Periodontitis.

BACKGROUND AND AIMS

extract (EA) exerts various biological effects, including anti-inflammatory activity. The effect of EA on alveolar bone destruction has not been reported; therefore, we aimed to determine whether EA could inhibit alveolar bone destruction associated with periodontitis in a rat model in which periodontitis was induced using lipopolysaccharide from (. -LPS).

METHODS

Physiological saline or . -LPS or . -LPS/EA mixture was topically administered into the gingival sulcus of the upper molar region of the rats. After 3 days, periodontal tissues of the molar region were collected. Immunohistochemistry was performed for cathepsin K, receptor activator of NF-B ligand (RANKL), and osteoprotegerin (OPG). The cathepsin K-positive osteoclasts along the alveolar bone margin were counted. EA effects on the expression of the factors regulating osteoclastogenesis in osteoblasts with . -LPS-stimulation were also examined .

RESULTS

Treatment with EA significantly reduced the number of osteoclasts by decreasing the RANKL-expression and increasing OPG-expression in the periodontal ligament in the treatment group compared to the . -LPS group. The study showed that the upregulation of p-IB kinase and (p-IKK/), p-NF-B p65, TNF-, interleukin-6, and RANKL and downregulation of semaphorin 3A (Sema3A), -catenin, and OPG in the osteoblasts with . -LPS-stimulation improved with EA-treatment.

CONCLUSION

These findings demonstrated that topical EA suppressed alveolar bone resorption in the rat model with . -LPS-induced periodontitis by maintaining a balance in RANKL/OPG ratio via the pathways of NF-B, Wnt/-catenin, and Sema3A/Neuropilin-1. Therefore, EA possesses the potential to prevent bone destruction through inhibiting osteoclastogenesis attributed to cytokine burst under plaque accumulation.