Inhibitory Effects of Standardized Boesenbergia pandurata Extract and Its Active Compound Panduratin A on Lipopolysaccharide-Induced Periodontal Inflammation and Alveolar Bone Loss in Rats.

Periodontitis, an inflammatory disease of the gingival tissue, triggered by microbial-derived elements, such as lipopolysaccharide (LPS), collapses the periodontal tissues and resorbs the alveolar bone. This study evaluated the inhibitory effects of standardized Boesenbergia pandurata extract (BPE) and panduratin A (PAN) on periodontitis-induced inflammation and alveolar bone loss. Sprague-Dawley rats with LPS-induced periodontitis were orally administered BPE (50 and 200 mg/kg/day) and PAN (20 mg/kg/day) for 8 days. Histological analysis revealed that BPE- and PAN-administered groups showed decreased cell infiltration and alveolar bone resorption. Furthermore, the BPE and PAN significantly alleviated the mRNA and protein expression levels of nuclear factor kappa B (NF-κB), interleukin-1ß, matrix metalloproteinase (MMP)-2, and MMP-8. BPE and PAN also inhibited the expression of nuclear factor of activated T cells, cytoplasmic 1, c-Fos, and ostoclastogenesis-related enzymes, including cathepsin K and tartrate-resistant acid phosphatase (ALP). BPE and PAN not only upregulated the osteoblastogenesis-associated markers, such as collagen type I (COL1A1) and ALP, but also increased the ratio of osteoprotegerin to receptor activator of NF-κB ligand. Collectively, BPE and PAN efficiently prevent destruction of periodontal tissues and stimulating the loss of alveolar bone tissues, strongly indicative of their potential as natural antiperiodontitis agents.

Inhibitory Effects of Boesenbergia pandurata on Age-Related Periodontal Inflammation and Alveolar Bone Loss in Fischer 344 Rats.

Periodontitis, an infective disease caused by oral pathogens and the intrinsic aging process, results in the destruction of periodontal tissues and the loss of alveolar bone. This study investigated whether Boesenbergia pandurata extract (BPE) standardized with panduratin A exerted anti-periodontitis effects, using an aging model representative of naturally occurring periodontitis. In aged rats, the oral administration of BPE (200 mg·kg-1·day-1) for 8 weeks significantly reduced the mRNA and protein expression of interleukin-1ß, nuclear factor-kappa B, matrix metalloproteinase (MMP)-2, and MMP-8 in gingival tissues (p < 0.01). In alveolar bone, histological analysis with staining and micro-computed tomography revealed the attenuation of alveolar bone resorption in the BPE-treated aged group, which led to a significant reduction in the mRNA and protein expression of nuclear factor of activated T-cells c1 (NFATc1), c-Fos, tartrate-resistant acid phosphatase, and cathepsin K (p < 0.01). BPE not only increased the expression of osteoblast differentiation markers, such as alkaline phosphate, and collagen type I (COL1A1), but also increased the ratio of osteoprotegerin to RANKL. Collectively, the results strongly suggested that BPE is a natural resource for the prevention or treatment of periodontal diseases.

Inhibitory Effects of Panduratin A on Periodontitis-Induced Inflammation and Osteoclastogenesis through Inhibition of MAPK Pathways In Vitro.

Periodontitis is an inflammatory disease caused by microbial lipopolysaccharide (LPS), destroying gingival tissues and alveolar bone in the periodontium. In the present study, we evaluated the anti-inflammatory and anti-osteoclastic effects of panduratin A, a chalcone compound isolated from Boesenbergia pandurata, in human gingival fibroblast-1 (HGF-1) and RAW 264.7 cells. Treatment of panduratin A to LPS-stimulated HGF-1 significantly reduced the expression of interleukin-1ß and nuclear factor-kappa B (NF-κB), subsequently leading to the inhibition of matrix metalloproteinase-2 (MMP-2) and MMP-8 compared with that in the LPS control (**p < 0.01). These anti-inflammatory responses were mediated by suppressing the mitogen-activated protein kinase (MAPK) signaling and activator protein-1 complex formation pathways. Moreover, receptor activator of NF-κB ligand (RANKL)-stimulated RAW 264.7 cells treated with panduratin A showed significant inhibition of osteoclastic transcription factors such as nuclear factor of activated T-cells c1 and c-Fos as well as osteoclastic enzymes such as tartrate-resistant acid phosphatase and cathepsin K compared with those in the RANKL control (**p < 0.01). Similar to HGF-1, panduratin A suppressed osteoclastogenesis by controlling MAPK signaling pathways. Taken together, these results suggest that panduratin A could be a potential candidate for development as a natural anti-periodontitis agent.