Abstract
Periodontal disease characterized by alveolar bone resorption and bacterial pathogen-evoked inflammatory response has been believed to have an important impact on human oral health. The aim of this study was to evaluate whether magnolol, a main constituent of Magnolia officinalis, could inhibit the pathological features in ligature-induced periodontitis in rats and osteoclastogenesis. The sterile, 3–0 (diameter; 0.2 mm) black braided silk thread, was placed around the cervix of the upper second molars bilaterally and knotted medially to induce periodontitis. The morphological changes around the ligated molars and alveolar bone were examined by micro-CT. The distances between the amelocemental junction and the alveolar crest of the upper second molars bilaterally were measured to evaluate the alveolar bone loss. Administration of magnolol (100 mg/kg, p.o.) significantly inhibited alveolar bone resorption, the number of osteoclasts on bony surface, and protein expression of receptor activator of nuclear factor-κB ligand (RANKL), a key mediator promoting osteoclast differentiation, in ligated rats. Moreover, the ligature-induced neutrophil infiltration, expression of inducible nitric oxide synthase, cyclooxygenase-2, matrix metalloproteinase (MMP)-1 and MMP-9, superoxide formation, and nuclear factor-κB activation in inflamed gingival tissues were all attenuated by magnolol. In the in vitro study, magnolol also inhibited the growth of Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans that are key pathogens initiating periodontal disease. Furthermore, magnolol dose dependently reduced RANKL-induced osteoclast differentiation from RAW264.7 macrophages, tartrate-resistant acid phosphatase (TRAP) activity of differentiated cells accompanied by a significant attenuation of resorption pit area caused by osteoclasts. Collectively, we demonstrated for the first time that magnolol significantly ameliorates the alveolar bone loss in ligature-induced experimental periodontitis by suppressing periodontopathic microorganism accumulation, NF-κB-mediated inflammatory mediator synthesis, RANKL formation, and osteoclastogenesis. These activities support that magnolol is a potential agent to treat periodontal disease.
Highlights
Periodontitis, a chronic infectious inflammatory disease, is highly prevalent among world populations [1]
The bacterial pathogen is known to play a critical role in the initiation of inflammatory processes in periodontal tissues and host immune response by releasing several inflammatory mediators such as proinflammatory cytokines, prostaglandin E2 (PGE2), and reactive oxygen species (ROS), as well as upregulating periodontitis-related gene expression including inducible nitric oxide synthase, cyclooxygenase2 (COX-2), and matrix metalloproteinases (MMPs) [6,7,8,9]
Our results showed that there was a severe bone resorption evidenced by a marked increase of amelocemental junction (ACJ)-alveolar crest (AC) distances both at buccal and palatal aspects in the ligation group when compared to the nonligation group (Figures 1(a) and 1(c))
Summary
Periodontitis, a chronic infectious inflammatory disease, is highly prevalent among world populations [1]. The bacterial pathogen is known to play a critical role in the initiation of inflammatory processes in periodontal tissues and host immune response by releasing several inflammatory mediators such as proinflammatory cytokines, prostaglandin E2 (PGE2), and reactive oxygen species (ROS), as well as upregulating periodontitis-related gene expression including inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), and matrix metalloproteinases (MMPs) [6,7,8,9]. The increased host inflammatory process in response to bacteria is often accompanied by an uncoupling
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