Quercetin, a plant flavonoid found in apples, dark berries and red wine, relieves periodontitis caused by cigarette smoke, according to an animal study.
By restoring autophagy levels and reducing the accumulation of reactive oxygen species, quercetin effectively restored and impaired osteogenic differentiation of human periodontal ligament cells (hPDLCs) and facilitated bone resorption after exposure to cigarette smoke, the authors wrote.
“Our results showed that autophagy dysfunction and damage from oxidative stress are significant mechanisms in the development of cigarette smoking-related periodontitis (CSRP) and demonstrated quercetin as a promising approach for future prevention and treatment of CSRP,” – write the authors led by Dr. Sheng Yang from Chongqing Medical University Dental Hospital (China).
Recently, a study of the relationship between human transcriptomes showed that smoking is closely associated with bone mineral density. The study also found that the MAP1LC3B gene, an autophagy biomarker that mediates the degradation of cellular components, including damaged organelles and invading microbes, is significantly important for bone mineral density and smoking. Therefore, the authors of this study hypothesized that cigarette smoke may aggravate CSRP by causing the accumulation of reactive oxygen species, impairing autophagy, and inhibiting osteogenic differentiation of periodontal cells.
Quercetin, which is known to have antioxidant and anti-inflammatory properties, is found in many foods, including parsley, apples and onions. Previous studies have shown that the plant flavonoid may protect osteoblasts from oxidative damage, reducing the toxic effects of smoking on bone. In addition, previous studies have already shown that quercetin can stop hydrogen peroxide-induced damage to human periodontal ligament cells and ligature-induced alveolar bone resorption in mice. For these reasons, the authors wondered whether quercetin could have a major impact in reducing smoking-related gum disease.
To evaluate the effect of quercetin on CSRP, human periodontal ligament cells were exposed to a cigarette smoke extract that was obtained by inhaling cigarette smoke into a syringe and prepared in the laboratory to create a cell model. This model was used to test the therapeutic effects of quercetin on oxidative stress and osteogenic differentiation. In addition, a mouse model of ligature-induced CSRP was established and the therapeutic effect of quercetin was analyzed.
After the mouse model was exposed to cigarette smoke, alveolar bone resorption was enhanced and the osteogenic differentiation potential of human periodontal ligament cells was suppressed. The authors write that quercetin effectively protected the osteogenic differentiation of human periodontal ligament cells (hPDLCs) and periodontal tissues by increasing the expression of beclin-1, which plays a vital role in autophagy and cell death.
In addition to increasing beclin-1 expression, quercetin treatment decreased the accumulation of p62, a protein that targets other proteins that attach to it for selective autophagy.
However, the study was not without limitations. Although quercetin has demonstrated good therapeutic effects, its lower water solubility, poor bioavailability, and inactive metabolites need to be better optimized in the treatment of CSRP, Young and colleagues write.
“However, quercetin is a natural candidate for the prevention and treatment of CSRP by stimulating HPDLC cell autophagy, reducing damage from oxidative stress, and restoring osteogenic differentiation potential,” the authors write.