Archives of oral biology · 2025
Branched-chain amino acids promote gelatinase secretion from human periodontal ligament stem cells through nuclear factor kappa-B signaling.
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Ning Xinjie, Zheng Huiling, Tu Ying, Guo Qiang, Ren Biao, Wu Leng, Xie Jing, Liu Chengcheng
Аннотация
OBJECTIVE: To explore the effects of branched-chain amino acids (BCAAs) on periodontal tissues and regulation of gelatinase secretion by human periodontal ligament stem cells (hPDLSCs).
DESIGN: The salivary BCAA levels (leucine, isoleucine, and valine) in the clinical participants were measured using mass spectrometry. A local injection model in the periodontium of Sprague Dawley rats was established to investigate the periodontal destruction induced by BCAAs. A BCAA-treatment model of hPDLSCs was established to detect the expression and activity of gelatinase and further explore the potential mechanism by which BCAAs enhance gelatinase secretion.
RESULTS: Compared to the healthy controls, the salivary levels of leucine (p = 0.0190), isoleucine (p = 0.0351), and valine (p = 0.0072) were significantly elevated in individuals with periodontitis. In vivo experiments revealed that BCAAs aggravated periodontal extracellular matrix degradation and alveolar bone resorption in rats. Three-dimensional reconstruction of the rat maxilla demonstrated an increase in the distance from the cementoenamel junction to the alveolar bone crest (p < 0.0001), and a decrease in the bone volume fraction (p < 0.0001). In vitro experiments demonstrated that BCAAs activate the phosphorylation of nuclear factor kappa-B (NF-κB) signaling pathway in the hPDLSCs and consequently induce the secretion of gelatinases. The absence of any of the components in the BCAAs attenuated this effect.
CONCLUSION: BCAAs increase gelatinase secretion through the NF-κB (p-p65) signaling pathway, consequently exacerbating periodontal tissue destruction. This provides a novel insight on the role of BCAAs in the host immune-inflammatory response and increases our understanding of the possible involvement of BCAAs in the periodontitis development.
DESIGN: The salivary BCAA levels (leucine, isoleucine, and valine) in the clinical participants were measured using mass spectrometry. A local injection model in the periodontium of Sprague Dawley rats was established to investigate the periodontal destruction induced by BCAAs. A BCAA-treatment model of hPDLSCs was established to detect the expression and activity of gelatinase and further explore the potential mechanism by which BCAAs enhance gelatinase secretion.
RESULTS: Compared to the healthy controls, the salivary levels of leucine (p = 0.0190), isoleucine (p = 0.0351), and valine (p = 0.0072) were significantly elevated in individuals with periodontitis. In vivo experiments revealed that BCAAs aggravated periodontal extracellular matrix degradation and alveolar bone resorption in rats. Three-dimensional reconstruction of the rat maxilla demonstrated an increase in the distance from the cementoenamel junction to the alveolar bone crest (p < 0.0001), and a decrease in the bone volume fraction (p < 0.0001). In vitro experiments demonstrated that BCAAs activate the phosphorylation of nuclear factor kappa-B (NF-κB) signaling pathway in the hPDLSCs and consequently induce the secretion of gelatinases. The absence of any of the components in the BCAAs attenuated this effect.
CONCLUSION: BCAAs increase gelatinase secretion through the NF-κB (p-p65) signaling pathway, consequently exacerbating periodontal tissue destruction. This provides a novel insight on the role of BCAAs in the host immune-inflammatory response and increases our understanding of the possible involvement of BCAAs in the periodontitis development.