Journal of periodontal & implant science · 2026
Role of the CXCL12/CXCR4 axis in periodontitis: bioinformatic and clinical evidence.
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Mei Jie, Shuai Renjie, Feng Xiaosong, Nan Kaiwen, Tang Changlin, Jin Fu, Duan Jun
Аннотация
PURPOSE: This study aimed to identify key genes associated with periodontitis using bioinformatic approaches and to validate the expression of the candidate molecules CXCL12 and CXCR4 in gingival tissue samples from patients with periodontitis.
METHODS: Two large periodontitis-related gene-expression datasets, GSE16134 and GSE10334, were retrieved from the Gene Expression Omnibus database. The datasets were processed, integrated, and screened to identify genes associated with periodontitis. The 10 genes with the highest node degrees were designated hub genes. Least absolute shrinkage and selection operator (LASSO) regression and support vector machine-recursive feature elimination (SVM-RFE) were then used to select signature genes, followed by correlation analysis. Gingival tissues discarded during periodontal surgery were collected from patients with stage III-IV chronic periodontitis. Morphological changes were evaluated using hematoxylin and eosin (H&E) staining, and CXCL12 and CXCR4 protein expression was assessed using immunohistochemistry (IHC). Quantitative polymerase chain reaction (qPCR) was performed to measure CXCL12 and CXCR4 mRNA expression.
RESULTS: Bioinformatic analysis identified CXCL12 and CXCR4 as the leading signature genes. CXCL12 ranked first in both the LASSO and SVM-RFE analyses, and CXCR4 showed the strongest correlation with CXCL12 among the hub genes. H&E staining demonstrated markedly greater inflammatory-cell infiltration in the gingival lamina propria of the periodontitis group than in the control group. IHC and qPCR confirmed that CXCL12 and CXCR4 protein and mRNA levels, respectively, were significantly higher in the periodontitis group than in the control group (P<0.05).
CONCLUSIONS: Upregulation of CXCL12 and CXCR4 was significantly associated with periodontitis. These molecules may participate in the periodontal inflammatory response, although their causal and mechanistic roles require further functional investigation.
METHODS: Two large periodontitis-related gene-expression datasets, GSE16134 and GSE10334, were retrieved from the Gene Expression Omnibus database. The datasets were processed, integrated, and screened to identify genes associated with periodontitis. The 10 genes with the highest node degrees were designated hub genes. Least absolute shrinkage and selection operator (LASSO) regression and support vector machine-recursive feature elimination (SVM-RFE) were then used to select signature genes, followed by correlation analysis. Gingival tissues discarded during periodontal surgery were collected from patients with stage III-IV chronic periodontitis. Morphological changes were evaluated using hematoxylin and eosin (H&E) staining, and CXCL12 and CXCR4 protein expression was assessed using immunohistochemistry (IHC). Quantitative polymerase chain reaction (qPCR) was performed to measure CXCL12 and CXCR4 mRNA expression.
RESULTS: Bioinformatic analysis identified CXCL12 and CXCR4 as the leading signature genes. CXCL12 ranked first in both the LASSO and SVM-RFE analyses, and CXCR4 showed the strongest correlation with CXCL12 among the hub genes. H&E staining demonstrated markedly greater inflammatory-cell infiltration in the gingival lamina propria of the periodontitis group than in the control group. IHC and qPCR confirmed that CXCL12 and CXCR4 protein and mRNA levels, respectively, were significantly higher in the periodontitis group than in the control group (P<0.05).
CONCLUSIONS: Upregulation of CXCL12 and CXCR4 was significantly associated with periodontitis. These molecules may participate in the periodontal inflammatory response, although their causal and mechanistic roles require further functional investigation.