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Detection of orthodontically induced inflammatory root resorption-associated biomarkers from the gingival crevicular fluid by proteomics analysis: a randomized-controlled clinical trial
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Detection of orthodontically induced inflammatory root resorption-associated biomarkers from the gingival crevicular fluid by proteomics analysis: a randomized-controlled clinical trial
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Detection of orthodontically induced inflammatory root resorption-associated biomarkers from the gingival crevicular fluid by proteomics analysis: a randomized-controlled clinical trial
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Journal Article
Detection of orthodontically induced inflammatory root resorption-associated biomarkers from the gingival crevicular fluid by proteomics analysis: a randomized-controlled clinical trial
2023
Overview
Orthodontically induced inflammatory root resorption (OIIRR) is an undesirable complication of orthodontic treatment (OT) with an ambiguous aetiologic mechanism. This study aimed to identify OIIRR-associated biomarkers in the gingival crevicular fluid (GCF) using proteomic analysis. In this randomized clinical trial, the upper first premolars (UFP) were exposed either to light or heavy force. The GCF was collected at 1 h, 1 day, 7 days, 14 days, 21 days, and 28 days following force application. After extraction of UFP, roots were imaged and resorption premolar, was used to deliver either light forcecraters were measured. Proteomic analysis of GCF was performed using 2D gel electrophoresis with MALDI-TOF/TOF MS/MS. Results were further analyzed by bioinformatics analyses showing the biological functions and predicted pathways. The predicted canonical pathways showed that the expression of immunoglobulin kappa (IGKC), neutrophil gelatinase-associated lipocalin (NGAL), neurolysin mitochondrial (NEUL), keratin, type II cytoskeletal 1 (K2C1), S100-A9, and the extracellular calcium-sensing receptor (CASR) were significantly associated with a range of biological and inflammatory processes. In conclusion, up-regulation of S100A9, CASR, and K2C1 suggested a response to force-related inflammation, chemotactic activities, osteoclastogenesis, and epithelial cell breakdown. Meanwhile, the up-regulation of IGKC, NGAL, and K2C1 indicated a response to the inflammatory process, innate immunity activation, and epithelial cell breakdown.
