Abstract
Peri-implant disease is a chronic inflammation of the soft and hard tissues around a dental implant, resulting from bacterial infection. Recent evidence indicates that some pro-inflammatory cytokines and chemokines released by immunocytes are substantially responsible for the progress and consequence of inflammation. High mobility group box 1 (HMGB1) is released into the extracellular matrix and acts as a key pro-inflammatory factor during injury, necrosis and inflammation. A higher concentration of HMGB1 has been found in gingival crevicular fluid from inflammatory gingival tissue than from healthy sites. HMGB1 mRNA and protein are overexpressed in murine periodontal ligament fibroblasts stimulated with lipopolysaccharide (LPS) and IL-1β. Thus, this study sought to assess HMGB1 expression in peri-implant crevicular fluid (PICF) at each stage of peri-implant disease and to investigate the correlation between HMGB1 and peri-implant disease progress. The results demonstrated that the HMGB1 expression level in PICF is indicative of the progress of peri-implant disease and hence may be a useful diagnostic and prognostic biomarker for peri-implant tissue.
Highlights
Contemporary peri-implant pathological models use immunobiology concepts to explain the disease development process, which is similar to that of gingivitis and periodontitis[3, 4]
A higher concentration of High mobility group box 1 (HMGB1) has been found in gingival crevicular fluid from inflammatory gingival tissue compared with healthy sites[14]
These data showed an increasing tendency of simplified gingival index (sGI), modified plaque index (mPI), modified Sulcus Bleeding Index (mBI) and probing depth (PD) accompanied by the progress of inflammation
Summary
Contemporary peri-implant pathological models use immunobiology concepts to explain the disease development process, which is similar to that of gingivitis and periodontitis[3, 4]. Bacterial products, such as lipopolysaccharide (LPS) and endotoxin, recruit neutrophils to the peri-implant pocket, which act as phagocytes and remove bacteria. HMGB1 is released into the extracellular matrix and act as a key pro-inflammatory factor during injury, necrosis and inflammation[5, 6]. A few studies have investigated the role of HMGB1 in the pathological process of periodontitis. HMGB1 mRNA and protein are overexpressed in murine periodontal ligament fibroblasts stimulated with LPS and interleukin (IL)-1β12. These observations suggest that HMGB1 plays a role in www.nature.com/scientificreports/. Several pro-inflammatory factors have been found to be related to the progress of periodontitis[15, 16], such as IL-1β, IL-6, IL-8 and tumor necrosis factor (TNF)-α. The higher expression of HMGB1 combined with IL-1β and TNF-α results in alveolar bone loss in periodontitis[12]
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