Progranulin is highly expressed in patients with chronic periodontitis and protects against experimental periodontitis in rats

Background The autocrine growth factor progranulin (PGRN) plays a crucial role in the physiological and pathological processes. However, its function in chronic periodontitis (CP) remains unclear. Methods Results Forty-five CP patients and 43 healthy controls were recruited. Expressions of PGRN in gingival biopsies were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry, respectively. The levels of PGRN, tumor necrosis factor alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta) in the gingival crevicular fluid (GCF) before and after non-surgical periodontal treatment were quantified by ELISA. In addition, recombinant human PGRN (rhPGRN) or its vehicle was injected into the gingiva of rats with ligature-induced experimental periodontitis to test its influence on the disease process. Local inflammatory cell infiltration and alveolar bone loss were assessed by histomorphometric analysis, and the expression levels of TNF-alpha and IL-1 beta in the gingiva were determined by RT-qPCR and ELISA. PGRN expression was increased in the gingiva and GCF of patients with CP compared with healthy controls. With the decline of periodontal clinical indices, the molar ratio of PGRN to TNF-alpha in GCF at 1 month after non-surgical treatment was significantly higher than at baseline (35.31 +/- 22.09 vs 25.67 +/- 16.19, P < 0.01). In rats with experimental periodontitis, local administration of rhPGRN attenuated inflammatory cell infiltration (P < 0.05), inhibited alveolar bone loss (P < 0.05) and decreased TNF-alpha and IL-1 beta levels (both P < 0.01) compared with the vehicle treatment group. Conclusion These findings suggest that progranulin is highly expressed in the gingiva and GCF of patients with CP and protects against experimental periodontitis in rats.