The mechanism underlying the remodeling effect of lactoferrin on midpalatal sutures during maxillary expansion and relapse in rats

Abstract

The remodeling effects of intragastric administration and intramaxillary injection of lactoferrin (LF) on midpalatal sutures (MPS) during maxillary expansion and relapse in rats were studied to explore the underlying bone remodeling mechanism. Using a rat model of maxillary expansion and relapse, rats were treated with LF by intragastric administration (1 g·kg-1·d-1) or intramaxillary injection (5 mg·25 μl-1·d-1). The effects of LF on the osteogenic and osteoclast activities of MPS were observed by microcomputed tomography, histologic staining, and immunohistochemical staining, and the expressions of key factors in the extracellular regulated protein kinase 1/2 (ERK1/2) pathway and osteoprotegerin (OPG)-receptor activator of nuclear factor-KB ligand (RANKL)-receptor activator of nuclear factor-KB (RANK) axis were detected. Compared with the group with maxillary expansion alone, osteogenic activity was relatively enhanced, whereas osteoclast activity was relatively weakened in the groups administered LF, and the phosphorylated-ERK1/2: ERK1/2 and OPG: RANKL expression ratios increased significantly. The difference was more significant in the group administered LF intramaxillary. Administration of LF promoted osteogenic activity at MPS and inhibited osteoclast activity during maxillary expansion and relapse in rats, which may have occurred through regulation of the ERK1/2 pathway and the OPG-RANKL-RANK axis. The efficiency of intramaxillary LF injection was greater than that of intragastric LF administration.