IL-1α regulates osteogenic differentiation and osteoclastic activity of dental follicle cells via JNK and p38 MAPK pathways

Background The expression of interleukin-1α (IL-1α) is increased in tooth with periapical lesion and the eruption of the permanent successor is accelerated in the presence of an infected deciduous tooth with abscess formation. Dental follicle (DF) plays a central role in tooth eruption through regulating alveolar bone resorption and formation. However, whether the increased IL-1α can disturb functions of DF and influence tooth eruption remains unknown. Herein, we studied the effect and possible mechanism of IL-1α on osteogenic differentiation, osteoclastic activity and matrix remodeling of the DF cells (DFCs). Methods Rat DFCs were treated with IL-1α. Quantitative real-time PCR and western blot were performed to analyze the expressions of osteogenesis, osteoclast formation and matrix remodeling related genes and proteins. DFC–bone marrow cell co-cultures, osteogenic differentiation and transwell matrigel invasion assay were used to determine the effect of IL-1α on DFCs further. Phosphorylation of JNK, ERK, p65 and p38 were evaluated in the IL-1α-treated group. Specific inhibitors of signal pathways were added to confirm their roles in this process. Results IL-1α decreased the expression of osteogenesis-related genes and proteins, and increased the expression of MMP9 and ratios of RANKL/OPG. DFCs cultured with IL-1α showed weaker osteogenic capacity, higher osteoclastogenic and invasive ability. Moreover, phosphorylation of JNK and p38 were up-regulated and pretreatment with specific inhibitors reversed the effect of IL-1α on DFCs. Conclusions IL-1α suppresses osteogenic differentiation, promotes osteoclastogenic ability and matrix remodeling of DFCs by activating JNK and p38 MAPK signaling pathways.