[Effects of Bruton's tyrosine kinase on the proliferation and differentiation of osteoclasts].

Objective: To observe the effect of Bruton's tyrosine kinase (BTK) on the proliferation and differentiation of osteoclasts and to explore the mechanism of BTK on bone destruction in periapical periodontitis.

Methods: After RAW264.7 cells induced with 100 ng·L⁻¹ receptor activator for nuclear factor-κB ligand (RANKL) for 5 days, osteoclast induction was confirmed by light microscopy, tartrate-resistant acid phosphatase (TRAP) staining, and quantitative real-time PCR (RT-qPCR).

Role of the Btk-PLC2 Signaling Pathway in the Bone Destruction of Apical Periodontitis.

Chronic apical periodontitis is characterized by alveolar bone absorption in the apical region and is the result of the participation of various inflammatory mediators. Studies have shown that the Bruton tyrosine kinase- (Btk-) phospholipase C2 (PLC2) signaling pathway plays an important role in bone absorption, but it is unknown whether it plays a role in apical periodontitis bone destruction. Therefore, this study verified the role of Btk and PLC2 in bone resorption of apical periodontitis by and experiments.

The potential effect of Bruton's tyrosine kinase in refractory periapical periodontitis.

To determine the expression of Bruton's tyrosine kinase (BTK) in refractory periapical periodontitis and analyze the relationship between BTK and bone resorption in refractory periapical periodontitis. The mechanism of bone resorption is also discussed. The OneArray Plus expression microarray was used to screen for genes related to refractory periapical periodontitis.