Lidocaine inhibits osteoclast activity in vitro.

Local anesthetics such as lidocaine have anti-inflammatory effects. However, the anti-inflammatory mechanism remains vague, but phagocytosis, migration, exocytosis, cellular metabolism and cellular pH levels seem to be affected. During COVID-19 pandemic was found that pro-inflammatory serum levels of IL-1, IL-6, TNF-α were reduced when lidocaine was given to these patients. These pro-inflammatory markers are also elevated in periodontitis and osteoporosis. IL-1 is known as an osteoclast activating factor. To investigate if lidocaine can inhibit osteoclast activity lidocaine was added to osteoclast precursors (PBMCs) alone or in co-cultures with GF cells. Lidocaine was added in a concentration of 3 mM for 6 h and 6 mM for 24 h. After 3 weeks of culture osteoclast formation, gene expression of RANKL, and inflammatory cytokines and resorption activity were measured. Exposure for 24 h to 6 mM lidocaine showed large vacuoles in both cell types. After three weeks of culture osteoclasts were formed but their number was significantly lower in the with 6 mM lidocaine treated co-cultures. Also, gene expression of RANKL, MCP-1, IL-1 and TNF-α was lower. When a 3 mM lidocaine concentration was added for 6 h the vacuoles were only visible in the GF cells and not in the PBMCs and after 3 weeks the number of osteoclasts formed was not reduced. When osteoclasts cultured on bone their resorptive activity was significantly lower. The lower lidocaine concentration and shorter incubation time showed that cell number was not affected but resorption activity of the osteoclasts was decreased. This indicates that lidocaine can inhibit osteoclast activity.