Sodium fluoride accelerates apoptosis, oxidative stress and matrix degradation of condylar chondrocytes by upregulating MMP-13 and RANKL

Fluoride exposure induces pathologic changes in condylar cartilage and subchondral bone in rats, possibly by upregulation of matrix metalloproteinase-13 (MMP-13) and RANKL.

Condylar chondrocytes and subchondral osteoblasts were treated with 5 mg/L and 50 mg/L NaF, respectively, and cell viability was detected. Chondrocyte apoptosis was detected by flow cytometry and western blotting. Oxidative stress, inflammatory factor secretion, and cell matrix degradation were detected using specific kits. RT-qPCR was used to detect the expression of osteoblast phenotype genes. A rat model of fluorosis was established to study the effects of fluoride exposure on condylar cartilage and subchondral bone in vivo.

To explore the regulatory effects of sodium fluoride (NaF) exposure on apoptosis, oxidative stress, and matrix degradation in condylar chondrocytes and subchondral osteoblasts using in vitro and in vivo experiments.

Low concentration of NaF enhanced the activity of chondrocytes and osteoblasts, but high concentration of NaF inhibited cell activity. Fluoride exposure induced chondrocyte apoptosis, oxidative stress, inflammatory response, and matrix degradation. It also decreased the expression of osteoblast phenotype gene osteoprotegerin (OPG) and increased the expression of osteoclast phenotype gene receptor activator of nuclear factor κB ligand (RANKL). In fluorosis rats, urinary and bone fluoride levels were increased, cartilage damage was aggravated, and the number of osteoclasts in subchondral bone was increased.