Abstract
BackgroundCartilage regeneration is a key step in functional reconstruction for temporomandibular joint osteoarthritis (TMJ-OA) but is a difficult issue to address. Strontium ranelate (SrR) is an antiosteoporosis drug that has been proven to affect OA in recent years, but its effect on chondrogenesis and the underlying mechanism are still unclear.MethodsBone mesenchymal stem cells (BMSCs) from Sprague–Dawley (SD) rats were induced in chondrogenic differentiation medium with or without SrR, XAV-939, and LiCl. CCK-8 assays were used to examine cell proliferation, and alcian blue staining, toluidine blue staining, immunofluorescence, and PCR analysis were performed. Western blot (WB) analyses were used to assess chondrogenic differentiation of the cells. For an in vivo study, 30 male SD rats with cartilage defects on both femoral condyles were used. The defect sites were not filled, filled with silica nanosphere plus gelatine-methacryloyl (GelMA), or filled with SrR-loaded silica nanosphere plus GelMA. After 3 months of healing, paraffin sections were made, and toluidine blue staining, safranin O/fast green staining, and immunofluorescent or immunohistochemical staining were performed for histological evaluation. The data were analyzed by SPSS 26.0 software.ResultsLow concentrations of SrR did not inhibit cell proliferation, and the cells treated with SrR (0.25 mmol/L) showed stronger chondrogenesis than the control. XAV-939, an inhibitor of β-catenin, significantly promoted chondrogenesis, and SrR did not suppress this effect, while LiCl, an agonist of β-catenin, strongly suppressed chondrogenesis, and SrR reversed this inhibitory effect. In vivo study showed a significantly better cartilage regeneration and a lower activation level of β-catenin by SrR-loaded GelMA than the other treatments.ConclusionSrR could promote BMSCs chondrogenic differentiation by inhibiting the Wnt/β-catenin signaling pathway and accelerate cartilage regeneration in rat femoral condyle defects.
Highlights
Cartilage regeneration is a key step in functional reconstruction for temporomandibular joint osteoarthritis (TMJ-OA) but is a difficult issue to address
Temporomandibular joint osteoarthritis (TMJ-OA) is a joint degenerative disease characterized by cartilage lesions along with changes in the synovium and degradation of subchondral bone
Cell proliferation assay of Bone mesenchymal stem cells (BMSCs) CCK-8 assays showed a clear dose-dependent effect of Strontium ranelate (SrR) on cell proliferation, and high concentrations (0.5, 1.0, and 2.0 mmol/L) of SrR significantly suppressed cell viability at days 3, 5, and 7 (P < 0.05)
Summary
Cartilage regeneration is a key step in functional reconstruction for temporomandibular joint osteoarthritis (TMJ-OA) but is a difficult issue to address. Subchondral osteosclerosis can lead to dysfunction of the cartilage tissue and cartilage degeneration; cartilage degeneration can lead to subchondral bone metabolic disorders, subchondral bone remodeling, and sclerosis [4, 5]. This vicious cycle strongly promotes the development of OA. Inhibition of this vicious cycle and regeneration of the degraded or even exfoliated cartilage are key to the treatment of OA and the reconstruction of joint function
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