Effect Of Ibandronate Sodium On Artilage Cartilage And Subchondral Bone In Rat Model Of Knee Osteoarthritis

Objective:To observe the effects of Ibandronate sodium on articular cartilage and the subchondral bone in a rat model of knee osteoarthritis,and investigate whether the mechanism of Ibandronate sodium is via the MAPKs signal pathway.Methods:30 3-month-old male SD rats were randomly divided into 3 groups(each group of 10 only): Sham-operated group,anterior cruciate ligament transection(ACLT)with intraperitoneal injection of saline(ACLT group),anterior cruciate ligament transection with ntraperitoneal injection of ibandronate sodium(the treatment group).One week after ACLT,rats in the treatment group were treated with intraperitoneal injection of ibandronate sodium 10ug/kg once a week for 12 weeks;Rats in the ACLT group were injected with saline Micro-computed tomography and histology analysis were performed to evaluate subchondral bone mass and microarchitecture,and cartilage degeneration.Results:(1)The bone volume fraction(BV/TV)and trabecular bone number(Tb.N)in ACLT group were significantly lower than that of in Sham-operated Group(P<0.05,and P<0.05),no statistically significant difference was found between the two groups' trabecular plate thickness(Tb.Th),but trabecular separation(Tb.Sp)was significantly higher than that of in Sham-operated Group(P<0.01);The bone volume fraction(BV/TV)and trabecular bone number(Tb.N)in treatment group were significantly higher than that of in ACLT Group(P<0.05,and P<0.05),no statistically significant difference was found between the two groups' trabecular plate thickness(Tb.Th),but trabecular separation(Tb.Sp)was significantly lower than that of in ACLT Group(P<0.05).(2)The mankin score in ACLT group was significantly higher than that of in Sham-operated Group(P<0.01);the mankin score in treatment group was significantly lower than that of in ACLT Group(P<0.05).(3)The MAPKs signal pathway(C-JUN and the P38 and ERK1)and MMP-13 levels in ACLT group were significantly higher than that of in Sham-operated Group(P<0.01,and P<0.01,and P<0.01,and P<0.01);the MAPKs signal pathway(C-JUN,ERK1 and P38)and MMP-13 levels in treatment group were significantly lower than that of in ACLT Group(P<0.01,and P<0.01,and P<0.01,and P<0.01).Conclusion:The results demonstrated that Ibandronate sodium can inhibit subchondral bone loss and protected articular cartilage in ACLT rats,at least partially,by inhibiting MAPKs signaling pathway.