Department of Orthopaedic Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, Japan.
Am J Sports Med. 2009 Nov;37 Suppl 1:139S-47S. doi: 10.1177/0363546509350984.
Cartilage and subchondral bone have recently been considered an osteochondral unit. The treatment of osteochondral lesions is still challenging, but better subchondral bone repair may result in higher quality repaired cartilage.
Alendronate accelerates bone formation in osteochondral defects and affects the quality of the repaired cartilage.
Controlled laboratory study.
Osteochondral defects were made on the left trochleas of 50 rabbits, which were assigned to 1 of 3 groups: control, ALN (weekly subcutaneous injection of 0.14 mg/mL alendronate), and ALN-S (alendronate injection in the first 8 weeks only). They were evaluated at 4, 8, 24, and 52 weeks. Bone repair was evaluated with microcomputed tomography and histologic evaluation. Cartilage repair was evaluated with ultrasound and histologic analyses.
At 4 weeks, the defects were filled, and cartilage-like repair tissue was observed in the ALN group, whereas the defects were incompletely filled in the control group. Alendronate treatment enhanced early bone formation and mineralization in the osteochondral defect for the first 8 weeks. The continuous injection of alendronate for 24 weeks resulted in delayed bone remodeling, but the rabbits in the ALN-S group showed good integrity of the subchondral bone plate, without delayed remodeling. At 52 weeks, the ALN-S group had a columnar arrangement of chondrocytes that had less fibrillation and looked superior to those in the ALN and control groups. Ultrasound analysis showed better quality of repaired cartilage of the ALN and ALN-S group than the control group.
Alendronate accelerated bone formation without inhibiting its mineralization but thereafter inhibited bone remodeling in an osteochondral defect. The withdrawal of alendronate at 8 weeks avoided the delayed remodeling and showed better subchondral bone repair. At 52 weeks, better subchondral bone repair resulted in better cartilage quality.
Alendronate administered in the early period accelerates bone formation and improves the quality of the repaired cartilage.
软骨和软骨下骨最近被认为是一个骨软骨单位。骨软骨病变的治疗仍然具有挑战性,但更好的软骨下骨修复可能会导致更高质量的修复软骨。
阿仑膦酸钠加速骨软骨缺损中的骨形成,并影响修复软骨的质量。
对照实验室研究。
在 50 只兔子的左滑车处制造骨软骨缺损,将其分为 3 组之一:对照组、ALN(每周皮下注射 0.14mg/ml 阿仑膦酸钠)和 ALN-S(仅在前 8 周注射阿仑膦酸钠)。在 4、8、24 和 52 周时进行评估。采用微计算机断层扫描和组织学评估评估骨修复。采用超声和组织学分析评估软骨修复。
在 4 周时,缺陷被填充,并且在 ALN 组中观察到软骨样修复组织,而在对照组中缺陷未完全填充。阿仑膦酸钠治疗在最初的 8 周内增强了骨软骨缺损中的早期骨形成和矿化。连续注射阿仑膦酸钠 24 周导致骨重塑延迟,但 ALN-S 组的兔子显示出软骨下骨板的良好完整性,没有延迟重塑。在 52 周时,ALN-S 组的软骨细胞呈柱状排列,纤维化程度较低,外观优于 ALN 和对照组。超声分析显示 ALN 和 ALN-S 组的修复软骨质量优于对照组。
阿仑膦酸钠加速骨形成而不抑制其矿化,但随后抑制骨软骨缺损中的骨重塑。在 8 周时停用阿仑膦酸钠避免了延迟重塑,并显示出更好的软骨下骨修复。在 52 周时,更好的软骨下骨修复导致更好的软骨质量。
在早期给予阿仑膦酸钠可加速骨形成并改善修复软骨的质量。