Department of Orthopedics, Sports Medicine Center, People's Liberation Army General Hospital, Beijing 100853, China.
Chin Med J (Engl). 2011 May;124(9):1386-94.
Microfracture is a type of bone marrow stimulation in arthroscopic cartilage repair. However, the overall concentration of the mesenchymal stem cells is quite low and declines with age, and in the end the lesion is filled by fibrocartilage. The aim of this research was to investigate a novel method of enhancing microfracture by determining whether low-energy shock waves in microfracture holes would facilitate cartilage repair in a rabbit model.
Full-thickness cartilage defects were created at the medial femoral condyle of 36 mature New Zealand white rabbits without penetrating subchondral bone. The rabbits were randomly divided into three groups. In experimental group A, low-energy shock-wave therapy was performed in microfracture holes (diameter, 1 mm) at an energy flux density (EFD) of 0.095 mJ/mm² and 200 impulses by DolorClast Master (Electro Medical Systems SA, Switzerland) microprobe (diameter, 0.8 mm). In experimental group B, microfracture was performed alone. The untreated rabbits served as a control group. At 4, 8, and 12 weeks after the operations, repair tissues at the defects were analyzed stereologically, histologically, and immunohistochemically.
The defects were filled gradually with repair tissues in experimental groups A and B, and no repair tissues had formed in the control group at 12 weeks. Repair tissues in experimental group A contained more chondrocytes, proteoglycans, and collagen type II than those in experimental group B. In experimental group B, fibrous tissues had formed at the defects at 8 and 12 weeks. Histological analysis of experimental group A showed a better Wakitani score (P < 0.05) than in experimental group B at 8 and 12 weeks after the operation.
In the repair of full-thickness articular cartilage defects in rabbits, low-energy shock waves in microfracture holes facilitated the production of hyaline-like cartilage repair tissues more than microfracture alone. This model demonstrates a new method of improving microfracture and applying shock waves in vivo. However, longer-term outcomes require further study.
微骨折是关节镜下软骨修复的一种骨髓刺激类型。然而,间充质干细胞的总体浓度相当低,并随年龄增长而下降,最终病变部位会被纤维软骨填充。本研究旨在探讨一种通过确定微骨折孔中的低能量冲击波是否会促进兔模型中的软骨修复来增强微骨折的新方法。
在 36 只成熟新西兰白兔的股骨内侧髁上造成全层软骨缺损,不穿透软骨下骨。兔子被随机分为三组。在实验组 A 中,使用 DolorClast Master(瑞士 Electro Medical Systems SA)微探针(直径 0.8 毫米)在能量通量密度(EFD)为 0.095 mJ/mm²和 200 脉冲下对微骨折孔(直径 1 毫米)进行低能量冲击波治疗。实验组 B 仅进行微骨折。未处理的兔子作为对照组。术后 4、8 和 12 周,对缺陷处的修复组织进行体视学、组织学和免疫组织化学分析。
实验组 A 和 B 的缺陷逐渐被修复组织填充,而对照组在 12 周时仍未形成修复组织。实验组 A 的修复组织含有更多的软骨细胞、糖胺聚糖和 II 型胶原,而实验组 B 的修复组织则含有更多的纤维组织。实验组 A 的组织学分析显示,在术后 8 和 12 周时,Wakitani 评分优于实验组 B(P<0.05)。
在兔全层关节软骨缺损的修复中,微骨折孔中的低能量冲击波比单纯微骨折更能促进透明样软骨修复组织的产生。该模型为改善微骨折和体内应用冲击波提供了一种新方法。然而,需要进一步的长期研究来确定其效果。