Beck Aswin, Murphy David J, Carey-Smith Richard, Wood David J, Zheng Ming H
Centre for Orthopaedic Research (M508), School of Surgery, University of Western Australia, Crawley, Western Australia, Australia School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, Australia.
School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, Australia.
Am J Sports Med. 2016 Oct;44(10):2629-2643. doi: 10.1177/0363546516652619. Epub 2016 Jul 19.
Microfracture and the autologous matrix-induced chondrogenesis (AMIC) technique are popular for the treatment of articular cartilage defects. However, breaching of the subchondral bone plate could compromise the subchondral bone structure.
Microfracture and AMIC will cause deleterious effects on the subchondral bone structure.
Controlled laboratory study.
A total of 36 sheep received an 8-mm-diameter cartilage defect in the left medial femoral condyle. Control animals (n = 12) received no further treatment, and the rest received 5 microfracture holes either with a type I/III collagen scaffold implanted (n = 12; AMIC group) or without the collagen scaffold (n = 12; microfracture group). Macroscopic infill of defects, histology, and histomorphometry of the subchondral bone were performed at 13 and 26 weeks postoperatively, and micro-computed tomography (CT) was also performed at 26 weeks postoperatively.
Microfracture and AMIC resulted in subchondral bone cyst formation in 5 of 12 (42%) and 11 of 12 (92%) specimens at 13 and 26 weeks, respectively. Subchondral bone changes induced by microfracture and AMIC were characterized by an increased percentage of bone volume, increased trabecular thickness, and a decreased trabecular separation, and extended beyond the area below the defect. High numbers of osteoclasts were observed at the cyst periphery, and all cysts communicated with the microfracture holes. Cartilage repair tissue was of poor quality and quantity at both time points and rarely reached the tidemark at 13 weeks.
Microfracture technique caused bone cyst formation and induced severe pathology of the subchondral bone in a sheep model.
The potential of microfracture technique to induce subchondral bone pathology should be considered.
微骨折术和自体基质诱导软骨形成（AMIC）技术在治疗关节软骨缺损方面很受欢迎。然而，软骨下骨板的破坏可能会损害软骨下骨结构。
微骨折术和AMIC会对软骨下骨结构产生有害影响。
对照实验室研究。
总共36只绵羊的左股骨内侧髁出现直径8毫米的软骨缺损。对照组动物（n = 12）未接受进一步治疗，其余动物接受5个微骨折孔治疗，其中12只植入I/III型胶原支架（AMIC组），12只未植入胶原支架（微骨折组）。术后13周和26周进行缺损的宏观填充、组织学检查以及软骨下骨的组织形态计量学分析，术后26周还进行了微型计算机断层扫描（CT）。
微骨折术和AMIC分别在术后13周和26周导致12个标本中的5个（42%）和11个（92%）出现软骨下骨囊肿形成。微骨折术和AMIC引起的软骨下骨变化的特征是骨体积百分比增加、小梁厚度增加、小梁间距减小，且超出缺损下方区域。在囊肿周边观察到大量破骨细胞，所有囊肿均与微骨折孔相通。在两个时间点，软骨修复组织的质量和数量都很差，在13周时很少达到潮线。
在绵羊模型中，微骨折技术导致骨囊肿形成并诱发软骨下骨的严重病变。
应考虑微骨折技术诱发软骨下骨病变的可能性。
