Bone Formation During Correction of Vertebral Rounding Deformity in a Rat Model of Pediatric Spondylolisthesis

医学 软骨内骨化 畸形 软骨 骨化 解剖 脊椎滑脱 Ⅰ型胶原 松质骨 病理 腰椎 外科
作者
Hiroaki Manabe,Kazuta Yamashita,Kosaku Higashino,Masatoshi Morimoto,Kosuke Sugiura,Yoshihiro Ishihama,Fumitake Tezuka,Yoichiro Takata,Toshinori Sakai,Koichi Sairyo
出处
期刊:Spine [Lippincott Williams & Wilkins]
卷期号:46 (5): E294-E302 被引量:1
标识
DOI:10.1097/brs.0000000000003779
摘要

Study Design. A study using rat spondylolisthesis models. Objective. The aim of this study was to elucidate the mechanism for correction of vertebral rounding deformity. Summary of Background Data. Vertebral rounding deformity is the strongest risk factor for high-grade slippage associated with spondylolisthesis in adolescents. We previously reported that inadequate endochondral ossification of the anterior upper corner of the vertebral growth plate in response to mechanical stress could be the pathological mechanism of vertebral rounding deformity. Methods. We created a model of spondylolisthesis using 4-week-old rats. They were divided into a tail suspension group that underwent tail suspension to decrease mechanical stress starting at 2 weeks postoperatively and a ground control group with no intervention. Radiographs and microcomputed tomography scans were obtained once weekly for 6 weeks postoperatively. The lumbar spines were then harvested for histological analysis. Immunohistochemical studies detected types I, II, and X collagen in the growth plate cartilage. Bone histomorphometrical analysis was also performed. Results. Radiological and histological evidence in the ground control group showed progress the rounding deformity with time as previously reported. Formation of normal cancellous bone was observed radiologically over time in the tail suspension group, indicating correction of rounding deformity. Histologically, the site showing radiological evidence of correction was derived from cartilage tissue. After starting tail suspension, the growth plate stained positive for type X collagen and the corrected site stained for types II and X collagen in a mosaic pattern. Chondrocytes expressing types I and II collagen and tartrate-resistant acid phosphatase-positive cells were also present at the corrected site. Histomorphometrically, more endochondral bone was detected at the corrected site than in the posterior aspect of the normal growth plate. Conclusion. Correction of vertebral rounding deformity was associated with improvement of chondrocyte differentiation; furthermore, there is possible involvement of a third mechanism, namely transchondroid bone ossification. Level of Evidence: N/A
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