Jinliang Lai1, Guanglin Ji2, Yuqiao Zhou3, Jincai Chen2, Min Zhou2, Jianwen Mo4, Tiansheng Zheng5. 1. Emergency Department, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China. 2. Department of Orthopedics, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China. 3. Gannan Medical University, Ganzhou, 341000, China. 4. Department of Orthopedics, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China. mjw1997@126.com. 5. Department of Orthopedics, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China. zhengtiansheng2001@163.com.
Abstract
BACKGROUND: This study was undertaken to establish a rat bipedal walking model of cervical kyphosis (CK) associated with chronic forward flexed neck and assess the effects of chronic forward flexed neck on endplate chondrocytes. METHODS: Forty-eight 1-month-old Sprague-Dawley rats were randomly divided into 3 groups: forward flexed neck group (n = 16), bipedal group (n = 16), and normal group (n = 16). Cervical curves were analyzed on a lateral cervical spine X-ray using Harrison's posterior tangent method before the experiment and at 2-week intervals for a 6-week period. Histologic changes in cartilaginous endplate chondrocytes were observed using hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), and terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling. RESULTS: Radiographic findings suggested a significantly decreased cervical physiological curvature in the forward flexed neck group over the 6-week follow-up; normal cervical curves were maintained in other groups. The average cervical curvature (C2-C7) was - 7.6 ± 0.9° in the forward flexed neck group before the experiment, - 3.9 ± 0.8° at 2 weeks post-experiment, 10.7 ± 1.0° at 4 weeks post-experiment, and 20.5 ± 2.1° at the last follow-up post-experiment. Histologically, results of H&E staining unveiled that cartilaginous endplate chondrocytes were arranged in an irregular fashion, with the decreased number at the observation period; the incidence of apoptotic cells in the forward flexed neck group was noticeably higher at the 6-week follow-up than that in other groups. CONCLUSIONS: CK developed as the result of chronic forward flexed neck. Histologic changes suggested that chondrocyte apoptosis may play a critical role in the development of cervical kyphotic deformity associated with chronic forward flexed neck.
BACKGROUND: This study was undertaken to establish a rat bipedal walking model of cervical kyphosis (CK) associated with chronic forward flexed neck and assess the effects of chronic forward flexed neck on endplate chondrocytes. METHODS: Forty-eight 1-month-old Sprague-Dawley rats were randomly divided into 3 groups: forward flexed neck group (n = 16), bipedal group (n = 16), and normal group (n = 16). Cervical curves were analyzed on a lateral cervical spine X-ray using Harrison's posterior tangent method before the experiment and at 2-week intervals for a 6-week period. Histologic changes in cartilaginous endplate chondrocytes were observed using hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), and terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling. RESULTS: Radiographic findings suggested a significantly decreased cervical physiological curvature in the forward flexed neck group over the 6-week follow-up; normal cervical curves were maintained in other groups. The average cervical curvature (C2-C7) was - 7.6 ± 0.9° in the forward flexed neck group before the experiment, - 3.9 ± 0.8° at 2 weeks post-experiment, 10.7 ± 1.0° at 4 weeks post-experiment, and 20.5 ± 2.1° at the last follow-up post-experiment. Histologically, results of H&E staining unveiled that cartilaginous endplate chondrocytes were arranged in an irregular fashion, with the decreased number at the observation period; the incidence of apoptotic cells in the forward flexed neck group was noticeably higher at the 6-week follow-up than that in other groups. CONCLUSIONS:CK developed as the result of chronic forward flexed neck. Histologic changes suggested that chondrocyte apoptosis may play a critical role in the development of cervical kyphotic deformity associated with chronic forward flexed neck.
Authors: Justin S Smith; Eric Klineberg; Christopher I Shaffrey; Virginie Lafage; Frank J Schwab; Themistocles Protopsaltis; Justin K Scheer; Tamir Ailon; Subaraman Ramachandran; Alan Daniels; Gregory Mundis; Munish Gupta; Richard Hostin; Vedat Deviren; Robert Eastlack; Peter Passias; D Kojo Hamilton; Robert Hart; Douglas C Burton; Shay Bess; Christopher P Ames Journal: World Neurosurg Date: 2016-04-13 Impact factor: 2.104
Authors: F Kandziora; R Pflugmacher; M Scholz; K Schnake; M Lucke; R Schröder; T Mittlmeier Journal: Spine (Phila Pa 1976) Date: 2001-05-01 Impact factor: 3.468