Apoptosis of endplate chondrocytes in cervical kyphosis is associated with chronic forward flexed neck: an in vivo rat bipedal walking model

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.