Abstract
BackgroundThis 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.MethodsForty-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.ResultsRadiographic 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.ConclusionsCK 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.
Highlights
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
Under general anesthesia induced by intraperitoneal injection of chloral hydrate (0.3 g/kg body weight), bipedal rats were created by tail and forelimb amputation close to the shoulder joint in the forward flexed neck group and bipedal group and served in height-regulated cages that allowed for ample movement and upright stance [18]
We found that the number of cartilaginous endplate (CEP) chondrocytes decreased over time in the forward flexed neck group compared with that in the bipedal group and the normal group
Summary
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. Cervical kyphotic deformity (CKD) is the most common deformity in the cervical spine [1]. Numerous surgeons have reported a rise of outpatients with kyphotic alignment of the cervical spine, in which their pathogenesis was different from any of the abovementioned causes [5,6,7]. Recent studies demonstrated that the majority of patients are youth, and they have a common prolonged smartphone use with a flexion of the cervical spine [5, 8, 9]. It appears to rather clear that forward flexed neck activity, like repetitive texting and sewing operations, including garment sewing, shoe sewing, and hand-woven carpet weaving, are assumed to be the causes of neck pain or similar symptoms [5, 8, 10,11,12]. It is noteworthy to elucidate whether chronic forward inclined head contributes to the development of CKD, and clarify the exact mechanism
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