To investigate cigarette smoking's relevance with cervical disc degeneration. We randomly selected 320 patients who came to our spine disease department outpatient clinic with chief complaint of neck-shoulder pain during June 2014-June 2016. According to the detailed smoking history, these patients were divided into 3 different groups, which were active smoker group (AS), passive smoking group (PS) and never-smoker group (NS). Each patient's Miyazaki's magnetic resonance imaging (MRI) classification of cervical disc degeneration was analyzed based on their cervical MRI films. In addition, VAS scores were applied to evaluate the degree of patients' neck-shoulder pain. With the help of statistical techniques, relevance between cigarette smoking, cervical disc degeneration and neck-shoulder pain were analyzed. In the NS group, the overall Miyazaki score, especially for C2/3, C3/4, C5,6 segments, are superior to those in the PS group, in addition, the Miyazaki scores for C1/2 - C6/7 segments in NS group beat the same segments in AS group with statistical significance (P < 0.05). In the AS and PS group, discs from C4/5 to C5/6 segments which score IV and V on Miyazaki classification account for a larger proportion than those discs from C1/2 to C3/4 segments with statistical significance (P < 0.05). In the AS group, male cases have larger proportion of Miyazaki level IV and V discs than female with statistical significance (P < 0.05). While in the AS and PS group, Miyazaki scores of patients whose smoking history ranges from 5 to 10 years are superior to those with smoking history longer than 10 years, with statistical significance (P < 0.05). In addition, VAS scores also vary among the three groups, in which, VAS scores in AS group are higher than those in the NS group. Smoking could accelerate the process of cervical disc degeneration, presenting with more severe neck-shoulder pain on the patients. In addition, the impact of smoking on the lower cervical discs is greater than the upper cervical discs.

Background: The leptin receptor-deficient knockout (db/db) mouse is a well-established model for studying type II diabetes mellitus (T2DM). T2DM is an important risk factor of intervertebral disc degeneration (IVDD). Although the relationship between type I diabetes and IVDD has been reported by many studies, few studies have reported the effects of T2DM on IVDD in db/db mice model. Methods: Mice were separated into 3 groups: wild-type (WT), db/db, and IGF-1 groups (leptin receptor-deficient mice were treated with insulin-like growth factor-1 (IGF-1). To observe the effects of T2DM and glucose-lowering treatment on IVDD, IGF-1 injection was used. The IVD phenotype was detected by H&E and safranin O fast green staining among db/db, WT and IGF-1 mice. The levels of blood glucose and weight in mice were also recorded. The changes in the mass of the trabecular bone in the fifth lumbar vertebra were documented by micro-computed tomography (micro-CT). Tunnel assays were used to detect cell apoptosis in each group. Results: The weight of the mice were 27.68 ± 1.6 g in WT group, which was less than 57.56 ± 4.8 g in db/db group, and 52.17 ± 3.7 g in IGF-1 injected group (P < 0.05). The blood glucose levels were also significantly higher in the db/db mice group. T2DM caused by leptin receptor knockout showed an association with significantly decreased vertebral bone mass and increased IVDD when compared to WT mice. The db/db mice induced by leptin deletion showed a higher percentage of MMP3 expression as well as cell apoptosis in IVDD mice than WT mice (P < 0.05), while IGF-1 treatment reversed this situation (P < 0.05). Conclusions: T2DM induced by leptin receptor knockout led to IVDD by increasing the levels of MMP3 and promoting cell apoptosis. IGF-1 treatment partially rescue the phenotype of IVDD induced by leptin receptor knockout.