The cervical spine naturally maintains a lordotic curvature to compensate for the thoracic kyphotic curvature.[8] As the loss of cervical lordosis progresses, the deformity also tends to progress rapidly by producing abnormal forces to the head and neck.[2, 30] Even with mild sagittal imbalance, detrimental symptoms can develop, which worsen with sagittal imbalance progression.[9] The vertebral disc is designed to maintain an isotropic form by transmitting axial load uniformly across the disc and vertebral endplate.[22, 23] In cervical spinal positions, such as extension, flexion, or lateral bending, the load of the disc is transmitted uniformly over the endplates.[23] Loss of cervical lordosis may alter this isotropic nature of disc loading and consequently contribute to continuous irregular loading, which accelerates disc degeneration.[23, 31] This degeneration can be aggravated by normal aging, calcification of the endplate, or decreased peripheral blood supply.[5] Abnormally increased mechanical pressure has also been shown to reduce the nutritional support of the disc and lead to disc degeneration.[29] Our results demonstrate a correlation between loss of cervical lordosis and cervical disc degeneration. In this study, cervical disc degeneration was evaluated using both Pfirrmann grades and the modified Matsumoto scoring system, whereas most previous studies have only used either of them.[4, 15, 25, 26] Pfirrmann grading assesses the homogeneity of disc structure and includes a distinction between the annulus and nucleus, whereas the modified Matsumoto scoring system considers the degree of the posterior disc protrusion and narrowing of disc space without considering the homogeneity of the disc. This difference in the evaluation criteria may explain the different relationship between the C1-C2 angle and disc degeneration, which the C1-C2 angle is only correlated with the Pfirrmann grades.
Changes in sagittal cervical alignment, such as FHP, may cause or result in adaptive mechanisms to global alignment change, which affects all spinal levels (including the cervical, thoracic, and lumbar regions).[18, 30] Contractions of the neck muscles due to vestibulocollic or cervicocolic reflexes induce anterior shifting of the head/neck center of gravity, resulting in a change in the spinal alignment.[27, 36] These reflexes cause cervical muscle spasm, representing shortening of the posterior neck extensor muscles and the tightening of the anterior neck muscles, which may increase the SVA.[6] Previous studies have shown that a larger C2-C7 SVA is related to higher Neck Disability Index scores [35] and demonstrated a correlation between the C2-C7 SVA and the C1-C2 angle.[35] The results of this study also showed that the C2-C7 SVA was significantly correlated with the O-C2 angle and the C1-C2 angle. However, to date, the clinical consequences of increased cervical SVA on cervical disc degeneration have not been described. In this study, the change in SVA was not correlated with cervical disc degeneration. Both in the lordotic and non-lordotic groups, the SVA was not correlated with cervical disc degeneration. These findings indicate that the SVA, which has been suggested to be related to FHP in previous studies, has little effect on disc degeneration. Cervical disc degeneration progressing with normal aging could be aggravated by the loss of natural sagittal angles rather than increased cervical SVA. Recently, one study showed significant correlation between cervical lordosis and C2-C7 SVA in asymptomatic Chinese population.[37] In this study, there was no significant correlation between C2-C7 angle and C2-C7 SVA. This may mean that the rate of disc degeneration is greater than that of FHP when clinical symptoms occur.
The optimal position and angle of the occipital bone and the cervical axis have been topics of discussion.[20, 21, 24] In this study, there was a negative correlation between the O-C2 and C1-C2 angle and the C2-C7 angle, as well as a significant correlation with the SVA. These results suggest a correlation between the occipital-cervical axis, cervical kyphosis, and FHP. There was a significant correlation between the occipito-cervical angle and cervical disc degeneration in this study. A recent cohort study showed that an increased occipito-cervical angle may result in large biomechanical stress on the adjacent structures or deformation of cervical alignment.[21] A previous study has shown that the loss of the natural C2-C7 angle facilitates cervical disc degeneration.[26] In addition, our findings suggest that a more negative occipito-cervical angle may accelerate disc degeneration. In summary, the SVA, the occipito-cervical angle, and the loss of cervical lordosis, expressed easily as the “forward head posture”, “the jaw lifting posture” and “the cervical kyphosis”, were correlated with each other. Also, only the latter two, the jaw lifting posture and the cervical kyphosis had were correlated with disc degeneration. Although the cause-and-effect relationship is unknown, it can be interpreted that FHP worsens the jaw lifting posture and cervical kyphosis, which may cause disc degeneration.
This study has some limitations. The pathophysiological mechanism of disc degeneration due to the loss of cervical lordosis remains unknown. As the analyses were cross-sectional, determining a cause-and-effect relationship is difficult. Furthermore, neck pain was not classified as causal factor in this study. As cervical disc degeneration progresses, neck pain or uneven loading to the cervical disc can induce deformity of the sagittal alignments, including both cervical and occipito-cervical angles. Long-term changes in the sagittal cervical parameters and disc degeneration were also not evaluated. Prospective longitudinal studies with long-term follow-up are necessary to investigate the clinical implications and the interactions between the alignment of cervical spines and the discs. Finally, as we did not include an asymptomatic group of participants, the results may not be generalizable to whole populations. Future long-term longitudinal studies in a general asymptomatic population are needed.