Neck Solutions

August 11, 2008

Association between cervical pillar hyperplasia and degenerative joint disease

Filed under: Neck Pain, Disc Problems, Arthritis — Administrator @ 5:45 pm

Segment-specific association between cervical pillar hyperplasia and degenerative joint disease

From: Chiropractic & Osteopathy 2006, 14:21

Cervical pillar hyperplasia is a radiological finding which first made its appearance in the literature less than 30 years ago. Its etiology and clinical significance are presently unknown; nevertheless, studies have shown that cervical pillar hyperplasia is a frequently overlooked etiology for the loss of the cervical lordosis. While these findings were disputed by several authors, other consequences of cervical pillar hyperplasia are not known at the present time. It has been theorized that the architectural difference that the presence of hyperplasia introduces into the cervical pillar may cause segmental biomechanical changes and may lead to a higher prevalence of degenerative joint disease at the hyperplastic or adjacent cervical levels. The clinical significance of this phenomenon, if found to be related to degenerative joint disease, should prompt an astute clinician into evaluating the articular pillars on all cervical spine radiographs – particularly because there could be a chance that the patient may develop degeneration at the specific cervical levels and may experience associated neck pain. The architecture of the cervical pillars cannot be modified by conservative therapy; therefore, clinicians should be aware that some of the symptoms may be attributed to degeneration and may influence the expected prognosis of the management of neck pain in those particular patients.

Currently, it is unknown whether the architecture of the articular pillars has a clinically important effect on segmental biomechanics and subsequent degeneration. The axis around which segmental flexion/extension occurs is principally influenced by the orientation of the facet joint in relation to the horizontal plane. A more horizontal facet in comparison to the plane of the superior endplate will shift the instantaneous center of rotation anteriorly, resulting in an increased load on the intervertebral disc (with changes in lateral flexion motion) and an increased risk of anterolisthesis. A straightening of the cervical curve, possibly caused by cervical pillar hyperplasia, results in a redistribution of the loads, favouring the facet joints, and therefore increasing the load on the associated intervertebral disc. Although this has only been demonstrated in a mechanical model, the evidence to-date suggests that an increase of the stress-load on the intervertebral disc locally may enhance the degenerative process in the intervertebral compartment. The possibility that a change in architecture may change the biomechanics of the cervical spine has led to the hypothesis that individuals who have cervical pillar hyperplasia may be predisposed to more biomechanical stress, as is involved in the predominantly accepted theory of the development of degenerative joint disease.

In our preliminary study, although we found no clinically important difference between the global presence/absence of cervical pillar hyperplasia and prevalence of degenerative joint disease, a more sensible explanation of the architectural influence of cervical pillar hyperplasia on cervical spine biomechanics may be segment-specific, meaning that a hyperplastic pillar at a specific cervical level may be related to a higher prevalence of degenerative joint disease at that specific level and/or one segment above or below. We therefore recommended that follow-up research evaluate the segment specific contribution of pillar hyperplasia to the development and severity of degenerative joint disease, because a segmental effect on the biomechanics of the cervical spine is more probable. We assume that the degenerative processes would be a result of the cervical pillar hyperplasia and not the opposite, since cervical pillar hyperplasia has been observed at all ages.

The cervical spine experiences a combination of active mobility and loading stresses, and is therefore, a region of the spine that is frequently affected by progressive degenerative processes. These processes lead to the condition called degenerative disc disease characterized by narrowing of the intervertebral discs, development of osteophytes, intercalary bones and surrounding subchondral sclerosis. Similar radiographic findings affecting the facet and uncovertebral joints can also be present in facet arthrosis and uncovertebral arthrosis, respectively.

Several grading systems have been developed to determine the degree of degeneration radiographically, using signs of subchondral sclerosis, joint space irregularity, decreased joint space and anterior and/or posterior osteophyte formation. degenerative joint disease, osteoarthrosis, or cervical spondylosis, are terms attributed to one or a combination of these findings affecting the disc (degenerative disc disease), uncovertebral, and facet joints (uncovertebral and facet arthrosis) at a particular spinal segment.

Degenerative joint disease is a common, age-related, multi-factorial condition with several theorized etiologies including metabolic, mechanical, inflammatory, and genetic components. This condition affects all joints, especially those that experience chronic biomechanical stresses such as frequent repetitive use and strain, previous trauma and frequent weight-bearing.

The clinical implications of these degenerative processes may include: limitation of head and neck mobility, with or without pain; possible intervertebral foramen encroachment and central canal stenosis, which can result in nerve root or spinal cord compression (radiculopathy and myelopathy respectively); and, although less common, extensive anterior osteophytosis can lead to dysphagia or even vocal fold paralysis. Some controversy exists in the literature with regard to whether radiological findings are related to the patient’s symptoms to a clinically important degree. One long-term follow-up study found that patients’ symptoms correlate with radiographic findings; however, the majority of authors to-date found only a weak relationship between radiographic degenerative changes and pain.

The presence of degenerative joint disease is often confirmed using plain film radiographic findings, with the lateral view being the most informative. The reliability of determining the severity of degenerative joint disease on plain film radiographs in the cervical spine has not been established, but the reliability of detecting the presence or absence of degenerative joint disease has a substantial-to-almost-perfect agreement when assessing the presence/absence of intervertebral disc narrowing, osteophyte formation, zygapophyseal joint, and uncinate process degeneration.

Since the relationship between cervical spine degenerative joint disease and cervical pillar hyperplasia has only been studied ‘globally’ (i.e. cervical pillar hyperplasia was judged to be generally present/absent within the cervical spine as a whole, regardless of whether hyperplastic pillars were detected at one or more levels from C3 to C6), the etiology and clinical relevance of cervical pillar hyperplasia remain unknown. The purpose of this paper, therefore, is to determine if there is a clinically important association between cervical pillar hyperplasia and degenerative joint disease at specific cervical levels, in an age and gender matched sample, and how strong this relationship is between the two conditions, on a by level basis.

The only known clinically relevant result of cervical pillar hyperplasia, as demonstrated in the literature, is its straightening effect on the cervical spine lordosis. Therefore, with such little research on what effect cervical pillar hyperplasia may potentially have on cervical spine biomechanics, it is important to explore any possible clinical consequences of this condition. In our preliminary study, we assessed the possibility that altered spinal biomechanics due to cervical pillar hyperplasia may lead to degenerative changes.

Our present study suggests that a generally weak to moderate segmental association exists between C4 and C5 cervical pillar hyperplasia and adjacent level degenerative disc disease, with the strongest (overall) association demonstrated between C5 cervical pillar hyperplasia and C5–6 degenerative disc disease. The odds of segmental degenerative disc disease occurring together with the adjacent presence of cervical pillar hyperplasia for the overall age categories are approximately two-to-one. Age stratified results demonstrated the same pattern of association (with one exception), even reaching the initially hypothesized moderately-strong association levels in some age categories. Pillar hyperplasia at C4 and C4–5 degenerative disc disease in the 50–54 year age category had the strongest stratified association; nevertheless, generally, the segmental relationship between cervical pillar hyperplasia and degenerative joint disease did not reach the initially proposed association of clinical importance across all age categories.

As mentioned previously, the discrepancies between the C-coefficients and ORs in the younger age subgroups (e.g. 40–54 years) for C4 cervical pillar hyperplasia and C3–4 degenerative disc disease may be due to sample size and/or cervical pillar hyperplasia and degenerative joint disease prevalence inadequacies; these, in turn, can sometimes amplify limitations of the computational formulas themselves. More specifically, naturally occurring low pillar hyperplasia prevalence at C3 and low degenerative joint disease prevalence in adjacent segments, were likely the cause of the lack of statistically significant associations at those respective levels, which in turn, may be due to the likelihood that there are other known contributors to the development of degenerative joint disease; these include trauma, genetic, metabolic, and inflammatory processes, but they were not tested in our study. Nevertheless, our results suggest that cervical pillar hyperplasia is only weakly-to-moderately correlated with the presence of degenerative joint disease; therefore, it may contribute somewhat to the development of degenerative joint disease, but the body may also compensate to some extent for the changes resulting from its slightly aberrant biomechanics. Considering that there are likely several clinically important contributing factors leading to the development of degenerative joint disease, hyperplasia may be but one of several of these. Our findings, when subjected to Coefficient of Determination analysis, suggest that at least in some cervical-spine levels, and in some age categories, cervical pillar hyperplasia may contribute to approximately 9–18% of the development of degenerative joint disease.

Some limitations encountered in this study were poor visualization of C2–3 when assessing films for cervical pillar hyperplasia and degenerative joint disease, poor visualization of C1–2 while assessing for degenerative joint disease, and the sometimes inconsistent presence of hyperplasia in the right and left pillar at a single cervical level. Due to diverging rays of the x-ray beam and small variances in patient positioning, the two articular pillars at any particular level may not be perfectly superimposed on the lateral cervical radiograph, thus allowing the evaluation of each pillar separately for cervical pillar hyperplasia. We were also limited by the lack of any peer-reviewed literature confirming the reliability of evaluating degenerative joint disease severity. Another potential assessment bias in the present study was the fact that one of the assessors, an experienced radiologist, could not be blinded to the presence/absence of cervical pillar hyperplasia while assessing for degenerative joint disease. A future study could eliminate this bias by blinding the assessing radiologist to the purpose of the study.

Another limitation is that the OR sample size estimate was performed ex post facto (after the data were collected), and this, as well as the data analysis (the hypothesis testing part) itself, revealed that the sample sizes in most of the age-specific categories were too small to yield adequate power i.e. statistical significance. Age categories were combined in an attempt to compensate for this, but future studies should endeavour to collect larger samples.

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