In the cervical spine, Wilder et al13 reported a baseline prevalence of 21.7% among their population. In their follow-up study, the authors reported the progression of cervical disc degeneration during a mean follow-up period of 5.8 years.12 The proportion of individuals who had evidence of progression was 47.9% and was similar between males (49.4%) and females (47.2%). The overall rate of progression of cervical disc degeneration per 100 person-years was also similar for males and females (8.9% and 8.0%, respectively); however, the age and sex-specific rates of progression per 100 person-years reveal that between ages 40 and 60 years, cervical disc degeneration progresses at a greater rate in females than in males. However, between ages 60 and 79, males had a faster rate of cervical degeneration progression than females (Figure 6). Similar progression rates were seen between males and females during the eighth (and greater) decade of life.
Regarding age-specific risk, the prevalence of lumbar disc degeneration increased with age across both cross-sectional studies (Figure 7). In one study, the proportion of participants aged 18 to 29, 30 to 39, 40 to 49, and 50 years or older with any degeneration was 42%, 48%, 70%, and 88%, respectively, and those with moderate to severe degeneration was 28%, 31%, 35%, and 60%, respectively.14 The second study looked at the prevalence of 4 different features of lumbar degeneration across 4 age groups in their population.15 Evidence of disc space narrowing was seen in only 21% of participants who were less than 40 years of age but by the fourth decade the prevalence had more than doubled to 52% and continued to increase to 68% in the fifth decade and to 81% in those aged 60 years and older. The prevalence of facet joint OA followed a similar pattern among the age groups: 24%, 45%, 74%, and 84%, respectively. Degenerative spondylolisthesis was rarely seen in patients younger than 50 years (range: 0%–2%); between the ages of 50 and 59, the prevalence was 11%, increasing to 34% in those aged 60 and older. Spinal stenosis was most prevalent in those aged 60 years and older (12%) with younger participants at a lower risk (range: 1%–5%).
Among Patients Who Receive Fusion for Lumbar or Cervical Degeneration, What Is the Risk of RASP Over Time?
The definition of RASP varied across 7 studies17–23 (Table 3 and Figure 8). Regardless of how degeneration was defined, the cumulative incidence of RASP following fusion ranged from 6.3% to 44.4% during 1.6 to 12.6 years of mean follow-up. The risk of cervical RASP was higher than that of lumbar RASP despite the shorter mean follow-up periods.
Among Patients Who Do Not Receive Fusion for Lumbar or Cervical Degeneration, but Who Were Eligible, What Is the Risk of Further Degeneration Over Time?
The cumulative incidence of additional degeneration in the lumbar spine in patients who did not receive (but were eligible for) lumbar fusion was low during a mean follow-up of 12.6 years in the only comparative study of nonoperative care that reported this outcome (Figure 9).17 Both posterior disc height reduction (>2 SD over the mean of the posterior disc height reduction in the entire nonoperative group) and remaining mean disc height (<20% of anterior vertebral height) had cumulative incidences of only 5.9%. No incidences of worsening of the University of California Los Angeles score or totally reduced posterior disc height (0 mm) were seen in these patients during 12.6 years. However, it must be noted that only 50% of the nonoperative patients from this study were available for the 12-year follow-up. Although it is unknown how many of those unavailable for follow-up ended up having surgery because of additional degeneration, any cases requiring surgery would not be reflected in these data. As a result, the risk of additional degeneration in this population is likely underestimated.
The overall strength of evidence evaluating the population risk of radiographical degeneration in the lumbar and cervical spine is “low,” that is, we have low confidence in the estimate of the absolute risk and further research may change the estimate. Regarding age-specific risk, the overall strength of evidence that the prevalence increases with age is moderate, that is, we have moderate confidence that evidence reflects the true effect and further research may change the estimate. The overall strength of evidence evaluating the risk of RASP among patients who receive fusion for lumbar or cervical degeneration and among patients who do not receive fusion for lumbar or cervical degeneration, but who were eligible, is “low.”
The etiology for ASP has been suggested to be either a natural progression of arthritic disease or an iatrogenic biomechanical effect of the fusion. The purpose of this systematic review was to assess the rate of spinal degeneration in patients without fusion and compare it to the rate of ASP in patients with fusion. If found to be comparable, it may suggest that the etiology of ASP is a natural progression of cervical spondylosis. If the ASP rate was substantially greater than the rate of spinal degeneration in patients without fusion, this may suggest that another factor (such as biomechanical effects) may be contributing to ASP.
There are limitations to this systematic review. First, there is no consensus on definition or classification of spine degeneration. As a result, authors use different outcome measures for degeneration that make comparisons from study to study not possible. Second, the outcome we used was radiographical degeneration. Although clinically symptomatic degeneration is of more interest, we chose to use radiographical degeneration as our outcome because population studies examining the risk of symptomatic degenerative disease were largely lacking in the literature. In an effort to maintain similar outcomes of measure in each group, we opted to examine radiographical outcomes as these were more readily available within the literature. However, radiographical degeneration may not necessarily correlate with clinically symptomatic disease. One strength of this review includes the use of longitudinal population studies that estimate the incidence of degeneration.
We found that the population risk of radiographical spinal degeneration ranged from 12.7% to 51.5% during a 5- to 25-year follow-up period. Among those who had spine fusion for degenerative disease, the risk of RASP in the spine ranged from 6.3% to 44.4% during a 1.6- to 12.6-year follow-up period. Among individuals who did not receive fusion for lumbar or cervical degeneration, but who were eligible, the risk of degeneration in this population was 5.9% during 12 years. However, it must be noted that more than 50% of the study population were unavailable for follow-up. It is likely that some of those not returning for follow-up had subsequent surgical procedures for spine degeneration making these estimates suspect.
These data suggest that although the overall risk of RASP is comparable to the rate of spinal degeneration, the follow-up period ranges were different. Specifically the follow-up in the spinal degeneration group was substantially longer. This suggests that the rate of RASP may be greater than the rate of natural degeneration; however, this statement should be interpreted cautiously. As noted, there is substantial variation in the follow-up and the definition of what constituted ASP. As with many clinical questions, further investigation is needed to better answer our key questions. To that end, a clear, universally agreed upon definition of ASP needs to be established. Secondly, parity between radiographical measures between the 2 groups needs to be established. Assessing the rate of adjacent segment disc degeneration to the rate of de novo spondylolisthesis will likely not provide valuable comparative information. However, comparing the rate of de novo spondylolisthesis versus the rate of adjacent segment spondylolisthesis may provide improved clinical insight. Furthermore, controlling for other variables such as the region of the spine (cervical vs. lumbar) and other potential covariates (i.e., age, sex, comorbidity) is needed for an accurate assessment. Finally and most importantly, parity between clinical measures between the 2 groups needs to be established. It may be challenging to interpret a comparison between patients with ASP and radiculopathy versus patients with ASP and axial back pain.
ASP may occur at a higher rate than the rate of natural spinal pathology and suggests that another factor (such as biomechanical effect of fusion) may accelerate pathologic changes.
Strength of Statement: Weak
- Reported rates of ASP in patients with fusion seem to be higher than the rates of de novo degeneration in patients without fusion, suggesting that the fusion itself may have a contributory effect in the development of ASP.
- These studies have significant variation in follow-up, definitions of radiographical degeneration and other covariates.
- Clarification of ASP definitions and classification is needed to optimally compare different patient populations.
The authors are indebted to Ms. Nancy Holmes, RN, for her administrative assistance.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.spinejournal.org).
1. Ghiselli G, Wang JC, Bhatia NN, et al. Adjacent segment degeneration
in the lumbar spine. J Bone Joint Surg Am 2004;86-A:1497.
2. Hilibrand AS, Carlson GD, Palumbo MA, et al. Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg Am 1999;81:519.
3. Wright JG, Swiontkowski MF, Heckman JD. Introducing levels of evidence to the journal. J Bone Joint Surg Am 2003;85-A:1.
4. Norvell DC, Dettori JR, Fehlings MG, et al. Methodology for the systematic reviews on an evidence based approach for the management of chronic LBP. Spine (Phila Pa 1976) 2011;36:S10–8.
5. Atkins D, Best D, Briss PA, et al. Grading quality of evidence and strength of recommendations. BMJ 2004;328:1490.
6. West S, King V, Carey TS, et al. Systems to Rate the Strength of Scientific Evidence. Maryland: Agency for Healthcare Research and Quality; 2002.
7. Norvell DC, Dettori JR, Skelly AC, et al. Methodology for the systematic reviews on adjacent segment pathology. Spine 2012;37:S10–S17.
8. Aono K, Kobayashi T, Jimbo S, et al. Radiographic analysis of newly developed degenerative spondylolisthesis in a mean twelve-year prospective study. Spine (Phila Pa 1976) 2010;35:887.
9. Hassett G, Hart DJ, Manek NJ, et al. Risk factors for progression of lumbar spine disc degeneration: the Chingford Study. Arthritis Rheum 2003;48:3112.
10. Kauppila LI, Eustace S, Kiel DP, et al. Degenerative displacement of lumbar vertebrae. A 25-year follow-up study in Framingham. Spine (Phila Pa 1976) 1998;23:1868.
11. Kauppila LI, McAlindon T, Evans S, et al. Disc degeneration/back pain and calcification of the abdominal aorta. A 25-year follow-up study in Framingham. Spine (Phila Pa 1976) 1997;22:1642.
12. Wilder FV, Fahlman L, Donnelly R. Radiographic cervical spine osteoarthritis progression rates: a longitudinal assessment. Rheumatol Int 2011;31:45.
13. Wilder FV, Hall BJ, Barrett JP. Smoking and osteoarthritis: is there an association? The Clearwater Osteoarthritis Study. Osteoarthritis Cartilage 2003;11:29.
14. Cheung KM, Karppinen J, Chan D, et al. Prevalence and pattern of lumbar magnetic resonance imaging changes in a population study of one thousand forty-three individuals. Spine (Phila Pa 1976) 2009;34:934–40.
15. Kalichman L, Guermazi A, Li L, et al. Association between age, sex, BMI and CT-evaluated spinal degeneration
features. J Back Musculoskelet 2009;22:189.
16. Kellgren J H, Jeffrey M R, Ball J, et al. Atlas of Standard Radiographs. Vol II. The Epidemiology of Chronic Rheumatism. Oxford: Blackwell Scientific, 1963.
17. Ekman P, Moller H, Shalabi A, et al. A prospective randomised study on the long-term effect of lumbar fusion on adjacent disc degeneration. Eur Spine J 2009;18:1175.
18. Kanayama M, Hashimoto T, Shigenobu K, et al. Adjacent-segment morbidity after Graf ligamentoplasty compared with posterolateral lumbar fusion. J Neurosurg 2001;95:5–10.
19. Satoh I, Yonenobu K, Hosono N, et al. Indication of posterior lumbar interbody fusion for lumbar disc herniation. J Spinal Disord Tech 2006;19:104–8.
20. Coric D, Nunley PD, Guyer RD, et al. Prospective, randomized, multicenter study of cervical arthroplasty: 269 patients from the Kineflex C artificial disc investigational device exemption study with a minimum 2-year follow-up: clinical article. J Neurosurg Spine 2011;15:348–58.
21. Kim SW, Limson MA, Kim SB, et al. Comparison of radiographic changes after ACDF versus
Bryan disc arthroplasty in single and bi-level cases. Eur Spine J 2009;18:218–31.
22. Maldonado CV, Paz RD, Martin CB. Adjacent-level degeneration after cervical disc arthroplasty versus
fusion. Eur Spine J 2011;20(suppl 3):403.
23. Park SB, Jahng TA, Chung CK. Remodeling of adjacent spinal alignments following cervical arthroplasty and anterior discectomy and fusion. Eur Spine J 2012;21:322.
adjacent segment degeneration; radiographical; natural history; spinal degeneration
Supplemental Digital Content
© 2012 Lippincott Williams & Wilkins, Inc.