A Three-Year Follow-up of Lumbar Spine Endplate (Modic) Changes

Mari Kuisma, MD; Jaro Karppinen, MD, DMSc; Jaakko Niinimäki, MD; Mauno Kurunlahti, MD, DMSc; Marianne Haapea, MSc; Heikki Vanharanta, MD, DMSc; Osmo Tervonen, MD, DMSc


Spine. 2006;31(15):1714-1718. 

In This Article


Modic changes are bone marrow and endplate changes adjacent to degenerative lumbar intervertebral discs. Three different Modic types (I, II, and III) were initially described by Modic.[2,3] Since then, mixed Modic lesions (I/II and II/III) have been identified, suggesting that all Modic changes can progress from one type to another and that they all present different stages of the same pathologic process.[4] A prevalence of 22% to 50% of disc levels affected by Modic changes has been observed in patients with degenerative intervertebral disc disease.[1,2,4] However, despite their high prevalence, there is limited knowledge about the natural course of Modic changes.

To the authors' knowledge, this is the largest study assessing the natural course of Modic changes. At baseline, the prevalence of Modic changes in sciatica patients was 23%, with Type II dominant. These findings accord with the earlier findings in symptomatic patient populations.[1,2,4] In asymptomatic subjects, Modic changes are claimed to be uncommon.[8] In a recent cohort study of 40-year-old Danes, Type I lesions were more common than Type II lesions.[9] The current results of Type II predominance were, however, confirmed in a Finnish cohort study of male train engineers and sedentary controls.[10] In the present study, the occurrence of Modic changes at baseline increased with age, as observed earlier,[11] indicating that disc degeneration and intradiscal destruction are age-related phenomena.

We observed that Modic changes were most likely to occur at L4-L5 and L5-S1, and there was a clear association with degenerative disc disease. Changes were usually identified at both sides of the disc margin, and they usually involved the whole anteroposterior length of the disc margin, as previously observed.[2] The vertical depth of Modic changes was observed to vary between 3 and 30 mm, in accordance with earlier findings.[2]

An association between Type I and Type II changes has been suggested.[2] Modic observed that 5 of 6 patients with Type I converted to Type II over a 14- to 36-month interval. One patient continued to show Type I changes.[2] In the same report, 10 patients with Type II changes remained stable over a 1- to 3-year period. In the present study, Modic changes in 10 of 70 discs (14%) at baseline converted to another type within the 3-year follow-up. Development of mixed Modic changes supports Braithwaite's notions about the natural history of these changes.[4] Mixed changes are assumed to develop before conversion to one of the true Modic Types.[12]

A new finding was that we observed eight conversions of Type II change to another Modic type (two to Type I and six to Type I/II). We speculate that an acute ongoing inflammatory process in some Type II changes causes the conversion of yellow to red marrow, resulting in Type I or Type I/II Modic change. This is supported by the progression of disc degeneration (loss of signal or disc height or even disc collapse in two cases). Furthermore, in support of an ongoing process, the vertical depth and the extent increased most significantly among lesions that did not convert to another type. In contrast to previous findings,[2] our data suggest that Type II changes may be less stable than previously assumed.

The incidence of new Modic changes in this study was 6% over the 3-year follow-up period. Most of these new changes were of Type I. All of the discs with new Modic changes were already degenerated at baseline, suggesting a discogenic origin rather than sequelae of an endplate defect. The new changes occurred in most cases adjacent to herniated discs and very seldom in association with an endplate defect. Furthermore, Modic changes in the nonherniated discs were constantly more restricted in size (data not shown). Previously, Type I changes have been detected after intradiscal chymopapain treatment, which may be considered as a model of acute disc degeneration.[13] Histopathologic sections of Type I changes have demonstrated destruction and fissuring of the endplates, and vascularized fibrous tissue within adjacent bone marrow. Type I changes are assumed to be associated with an ongoing active degenerative process,[2] and our data support this hypothesis.

Three of 13 new Modic changes were mixed Type I/II. It has been suggested that Type I Modic lesions represent an acute stage and may transform to Type II as the subchondral bone heals.[14] Our study supports this hypothesis because mixed Type I/II changes are assumed to develop just before conversion to the true Type II change.[4,12] Type II changes are usually thought to be associated with more stable and chronic degenerative processes,[2] and they are generally assumed to develop from Type I changes. Because we had only baseline and 3-year images, we cannot say with certainty whether Type II changes developed directly from normal bone marrow or whether they were preceded by Type I changes.

The association of Modic changes with clinical symptoms has been evaluated in several studies. Toyone et al[15] found an association between Modic Type I change and low back pain. They stated that 73% of patients with a Type I change, but only 11% of patients with Type II, had significant low back pain. In a recent study, Mitra et al[16] found a positive trend between the evolution of Type I to Type II change and symptom improvement. These authors also think that Type I is painful, at least at some stage of the process. The etiology of Type I change remains unclear. It has been suggested that repeated trauma to the intervertebral disc results in upregulation of inflammatory mediators in the nucleus pulposus. Diffusion of such toxic chemicals through the vertebral endplates could then result in a local inflammatory reaction resulting in low back pain.[17] Vital et al[12] suggested that Modic Type I changes appear to be a good indicator of satisfactory surgical outcome after arthrodesis. However, it is probably premature to assume that Modic changes are themselves indicative of need for a specific intervention. As the next step, we are going to analyze the association of new Modic changes with clinical symptoms in a larger sciatica patient population.

The limitation of our study is that the study population consisted of sciatica patients; therefore, these results cannot be generalized to an asymptomatic population. It would be valuable to investigate Modic changes in an occupational, nonpatient population. Likewise, further high-quality prospective cohort studies are warranted to find the association of Modic changes with clinical symptoms. Another limitation of the current study is the lack of T1-weighted sagittal images as we used axial T1-weighted images to evaluate the extent of the changes in the transverse plane. This is not suggested for clinical practice, since we think that the sagittal plane best illustrates the presence or absence of Modic changes and is sufficient to evaluate the superior-inferior extent of the degenerative endplate changes.


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