Modic type I change may predict rapid progressive, deforming disc degeneration: a prospective 1

1Department of Radiology, Helsinki University Central Hospital, Topeliuksenkatu 5, HUS, 00029 Helsinki, Finland

1Department of Radiology, Helsinki University Central Hospital, Topeliuksenkatu 5, HUS, 00029 Helsinki, Finland

2Institute of Occupational Health, Helsinki, Finland

3Departments of Physical Medicine and Rehabilitation, Helsinki and Uudenmaa District University Hospitals, Helsinki, Finland

3Departments of Physical Medicine and Rehabilitation, Helsinki and Uudenmaa District University Hospitals, Helsinki, Finland

This prospective magnetic resonance imaging (MRI) study in chronic low-back pain (CLBP) patients evaluated the natural course of degenerative lumbar spine changes in relation to Modic 1 type changes (M1) within 1 year.

From 3,811 consecutive CLBP patients referred to lumbar spine MRI 54 patients with a large M1 were selected using strict exclusion criteria to exclude specific back disorders. Follow-up MRI was obtained within 11–18 months.

At baseline M1 was associated with an adjacent endplate lesion in 96% of the cases. In follow-up, an unstable M1 was associated both with an increase of endplate lesions, decrease of disc height and change in disc signal intensity, most found at L4/5 or L5/S1. In disc spaces without M1, progression of degenerative changes was rare.

Endplate deformation, decreasing disc height and change of disc signal intensity appear essential features of accelerated degenerative process associated with M1.

The importance of Modic changes has been pointed out in many studies due to their association with chronic low-back pain (CLBP) [1–3]. They are quite uncommon among asymptomatic people [4]. Three types of subchondral signal abnormalities in vertebral body marrow were originally described by Modic et al. [5]. Modic 1 type change (M1) was hypointense on T1-weighted magnetic resonance imaging (MRI) and hyperintense on T2-weighted MRI. Fibrovascular tissue was found in such lesions. Modic 2 type change (M2), hyperintense on both T1-weighted image and T2-weighted image was detected in lesions with fatty degeneration. Modic 3 type change (M3) was hypointense on both T1-weighted image and T2-weighted image and detected in lesions with sclerosis. Modic changes are closely related to the degenerative process affecting the disc, including disc herniation [6–8]; their prevalence increases with age [9].

M1 that is associated with fibrovascular tissue has been noted to convert to M2 reflecting fatty degeneration [5]. The conversion may be slow since M1s have been found to enlarge even during several years’ follow-up [10, 11]. Reconversion from M2 to M1 has also been reported [7].

The etiology and pathomechanism of Modic changes and their role in the process of disc degeneration is poorly understood so far. Therefore, studies on various subgroups of patients with Modic changes are needed.

In previous studies an association between M1 and bony endplate lesion and an accelerated progress of disc degeneration was found [11, 12]. The patient sample was, however, small and the span of follow-up period quite variable (18–72 months). A shorter and more homogeneous follow-up interval is needed to study the velocity of progress and interval of appearance of degenerative disc changes.

The aim of this study was to evaluate the association of M1 in the lumbar spine with degenerative disc changes and bony endplate lesions and the short term-evolution of these variables.

The patients were selected from 3,811 consecutive CLBP patients referred during six consecutive years to a standard lumbar spine magnetic resonance imaging (MRI) study at a university hospital. Patients with nonspecific CLBP of at least 3 months’ duration and a definite M1 or a mixed Modic change (M1/M2 or M1/M3) occupying an area of at least 15% of that of the vertebral body in sagittal MR (T1- and T2-weighted) images were included. The slice with the largest Modic change in T1-weighted image was chosen for measurement of the lesion. The strict exclusion criteria were: age older than 65 years, any specific back disease such as fracture, neoplasm, infectious or rheumatic spine disease, spondylolisthesis (4 mm or more), spinal stenosis, disc extrusion or any other finding with neural compression. In addition, patients with any major or a recent (Open in a separate windowFig. 1

On T1-weighted image, a “dark spot” type focal subchondral hypointensity (arrow) surrounded by a mixed type (M1/M2) signal abnormality adjacent to the upper endplate of L3/4 disc

The presence of anterior and posterior bulging or protrusion reaching definitely beyond the intervertebral disc space was assessed at baseline on axial and sagittal images and recorded in a dichotomous manner as present or absent.

Disc height, the distance between the upper and the lower endplate of the adjacent vertebrae, was visually graded as normal (higher than or as high as the upper normal disc space), slightly decreased (33% lower than the upper, normal disc space), decreased (34–66% lower than the upper, normal disc space) or severely decreased (>66% lower than the upper, normal disc space) at levels L1/2–L4/5. Since L5/S1 is normally lower than upper disc space different criteria were applied to L5/S1 disc; normal bright signal intensity of nucleus pulposus was regarded always as normal disc height and degenerated disc was visually graded as slightly decreased, decreased or severely decreased.

Signal intensity of the nucleus pulposus (disc signal intensity) was estimated in each disc (n = 270) as normal (bright), fair (slightly decreased), dark (clearly decreased), black (annulus fibrosus and/or nucleus pulposus region similar to that of cortical bone) and black/white disc (dark annulus fibrosus but bright signal in nucleus pulposus in an otherwise severely degenerated disc with decreased disc height).

Comparative variables were created for the final analysis by comparing the size and signal intensity of the original lesion with that of the corresponding lesion in the follow-up image. The presence and change in size of M1 type lesion during the follow-up was classified as absent, constant, decreased, disappeared, increased and appearance of a new M1. The development of the M1 lesion into M2 or M3 type was classified accordingly. The presence and stability of endplate lesions was classified as absent, constant, decreased or disappeared, increased and appearance of a new finding. Disc height and its change were classified as constantly normal, constantly decreased (unchanged) and further decreased. A visually estimated decrease of disc height at least 20% between baseline and follow-up image was accepted. The change of disc signal intensity was evaluated as follows: constantly normal, constantly decreased (unchanged), further decreased, and increased (change from a dark or black to a bright nucleus pulposus or an increase of the bright area in the nucleus pulposus region in a black/white disc). The presence and change in size of the disc bulge (bulging or protrusion) was assessed on the sagittal image as absent, constant, decreased, disappeared and appeared.

The associations between baseline subchondral signal abnormalities and degenerative variables were evaluated by cross-tabulating. The association between the development of M1s and other degenerative changes was evaluated by cross-tabulating the comparative variables created to classify changes in M1, disc signal intensity, disc height and endplate lesions. Chi-square tests were run to detect significant differences in cell frequencies. Due to multiple observations per patient, intracluster correlation between these changes was computed [15]. Intracluster correlation coefficient compares the within-group variance (in this case, the progression of M1 changes within a single individual) with the between-group variance (the corresponding changes between patients) [16]. As the intracluster correlation was negative (ρ = −0.06), the conversion coefficient for Chi-square statistics was smaller than 1. The resulting adjusted Chi-square test statistic would be larger than the crude one and the corresponding adjusted p-values (not given) even smaller than the crude values (p Open in a separate windowFig. 2

On T1-weighted image, irregularity of the both endplates and defects in the adjacent subchondral bone surrounded by M1 type hypointensities in L5/S1 disc with decreased disc height and posterior bulge (arrow)

Posterior and anterior bulging/protrusion was observed in 100 (37%) and 93 (34%) of the 270 disc spaces, respectively. Fifty-one (51%) of the posterior and 47 (51%) of the anterior bulges were found in discs with an adjacent M1 (Fig. 3a).

a At baseline on T1-weighted image, the L5/S1 disc has a decreased disc height and an anterior bulge (broad arrow). There is an M1 type hypointensity adjacent to the both endplates and only slight depression in the upper endplate of L5/S1 disc (thin arrow). b After 1-year follow-up, on T1-weighted image, M1 has enlarged and there is still an anterior bulge. A focal defect has appeared in the upper endplate of L5/S1 disc anteriorly (arrow)

Disc height was normal in 169 (63%) of discs, slightly decreased in 58 (21%), decreased in 25 (9%), and severely decreased in 18(7%). Only 3 (0.6%) of M1s were found adjacent to a disc with a normal disc height.

Disc signal intensity was normal in 17%, slightly decreased in 35%, decreased in 35%, severely decreased in 3% and black/white in 10% of the 270 lumbar discs. None of the discs with a normal or only slightly decreased signal intensity had an adjacent M1 while 29% of discs with a decreased disc signal intensity and 93% of the 28 black/white discs had.

During the 1-year follow-up most of the M1s changed regarding their signal intensity, shape and size. 10 (9%) M1s remained constant, 44 (40%) increased, 49 (45%) decreased, seven (6%) disappeared, and 10 new M1s appeared. Sixty-four (58%) M1s converted partly and five (6%) totally to M2s, larger M1s more likely than small ones. 5/81 (6%) of M2s reconverted to M1s. Signal intensity did not change at the same pace in all regions and heterogeneous, mixed signal abnormalities were observed adjacent to most disc spaces after follow-up. In disc spaces with an absent or constant adjacent M1 a slighter progress of degenerative changes was noted than in those with a changing or appearing M1 (Tables 1, ​,2,2, ​,3,3, ​,44).

Modic 1 type change in relation to the change in endplate lesion after 1-year follow-up

EPL endplate lesion, M1 Modic 1 type change

p Table 2

Modic 1 type change in the upper endplate in relation to the change of posterior bulge after 1-year follow-up

M1 Modic 1 type change

Modic 1 type change in the upper endplate in relation to the change of disc height after 1-year follow-up

M1 Modic 1 type change

p Table 4

M1 in the upper endplate in relation to the change of disc signal intensity after 1-year follow-up

M1 Modic 1 type change

p Open in a separate windowFig. 4

a At baseline, there is M1 adjacent to the both endplates and a bony endplate defect (broad arrow) adjacent to the upper endplate of L4/L5 disc on T2-weighted image. The L4/L5 disc has a posterior (thin black arrow) and anterior (thin white arrow) bulge and a decreased disc signal intensity. b After 1 year, both M1s and the endplate defect have enlarged (thin arrow). Disc height has decreased, anterior and posterior bulge have increased and the disc signal intensity has increased (turned to black/white)

a On T1-weighted image at baseline, L4/L5 disc has an anterior (thin arrow) and posterior (thick arrow) extrusion and a large hypointensity (M1) in the subchondral bone adjacent to the both endplates with irregularities posteriorly. b After follow-up, M1 type hypointensity adjacent to the both endplates has changed into a mixed type (M1/M2) subchondral hypo- and hyperintensity (small arrows). Disc height and extrusions have decreased and irregularities of the endplates have increased

The change of M1 was associated with the decrease of disc height (Table 3, p