Similar marrow changes have also been noted in the pedicles. While originally described as being associated with spondylolysis, they have also been noted in patients with degenerative facet disease and pedicle fractures [7, 8] (Fig. 10.4). We do not know the exact mechanism by which these marrow changes occur. Their association with degenerative disk disease, facet changes, and pars and pedicle fractures suggest they are a response to biomechanical stress. This then suggests the first and likely most common etiology – mechanical.

The bone is a dynamic architectural substance that responds to changes imposed upon it. When stressed, the bone behaves according to Wolff’s law [9]. Wolff’s law of bone states that the architecture of a bone is determined by the mechanical stresses placed upon it and the bone’s adaptation to withstand these stresses. Wolff’s law is an example of the complementarity of form and function, showing that the form of a bone is shaped by its functional experience. The trabeculae of spongy bone often develop along lines of stress. The major trabecular orientation in the vertebral bodies and pedicles is in-line with the principal direction of loading, whereas perpendicular laid-down support elements or “struts” increase the overall strength. As the bone comes under consistently applied stresses, it may react through the development of microfractures as well as osteoblast depositing new osseous tissues. The orderly remodeling of bone depends on a precise balance between deposition and resorption, between osteoblasts and osteoclasts, a process which repairs microfractures. The remodeled bone is known to contain microfractures that can demonstrate abnormal uptake at scintigraphy. It has been suggested that the type I MR signal intensity changes may be a reflection of remodeling trabecular bone with microfractures and associated marrow changes [10–12].

Of these three types, type I changes appear to be more fluid and variable, a reflection of some ongoing underlying pathological process such as continuing degeneration with resulting changing biomechanical stresses. Of the three types, type I is most often associated with ongoing low back symptomatology [13–17]. In a longitudinal study, the incidence of new degenerative marrow changes was 6 % over a 3-year period, most of these being of type I [15]. In a study of nonoperated patients with low back pain, Mitra [14] found that 92 % of type I changes converted either wholly or partially into type II (52 %), became more extensive (40 %), or remained unchanged (8 %). There was an improvement in symptoms in patients where type I changes converted to type II.

Some studies of diskography in patients with degenerative marrow changes have suggested that type I marrow changes are invariably associated with painful disks [18, 19]. Others [20, 21] have failed to be able to reproduce this association, and thus the relationship of degenerative marrow changes and diskogenic pain remains unproven.

In most cases, type II degenerative changes appear to be associated with a more stable state. Type II changes, however, are not always permanent and conversion between type II and I has been demonstrated. In general, when type II marrow changes convert to type I, there is usually a superimposed process such as continued or accelerated degeneration or vertebral osteomyelitis. Some authors have suggested that mixed lesions are more common than originally thought and indicative of overlap and progression of one type to another [15] (Fig. 10.5).

In most studies of marrow changes, type II are the most prevalent and the prevalence increases with age [15, 22, 23]. Others have suggested that type II changes are less stable and may be as active as type I and equipotent relative to symptomatology [15, 24, 25]. In a study by Määttä et al. [26], there was a 46 % prevalence of marrow changes in patients referred to spinal surgery. In a study by Jensen [25], this prevalence was 43 % in patients with low back pain seeking care. In fact, Marshman et al. [24] reject the contention that type I lesions are more active. They speculate that the bone marrow appearances are merely epiphenomena. As such, they detract one from the more important consideration that the de novo pain afferents have traversed the disk space providing a substrate for diskogenic pain which is a more important consideration than the gross histological appearance and MR signal intensity change of the vertebral body marrow. This last point is valid in that MR changes are likely a consequence of the biomechanical, cellular, and immunological factors that are primarily responsible for symptomatology. The signal intensity changes on MR are a secondary reflection. However, I believe the available data would support that type I marrow changes are more strongly associated with symptomatology than type II and more fluid, and their resolution or change is more common and associated with clinical improvement.

Type III degenerative marrow changes are the least common and probably are a reflection of end-stage degenerative disk disease. There is no enough data to make meaningful comments about its relationship to symptomatology or even the preceding two types.

In a study by Toyone [13], 70 % of patients with type I marrow changes had segmental hypermobility versus 16 % with type II. Probably the greatest support for suggesting these marrow changes, particularly type I, is related to biomechanical instability and is based on observations following fusion. Chataigner [27] has suggested that type I marrow changes have much better outcomes with surgery than those with isolated degenerative disk disease and normal or type II marrow changes. In addition, resolution of type I marrow changes to either normal or type II was associated with higher fusion rates and better outcomes. Other studies support the contention that persistence of type I changes after fusion suggests pseudoarthrosis and is associated with a greater percentage of patients with persistent symptoms. Conversely, resolution of type I marrow changes to either normal or type II was associated with higher fusion rates and better outcomes [28–30]. The conclusion then would be that fusion produces greater stability, reduces biomechanical stresses, and accelerates the improvement in the course of type I marrow changes (Fig. 10.6).

As further support for these fluid marrow changes reflecting biomechanical stress, we have seen similar marrow conversion in the pedicles of vertebral bodies associated with symptomatic pars and pedicle fractures as well as severe degenerative facet joint disease. Twenty-two patients with type I marrow changes of the pedicles and back pain were followed longitudinally. The type I pedicle marrow changes resolved in 17 patients but persisted in 5. Self-reported pain scores tended to improve over time with concordant resolution of marrow signal intensity, but this was not statistically significant – functional improvement was. Of the 17 patients with resolution of the type I marrow change, 6 converted to type II and 11 turned to normal marrow signal. This result suggests that the pedicle marrow type I conversion to a normal or type II appearance is associated with improved symptoms [31].

While the data is strong that there is a mechanical etiology to many of these marrow changes, there is a growing body of literature that suggests that in some there is a true infectious or inflammatory cause [32]. Multiple authors have observed a variety of inflammatory mediators in association with degenerative marrow changes. Burke et al. [21] observed an increase in proinflammatory mediators such as interleukin-6, interleukin-8, and prostaglandin E-2 in the disks of patients with type I marrow changes and in patients undergoing fusion for LBP. Ohtori et al. [33] found that the cartilaginous end plates of patients with type I marrow changes had more protein gene product (PGP) 9.5 immunoreactive nerve fibers and tumor necrosis factor (TNF) immunoreactive cells than those with normal end plates. PGP 9.5 immunoreactivity was seen exclusively in patients with diskogenic LBP. TNF immunoreactive cells in end plates with type I marrow changes were higher than those with type II marrow changes. These authors concluded that type I marrow changes represented a more active inflammation by mediated proinflammatory cytokines, whereas type II and type III changes appeared to be more quiescent [3]. Korhonen [34] in a study of infliximab, a monoclonal antibody against TNF-alpha, suggests it was most effective when there were degenerative type I marrow changes at the symptomatic level. Nevertheless, the relationship to immunobiologic and cellular response mechanisms, while probably important, remains unclear.