Lumbar osteochondrosis

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We use the term lumbar osteochondrosis to describe degenerative changes to the end plates of the vertebral body. The starting point is mechanical overload caused by intervertebral disc damage and degeneration.

End plate changes in the context of Scheuermann’s disease are also osteochondrotic lesions. However, these are due to an imbalance between pressure load and resistance of the end plates during ossification. They are not discussed here.

Natural course

In animal experiments, an osteochondrotic lesion could be seen after approx. 6-12 weeks after injecting chymopapain into healthy intervertebral discs.¹

The acute stage corresponds to bone marrow edema in the adjacent vertebral body endplate area, which can undergo fatty conversion over a period of 1-3 years and thus heal. The progression through these stages can be visualized by magnetic resonance imaging as so-called MODIC changes ²:

MODIC Changes of intervertebral endplates

Histologically, the progression from MODIC I to MODIC II and III is characterized by destruction of the cartilaginous endplate part with destruction of the intervertebral disc and increasing sclerosis of the endplate. Repair processes with sprouting of vessels and nerve fibers have been observed in this stage. It is postulated that this sprouting is the morphological basis for the development of discogenic pain. ³

The natural course is influenced by the general metabolic situation (blood circulation → smokers) as well as by interim complications (infection → spondylodiscitis) and instabilities (vacuum phenomenon, pseudospondylolisthesis).

Pathophysiology

The development of the inflammatory reaction is still not fully understood. It is possible that different pathways exist.

Mechanical damage

Disc degeneration (whether acute or chronic) is associated with a loss of height, which can be explained by a decrease in swellable material (aggrecan). The cartilaginous endplates are exposed to increased shear forces due to the continuous loading of the segment, which can lead to fissures into the bony interface.

Metabolic damage

The mechanical overloading of the bone leads to sclerosis, which per se worsens the local blood supply situation. In smokers, it can be assumed that there is an additional lack of blood flow, which massively restricts the diffusion of nutrients into the disc and leads to the death of the nucleus pulposus cells (NP cells). This results in a lack of aggrecan producers and the disc dries up.

In osteoporosis, damage to the sinusoidal trabecular structure results in a deficient supply to the endplate area and, consequently, to the adjacent intervertebral disc. → Article on intervertebral disc changes in osteoporosis.

Immunological reaction

The immunological response can be easily observed in the MODIC-I changes as bone marrow edema. It occurs when the nucleus pulposus tissue, which is otherwise protected from the immune system, comes into contact with the perfused bone. The immune response triggered here suggests an autoimmunological pathway. ⁴

Pathophysiology of osteochondrosis and associated inflammation.

Infection

In individual studies, bacterial contamination, particularly with Cutibacterium Acnes, was confirmed in more than 50% of the intraoperatively obtained herniated discs. This colonization was only seen in cases with a corresponding osteochondrotic MODIC type I reaction. The transition to spondylodiscitis could therefore be a fluid one. However, these data are also contrasted with multicentric data that were able to rule out bacterial colonization in the majority of cases. ⁵

Epidemiology

The prevalence of MODIC changes in the general population is 6%, in the population of back pain patients >40%. ⁶

Only MODIC type I changes are of clinical significance, as only they have been shown to be associated with back pain. The grading of the degree of bone marrow edema is also important here. This correlates positively with the extent of the pain.⁷

Graduation of MODIC changes according to the extent of vertebral body edema.

Clinic

Patients typically describe a breakthrough sensation, especially when standing for long periods. The main symptoms are back pain, sometimes also leg pain. If there is also instability, the symptoms can sometimes also exacerbate at night (=after exertion).

Tests of the anterior column (heel drop pain, axial compression) are usually positive, sometimes the segments are also locally painful due to pressure. The pain can usually also be provoked by rotation in this segment.

Diagnostics

A comprehensive picture of the metabolic situation of the intervertebral disc and end plates can only be obtained through a combination of magnetic resonance imaging and radiographic diagnostics.

MRI

The magnetic resonance imaging sequence is well described by the MODIC changes:

MODIC I: Edema. T2 light, T1 dark
MODIC II: greasy conversion. T2 less bright, T1 bright
MODIC III: Sclerosis. T2 and T1 dark

Spondylodiscitis can also be considered in the differential diagnosis of MODIC I changes. Differentiation is possible here by means of contrast agent application, which is useful for diagnosing the extent of abscesses. However, valuable information for differentiation can also be obtained from X-ray images.

X-ray

X-rays of the lumbar spine should be taken in a standing position, as valuable information on the mechanics can be read off here. If necessary, functional radiographs should be taken with the patient lying down, as a greater amplitude of movement can be observed here.

In particular, the following should be considered:

Contour of the end plates. If the end plates cannot be delimited, it could be spondylodiscitis after all
Vertebral body deformation due to fracture as the reason for the edematous endplate change
Vacuum phenomenon. A vacuum phenomenon is an expression of the final stage of disc destruction. Intraoperatively, an empty disc space is found here. The vacuum phenomenon also indicates the lack of stabilization of the degeneratively damaged segment.
Pseudolisthesis, scoliotic tilting, pathol. Hypermobility (>8° segmental mobility in the functional images) with a damaged intervertebral disc

Therapy

Therapy is only rarely planned for the treatment of osteochondrosis alone, as these lesions can also be clinically silent. Particularly in the case of multi-segmental changes, it may be difficult to identify the affected level clinically and also via infiltration testing.

Indications for adequate treatment planning come from the morphological and, if necessary, clinically leading concomitant pathology:

Stenosis: dermatome-related, claudication, neurology
Instability: radiographic evidence

If no index segments or underlying concomitant pathology can be identified from the current findings, follow-up images (e.g. in the case of deg. de novo scoliosis) or the comparison of prone and upright images may provide further valuable information.

According to the complete diagnosis made here, a prognosis (including knowledge of the natural course of the disease) and a treatment proposal should be made.

Conservative therapy includes supportive measures such as a lumbar brace. The analgesic benefit outweighs any possible side effects (?muscle atrophy). It has also been shown that this measure can reduce periods of incapacity for work. ⁸

Heterogeneous picture of possible treatment options for osteochondrosis. From Jensen et al. 2011 ⁹

Overall, there is no conclusive picture of the optimal form of treatment if one is guided by osteochondrosis alone. It is therefore essential – especially when surgical measures are involved – to identify a leading concomitant pathology on the basis of which further steps can be planned.

Lumbar osteochondrosis

Natural course