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Modic changes, possible causes and relation to low back pai.pdf

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Modic changes, possible causes and relation to low back pain

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H.B. Albert ^{, a,} , P. Kjaer^a, T.S. Jensen^a, J.S. Sorensen^a, T. Bendix^a and Claus Manniche^a

^aAll The Back Research Center, Part of Clinical Locomotion Science, University of Southern Denmark, Lindevej 5, 5750 Ringe, Denmark

Received 3 May 2007; 

accepted 4 May 2007. 

Available online 10 July 2007.

Summary

In patients with low back pain (LBP) it is only possible to diagnose a small proportion, (approximately 20%), on a patho-anatomical basis. Therefore, the identification of relevant LBP subgroups, preferably on a patho-anatomical basis, is strongly needed.

Signal changes on MRI in the vertebral body marrow adjacent to the end plates also known as Modic changes (MC) are common in patients with LBP (18–58%) and is strongly associated with LBP. In asymptomatic persons the preval‎ence is 12–13%. 

MC are divided into three different types. Type 1 consists of fibro vascular tissue, type 2 is yellow fat, and type 3 is sclerotic bone. The temporal evolution of MC is uncertain, but the time span is years.

Subchondral bone marrow signal changes associated with pain can be observed in different specific infectious, degenerative and immunological diseases such as osseous infections, osteoarthritis, ankylosing spondylitis and spondylarthritis. In the vertebrae, MC is seen in relation to vertebral fractures, spondylodiscitis, disc herniation, severe disc degeneration, injections with chymopapain, and acute Schmorl’s impressions.

The aim of this paper is to propose two possible pathogenetic mechanisms causing Modic changes. These are:

A mechanical cause: Degeneration of the disc causes loss of soft nuclear material, reduced disc height and hydrostatic pressure, which increases the shear forces on the endplates and micro fractures may occur. The observed MC could represent oedema secondary to the fracture and subsequent inflammation, or a result of an inflammatory process from a toxic stimulus from the nucleus pulposus that seeps through the fractures.

A bacterial cause: Following a tear in the outer fibres of the annulus e.g. disc herniation, new capilarisation and inflammation develop around the extruded nuclear material. Through this tissue it is possible for anaerobic bacteria to enter the anaerobic disc and in this environment cause a slowly developing low virulent infection. The MC could be the visible signs of the inflammation and oedema surrounding this infection, because the anaerobic bacteria cannot thrive in the highly aerobic environment of the MC type 1.

Perspectives: One or both of the described mechanisms can – if proven – be of significant importance for this specific subgroup of patients with LBP. Hence, it would be possible to give a more precise and relevant diagnosis to 20–50% of patients with LBP and enable in the development of efficient treatments which might be antibiotics, special rehabilitation programmes, rest, stabilizing exercise, or surgical fixation, depending on the underlying cause for the MC.

Helsinki, Finland: 28–29 June 2007

President: Dr P. Dolan

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MODIC CHANGES: THE PREVAL‎ENCE AND RELATIONSHIP TO LUMBAR DISC HERNIATION. A POSSIBLE NEW PATHOGENESIS OF LOW BACK PAIN

HB Albert; and C Manniche

The Back Research Centre, Part of Clinical Locomotion Science, University of Southern Denmark, Denmark

The study was founded by The Regional Institute of Health Sciences Research

Background: There is a need for identifying specific subgroups of LBP, Modic changes might be one of these subgroups. The aim is to describe the relationship between a previous herniated disc and the following Modic changes.

Methods: 181 patients with radicular pain below the knee, leg pain 3, duration of leg pain between 2 and 52 weeks, and age between 18 and 65 years were included. The patients were randomized into one of two active conservative treatment regimes lasting eight weeks. All included patients were scanned at baseline and again at 14 months follow-up. All MRI eval‎uation was carried out by the same experienced radiologist using a validated eval‎uation protocol.

Results: The preval‎ence of Modic changes type 1 increased more than 3 fold from 9 % at baseline to 29 % at follow-up; type 2 was respectively 14 % and 13 %. In patients with Modic changes at baseline, extremely few reduced in size or disappeared, on the contrary new type 1 changes developed after the herniation. In patients with a normal disc, 0 % developed Modic changes at follow-up, whereas in those with extrusions and sequestrations 56–63%. There exist a strong association between Modic changes and LBP, 67 % of those with Modic changes had LBP compared to 21 % of the patients without, OR 6.1, (p<0.0001).

Discussion: A lumbar disc herniation is a strong risk factor for developing Modic changes (especially type 1) during the following year. Furthermore, Modic changes are strongly associated with LBP.

Correspondence should be addressed to Mr J. O’Dowd, Honorary Secretary at SBPR c/o BOA, Royal College of Surgeons, 35–43 Lincoln’s Inn Fields, London, WC2A 3PE.