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Fundamentals of Intervertebral Disc Degeneration

Intervertebral Disc Degeneration

Goal of the Study?

In this review article from the Annals of Weill Cornell Neurological Surgery1 the authors’ goals were twofold:  a) Cover the underlying pathophysiology and risk factors of Degenerative Disc Disease and b) Provide a comprehensive summary of the development, structural, radiological and biomechanical properties of human Intervertebral discs.

 

Why are they doing this study?

The loss of the delicate balance between the two processes, Catabolic (Separation of components, releasing energy) and Anabolic (combining components, requiring energy) in InterVertebral Discs (IVD), signals the onset of Degenerative Disc Disease (DDD).  Risk factors such as genetics, aging, smoking and obesity accelerate the catabolic process, which can lead to drastic changes in the IVD such as decreased nutrient availability, structural changes, inflammation and ultimately back pain.  These changes occur in the extracellular matrix of the disc and compromise the anatomical structures and normal functions of the IVD. 

 

 

What was done?

In this review of the current literature, the authors outlined the pathophysiology of intervertebral disc degeneration, focusing on the differences between diseased discs and healthy discs.  An IVD consists of three anatomically distinct components; the gelatinous Nucleus Pulposus (NP) Core, the concentric Annulus Fibrosus (AF) layers surrounding the NP and the Cartilaginous EndPlates (CEPs).  In a young, healthy adult, the boundary between the NP and AF is distinct and highly organized.  The CEPs efficiently provide nutrients and oxygen to the NP and AF.  In patients with degenerated discs, the CEPs undergo structural changes such as ossification and porosity that impair their efficient transportation of essential nutrients to the discs.

 

What did they find?

From existing literature, it appears that only a small fraction of LBP can be attributed to a specific etiology such as osteoporosis, infections, fractures, structural deformity, neoplasms, radiculopathy or cauda equina syndrome.  It seems that over 85% of the DDD cases can not be attributed to a specific cause.  They also found that MRI findings consistent with high Pfirrman grades or significant Modic changes do not correlate well with the intensity or progression of chronic LBP.  They conclude that the direct associations between radiographic findings of DDD and chronic LBP remain unclear.

It also appears that current treatments for LBP and Lumbar Disc herniation (LDH), such as physical therapy, pain medication and surgical intervention, tend to treat the patients’ symptoms but do not treat the underlying disease in the disc.  As a result, newer biological treatments such as gene therapy, growth factors, stem cell injections and tissue-engineered methods are gaining popularity for their potential to restore the degenerated IVDs.

 

Why do these findings matter?

The socioeconomic consequences of Lower Back Pain (LBP) are severe and estimated to be in the neighbourhood of $100 billion per year in the USA alone.  Intervertebral disc degeneration and herniation is one of the leading causes of LBP.  Understanding the complex and numerous mechanisms that give rise to lumbar Degenerative Disc Disease is critical in designing novel therapies such as cell-based treatment, which aim to not only halt the DDD but reverse its damaging effects.  The ultimate goal being to restore the integrity and biomechanical function of the IVD.

 

At Dynamic Disc Designs, we have developed realistic intervertebral disc disease models to help explain to patients that suffer from related symptoms why, and what to do about it. Our models are used by thousands of doctors, chiropractors and other health care practitioners around the world.

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  1. […] rate cyclic loading at 2-second intervals demonstrated regeneration in the degenerated induced […]

  2. […] and natural physiological changes associated with aging, it is not possible to associate increased innervation solely with […]

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