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Disc Degeneration (aka: Degenerative Disc Disease)
The second thing that needs to be said is that there is still quite a debate over the origin Disc Degeneration (DD). Some feel that DD is inevitable in every spine and it's an extension of the natural ageing process of the disc. Others, including the number one Functional anatomist in the world, Dr. Nikolai Bogduk, feels that DD is NOT part of normal disc ageing but is an acquired condition with occurs as the result of structural damage and structural failure of the disc and/or vertebral end-plate. Therefore I will describe DD in terms of 'structural change' which affect the disc and are often the origin of discogenic pain. The first two photos are cadaver photos of two lumbar discs, vertebrae included. The photo on the left shows two normal and healthy discs. The right photo demonstrates moderate to severe Disc Degeneration. Note the desiccated and thinned discs, and anterior end-plate collapse. These are the tell-tale signs of DD. A basic understanding: DD is a condition of the intervertebral disc/s of the spine which is now believed to begin as a non-painful injury to the disc or vertebrae. Once set in motion, DD will sometimes progressively worsen and cause a change in the normal structure and make-up of the disc. Specifically, DD will lead to a progressive dehydration (desiccation, or drying out) of the disc which in turn leads to a thinning and weakening of the disc itself. This structural weakening is what gets us in trouble, for this weakening may allow the inner nucleus to herniate' its way out of the disc through developing 'anular tears'. When the nuclear material gets close to the outside of the disc, extreme discogenic pain may occur. The situation may worsen more by the nuclear material completely braking out of the disc and directly pinching and/or chemically irritating the sensitive neural structures which lye to the rear of the disc.
Who may develop Disc Degeneration? Researchers Battie et al. and Sambrook et al. have both confirmed that genetic inheritance plays a huge role in DD. In their award winning research, they concluded that 70% of DD cases are statistically genetically determined! To translate this into laymen's terms, this means that 70% of patient of DD sufferers may have been passed bad genes from their parents which have lead to the development of DD. The Genes do NOT cause DD directly but do so indirectly by produce sub-standard disc materials (proteoglycans and collagen) which leave the discs vulnerable to loading injuries at relatively light weights. (Sambrook PN, et al. Arthritis Rheum. 1999 Feb;42(2):366-72), (Battie MC, et al. Spine 1995 'Volvo Award for science',15;20(24): 2601-12) The type of work you do may also predispose you to the occurrence of DD. Jobs that require very heavy lifting, repetitive bending, repetitive twisting, and even 'vibration' type jobs also have a high association with DD. Dancers, Rodeo Cowboys, American Football players, and weight lifting athletes are also much more likely to develop DD (Videman T, et al. Spine. 1995 Mar 15;20(6):699-709). I am probably a statistic in this last study.
Cigarette smoking and any disc condition is just a bad idea. In her first Volvo Award winning study in 1991, Dr. Battie confirmed that smokers rate of DD was significantly higher than that of non-smokers (Battie MC, et al. 'Volvo award Science' 'smoking & lumbar IVD degeneration' Spine 1991 Sep;16(9):1015-21). Currently most neurosurgeons will not even perform spinal surgery on you until you have quite your habit for three months. Smoking seems to further impede the already terrible blood supply to the disc. The Origin of Disc Degeneration: Kirkaldy-Willis's Three Phases of Degeneration: The first theory of DD occurred back in the 1970s. "The Degenerative Cascade", was then proposed by the famous Dr. Kirkaldy-Willis MD. He recently describes 'three phases of degeneration' (1999) summarizes this as follows: Recurrent strains will cause small circumferential tears in the anulus. These circumferential tears coalesce with time and eventually form radial anular tears which give the nucleus a path to the outer - pain sensitive - anulus. In more time the disc may become completely disrupted - torn form front to back and side to side. A loss of disc height will begin as the degeneration process continues - mostly from a loss of proteoglycans. In the later stages of degeneration the disc may be virtually nonexistent, paper thin mass of fibrous tissue. In the very final stages severe disc reabsorption will occur and may even cause complete bony ankylosis (Kirkaldy-Willis WH, Bernard T, "Managing Low Back Pain - 4th edition; 1999). In modern times there are three other theories floating around, all of which are based upon the belief that micro-damage to the vertebral end-plates lead to degeneration of the nucleus. The first theorizes that an out of control nuclear inflammation reaction destroys the nucleus after the vertebral end-plate repair process had begun. Kind of an 'inflammation goes wild' type of situation. The second theorizes than an out of control autoimmune reaction destroyed the nucleus. It was felt the fracture of the end-plate exposed the virgin nucleus to the immune system of the body for the first time. Since the nucleus is avascular (has no blood supply) the immune system has never seen it before and therefore does not recognize it and attacks it. This particular theory seems to be on its way out for other studies have been disproving it. Bogduk's Theory of Disc Degeneration Evolution.
Figure #3: This demonstrates how a healthy disc distributes axial load evenly over the disc. Note how the healthy nucleus (pink) carries its share of the downward axial load of the body and pushes outward on the anulus - standing them up so to speak. In this configuration the anulus is at its maximum strength. The anulus relies on this high hydrostatic pressure within the nucleus and any drop in this pressure will structurally disrupt the disc.
This 'increased axial load' upon the anulus triggers a train of biochemical events (namely increased action of MMP's) that weaken's the anulus severely. Anular tears will now begin and finally we may begin to experience pain. That is enough for this page. I have included a page that take Dr. Bogduk's theories much deep for those of you who really want to understand this degeneration process. The next pages will discuss further end-stages of Disc Degeneration, beginning with anular tears and disc herniations. |
The
first thing that needs to be addressed is the actual term "degenerative
disc disease". This is a terribly confusing term that should be
completely done away with! Neither recent medical text books nor
any of the latest research papers use the term degenerative disc disease
(aka: DDD). Instead, modern researchers use the terms 'Disc
Degeneration' or 'Disc Degradation' which are the terms I will use as
well.
Figure
#1 DD can be easily identified on MRI (weighted T2 scan)
by the presents of very black looking disc/s. The blackness is
the result of the discs lost water content (desiccation). A normal
healthy disc appears very white on MRI because of the very high water
content. Structural damage to the vertebral end-plates or outer
fibers of the disc (anulus fibrosus) may also be seen. is a sagittal
'weighted T2 MRI' view of a 31 year old patient who has been suffering
lower back pain and lower extremity pains for 14 months. Note the
severely blackened (desiccated) L5 disc (white arrow) and the two white,
normal and healthy discs above. This is an example of moderate DD of
the L5 disc. Signs of structural disruption (damage) of the disc
are also visualized by the presents of a white HIZ lesion (black arrow)
in the back of that same disc. 
I
believe my DD and subsequent disc disruption, was the result of 11 years
of intense weight training and Olympic Level Hammer throwing. You
can plainly see past end-plate damage (Figure
2) on my recent T1 MRI, as well as DD throughout my
entire lumbar spine. This type of end-plate structural damage is
classified as a 'depression end-plate fracture' as classified by
The
third theory championed by Dr. Nikolai Bogduk MD, paints a much more
likely scenario. In a nut shell, he feels that sudden decrease
in nucleus hydrostatic pressure, which occurs as a result of End-Plate
fracture/indention or inner Anulus disruption, causes a series of inappropriate
cell-mediated responses within both the nucleus and anulus. These
inappropriate responses cause a progressive drying-out of the nucleus,
and a weakening of the anulus. The whole key of DD is a shift in
stress loads upon the disc
Figure
#4: Trauma has induced a micro-fracture of the vertebral
end-plate. An 'end-plate herniation' (aka: Schmorl's Node') has
occurred (pink arrow) into the end-plate defect and resulted in 'structural
change'. An instantaneous increase in nucleus volume occurs which
in turn decreases the nucleus hydrostatic pressure - like popping a
balloon. Now the nucleus does not have the pressure to stand up
the inner anulus and it collapses inward. The result is more structural
change as the inner anulus collapses inward. Now the disc no longer
has an even weight distribution and the anulus gets 'over-loaded'.