Some time ago, a question came up in the member discussion forum at FixYourOwnBack.com as to whether extruded lumbar disc herniations “went away” or whether they remained in the epidural space. This coincided with an older paper (Haro, 2000) that was discussed on Facebook as the potential mechanism for resorption of extruded disc fragments. I thought that would be a good topic to flesh out a bit with a literature search. I’ll attempt to summarize my reading of the past 13 years of investigation into this topic. In direct response to the above question, “Yes, resorption of the extruded herniated disc fragments is part of the natural history of disc injury.” The amount of time that takes to happen varies from person to person but here are a few cullings from several studies:
- Follow up MRI 6-12 months after initial injury demonstrates about 50% of patients see about 70% decrease in size of extruded material. (Fagerlund, 1990, Maigne, 1992, Bush, 1992; Jensen, 1996; Autio, 2006; Monument 2011)
- In a retrospective cohort study, Saal and Saal demonstrated that lumbar disc herniation with radiculopathy can be successfully treated nonoperatively, with nonoperative treatment resulting in “good to excellent” outcomes for approximately 90% of patients. (Saal, 1996)
- MRI findings lag behind improvement of leg symptoms (Ito, 1996)
- Larger extrusions and sequestrations are more likely to resorb. (Maigne 1992, Bush 1992, Jensen 1996)
That last point is interesting as all too often patients report to me that their neurosurgeon suggested surgery because to the large size of the herniated disc fragment. This is somewhat understandable as often a large herniation can cause not only chemical irritation of the nerve root (due to inflammation) but also mechanical compression of the nerve root. Often intense pain in the leg accompanies this scenario and sometimes motor weakness as well. Years ago, more than 3 days of progressive motor weakness in these cases drove the clinical decision to decompress the nerve surgically. These days, this 2011 review article sums it up the current “gray” zone we are in… “In the absence of serious neurologic deficits or for persistent non-radicular low back pain, consensus whether surgery is useful or not has not yet been established. Furthermore, the timing of the intervention with respect to prolonged conservative care has not been evaluated properly.” (Jacobs, 2011) In their review of randomized controlled trials comparing various interventions for herniated lumbar disc injury with sciatica Jacobs, et al found that after 1 year, there was no difference between surgical vs. conservative interventions. The primary benefit in surgery was quicker relief of the leg pain, with average time before resolution of leg pain averaging 4 weeks in quick surgical interventions, vs. 12 weeks for conservative care. For those who opt for conservative care and want to know how they can help the process of resorption of the herniated disc material, we are still learning what those variables are. One clear thing to not do is smoke. Tsarouhas et al in 2011 showed that smoking resulted in more severe pain with disc injury, longer time for resorption of herniated disc material and smokers have a longer duration of symptoms. Many might wonder what the actual mechanism is for resorption of an extruded disc. That discussion gets a bit technical with histochemistry and biochemistry. For those that are interested, let’s “suit up” and get to it!
The Role of Macrophages and Matrix Metalloproteinases (MMPs) in Disc Resorption
Remember those Pac-Man-like things under the microscope in cell biology class that were called macrophages? As it turns out, these differentiated white blood cells (WBC) play a key role in the process. In a very amoeba-like fashion, they sidle up to the extruded annulus and get to work with a toolbox of cytokines and proteolytic enzymes. Some of these macrophages are residents in a normal disc; others arrive if blood vessels in the outer third of the annulus or in the vertebral endplate are disrupted. The more blood vessels that are disrupted, the more macrophages that are on the scene. While we’re still learning a lot about this process, it resembles a lot of other common inflammatory cascades. Among the enzymes that the macrophages bring that have been studied a bit more, are the matrix metalloproteinases (MMPs)
At present, about 24 of these proteolytic enzymes have been discovered and they come not only from macrophages but also from chondrocytes in the disc. I like to think of the different MMPs as different types of cleaners you might use around the house. Maybe you use 409 to clean your kitchen counters, Windex to clean your windows, Clorox to brighten your white clothes and Tide to clean the color garments. Some of those cleaners in certain combinations might not be a good idea for health (ammonia in the Windex + bleach=chlorine gas) and we’ll discuss that analogy a bit more in a minute. Also, you might be able to get a really dirty window cleaner with 409, but Windex will be superior to get the job done. You get the drift? So those 24 MMPs have been divided up into groups depending on their function. 1. Collagenases (MMPs-1, -8, -13 and -18)– the only enzymes that can cleave intact interstitial collagen molecules. 2.Gelatinases (MMPs-2 and -9)–degrade denatured collagen molecules and basement membrane collagens. 3. Stromelysins (MMPs-3, -10 and -11)– cleaves cartilage matrix components, including aggrecan, proteoglycans, and fibronectin. 4. Membrane-type MMPs (MMPs-14, -16, -17 and -18)–responsible for the activation of other MMPs, but only play a secondary role in direct matrix degradation. One interesting finding is that a few of these MMPs are present in low quantities in even normal and young discs. As the disc shows signs of increased degeneration, the amount of MMPs and the variety of MMPs increases. So, if MMPs are needed to clean up a herniated disc, then more must be better…right? Well hold on sparky. These are catabolic proteins, they break stuff down. We have known since the late ‘90s that they are present in greater quantities in degenerated discs, and some suspect that their very presence is the CAUSE of the disc degeneration. As in most bodily reactions, a catabolic agent has an anabolic partner and homeostasis is maintained when we balance those reactions. It seems that when the scale tilts toward the catabolic agents, that’s when we see increased disc degeneration. At least that’s what the correlational studies suggest. Of course you can’t extrapolate causation from a correlation. It could be that the upregulation of MMPs is reflective of a response to injury (essentially a normal inflammatory response) rather than being the cause of the observed degeneration.
Current investigations into MMPs are attempting to manipulate the ratio of catabolic MMPs vs. anabolic agents. Some are also investigating the lifestyle issues that are correlated with low back pain, disc degeneration and with upregulation of certain MMPs. Among those lifestyle items that have been associated with higher levels of degeneration and with higher levels of MMP in the disc is hard physical labor, especially when it involves frequent lifting. The researchers often infer that that lifting equates only compressive load without regard to other vectors of load like torsion and shear. Adams demonstrated to us in 1982 that even in vivo discs are remarkably resistant to pure compressive force but they prolapse with additional flexion + compression. I personally think that an area worthy of investigation is in HOW the disc is compressed. Most of the studies I’m aware of infer compressive load by lifestyle questionnaires looking for employment that involves heavy physical loading of the discs. Some of that sample likely lifts with maintenance of the lumbar lordosis and some likely don’t. I suspect that those that don’t with the inherent flexion + compression moment on the disc, will experience more LBP and more disc degeneration. Indeed, I have noted for years the presence of habitual lumbar hinging (flexion + compression) with naïve and loaded movements toward the floor. Correction of this lumbar hinge by training a hip hinge stereotype has proven to be a remarkably simple intervention to help these painful backs improve.
In regards to disc resorption, what are we left with? The natural history after disc herniation is for resorption to occur at varying speeds and degrees dependent on a variety of other lifestyle factors. If you want to improve the resorption process, don’t smoke, exercise moderately but limit heavy physical labor. We still have more investigation to do on the specifics of dose and type of “physical labor” and “lifting”. As that comes up in the literature, I’ll try to keep you posted. Be well, and if you want my personal advice based on clinical experience…hip hinge when you bend towards the floor. If you need help figuring out how to do that hip hinge thingy, go here…
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