Research Review by Dr. Shawn Thistle©

Date:

Mar. 2007

Study Title:

Does facet inflammation induce radiculopathy? An investigation using a rat model of lumbar facet inflammation

Authors:

Tachihara H et al.

Publication Information:

Spine 2007; 32(4): 406-412.

Summary:

The relationship between herniated intervertebral discs and radiculopathy has been well established. Radicular pain associated with disc herniations is known to result from a combination of mechanical and chemical factors. Mechanically, disc degeneration or bulging in addition to extruded nucleus pulposus can physically compress a nerve root. Chemical mediators such as cytokines create an inflammatory cascade around the nerve root which can also cause radiculopathy. These two factors may coexist, but may occur in isolation.

Clinically, it has also been established that many patients with clear radiologic or advanced imaging evidence of nerve root compression experience no radicular symptoms, while others with seemingly no nerve root compromise on imaging do. Imaging studies on the general population and low back pain patients have demonstrated the lack of association between the presence of disc herniation and symptoms repeatedly. Similar evidence exists regarding spondylotic (degenerative) changes to the spine. Essentially, the prudent clinician must always remember to "..treat the patient, not the picture".

Facet joint spondylosis is a well documented pathological process that affects most people with age. It is well understood how structural changes in facet joints can mechanically compromise lumbar nerve roots (although as mentioned above, this does not always occur).

Recently, it has also been proposed that synovial inflammation of degenerating facets can create a chemical milieu similar to that of a herniated nucleus pulposus, which may lead to radicular pain and symptoms. Prior research on this particular topic has demonstrated that facet joint cartilage and synovioum contain inflammatory cytokines, one of the chemical mediators known to cause radiculopathy. What is not known is if inflammation in facet joints can reach the nerve roots to cause radiculopathy.

This study utilized a rat model to investigate this question. Many manual therapists would claim to have known this for years, despite a lack of supporting basic science or clinical evidence. (NOTE: There is evidence that lumbar facet joints can cause referred pain to the leg, foot and ankle - most are likely familiar with Bogduk's work in this area. This paper is investigating radiculopathy, not referred pain.)

This laboratory study utilized 130 female Sprague-Dawley rats that were divided into three groups:
  1. Arthritis Group (n = 60) - surgically induced facet inflammation was accomplished by inserting a gelatin sponge containing complete adjuvant into the L5-6 facet joint
  2. Control Group (n = 60) - a sponge containing saline solution was inserted surgically into the L5-6 facet joint
  3. Sham Group (n = 10) - a surgical incision was made through the L5-6 joint capsule, and was immediately sealed
At 1,3, 5, 7, 14, 21, and 28 days after surgery the rats underwent behavioural testing for mechanical allodynia. Sensitivity to non-noxious mechanical stimuli was tested by determining hind-paw withdrawal response using a previously validated technique (von Frey hair - Stoelting, Wood Dale IL). This technique involves acclimatizing the rats to a plastic cage for 15 minutes before touching the paw from below with the von Frey hair (basically a measurable filament of different "gauges") in the area innervated by the L5 nerve root. The main outcome measure was the 50% withdrawal threshold - representing the force of stimulation required to make the rat display pain behaviour (withdrawal) in 50% of trials.

Further, histochemical samples were taken at each measurement time to determine leukocyte infiltration into the epidural space, presence of cytokines and tumour necrosis factor alpha (TNF-α), and degenerative changes to the facet joint cartilage.

Pertinent Results:

  • animals in all three groups showed stable conditions before surgery in response to mechanical stimulation
  • a significant reduction in mechanical pain threshold was noted in the arthritis group on days 3, 5, and 7 compared to the other two groups
  • mechanical allodynia improved slowly over the 28-day period, but did not fully resolve
  • many inflammatory cells were present in the arthritis group at day 3, while very few were noted in the other groups (note from day 14 to 28 this difference was no longer significant)
  • macroscopic joint surface anomalies including erosions and abrasions, decreased cartilage matrix, hypocellularity, osteoblast proliferation, and hypertrophic synovium were noted in the arthritis group at day 3, while the control group cartilage was normal
  • the number of TNF-α positive neurons on days 1 and 3 was significantly larger in the arthritis group versus the control group

Conclusions & Practical Application:

In this study, surgically induced facet inflammation led to local inflammation that infiltrated the nerve root, degenerative changes to the facet, and signs of radiculopathy. This supports the hypothesis that inflammation from facet joints can reach the nerve roots, resulting in leg symptoms. It is also interesting to note that the chemical changes in this study correlated more closely with the allodynia than the degenerative changes. This may help to explain the inconsistent relationship noted above between imaging findings and symptomatology.

Animal models provide a starting point in the investigation of many medical conditions. Despite obvious limitations, they can provide useful insight into spinal pain. In this study a well designed animal model demonstrated the potential for facet joint inflammation to cause radiculopathy. Although future studies performed on humans would be ideal, this model would present many difficulties, and may not come to fruition. It is for this reason that manual therapists should be familiar with this type of research to gain a more in depth understanding of how these theories are developed and tested.

The interesting clinical application of this study is that radicular symptoms may be caused by disc pathology (herniation), or potentially by facet inflammation. Future studies should elucidate clinical methods to help clinicians distinguish between these two pathologies in order to appropriately guide treatment options.