disc inflammation

Disc Injury Triggers Neurogenic Inflammation of Adjacent Healthy Discs

More frequently than you may know, adults suffer from severe lower back pain that may sometimes incapacitate them. When spine discs degenerate, it is one of the most common clinically discovered causes of low back pain. 

Researchers are still working to understand fully how disc degeneration causes pain. However, some scientists think that inflammation from damaged discs, when it affects the nerve endings around the disc, the body translates it to pain affecting adjacent discs.1

disc inflammation

Disc Degeneration and Inflammation

Interleukin-1beta (IL-1β) and interleukin-6 (IL-6) are molecules actively involved in the body’s immunological response, resulting in pain and swelling. Researchers discovered that the injured disc generated these molecules. 

Surprisingly, the disc next to the damaged disc presented inflammation despite not being primarily injured. Scientists suspect that the release of neuropeptides like substance P and calcitonin gene-related peptide are responsible.

Study Methods

The researchers used male Sprague-Dawley rats for the study. The rats were divided into three groups: a sham group, a disc injury group, and a disc injury + TrkA antagonist group. The sham group rats underwent anesthesia and skin puncture but no disc injury. The disc injury group rats had a needle inserted into one of their tail discs. The disc injury + TrkA antagonist group rats received an injection of a drug that blocks the TrkA pathway before undergoing disc injury.

The researchers examined the rats at several time points after the disc injury. They collected tissue samples from the injured disc and the adjacent one. They then used various methods to measure the levels of inflammatory molecules, neuropeptides, and other molecules involved in disc degeneration.

 

 

Key Findings

The study found that the levels of the inflammatory molecules peaked on the first day after injury and then decreased over time.

Interestingly, the adjacent disc also showed inflammation. Similar quantities of inflammatory molecules were found in the two discs, indicating that the damaged disc could produce substances inflaming the healthy disc.

The researchers raised the possibility that neuropeptides like CGRP and SP are to blame for this behaviour. They discovered that, following injury, there were higher amounts of these neuropeptides in both the damaged and healthy discs. Since neuropeptides can pass through nerves, the researchers think that neuropeptides from the injured disc may be moving to the healthy disc and causing inflammation.

The study also examined the TrkA pathway. TrkA is a receptor for NGF, a molecule involved in pain signalling. The researchers found that the levels of TrkA were elevated in both the injured disc and the healthy disc after injury. This suggests that the neuropeptides released by the injured disc may activate the TrkA pathway in the healthy disc, further contributing to inflammation.

Implications for Treatment

The study also investigated the potential of targeting the TrkA pathway for treating disc degeneration. The researchers gave a TrkA antagonist drug to one group of rats before damaging their discs. They found that in both discs, the TrkA antagonist lowered the amounts of inflammatory chemicals and neuropeptides, meaning that a possible treatment approach for disc degeneration and back pain might involve inhibiting the TrkA pathway.

Discussion and Clinical Implications

This study affirmed that neurogenic inflammation significantly causes disc degeneration and back pain. Injured discs release neuropeptides that cause inflammation in healthy discs, damaging the disc and leading to pain.

The therapy of low back pain may be affected by these findings. Pain management and preventing future disc degeneration may be aided by medications that inhibit the TrkA pathway or other components of neurogenic inflammation. To create and evaluate these treatments on people, further study is necessary.

Limitations of the Study

The study used a rat model of disc degeneration, and it is important to note that this may not perfectly reflect what happens in humans. Rats have different spinal anatomy and pain mechanisms compared to humans. Additionally, the study only looked at the short-term effects of disc injury. It must be clear how these processes would play out over a longer period in a human spine.

Another limitation is that the study focused on disc degeneration caused by injury. However, disc degeneration can also be caused by other factors, such as aging and wear and tear. It is unclear whether neurogenic inflammation plays the same role in these cases.

Future Research

Scientists will need to do further research to determine exactly how much neurogenic inflammation is involved in low back pain and disc degeneration. They also need to uncover the therapies that hinder neurogenic inflammation and see how effective they are in humans compared to the rats in this experiment.

Also, studies need to be carried out on other variables that significantly cause disc generation and how they relate to neurogenic inflammation.