An intervertebral disc serves as a cushion between each of the vertebrae in the spinal column. The discs have a strong outer layer of collagen fiber that provides support (the annulus fibrosus) and a gel-like center that provides the cushioning (the nucleus pulposus).
A bulging disc occurs when the nucleus pulposus loses its structural integrity but remains within the annulus fibrosus. A herniated disc occurs when there is a tear in the annulus fibrosus causing the gel-like substance to leak through. The budged or herniated disc could cause abnormal pressure against the spinal nerve, and a patient may experience a range of symptoms including pain, numbness, tingling, burning, and weakness in certain areas depending on the location of the disc. In some cases, a patient may experience severe pain even in the absence of nerve root compression due to the nucleus pulposus releasing inflammatory chemical mediators.
The lumbar region of the spine is the most common for disc herniation with more than 90% located in the L4-L5 or L5-S1 regions. Although the main causes of a bulging and herniated disc are mechanical stress and physical injury, the disc degeneration has often occurred before hand rendering the disc more susceptible to any extra mechanical overload and more vulnerable to become bulged or herniated.
Cause of Disc Bulging and Herniation - Imbalance of Nutrient Supply and Demand
The nucleus pulposus undergo biomedical and phenotypic changes during aging and degeneration. For optimal function and survival, disc cells require a sufficient supply of nutrients and adequate removal of metabolic waste. Cells in the nucleus pulposus and the inner annulus fibrosus are often exposed to suboptimal microenvironments with low oxygen tension, limited glucose availability, relative low pH from lactic acid buildup, and high metabolic waste accumulation. Limited oxygen supply creates an avascular environment, ATP production from mitochondrion respiration was inhibited and disc cells predominately rely on glycolysis for energy production, which requires glucose although glucose supply is also limited and produces excessive amount of lactic acid. Low supply of nutrients and a decrease in pH thus affecting the ability of disc cells to synthesize and maintain the disc extracellular matrix and leads to disc degeneration.
One cause of reducing the nutritional supply is the calcification of the cartilaginous endplate, which is acting as a barrier of nutrient transport. Such calcification can be due to a loss of function of the matrix Gla protein caused by under carboxylation of the matrix Gla protein. Carboxylation of the matrix Gla protein in the chondrocyte is a Vitamin K dependent process. Liver produce bile which facilitate Vitamin K absorption. A liver deficiency can cause Vitamin deficiency and lead to under carboxylation of the matrix Gla protein.
Another factor affecting the nutritional supply is vasoactive drugs such as Norepinephrine that obstruct blood supply to the vertebral column or the capillary beds of the endplate. Post-contrast MRI studies of human intervertebral discs found that signal intensity increased inside the disc after administration of vasoactive drugs.
Increased cellular demand can also cause nutrient depletion. An increase in cellular consumption can be caused by cytokines and increased growth factor levels. Moderate levels of growth factors are essential for maintaining a healthy disc. Growth factors, such as basic fibroblast growth factor (bFGF), transforming growth factor (TGF) and insulin-like growth factor (IGF), stimulate the chondrocyte or fibroblast to produce more matrix and inhibit the production of the matrix metalloproteinases (MMPs). Cytokines, such as interleukin-1 (IL-1), interferon (IFN), and tumor necrosis factor- (TNF-) inhibit the synthesis of the matrix and promote the production of MMPs. These cytokines are produced by macrophages which enter the disc in response to injury. Macrophages also secrete superoxide (O-), which can degrade hyaluronic acid and proteoglycans, causing them to disaggregate, and can inhibit chondrocyte proliferation and synthesis. Upon loss of proteoglycans and an increased permeability of the matrix in degeneration increased levels of growth factors and cytokines infiltrate, affecting cellular metabolism and the balance between nutrient supply and demand causing the disc degeneration.
The effects of depleted nutrients and increased metabolites have a cumulative detrimental effect on survival of cells in the intervertebral disc as well as on the integrity of the disc matrix. The imbalance can fall to critical levels causing the disc degeneration. Such degeneration can reach a level that the disc can become very fragile and easily become herniated or bulged even under a normal load.
The ligaments including the Ligamentum Flavum, the Anterior Longitudinal Ligament and the Posterior Longitudinal Ligament are also important elements of the spine that hold the whole structure together. These ligament also rely on diffusion for nutrient supply. When the disc nutrients are under supply, the ligaments are also affected. Many herniated and bulging disc patients may also have chronic ligament injuries. Patients may still experience pain and muscle spasm in some case after the disc problem have been successfully treated.
