A study 1examining cadaveric intervertebral discs (IVD) indicates disc degeneration is more closely related to reduced pressure associated with mechanical loading than levels of endplate porosity or thickness. Though endplate porosity increases as the IVD degenerates, the results of the study demonstrated that IVD degeneration is caused by reduced pressure in the nucleus—not the reduction of nutrient transport caused by endplate thickening and a reduction of porosity—and that mechanical loading from nearby discs contributes to endplate porosity in age-related disc degeneration.
What’s at Stake?
Understanding the role of IVD endplate thickness and porosity and the role of mechanical loading, age, and sex on determining the efficacy of endplate function is important in the future diagnosis and treatment of disc degeneration. The enervated endplates, when damaged or degenerated, can cause back pain. When properly functioning, they are responsible for the transport of nutrients to the IVD, regulate fluid pressure and metabolite transport between the body of the vertebrae and its nucleus. Disruption in this process can contribute to disc degeneration, inflammation in the vertebrae, and possible infection to the disc.
The level of porosity inside the bony endplates affects the amount of nutrients delivered to the nucleus and the mechanical stability of the vertebrae. A porous endplate allows more nutrients and pressure-regulating fluid to flow into the nucleus of the IVD. A thickened, less porous endplate reduces the nutrient and fluid flow, but creates more structural stability in the IVD, reducing the potential for injury. The proper balance and porosity of the IVD unit is integral to the overall health of the disc, but understanding the mechanism by which the degenerative process occurs is essential in anticipating how a body’s mechanical functions might contribute to a disruption of disc health.
Researchers compared the relative thickness and porosity of IVD endplates in 40 cadaveric motion segments from 23 cadavers between the ages 48 to 98 years old. The segments were subjected to compression, and the intradiscal stresses were measured and analyzed. Stress profiles were created to determine the average nucleus pressure, as well as the maximum anterior and posterior annulus pressure. The segments were dissected, and discs with endplates on each side were scanned and analyzed for their thickness and porosity in the midsagittal regions. An average value was calculated for the anterior, central, and posterior regions of each of the endplates. A macroscopic and microscopic examination determined the scope and level of disc degeneration in each segment.
The results of the data sets indicated that nucleus pressure and posterior and anterior annular stresses decreased as the disc degeneration levels increased. There was a slight increase of intradiscal pressure (IDP) with age, but there was no maximum stress increase of the annulus with age. Lower spinal levels were associated with a decrease in IDP.
The endplates were thinner nearer the nucleus, with a 14 % reduction in thickness in the inferior endplates. An analysis of the averaged data set from the three regions of both endplates showed no association between age or level of degeneration and endplate thickness, but there was an inverse relationship between the disc degeneration and endplate thickness. There was a strong relationship between endplate thickness and IDP in an analysis of adjacent discs.
Endplate porosity was more pronounced in the center of the endplate and became less so opposite the annulus. This porosity was not age-dependent but—with the exception of the anterior endplate region— was positively correlated with disc degeneration levels. The levels of endplate porosity was inversely associated with adjacent disc pressure and stress.
Endplate thickness was the major determinant of endplate porosity levels. Disc degeneration and mechanical loading measures were also indicated as predictors. The most apparent predictors of endplate thickness (after porosity) included disc pressure and spinal level. IDP was the dominant predictor of disc degeneration.
The study found that disc degeneration was associated most often by disc stress, rather than porosity of the endplate or its thickness. As the levels of disc degeneration increased, porosity of the endplate increased. The porosity of the adjacent disc was inversely affected in terms of pressure and mechanical stress.
Wolff’s law posits that the body’s bone mass and design will compensate for the pressures of mechanical stresses and subsequent anatomical deformation, strengthening the endplates and vertebrae that are subjected to the most physical activity. Reduced loading can thin endplates that are not subjected to pressure. This eventually leads to them becoming more porous. The results of this study affirm this theory, as the lower central endplate regions were harder, thicker, and stronger than those of the anterior-posterior endplate regions. There is an apparent compromise between the strength of the outer bone and the porosity of the central endplate, which allows for stability and nutrient flow where they are needed the most.
There is an evident drop in nucleus pressure during progressive disc degeneration. The reduction of fluid pressure lessons the endplate’s thickness and makes it more porous, leading to bone degeneration and loss. The bone is more likely to buckle and further degrade as it becomes more porous and less stable, reducing nucleus pressure further. This cycle of abnormal pressure reduction is responsible for the continuation of the degenerative process—not the reduced metabolite transport. There is an increased risk of bone fracture with increased porosity and endplate thinning. A fracture would increase stress on the IVD and contribute to the cycle of degeneration, in spite of the increased availability of nutrients that can reach the nucleus through the endplate’s porosity.