The authors of a review
What’s at Stake
Chronic lower back pain (LBP) –particularly that due to intervertebral disc (IVD) disorders—is a frequent cause of disability in the workplace. The study of ergonomics is devoted to preventing or lessening LBP in workers. However, by using a “tissue tolerance” paradigm to determine which individuals may be at greater risk of developing disc degeneration, they neglect the effects of the biologic response in tissues to mechanical loading—including how the progression of disease affects the tissue’s ability to respond to those loads.
When mechanical forces are applied to the body, they are distributed through the spine, tissues, and cells. The mechanical integrity of the extracellular matrix is dependent upon the orientation, alignment, and composition of physical properties within its noncellular components. Any alterations of this matrix can affect the tissue’s ability to bear loads and will influence its levels of mechanical function. The tissue tolerance limits used in current ergonomic studies is based upon the point at which damage will occur, including the point at which compressive forces will cause endplate microfracture or the effects of shear loading, applied loading, or loading magnitude. The authors of this review propose that more universally applicable tolerance limits may be developed by including information about complex disc biology and biomechanical loading.
Factors contributing to LBP include biological, physical, and psychosocial components. Any of the factors involved in LBP may interact at different intensity levels to increase or decrease the risk of developing IVD disorders. Spinal loading cycles regulate the integrity of tissue and muscles. At the cellular level, mechanical loading can cause metabolic changes including a build-up or breakdown of the cellular matrix. A tissue will respond in different ways depending on the amount of tissue being acted upon. A thinner tissue is more likely to break than a thicker tissue, and there is an optimal physiologic range of mechanical loading for tissues within which the cellular response will support the matrix. When the mechanical loading stress limits fall outside of this range, the breakdown of the matrix occurs. Tissue integrity is a dynamic variable that is time-dependent throughout the day and in response to age-related degradation. These factors should be considered when determining risk factors for individuals at various times within the workplace.
The Cycle of Pain
Another factor that may influence the dynamic of LBP and disc degeneration is the perception of pain, which may stem from spinal cord or nerve impingement, nerve root growth into the IVD following disc herniation, and torn ligaments, facets or tissues. Though healthy IVDs do not contain a direct nerve root or blood supply, when degeneration occurs, spaces open through which nerves and vessels enter. They may attach themselves to the IVD and create and sustain a source of pain. A loss of proteoglycans because of the degeneration also contributes to this new nerve and blood vessel growth, compounding the problem. Because the fluid content within the IVD fluctuates in a time-dependent manner, degeneration and related inflammation/pain create a time-dependent loop of damage and discomfort that makes the study of interdependent elements of spinal biology and mechanics valuable in ergonomics research.
The interdependency of mechanical and biological factors in determining rates of disc disruption, damage, and associated pain, and the time-dependent nature of cycles of disc strengthening and weakening, indicate that future effective ergonomics studies seeking to develop new tolerance limit paradigms should be based upon a holistic biochemical/mechanical approach, rather than any one single factor alone.
KEYWORDS: ergonomics, IVD pain, biological and mechanical forces of the spine, disc disruption, loss of proteoglycans, spinal biology, disc herniation, torn ligaments, facets or tissues, mechanical integrity of the extracellular matrix, interdependent elements of spinal biology