Degenerative Disk Disease (DDD)
DDD is a progressive condition in which discs lose their normally high degree of hydration and flexibility, and thus can become compromised in their ability to cushion the spine. Because discs don’t have a good blood supply, once injured they are unable to repair themselves well and the result from damage may become progressive. Progressive changes characteristic of disc degeneration, at various stages, include one or more of: disc dehydration, in particular in the normally well hydrated disc nucleus; tears at the outer fibrous annulus; reduced disc height; growth of bone spurs (osteophytes); and/or narrowing of the spinal canal (e.g. spinal stenosis).
DDD becomes fairly common as early as 40 years old and progresses with increasing prevalency with age thereafter - though it does not necessarily become symptomatic. In fact, >50% of people >40 years old and without any significant low back pain have evidence of degenerative disc disease of their lower spine that may be seen on MRI. However, some degenerative lumbar spines do become pathologic and can cause severe pain. While DDD incidence and degree increases with age beyond 40 years old, conversely the incidence of (and treatments for) chronic, severe axial discogenic LBP peak around 40 years old, and decrease with age thereafter. Furthermore, while disc hydration and thus DDD are directly correlated to the extent of "proteoglycan" (PG) content - the chemical which holds water in discs - neither evidence or extent of DDD nor proteoglycan content have been sufficient correlated to distinguish painful vs. non-painful discs for these measures alone to provide a reliable discogenic pain diagnostic.
Chronic, severe axial discogenic low back pain is believed to arise from a potent combination of increased nociceptors (pain reporting nerves) and acidity associated with hypoxia within the disc nucleus (inner region of the disc). Both of these factors have been uniquely observed in painful (vs. non-painful) discs, and may in fact indirectly relate to DDD and PG content despite the failure of these indications to reliably predict pain alone. PG is a known inhibitor against nerve ingrowth, and its decrease is expected to enhance a permissive environment for innervation into discs. This appears to manifest in nerve in-growth that is observed in the nuclei of discs that are painful, but not of discs that are non-painful. Also, in response to damage accumulation and inflammation in some discs, repair mechanisms become defective due to overworked disc cells in a particularly poorly vascularized, and thus hypoxic environment. This leads to abnormal cellular metabolism and glycolysis, which produces lactic acid (and also alanine) byproduct that drives increased acidity in the disc nucleus. Acidity is a known stimulant to nociceptors by activating ion channels, and it thus follows that nociceptors + acid = pain in discs. Thus, painful discs appear to be identified by in-growth of nociceptors and increased hypoxic acidity in disc nuclei, as may be reliably indicated by changes in disc chemistry per the combination of related chemical biomarkers: PG and LA (and perhaps alanine or "AL").
Any patient suffering from LBP should consult their own doctor, including possible specialists when indicated, to determine the recommended course of diagnostic or therapeutic options available to that patient for their particular condition, and should not direct any decision with respect to their medical care in any way based upon this summary or information on this site - which is intended for general background purposes of our company's direction and mission only.
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