Free Radical Theory:  The free radical theory, proposes that tissue damage occurs in the presence of highly reactive oxygen species called free radicals.  These free radicals are produced during various stages of cellular metabolism of our environmental sources.  Reactive oxygen compounds may cause ageing by destroying essential body chemicals that help repair cell components.  Major underlying state, which induces free radical protection, is reduced blood supply or ischemia.

The Programmed Cellular Senescence Theory:  Ageing may be an entirely an intrinsic process according to the program cellular senescence theory.  There may be a genetic reproduction program, which has spelled out at conception in the DNA within the fertilized egg.  This theory suggests that cellular division may eventually reach termination points and cease to continue.  Normal differentiated cells have been shown in some studies to possess limited capacity to multiply.  The senescent changes may be accelerated by combined system degeneration.

The Cross-Linking Theory:  The crossed-linking theory refers to progressive tissue dehydration, collagen approximation, and the development of insoluble bonds between collagen fibers.  The collagen crossed-linking occurs outside the cell.  Some of the crossed-linking responses induce to facilitate it by non-enzymatic glycation.

Bioenergetic Theory:  The bioenergetic theory of ageing relates to belief that the initial capacity for oxidative phosphorylation decline steadily as a result of ageing.  This has also been referred to as metabolic theory of ageing.  Evidence for complex interrelationship between defects and energy metabolism excitotoxicity oxidative damage has been identified.  Mitochondrial DNA is particularly sensitive to oxidative damage.  There is evidence that mitochondrial function declines with age.  This dysfunction also contributes to free radical generation leading to changes in the cell.

Disc Degeneration

One of the most common age-related changes involving the spine is that of disc degeneration.  As intervertebral discs age, they tend to become dehydrated or dried out.  Subsequently, they lose volume, become stiffer and generally lose their ability to act as efficient shock absorbers.  Paralleling this process the joint tissues and ligaments of the spine become less flexible.  The loss of vertical disc height leads to a shift of weight-bearing stress upon the vertebral segment, typically resulting in greater wear and tear on the spinal joints (facets).  This contributes to thickening of the joint capsule and osteoarthritis of the spinal joints.  Bone hypertrophy (bone spur development) combined with the loss of vertebral disc height contributes to narrowing of the openings where nerves exit the spine.  This process can lead to symptoms associated with nerve compression such as radiating extremity pain, extremity numbness and weakness.