Table 1.

Intervertebral disc pathology.

Internal disc disruption (IDD)	(i) Defined by the development of focal fissures extending outward from the nucleus into the annulus (radial fissure) or along annular lamellae (circumferential fissure) [1, 7].
	(ii) Annular fissures provide a conduit for inflammatory chemical mediators to trigger nociceptive nerve endings in the outer AF [1, 7]. Additionally, “nerve ingrowth” along fissure sites can increase exposure to nociceptive and mechanical stimuli [1, 7]
	(iii) Discogenic pain may develop when annular pain fibers are directly stimulated by inflammatory mediators or are indirectly stimulated secondary to increased mechanical loading pressures [1, 4, 6].
	(iv) Though nuclear degeneration is minimal in early stages of IDD, it is believed to trigger a catabolic cascade within the microenvironment of the disc, which serves as a precursor to overt disc herniation and DDD at later stages [1, 7].
	(v) IDD is considered to be the most common detectable cause of LBP (estimated prevalence of 39%) [1, 8].
Degenerative disc disease (DDD)	(i) Defined as a diffuse, progressive, and age-related phenomenon defined by nuclear dehydration and fibrosis and resultant disc space narrowing (3-4% loss per year) [1, 4, 9, 10].
	(ii) Mechanical, biochemical, nutritional, and genetic factors contribute to a shift towards catabolic metabolism within the disc microenvironment. Hallmarks include increased metalloproteinase (MMP) activation, decreased IVD cell viability, and decreased proteoglycan (PG) production [4, 9, 11, 12].
	(iii) Resultant increased disc space narrowing can cause a redistribution of axial mechanical forces on nearby structures (e.g., vertebral body endplates, facet joints) causing tissue irritation and degeneration (i.e. osteophytes, buckling) [1, 13].
	(iv) DDD may or may not result in discogenic LBP but almost universally compromises disc integrity, predisposing the disc to further injury [4, 12, 13].
Disc herniation	(i) Defined by a displacement of nuclear disc material beyond the normal contours of the outer nucleus [1, 5].
	(ii) Stages include bulge, protrusion, extrusion, and sequestration
	(iii) It is the most common etiology of radicular leg pain, via chemical radiculitis or mechanical compression of nerve roots [1].
	(iv) May contribute to focal LBP as a result of inflamed dura of a surrounding nerve root sleeve (somatic referred pain) or from activation of outer annular pain fibers within the injured disc [1].
	(v) Data suggests an alteration of the annulus may contribute to decreased disc integrity and accelerated DDD [13–17].