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| 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]. |
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| 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]. |
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| 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]. |
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