Lumbar Degenerative Disk Disease

Updated: Apr 26, 2016
  • Author: Rajeev K Patel, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Descriptions of treatment for low back pain (LBP) date to Hippocrates (460-370 BCE), who reported joint manipulation and use of traction. Onset of LBP often is associated with bipedal ambulation. Theories propose that this transformation in the mechanics of locomotion is the inciting evolutionary event that made the lumbar spine susceptible to degenerative disease. Degeneration is universal to structures that comprise the functional spinal unit, composed of 2 adjacent vertebral bodies and the intervertebral disk. The disk and 2 zygapophyseal joints at the same level function as a trijoint complex.

As humans age, they endure both macrotraumas and microtraumas and undergo changes in body habitus that alter and redistribute biomechanical forces unevenly on the lumbar spine. Natural progression of degeneration of the lumbar segment with motion proceeds with characteristic anatomic, biomechanical, radiologic, and clinical findings in lumbar degenerative disk disease (LDDD). [1]



Posterior elements of the lumbar spinal functional unit typically bear less weight than anterior elements in all positions. Anterior elements bear over 90% of forces transmitted through the lumbar spine in sitting; during standing, this portion decreases to approximately 80%. As the degenerative process progresses, relative anterior-to-posterior force transmission approaches parity. The spine functions best within a realm of static and dynamic stability. Bony architecture and associated specialized soft tissue structures, especially the intervertebral disk, provide static stability. Dynamic stability, however, is accomplished through a system of muscular and ligamentous supports acting in concert during various functional, occupational, and avocational activities.

The overall mechanical effect of these structures maintains the histologic integrity of the trijoint complex. Net shear and compressive forces must be maintained below respective critical minima to maintain trijoint articulation integrity. Persistent, recurrent, nonmechanical, and/or excessive forces to the motion segment beyond minimal thresholds lead to microtrauma of the disk and facet joints, triggering and continuing the degenerative process. [2] Degenerative cascade, described by Kirkaldy-Willis, is the widely accepted pathophysiologic model describing the degenerative process as it affects the lumbar spine and individual motion segments. [3] This process occurs in 3 phases that comprise a continuum with gradual transition, rather than 3 clearly definable stages.

Phase I

The dysfunctional phase, or phase I, is characterized histologically by circumferential tears or fissures in the outer annulus. Tears can be accompanied by endplate separation or failure, interrupting blood supply to the disk and impairing nutritional supply and waste removal. Such changes may be the result of repetitive microtrauma. Since the outer one third of the annular wall is innervated, tears or fissures in this area may be painful. Strong experimental evidence suggests that most episodes of LBP are a consequence of disk injury, rather than musculotendinous or ligamentous strain. Circumferential tears may coalesce to form radial tears. The nucleus pulposus may lose its normal water-imbibing abilities as a result of biochemical changes in aggregating proteoglycans.

Studies suggest proteoglycan destruction may result from an imbalance between the matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1). [4, 5, 6] This imbalance results in diminished capacity for imbibing water, causing loss of nuclear hydrostatic pressure and leading to buckling of the annular lamellae. This phenomenon leads to increased focal segmental mobility and shear stress to the annular wall. Delamination and fissuring within the annulus can result. Annular delamination has been shown to occur as a separate and distinct event from annular fissures.

Microfractures of collagen fibrils in the annulus have been demonstrated with electron microscopy. MRI at this stage may reveal desiccation, disk bulging without herniation, or a high-intensity zone (HIZ) in the annulus. Structural alteration of the facet joint following disk degeneration is acknowledged widely, but this expected pathologic alteration does not necessarily follow. Changes associated with zygapophyseal joints during the dysfunctional phase may include synovitis and hypomobility. The facet joint may serve as a pain generator.

Phase II

The unstable phase, or phase II, may result from progressive loss of mechanical integrity of the trijoint complex. Disk-related changes include multiple annular tears (eg, radial, circumferential), internal disk disruption (IDD) and resorption, or loss of disk-space height. Concurrent changes in the zygapophyseal joints include cartilage degeneration, capsular laxity, and subluxation. The biomechanical result of these alterations leads to segmental instability. Clinical syndromes of segmental instability, IDD syndrome, and herniated disk seem to fit in this phase.

Phase III

The third and final phase, stabilization, is characterized by further disk resorption, disk-space narrowing, endplate destruction, disk fibrosis, and osteophyte formation. Diskogenic pain from such disks may have a higher incidence than that of the pain from the disks in phases I and II; however, great variation of phases can be expected in different disks in any given individual and individuals of similar ages vary greatly.




United States

Lifetime incidence of LBP is reported to be 60-90% with annual incidence of 5%. Each year, 14.3% of new patient visits to primary care physicians are for LBP, and nearly 13 million physician visits are related to complaints of chronic LBP, according to the National Center for Health Statistics. [7, 8]


The natural history has been reported to be favorable in some studies and is frequently quoted to patients. Reports indicate that 40-50% of patients are symptom-free within 1 week and up to 90% of symptoms resolve without medical attention in 6-12 weeks.

  • Deyo and Tsui-Wu reported that 33.2% of patients with LBP reported symptoms for less than 1 month, 33% reported pain for 1-5 months, and 32.7% reported pain for longer than 6 months. [9] Later, over a 2-year follow-up, 44% of patients reported chronic symptoms (defined as back pain for >90 d in the previous 6 mo). Most patients had low levels of back pain, with 20% rating their pain at 4 or greater on a scale of 0-10 (where 0 indicates no pain), 13% rated their pain as 5 or greater, and 8% reporting pain of 6 or greater.
    • Von Korff and colleagues reported that 15-20% of primary care patients with LBP had moderate-to-severe limitations in activity during a 1-year follow-up after their initial episode resolved. Recurrence rates of 60-85% have been reported in the first 2 years after an acute episode of LBP. [10]
  • Although incidence of LBP has remained relatively static, disability from LBP has increased 14 times the rate of population growth. Back pain results in more lost productivity than any other medical condition and is second only to upper respiratory complaints as cause of time lost from work. Back pain accounts for approximately 175.8 million days of restricted activity each year in the United States. At any given time, 2.4 million Americans are disabled because of LBP, with 1.2 million on a chronic basis. As of 2005, lower back pain ranks as the number one cause of disability in individuals under the age of 45.
  • In 1990, 400,000 industrial low back injuries resulted in disability in the United States. This number represents approximately 21% of injuries in the workplace but accounted for 31% of compensation payments. After a patient receiving worker's compensation is out of work for more than 6 months, the likelihood of his or her returning to work is only 50%. After 1 year, the likelihood is only 25%, and after 2 years, the individual will likely never return to productive work. In 1990, direct medical cost of spinal disorders was estimated to than $23 billion in the United States. Furthermore, plausible estimates of total costs of low back disorders ranged from $25 billion to almost $85 billion in 1990. [11]
  • Looking at 1998 statistics, Luo and colleagues found total health care expenditures incurred by individuals with back pain in the United States to have reached $90.7 billion; total incremental expenditures attributable to back pain among these persons were approximately $26.3 billion. On average, individuals with back pain incurred health care expenditures that were approximately 60% higher than individuals without back pain ($3498 vs $2178). Of service expenditures, 75% were attributed to those individuals within the top 25% of expenditure. Disk disorders were also found to be associated with higher medical costs. [12]


LBP secondary to degenerative disk disease affects men and women equally. Gautschi et al found in a cohort of 214 patients with lumbar degenerative disk disease that preoperatively, females scored worse than males on measurement of subject functional impairment but that males and females scored similarly in terms of objective functional impairment. The investigators also found that postoperative results did not differ between the sexes at 6-week, 6-month, and 1-year follow-up. [13]


LBP secondary to degenerative disk disease is a condition that affects young to middle-aged persons with peak incidence at approximately 40 years. With respect to radiologic evidence of LDDD, the prevalence of disk degeneration increases with age, but degenerated disks are not necessarily painful.