Degenerative disc disease
# Degenerative disc disease
If you have been diagnosed with degenerative disc disease, here is what you need to know. Degenerative disc disease is the normal aging of the intervertebral discs, not a disease. It affects 90% of people aged 60 and older, but most have no pain.1 The term "disease" in degenerative disc disease is misleading: these changes are similar to gray hair or wrinkles. Exercise and movement remain the best treatments for maintaining your function and quality of life.
What is degenerative disc disease?
Degenerative disc disease describes age-related changes in the intervertebral discs: dehydration, loss of height, and structural deterioration. These changes occur in almost all adults and represent normal aging, not a disease.
The intervertebral discs are located between the vertebrae of your spine. They function as shock absorbers with a gelatinous center called the nucleus pulposus surrounded by tough outer layers called the annulus fibrosus.2 With age, the nucleus loses its water content, dropping from about 90% in youth to as low as 70% in older adults. This loss of water decreases the height of the disc and its ability to cushion.
Research by Brinjikji and colleagues shows that 30% of people in their twenties have disc degeneration on MRI scans. This figure rises to 90% at age sixty. However, most of them have no pain.1 This discrepancy between structural changes and symptoms challenges the idea that degeneration always causes pain.
Physical therapy for back pain plays a central role in managing this condition. It treats symptoms through exercise and education rather than focusing on structural outcomes that cannot be changed.Why do discs degenerate with age?
Discs gradually lose water as proteoglycans break down over time. Genetic factors account for 60 to 75% of the variation between individuals.3 Smoking, obesity, and repetitive strain accelerate the process.
The main mechanism involves biochemical changes in the nucleus pulposus. Proteoglycans, which are responsible for attracting and retaining water, break down with age. Unlike most tissues, discs do not have a direct blood supply after early childhood. They receive their nutrients through the movement of adjacent vertebral plates, like a sponge that feeds itself through compression and decompression.
| Postman | Impact on degeneration | Editable? |
|---|---|---|
| Genetics | 60 to 75% of the variation between individuals | No |
| Age | Universal natural progression | No |
| Smoking | Reduced disc nutrition via nicotine | Yes |
| Obesity | Increases stress and inflammation | Yes |
| Inactivity | Reduced nutrient pumping | Yes |
| Repetitive tasks | Accumulated microtrauma | Partially |
Studies on twins suggest that genetic inheritance accounts for 60 to 75% of the variation in disc degeneration.3 Specific genes affect collagen structure, proteoglycan metabolism, and inflammatory responses. This genetic influence explains why some people develop extensive degeneration in their thirties while others maintain relatively healthy discs into their sixties.
Smoking particularly damages the discs by reducing the delivery of nutrients through the effects of nicotine on blood vessels.5 Obesity increases the load on the lumbar discs and promotes inflammation throughout the body. Excessive loads and prolonged inactivity both contribute to degradation.
What symptoms do you experience with disc disease?
Symptoms include lower back pain that worsens when sitting, morning stiffness lasting 15 to 30 minutes, and occasional flare-ups. If you recognize these symptoms, know that this is a common condition that responds well to treatment. Importantly, many people with visible degeneration on MRI scans have no pain at all.
Chronic lower back pain is the most common symptom. It is characterized by axial pain centered in the lumbar spine that does not usually radiate down the legs. The pain often worsens with prolonged sitting, bending forward, or lifting heavy objects.
Morning stiffness lasting fifteen to thirty minutes often accompanies the condition. The discs rehydrate during the night due to pressure changes when you are lying down. This increase in disc volume can stretch the sensitive outer fibers, creating temporary discomfort until the day's activity slowly expels the excess fluid.
Acute pain flare-ups interrupt the pattern of chronic symptoms. These flare-ups usually follow specific movements or activities and last for days to weeks before subsiding.8 Understanding that flare-ups are temporary aggravations rather than deterioration helps you maintain confidence in active management approaches.
Pain that spreads to the buttocks or back of the thighs sometimes accompanies disc disease, but without the specific nerve patterns characteristic of nerve root compression.9 When pain extends below the knee or includes numbness and tingling, consult our guide to lumbosciatica to understand the differences.
10 mini-tips to understand your pain
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How is the diagnosis made?
Diagnosis is based on clinical examination of symptoms and movements, plus imaging showing disc height loss and MRI signal changes. Functional assessment remains more important than imaging results in guiding treatment.
The clinical examination provides the basis for diagnosis. Physical therapists and physicians assess the location and quality of pain, what improves or worsens symptoms, and how symptoms affect daily activities. This clinical information is often more valuable than imaging in guiding treatment decisions.
Plain radiographs show basic degenerative changes such as reduced disc height, bone spurs at the vertebral margins, and hardening of the vertebral plate.11 These findings indicate that degenerative processes have occurred, but they do not correspond well with the symptoms.
MRI is the gold standard for visualizing the internal structure of the disc. If you have an MRI, don't be discouraged by the results. T2 sequences show normal discs as bright white due to their high water content. Degenerated discs appear dark gray or black when proteoglycan degradation reducesthe watercontent.
| Pfirrmann grade | MRI signal | Disc height | Description |
|---|---|---|---|
| I | Bright white | Normal | Normal disc, well hydrated |
| II | White and gray | Normal | Minor changes for beginners |
| III | Gray | Slightly reduced | Moderate degeneration |
| IV | Dark gray | Moderately reduced | Advanced degeneration |
| V | Black | Devastated | Severe degeneration |
The MRI grade does not predict the severity of pain. Many people with advanced degeneration (Grade IV to V) remain pain-free, while others with mild changes report significant symptoms.
Why don't MRI results predict pain?
Most disc tissue has no nerve endings. Only the outer third of the annulus can cause pain.13 Psychological factors, nervous system sensitization, and physical conditioning influence symptoms more than structural appearance.
The poor correlation between MRI findings and pain severity can be explained by several factors. Disc tissue contains few nerve endings, which are limited to the outer third of the annulus fibrosus. Most of the structural changes visible on imaging occur in areas without nerves that cannot generate pain.
Brinjikji's systematic review of imaging studies in pain-free individuals found that 40% of 30-year-olds and 96% of 80-year-olds showed disc degeneration on MRI despite having no back pain.1 This finding demonstrates that degenerative changes represent normal aging that often occurs without symptoms.
Age group% with MRI degeneration% with pain
| 20 to 29 years old | 30% | Variable, often low |
|---|---|---|
| 30 to 39 years old | 40% | Variable |
| 50 to 59 years old | 80% | Variable |
| 60 years old and older | 90% | Variable |
| 80 years old and older | 96% | Painless majority |
Pain does not come from structural degeneration itself. It comes from secondary processes such as inflammation, mechanical instability, or altered movement patterns.14 Psychological factors, particularly avoidance beliefs based on fear and catastrophizing about pain, are better predictors of functional limitations than imaging results.15
How does physical therapy treat disc disease?
Physical therapy improves mobility, strengthens core muscles, and teaches pain management principles. Exercise nourishes the discs through movement and reduces pain more effectively than passive or structural treatments.
Physical therapy addresses degenerative disc disease through comprehensive assessment and individualized treatment. The initial assessment identifies specific limitations in spinal mobility, muscle strength imbalances, and functional restrictions that contribute to symptoms. This assessment guides personalized treatment plans that target each patient's unique presentation.
Exercise therapy is the cornerstone of management. Controlled movement improves disc nutrition through a pumping action that circulates fluids and nutrients between the discs and surrounding blood vessels.4 Strengthening exercises targeting the core muscles and hip stabilizers reduce mechanical stress on degenerated discs.17
Manual therapy techniques, including mobilization, provide short-term pain relief and restore movement, making it easier to participate in exercises.18 Combining manual therapy with exercise and education yields better long-term results.
Education about the neuroscience of pain changes how patients understand and respond to degenerative disc disease. Education emphasizes that disc degeneration represents normal aging rather than ongoing damage.19 Understanding that pain intensity reflects the sensitivity of the nervous system rather than tissue damage empowers you to slowly increase activity despite discomfort.
Our approach to physical therapy for back pain incorporates this modern perspective to optimize your results.What exercises help despite degeneration?
Core stabilization exercises, extension-based movements, and aerobic conditioning are most beneficial. Movement creates a pumping effect that nourishes the discs. Moving may seem counterintuitive, but it is the best medicine for your discs.
Exercise benefits degenerative discs through several mechanisms. Movement creates pressure changes within the discs that circulate nutrients from the vertebral plates into the disc tissue and expel waste products. This pumping action becomes particularly important as discs age. Even degenerated discs retain the ability to exchange nutrients and perform cellular metabolism.
| Type of exercise | Profits | Examples |
|---|---|---|
| Core stabilization | Protects the spine during movement | Plank, bird dog, dead bug |
| Extension | Counteracts daily bending activities | McKenzie, prone press-up |
| Aerobics | Reduces inflammation, improves well-being | Walking, swimming, cycling |
| Flexibility | Reduces compensatory stress | Hip and hamstring stretches |
The principles of load management guide exercise prescription. Starting with tolerable intensities and then progressing slowly as capacity improves allows for tissue adaptation while building confidence.20 Some discomfort during and immediately after exercise often occurs and does not indicate damage, provided that symptoms return to normal within twenty-four hours.
Long-term adherence to exercise determines ultimate success. Benefits accumulate with consistent participation but quickly disappear when activity stops.21 Finding enjoyable activities and setting realistic goals helps maintain commitment.
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Book an appointmentHow does disc disease progress over time?
The good news is that symptoms do not inevitably worsen. Many people improve as the discs stabilize and the body adapts. Occasional flare-ups are normal, but the overall trend is often favorable with active management.
The natural history of disc degeneration follows an expected pattern of structural changes that begins in early adulthood and progresses throughout life.2 This progression occurs in everyone regardless of symptoms and represents normal aging rather than disease progression.
Symptom patterns generally do not follow structural progression. Many patients experience symptom improvement over time despite ongoing structural degeneration.22 This paradoxical improvement occurs when discs collapse and stabilize, reducing mechanical irritation and inflammatory responses. The nervous system adapts to persistent structural changes and reduces sensitivity to signals from degenerated discs.
The majority of people with disc degeneration maintain productive work, leisure activities, and quality of life throughout their lives.23 Disability stems less from structural degeneration than from deconditioning, avoidance behaviors due to fear, and ineffective coping strategies.
Links to other back conditions
Degenerative disc disease is part of a continuum of changes that can affect several structures of the spine. Understanding these relationships helps to better interpret your symptoms.
The relationship between disc degeneration and disc herniation involves structural weakening. Degeneration creates cracks and tears in the annulus fibrosus, which provide pathways for the nucleus material to migrate outward. However, not all degenerated discs herniate.
Spinal stenosis sometimes develops secondary to disc degeneration. The loss of height alters the dimensions of the spinal canal and the alignment of the joints. Symptoms of stenosis typically include leg pain when walking, which improves when leaning forward. Osteoarthritis of the facet joints accelerates when disc degeneration alters load distribution. When discs lose height and cushioning capacity, the facet joints assume higher percentages of the load.When should other treatments be considered?
Additional treatments are considered after 12 weeks of physical therapy without sufficient improvement. Options include anti-inflammatory drugs for flare-ups, occasional epidural injections, and, in rare cases, surgery for severe refractory instability.
| Treatment | Role | When to consider |
|---|---|---|
| Anti-inflammatory drugs | Relief from acute flare-ups | Short term only |
| Epidural injections | Temporary relief, rehabilitation window | Severe refractory flare-ups |
| Surgery (fusion) | Last resort | After 6 to 12 months of complete conservative treatment |
Nonsteroidal anti-inflammatory drugs reduce pain and inflammation during acute flare-ups.24 Short-term use for several days to weeks is appropriate. Chronic daily use raises concerns about side effects.
Epidural steroid injections can provide temporary relief for weeks to months during severe flare-ups, creating a window for exercise rehabilitation.
The good news: the vast majority of cases of degenerative disc disease can be managed without surgery. Surgical options remain controversial, with inconsistent evidence supporting their superiority over conservative management. Structured exercise programs produce improvements that often equal or exceed those achieved with more invasive interventions.
What lifestyle changes help?
Maintain a healthy weight to reduce the load on your discs. Stop smoking, as nicotine impairs disc nutrition. Stay active with regular exercise and improve your workplace ergonomics to prevent flare-ups.
Weight management has a significant impact on the load on the lumbar discs. Each kilogram of excess body weight increases the compressive forces on the lumbar discs.28 Modest reductions of 5 to 10% in body weight provide noticeable benefits.
Quitting smoking ranks among the most important modifiable factors. Nicotine constricts the blood vessels supplying the spinal discs, reducing the delivery of nutrients to the disc tissue.5 The benefits of quitting accumulate over months to years.
Ergonomic improvements address activities that contribute to disc load. Proper sitting posture with lumbar support reduces pressure inside the disc.29 Sit-stand workstations allow for position changes throughout the day, promoting disc nutrition through movement.
Stress management influences pain perception. Chronic psychological stress increases muscle tension and amplifies pain signaling through central sensitization.30
Ready to manage your degenerative disc disease?
Degenerative disc disease does not have to limit your activities or define your future. Our physical therapists at Physioactif help you understand and manage this condition with personalized exercise programs, manual therapy, and education. We focus on maintaining function and quality of life despite disc changes.
Our team specializing in back pain translates pain science research into practical treatment plans. We create personalized programs that target modifiable factors rather than structural outcomes. We teach you exercises that improve disc nutrition, strengthen supporting muscles, and restore confidence in movement.Contact Physioactif today to begin your journey toward improved function, focusing on what you can do rather than structural changes beyond your control.
References
1. Brinjikji W, Luetmer PH, Comstock B, et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol. 2015;36(4):811-816.
2. Roughley PJ. Biology of intervertebral disc aging and degeneration: involvement of the extracellular matrix. Spine. 2004;29(23):2691-2699.
3. Battié MC, Videman T, Levalahti E, et al. Genetic and environmental effects on disc degeneration by phenotype and spinal level. Spine. 2008;33(25):2801-2808.
4. Urban JP, Smith S, Fairbank JC. Nutrition of the intervertebral disc. Spine. 2004;29(23):2700-2709.
5. Akmal M, Kesani A, Anand B, et al. Effect of nicotine on spinal disc cells: a cellular mechanism for disc degeneration. Spine. 2004;29(5):568-575.
6. Peng B, Wu W, Hou S, et al. The pathogenesis of discogenic low back pain. J Bone Joint Surg Br. 2005;87(1):62-67.
7. Adams MA, Dolan P. Spine biomechanics. J Biomech. 2005;38(10):1972-1983.
8. Peng B, Chen J, Kuang Z, et al. Diagnosis and surgical treatment of back pain originating from endplate. Eur Spine J. 2009;18(7):1035-1040.
9. Bogduk N. On the definitions and physiology of back pain, referred pain, and radicular pain. Pain. 2009;147(1-3):17-19.
10. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760-765.
11. van Tulder MW, Assendelft WJ, Koes BW, et al. Spinal radiographic findings and nonspecific low back pain. Spine. 1997;22(4):427-434.
12. Pfirrmann CW, Metzdorf A, Zanetti M, et al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine. 2001;26(17):1873-1878.
13. Freemont AJ, Peacock TE, Goupille P, et al. Nerve ingrowth into diseased intervertebral disc in chronic back pain. Lancet. 1997;350(9072):178-181.
14. Adams MA, Roughley PJ. What is intervertebral disc degeneration, and what causes it? Spine. 2006;31(18):2151-2161.
15. Wertli MM, Rasmussen-Barr E, Weiser S, et al. The role of fear avoidance beliefs as a prognostic factor for outcome in patients with nonspecific low back pain. Spine J. 2014;14(5):816-836.
16. Delitto A, George SZ, Van Dillen L, et al. Low back pain: clinical practice guidelines. J Orthop Sports Phys Ther. 2012;42(4):A1-A57.
17. Searle A, Spink M, Ho A, et al. Exercise interventions for the treatment of chronic low back pain: a systematic review and meta-analysis. Clin Rehabil. 2015;29(12):1155-1167.
18. Rubinstein SM, van Middelkoop M, Assendelft WJ, et al. Spinal manipulative therapy for chronic low-back pain. Cochrane Database Syst Rev. 2011;(2):CD008112.
19. Louw A, Zimney K, Puentedura EJ, et al. The efficacy of pain neuroscience education on musculoskeletal pain. Physiotherapy Theory and Practice. 2016;32(5):332-355.
20. O'Sullivan PB, Caneiro JP, O'Keeffe M, et al. Cognitive functional therapy: an integrated behavioral approach for the targeted management of disabling low back pain. Phys Ther. 2018;98(5):408-423.
21. Jordan JL, Holden MA, Mason EE, et al. Interventions to improve adherence to exercise for chronic musculoskeletal pain in adults. Cochrane Database Syst Rev. 2010;(1):CD005956.
22. Elfering A, Semmer N, Birkhofer D, et al. Risk factors for lumbar disc degeneration: a 5-year prospective MRI study in asymptomatic individuals. Spine. 2002;27(2):125-134.
23. Henschke N, Maher CG, Refshauge KM, et al. Prognosis in patients with recent onset low back pain in Australian primary care. BMJ. 2008;337:a171.
24. Roelofs PD, Deyo RA, Koes BW, et al. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev. 2008;(1):CD000396.
25. Chou R, Hashimoto R, Friedly J, et al. Epidural corticosteroid injections for radiculopathy and spinal stenosis. Ann Intern Med. 2015;163(5):373-381.
26. Mannion AF, Brox JI, Fairbank JC. Comparison of spinal fusion and nonoperative treatment in patients with chronic low back pain. Spine J. 2013;13(11):1438-1448.
27. Foster NE, Anema JR, Cherkin D, et al. Prevention and treatment of low back pain: evidence, challenges, and promising directions. Lancet. 2018;391(10137):2368-2383.
28. Liuke M, Solovieva S, Lamminen A, et al. Disc degeneration of the lumbar spine in relation to being overweight. Int J Obes. 2005;29(8):903-908.
29. Robertson MM, Ciriello VM, Garabet AM. Office ergonomics training and a sit-stand workstation: effects on musculoskeletal and visual symptoms. Appl Ergon. 2013;44(1):73-85.
30. Linton SJ, Shaw WS. Impact of psychological factors in the experience of pain. Phys Ther. 2011;91(5):700-711.
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