Degenerative lumbar spondylosis


Spondylosis is part of the normal aging process of the spine. Dixon (1980) refers to the sequence of changes affecting one of more levels of disc degeneration, disc narrowing, osteophyte formation and osteoarthritis of the facet joints. Degeneration is characterized by slow, destructive changes which are not balanced by the regeneration that occurs in younger tissues (Grieve, 1981).


Roland and Van Tulder (1998) found that roughly 40% of patients with advanced disc degeneration on radiography do not have backpain, indicating that symptoms and radiographic changes may be unrelated.


In old age, the range of lumbar movement decreases. Originally this was thought to be due to the thinning of the intervertebral discs, however, it is now thought that only 30% of discs become thinner and in old age most discs increase in volume, become thicker centrally and more convex. Loss of vertebral column height is caused by loss of vertebral body height. The reason for loss of movement is thought to be due to disc stiffness or reduction of the elasticity of the disc (Twomey and Tayler 1983). The histological and biochemical changes include an increase in the total number of collagen fibres, a decreased in water content and a change in the prosteoglycagen ratios. There is also an increase in the “failure fatigue” of collagen in the older cartilage. These changes lead to a decrease in compliance of the disc fibrocartilage therefore making it less capable as acting as an efficient shock absorber. If the disc becomes vascularised, which can occur when the end plates are damaged, disc degeneration is accelerated. Nerve fibres then accompany the blood vessels into the disc and may serve a nocioceptive function.


Aging is accompanied by loss of both trabecular and cortical bone which results in a decrease in bone strength. The rate at which bone loss occurs is influenced by such factors as the menopause, declining calcium absorption, smoking and reduced physical exercise. The height of the vertebral bodies declines in old age, principally due to the reduction of transverse trabeculae which acts as “cross-braces” to the vertical trabeculae. As the trabeculae weaken, the vertebral body becomes less resistant to deformation and injury.


Osteophytes are outgrowths of healthy bone from the vertebrae. Their development is an important defensive mechanism against compressive forces which exceed the capacity fo the bone to resist them. They are composed of more compact, stronger bone, than the rest of the vertebral body. A young person with normal vertebrae may develop osteophytes when the pressure on the vertebral body is excessive, as in heavy manual work. Disc degeneration and the subsequent impaired shock-absorbing capacity of the vertebral column can also lead to their formation, as can pathological processes such as osteoporosis. Quite marked osteophytosis may be present without giving rise to symptoms.


Progressive resorption and thinning of the articular cartilage in the end plates occurs, with replacement by bone, so that over the age of 60 there is often only a thin layer of calcified cartilage separating the disc from the vertebral body. With increasing age, it is likely that there is a decrease in the diffusion of substances though the end plates. Since the cells in the disc are dependent on this route for the supply of nutrients and the removal of waste products, closure of the end plate route leads to nutritional deficiencies and a build up of metabolic products.


The epidemiology of spondylosis increases markedly with age and is uncommon below 45years of age. The normal aging process can be accelerated by increased exposure to mechanical stresses, which then give rise to degenerative changes. Which part of a motion segment is initially affected depends on the particular mechanical stresses or postures to which the spine is subjected and the integrity of the tissues themselves.


With age, there is a progressive decrease in the water-biding capacity of the nucleus of the disc.

Degenerative changes of intervertebral discs were classified in 1966 by Rolander based on their appearance on mid-dagital sections.


Grade 0 – Macroscopically normal / juvenile discs

Grade 1 – Normal adult discs, white in colour, the nucleus bulges.

Grade 2 – Age changes, less distinct boundary between nucleus and annulus, yellowish colour.

Grade 3 – Frank disc dessication, multiple fissures in nucleus and annulus, disc thinning.



The incidence of disc degeneration does increase in old age and the lower two lumbar levels are most affected as these levels are subject to greatest physical stress. Fissuring of the annulus is seen with increasing frequency in old age. The etiology of degerative disc disease includes both genetic and environmental factors. The incidence of disc degeneration in the spine as a whole is highest at the lowest two lumbar levels, particularly in the lumbosacral disc. This is because there is a large amount of movement at this level and the shear forces acting on the disc with the lordotic posture in the standing posture also increase the forces on the disc. Degenerative changes may predominantly affect the disc in some individuals, while in others they affect the facet joints, at least in the initial stages of degeneration.


Secondary chondrosis interverbralis (osteochondrosis intervertebralis) describes parthological changes outside the intervertebral disc and is characterized by changes in the cartilage end plates and sclerosis of the adjacent spongiosa of the vertebral bodies resulting in erosive chondrosis. Bony osteophytes develop in the region of the vertebral bodies (Spondylosis deformans).


As a result of the changes in the intervertebral discs and subsequent decrease in height, there are degenerative changes in the zygopophyseal joints (spondyloarthrosis). The decrease in height of the vertebral column causes a caudal dislocation of the inferior articular process and stresses the capsule of the joints.


Clinical Presentation

Age onset

  • Usually middle aged and older
  • Often heavy manual work
  • Gradual onset



  • Can be confined to lumbar region but may experience symptoms referred to the lower limbs


Diurnal Pattern

  • worse first thing am./ stiffness, eases off fairly quickly
  • activity dependent.




  • Variable, vague, ache, dull
  • Low back pain, unilateral or bilateral lower limbs
  • Often aggravated with walking, standing (extension activities)
  • Often eased by flexion
  • Eased by movement / resting in neutral



Posture – Flattened lumbar lordosis

Rom – Stiff lumbar segments, usually in an articular restriction

  • Extension and side flexions usually worse than flexion

Neuro – Depends on whether nerve roots are involved.



Postural correction / Back care advice / use of heat/ice.

Isometric exercises to strengthen the abdominal and spinal muscles.

Advise re: medication (analgesia, NSAIDS, glucosamine sulphate, amitriptyline)

Address muscle imbalance / stability as appropriate

Address joint restriction as appropriate, spinal mobilization techniques, often starting in the direction opposite to that of pain aggravation. Most effective in the first 6 weeks.

General activity programme / pacing advice.

Weight reduction if appropriate.

Erganomic adjustments if appropriate.



Dependent upon the level and degree of degeneration. Most cases of acute pain begin to settle within 6 weeks.



Adams, M., Bogduk, N., Burton, K., Dolan, P. The biomechanics of backpain. Churchill livingstone.


Andersson, G. (1997) The epidemiology of spinal disorders. The adult spine: principles and practice. Lippincott-Raven. Philadelphia 93-141


Dixon, A. (1980) Diagnosis of low back pain. The lumbar Spine and Backpain. 2nd Ed. Pitman Medical. P135


Fujiwara, A., Lim, T.H., An, H.S., Tanaka, N., Jean, C.H., Adesson, G., Houghton, V.M. (2000) The effect of disc degeneration and facet joint OA on the segmental flexibility of the lumbar spine. Spine. 25(3) 3036-3044


Grieve, G.P. (1988) Clinical features. In: Grieve, G.P., ed. Common Vertebral joint problems, 2nd ed. New York, Churchill Livingston 299-353.


Prescher, A. (1998) Anatomy of the aging spine. European Journal of Radiology. 181-195


Roland, M., Van Tulder. (1998) Should radiologists change the way they report plain radiographs of the spine. Lancet. 352, 229-230


Rolander, S.,D. (1996) Motion of the lumbar spine with special reference to the stability effect of posterior fusion. Orthopaedic Scandinavia.


Twomey, L.T., Taylor, J.R. (1993) Sagital movements of the human intervertebral lumbar column: a quantitative study of the role of the posterior vertebral elements. Archives of physical medicine and rehabilitation. 64, 322-325