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This page contains most of the knowledge we have on the subject at this time.
It has yet to be reviewed.
Standard descriptions of the lumbar spine refer to the healthy, young, adult spine. There is also variation to what is "normal" for the lumbar spine. With aging you see fairly uniform changes in the lumbar spine, and so normality changes with advancing age. Many changes in the lumbar spine are not associated with symptoms and are therefore not pathological, but rather part of the normal ageing process.
The changes in collagen, proteoglycans, and elastic fibres have major biomechanical effects on the disc. With age they become drier, and with an increase in collagen and reduction of elastin, they become more fibrous and less resilient. The increased collagen and collagen-proteoglycan binding leads the disc to become stiffer (more resistant to deformation), and the decreased water-binding capacity means they are less able to recover from creep deformation. This can lead to a change in mobility.
|Area of Change
- In childhood, the disc adapts to anaerobic metabolism after the regression in infancy of the meagre blood supply to the disc.
- synthesis, size, and the concentration in the nucleus pulposis (NP) decreases with age.
- Proteoglycans account for 65% of the dry weight in early adult life, decreasing to 30% by age 60.
- There is a reduction in large proteoglycan aggregates by adolescence
- The concentration of chondroitin sulphate falls, with keratan sulphate remaining constant. This means a rise in the keratan sulphate/chondroitin sulphate ratio.
- Collagen content increases, with an increase in collagen-proteoglycan binding, in both the anulus fibrosis (AF) and NP.
- Fibril diameter in the NP increases, so that the type II collagen of the NP resembles the type I collagen of the AF. Reciprocally, the average fibril diameter in the AF decreases. Overall, there is less distinction between the collagen of the NP and the AF
- Increase in the amount of type I collagen in the outermost laminae of the posterior quadrant of the AF, and a decrease in the type II collagen. This suggests some changes are not age related but related to internal stresses related to location.
- Reduction of elastic fibres in the AP from 13% at age 26 to 8% at age 62.
- Increase in concentration, with the appearance of distinctive non-collagenous proteins. Their function is unknown.
- Decrease in water content with age from 88% at birth, to 65-72% by age 75.
- Most of the dehydration occurs during childhood and adolescence, with a final reduction of AP water content by 6% from early adulthood to old age
- Factors leading to reduced water content: loss of proteoglycans, change in KS/CS ratio, increased collagen and collagen-proteoglycan binding leaving fewer polar groups of the PGs to bind water
- Viable cells decrease in the NP.
- Proportion of cells that exhibit necrosis rises from 2% in infancy, to 50% in young adults, to 80% in old age. Lipofuscin granules accumulate
|NP and AF distinction
- There is less distinction between the NP and AF as the disc becomes more fibrous.
- They coalesce, and the NP becomes encroached by the AF.
- The NP becomes more solid, dry, and granular after middle age. There is less ability to exert fluid pressure with a drier more fibrous NP, with it being less able ot transmit weight directly, and less able to exert radial pressure on the AF. There is therefore a greater vertical load borne by the AF.
- Collagen lamellae of the AF increases in thickness, and becomes more fibrillated, and cracks and cavities may develop.
- These can enlarge and become clefts and fissures. There is an increase in incomplete lamellae
- These changes can occur due to repeated minor insults with an overloaded AF during trunk movements over the course of activities of daily living.
- Reduction in the tensile strength of the AF, but no simple relationship between age and tensile properties.
|Intervertebral disc height
- Intervertebral disc height increases with age.
- There is an increase in AP diameter by 10% in females, and 2% in males, and a 10% increase in height of most discs. The upper and lower surfaces of the discs increase in convexity.
- Disc height maintenance with age is "normal."
- Any loss of trunk stature is due to decreases in vertebral body height.
- Disc narrowing is due to a process other than ageing.
Vertebral Endplate Changes
- The vertebral endplate is part of the growth plate of the vertebral body
- The articular region of the endplate is formed by fibrocartilage
- The vertebral body side of the endplate is formed by columns of proliferating cells that extend into the ossifying vertebral body
- The articular region of the endplate becomes thicker
- The growth zone decreases in thickness
- Proliferating cells become fewer
- Vertebral growth slows
- vertebral endplate is gradually sealed off from the vertebral body by development of the subchondral bone plate
- After age 20, only the articular region of the original growth plate persists
- The endplate becomes thinner
- Cell death in the superficial cartilage layers
- In the subchondral bone of the endplate, vascular channels are gradually occluded leading to a decrease in permeability of the endplate to nutrients for the disc
- Vertebral endplate strength decreases, but this depends on the underlying vertebral body so they should be considered together
Vertebral Body Changes
- Decrease in bone density in the lumbar vertebral bodies, and a decrease in bone strength
- Slowly absorbed, but those that persist are thickened
- Absorbed and not replaced.
- Therefore ageing is characterised by the loss of horizontal trabeculae, most marked in the central vertebral body (the part overlying the NP).
- This removes weakens their bracing effect on the vertical trabeculae, and the loadbearing capacity of the central vertebral body decreases.
- With the weakening of the trabecular system, a greater proportion of the compressive load on the vertebral bodies is borne by the cortical bone.
- Over the age of 40, trabecular bone bears only 35% of the load, but cortical bone fails at only 2% deformation, while trabecular bone fails at 9.5% deformation.
- The vertebral body is less resistant to deformation and injury with greater reliance on the cortical bone.
- With less support from the underlying bone, the vertebral bodies deform by microfractures.
- These gradually bow into the vertebral body, giving a concave shape to the superior and inferior surfaces of the vertebral body.
- The central vertebral endplate is more susceptible to fractures with excessive compressive load.
- With increasing age microfractures are found in the endplates and vertebral trabeculae of the vertebral bodies.
- These are more seen in the lower thoracic and thoracolumbar junction, rather than below L2.
- They are due to fractures that are large enough to allow nuclear material to extrude into the vertebral body.
- They are not symptomatic per se. They have highest incidence in adolescence, and don't increase in frequency with age.
- Small protrusions of disc material into the vertebral bodies may be of significance.
Facet Joint Changes
- Increases in thickness of the subchondral bone of the facet joints during growth, reaching a maximum between 20-50 years
- Thereafter it gets gradually thinner
- Steadily increases in thickness with age
- Focal changes start in the fourth decade related to stresses applied to the joints
- In the anteromedial third of curved facet joints, with repeated stresses of daily living, the cartilage cells hypertrophy (especially the midzone layer). This progresses to vertical fibrillation of the cartilage associated with sclerosis of the subchondral bone plate.
- Severe or repeated pressures may result in erosions and focal cartilage thinning
- Other regions may exhibit swelling that accounts for the general increase in thickness
- In locations of cartilage loss, the fibrofatty intra-articular inclusions may increase in size to fill the space vacated by the cartilage
- The posterior section of the joint shows parallel splitting of cartilage.
- A split piece of cartilage may remain attached to the joint capsule and form a false intra-articular meniscoid.
- Cell hypertrophy is almost universal in the fourth decade, and minor fibrillation is common in the fourth and fifth decades
- Older joints have gross thickening and irregularity of the calcified zone of cartilage and increased collagen in the superficial layers, with fewer and smaller cell nuclei.
- Cartilage changes are more severe in the polar regions than at the centre of the joint
- There is a loss of distinction between changes in the anteromedial and posterior portions of the joint with older joints
- Development of osteophytes and 'wrap-around bumpers'
- Osteophytes develop along attachment sites of the joint capsule and ligamentum flavum to the superior articular process
- Wrap-around bumpers are extensions of the edges of the articular cartilage curving around the dorsal aspect of the inferior articular process. Repeated stress during rotatory movements causes the cartilage to spread out to cover and protect the edges of the bony articular process
The biochemical and structure changes that occur have an effect on the mechanical properties and movements of the spine.
|Creep and hysteresis
- Increased creep and hysteresis
- Greater set after creep deformation
- Cause of change: Probably due to the decreased water-binding capacity of the intervertebral discs. They therefore take longer to resume their original structure following deformaiton
|Range of motion
- Decreased range of motion
- Evident in the entire lumbar spine and individual intervertebral joints
- Young children show the greatest lumbar mobility. They are between 50-300% more mobile than middle-aged people at various segmental levels.
- Decreases considerably by adolescence, and beyond the age of 30 there is then a gradual decline.
- Cause of change: The reduced mobility is principally due to the increased stiffness in the intervertebral discs with ageing. (proven with release experiments removing the posterior ligaments and facet joints). This is due to disc dehydration and fibrosis
Spondylosis and Degenerative Joint Disease
Spondylosis refers to the development of osteophytes along the junction of vertebral bodies and their intervertebral discs. Spondylosis is not a disease but a natural consequence of the stresses applied to the spine throughout life. They are reactive and adaptive changes that are due to compensation of biomechanical aberrations. It is an active and purposeful process, not a degenerative one.
With age, the NP becomes less resilient and stiffer, and the AF bears more of the compressive loads applied to the disc. Adaption occurs with the greater loads. Excessive compression can result in ossification of the terminal ends of the collagen fibres of the AF. This ossification can occur in the anterior and posterior margins of the disc where compressive strains are focused during flexion and extension. Excessive vertical load-bearing can result in the development of osteophytes along the entire margin of the vertebral body. This is the vertebral body trying to expand its articular surface area in order to distribute axial loads over a wider area, and therefore lessening the stress applied to the AF during load. In other words, osteophytosis is a natural response to the altered biomechanics of the lumbar spine that are itself due to biochemical changes in the disc. It is not a disease but rather an expected morphological change with age.
The terms osteoarthrosis and degenerative joint disease refer to changes seen in the facet joints. However again, these are morphological consequences of stresses applied to the facet joints over time. The changes are found in regions of greatest and repeated stresses. These are adaptive changes, the structure remodels to account for the applied stresses. However, with severe or repeated stresses, destructive features may occur.
The most pivotal reason that all these changes are not diseases, is the fact that they are irregularly associated with pain and disability. There is no correlation between spondylosis and osteoarthrosis in patients with or without symptoms. There is some additional factor that must be the cause of pain.
These are study notes taken from Chapter 13 of:
- Bogduk, Nikolai. Clinical and radiological anatomy of the lumbar spine. Edinburgh: Elsevier/Churchill Livingstone, 2012.