Age changes in the lumbar spine

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Chapter 13 Age changes in the lumbar spine

Textbook descriptions imply that the structure of the lumbar spine conforms to some sort of standard or even ideal form, and that a standard description is applicable to all individuals. However, such descriptions only reflect the average, healthy, young adult spine. Yet, even then the lumbar spine is subject to variations, e.g. in the shape and orientation of the zygapophysial joints (see Ch. 3), the shape of the lumbar lordosis (see Ch. 5) and the possible ranges of movement (see Ch. 8). What is considered the ‘normal’ lumbar spine is only a composite of the mean values, or most common form, of these and other possible variables.

In this regard, ‘normal’ is defined as the structure most commonly exhibited by individuals in a population. However, when defined in this way, normality is greatly influenced by age. As individuals age, their lumbar spines undergo changes that are fairly uniformly reflected by the population. Thus, what is ‘normal’ for a young adult population may not be ‘normal’ for an older population. Moreover, if changes uniformly exhibited by an older population are not associated with symptoms, then they cannot be regarded as pathological. They are simply part of the natural biological process of ageing. Each age group, therefore, defines its own normal standards, and in order that clinicians neither confuse age changes with pathological changes, nor misconstrue them as such, they should be aware of what constitutes the natural changes with age in the lumbar spine.

In this regard, the fundamental age changes of the lumbar spine occur at the biochemical level. In turn, these affect the microbiomechanical and overt biomechanical properties of the spine, which are ultimately reflected in the morphology of different components of the lumbar spine and its patterns of movement.

Biochemical changes

One of the most fundamental changes in the lumbar spine occurs in the nuclei pulposi. Changes in biochemistry are most dramatic from infancy to about the age of ten years.^1,² These seem to be triggered by the regression in infancy of the meagre blood supply to the disc, and they set the trend that occurs through later life as the disc adapts to anaerobic metabolism.^1,²

With ageing, the rate of synthesis of proteoglycans decreases ³ and the concentration of proteoglycans in the nucleus pulposus also decreases.⁴^–⁷ In early adult life, proteoglycans amount to about 65% of the dry weight of the nucleus (see Ch. 2) but by the age of 60 they constitute only about 30%.⁸ Those proteoglycans that persist are smaller in size^9,¹⁰ and have a smaller molecular weight.^11,¹² The proportion of aggregated proteoglycans decreases³ and the number of large proteoglycan aggregates decreases such that, by adolescence, the nucleus pulposus consists largely of clusters of short aggrecan molecules and non-aggregated proteoglycans.⁵ Associated with these latter changes is a decline in the concentration of functional link proteins.⁵

Apart from these changes in composition, the nature of the proteoglycans also changes. While the keratan sulphate content of the disc remains fairly constant, the concentration of chondroitin sulphate falls, and this results in a rise in the keratan sulphate/chondroitin sulphate (KS/CS) ratio.^6,¹²^–¹⁵

The other major change in the nucleus pulposus is an increase in its collagen content,^5,¹⁶ and an increase in collagen–proteoglycan binding.⁹ The collagen content of the anulus fibrosus also increases¹⁷ but the concentration of elastic fibres in the anulus drops, from 13% at the age of 26 to about 8% at the age of 62.¹⁸

The collagen of the intervertebral disc not only increases in quantity but also changes in nature. The fibril diameter of collagen in the nucleus pulposus increases,^5,¹⁹^–²² such that the type II collagen of the nucleus starts to resemble the type I collagen of the anulus fibrosus. Reciprocally, the average fibril diameter in the anulus fibrosus decreases.²⁰ Consequently, there is less distinction between the collagen of the nucleus pulposus and the anulus fibrosus.

The changes in collagen are related not only to age but also to location.²³ While the collagen content of the anulus in general increases with age, there is a significant increase in the amount of type I collagen in the outermost laminae of the posterior quadrant of the anulus, and a reciprocal decrease in type II collagen. This suggests that some of the changes in collagen are not generalised age changes but are active metabolic responses to changes in the internal stresses of the anulus.²³

The concentration of non-collagenous proteins in the nucleus pulposus increases,²⁴^–²⁸ and ageing is characterised by the appearance of certain distinctive non-collagenous proteins.²⁸ However, because the functions of non-collagenous proteins are not known (see Ch. 2), the significance of changes in these proteins remains obscure. In contrast, the changes in collagen, proteoglycans and elastic fibres have major biomechanical effects on the disc.

Because chondroitin sulphate is the major source of ionic radicals that bind water to proteoglycans (Ch. 2), it is tempting to expect that the change in the KS/CS ratio would result in a decrease in the water-binding capacity and the water content of the nucleus pulposus. Indeed, the water content of the nucleus does decrease with age.¹⁶ At birth, the water content of the nucleus pulposus is about 88%, and this drops to about 65–72% by the age of 75 years.^6,²⁹ However, most of this dehydration occurs during childhood and adolescence, and the water content of the nucleus pulposus decreases by only about 6% from early adult life to old age.³⁰

Sophisticated biochemical studies indicate that it is not simply the loss of proteoglycans or the change in the KS/CS ratio that decreases water-binding in the nucleus. Rather, the increased collagen and increased collagen–proteoglycan binding leave fewer polar groups of the proteoglycans available to bind water,¹⁶ and the decrease in water-binding capacity of the nucleus is a function of the complex way in which the ionic interactions between proteoglycans and proteins are altered.^10,¹¹

Regardless of the actual mechanism, the lumbar intervertebral discs become drier with age, and with the increase in collagen and the loss of elastin, they become more fibrous and less resilient. The increased collagen and increased collagen–proteoglycan binding render the discs stiffer, i.e. more resistant to deformation, and their decreased water-binding capacity renders them less able to recover from creep deformation. The clinical effect of these changes is expressed as changes in the mobility of the lumbar spine, and these are described in a later section below.

Structural changes in the intervertebral discs

As the disc ages, the number of viable cells in the nucleus decreases, and the proportion of cells that exhibit necrosis changes from 2% in infancy to 50% in young adults and 80% in elderly individuals.⁵ Lipofuscin granules accumulate with advanced age.³¹

Macroscopically, as the intervertebral disc becomes more fibrous, the distinction between nucleus pulposus and anulus fibrosus becomes less apparent. The two regions coalesce and the nucleus pulposus appears to be encroached by the anulus fibrosus.³² After middle life, the nucleus pulposus becomes progressively more solid, dry and granular.³²

As the nucleus pulposus dries out and becomes more fibrous, it is less able to exert fluid pressure.^33,³⁴ Thus, the nucleus is less able to transmit weight directly and less able to exert radial pressure on the anulus fibrosus (cf. Ch. 2). A greater share of any vertical load is therefore borne by the anulus fibrosus. Consequently, the anulus fibrosus is subject to greater stresses and undergoes changes reflecting the increasing and different strains it suffers.

With age, the collagen lamellae of the anulus increase in thickness and become increasingly fibrillated ³⁵^–³⁸ and cracks and cavities may develop,^5,³⁹ which may enlarge to become clefts and overt fissures.³² The number of incomplete lamellae increases.³⁷ Such changes are not necessarily due to externally applied injuries to the spine but can simply be due to repeated minor insults sustained by the overloaded anulus fibrosus during trunk movements in the course of activities of daily living. Although the tensile strength of the anulus decreases with degeneration of the disc, there is no simple relationship between age and tensile properties.⁴⁰

Narrowing of the intervertebral discs has previously been considered one of the signs of pathological ageing of the lumbar spine ^32,^41,⁴² but large-scale post-mortem studies have now refuted this notion. The dimensions of the lumbar intervertebral discs increase with age. Between the second and seventh decades, the anteroposterior diameter of the lumbar discs increases by about 10% in females and 2% in males,³⁰ and there is about a 10% increase in the height of most discs.³⁰ Furthermore, the upper and lower surfaces of the discs increase in convexity,³⁰ a change which occurs at the expense of the shape of the vertebral bodies (see below).

Maintenance of disc height is the ‘normal’ feature of ageing, and any loss of trunk stature with age is the result of decreases in vertebral body height.⁴³^–⁴⁶ Overt disc narrowing invites the consideration of some process other than ageing, and this is considered in Chapter 15.

Changes in the vertebral endplate

In the newborn, the vertebral endplate is part of the growth plate of the vertebral body. Towards the intervertebral disc, the articular region of the endplate is formed by fibrocartilage, while on the vertebral body side, columns of proliferating cells extend into the ossifying vertebral body (see Ch. 12). By the age of 10–15 years, the articular region of the endplate becomes relatively thicker, while the growth zone decreases in thickness, and proliferating cells become fewer.⁴⁷ As vertebral growth slows during the 17th–20th years, the vertebral endplate is gradually sealed off from the vertebral body by the development of the subchondral bone plate, and after the age of 20 only the articular region of the original growth plate persists.⁴⁷ Between the ages of 20 and 65, the endplate becomes thinner⁴⁷ and cell death occurs in the superficial layers of the cartilage.³⁸

In the subchondral bone of the endplate, vascular channels are gradually occluded,⁴⁷ resulting in a decrease in the permeability of the endplate region for nutrients to the disc. This impaired nutrition may be one of the factors that cause the biochemical changes in the nucleus pulposus, but it seems to come too late in life to be the fundamental cause.

With age, the apparent strength of the vertebral endplate decreases,^34,⁴⁸ but because the strength of the endplate depends on the strength of the underlying vertebral body, this change is better considered together with the other changes that affect the vertebral body.

Changes in the vertebral body

With age, there is an overall decrease in bone density in the lumbar vertebral bodies ^43,^44,⁴⁹ and a decrease in bone strength.^34,⁵⁰ These changes in density and strength correlate with changes in the size and pattern of trabeculae in the vertebral body.

Vertical trabeculae are slowly absorbed, although those that persist are said to be thickened.⁵¹ On the other hand, horizontal trabeculae are absorbed and not replaced.^49,⁵¹ Consequently, ageing of the vertebral bodies is characterised by the loss of horizontal trabeculae^49,⁵¹ and this is most marked in the central portion of the vertebral body (that part overlying the nucleus pulposus).

The loss of horizontal trabeculae removes their bracing effect on the vertical trabeculae (see Ch. 1), and the load-bearing capacity of the central portion of the vertebral body decreases. Overall, with weakening of the trabecular system, a greater proportion of the compressive load on vertebral bodies is borne by cortical bone. Over the age of 40, the trabecular bone bears only 35% of the load.^34,⁵⁰ However, cortical bone fails at only 2% deformation, whereas trabecular bone tolerates 9.5% deformation before failing.³⁴ Consequently, with greater reliance on cortical bone, the vertebral body becomes less resistant to deformation and injury.

Lacking support from the underlying bone, the vertebral endplates deform by microfracture ⁵² and gradually bow into the vertebral body, imparting a concave shape to the superior and inferior surfaces of the vertebral body.^30,⁴⁹ Moreover, the central portion of the vertebral endplate is rendered more liable to fracture in the face of excessive compressive loads applied to the disc, and with increasing age microfractures can be found in the endplates and vertical trabeculae of vertebral bodies.⁵³^–⁵⁸

Fractures in the vertebral endplates may be large enough to allow nuclear material to extrude into the vertebral body, forming so-called Schmorl’s nodes. Schmorl’s nodes, however, are more a feature of the lower thoracic and thoracolumbar spines and have a low incidence below the level of L2.^59,⁶⁰ Per se, they are not symptomatic, nor are they related to age; their incidence is greatest in adolescence and they do not increase in frequency with age.^59,⁶⁰ Nevertheless, smaller protrusions of disc material into the vertebral bodies are not without significance and this is described in Chapter 15.

Changes in the zygapophysial joints

The subchondral bone of the lumbar zygapophysial joints increases in thickness during growth and reaches a maximum between the ages of 20 and 50 years.^61,⁶² Thereafter, it gradually gets thinner.^61,⁶³ The articular cartilage, on the other hand, steadily increases in thickness with age but exhibits certain focal changes that start in the fourth decade and which can be related to the stresses applied to these joints.

In the anteromedial third of curved zygapophysial joints, the cartilage exhibits cell hypertrophy (particularly in the midzone layer), which progresses to vertical fibrillation of the cartilage associated with sclerosis of the subchondral bone plate.⁶² At any stage, these changes are more advanced in the concave, superior articular process than in the inferior articular process. It is the anteromedial, or backward-facing, portion of this facet that resists the forward shear stresses applied to the intervertebral joint during weight-bearing and flexion movements (see Chs 2 and 8), and it can be surmised that the fibrillation that develops with age in this region reflects the repeated stresses incurred in the course of normal activities of daily living.⁶²^–⁶⁴ Severe or repeated pressures may result in erosion and focal thinning of the cartilage, while other regions may exhibit swelling that accounts for the general increase in thickness of the articular cartilage.^63,⁶⁴ Where cartilage is lost, fibro-fatty intra-articular inclusions may increase in size to fill the space vacated by the cartilage.⁶²

The posterior section of the joint characteristically exhibits a different kind of splitting of cartilage – parallel to the joint surface. A split piece of cartilage may remain attached to the joint capsule and form a false intra-articular meniscoid.⁶²

Cell hypertrophy is almost universal in the fourth decade, and minor fibrillation is common in the fourth and fifth decades. Older joints exhibit gross thickening and irregularity of the calcified zone of cartilage and increased collagen in the superficial layers. The cells are fewer and have smaller nuclei. The changes in cartilage are more severe in the polar regions of the joint than at its centre. In older joints, the distinction between changes in the anteromedial and posterior portions of the joint is lost.⁶²

Other features exhibited by the joints are the development of osteophytes and ‘wrap-around bumpers’. Osteophytes develop along the 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. Presumably, as a result of repeated stresses at these sites during rotatory movements, the articular cartilage spreads out to cover and protect the edges of the bony articular process.

Changes in movements

The biochemical and structural changes in the joints of the lumbar spine have an inevitable effect on the mechanical properties, and therefore movements, of the spine. Older lumbar spines show a greater amount of creep and hysteresis, and a greater set after creep deformation,⁶⁵ but they show a decreased range of motion. A progressive decrease in range of motion with age has been demonstrated in cadavers^59,⁶⁶^–⁶⁸ and in living subjects using both clinical⁶⁷ and radiographic^59,^66,⁶⁹ methods, and is evident in the ranges of motion both of the entire lumbar spine^67,⁶⁸ and of individual intervertebral joints.^59,^66,⁶⁹

Young children, strikingly, show the greatest lumbar mobility. At various segmental levels, they are between 50% and 300% more mobile than middle-aged subjects.^67,⁶⁹ Mobility decreases considerably by adolescence, and beyond the age of 30 there is a gradual but definite decrease in mobility.^59,^66,^67,⁶⁹

Because ‘release’ experiments show that removing the posterior ligaments and zygapophysial joints does not greatly increase the range of flexion in older cadavers,⁶⁸ it appears that increased stiffness in the intervertebral discs is the principal cause of the reduction in mobility that develops with ageing. This can be readily ascribed to the dehydration and fibrosis of older intervertebral discs.

The greater hysteresis seen in older spines is probably due to the decreased water-binding capacity of their intervertebral discs.⁶⁵ Less able to attract water, these discs take longer to resume their original configuration and structure after deformation.

Spondylosis and degenerative joint disease

It has been customary to describe certain changes in the intervertebral discs and zygapophysial joints as features of a disease. In the case of the intervertebral discs, the disease has been ‘spondylosis’, and in the case of the zygapophysial joints it has been called ‘osteoarthrosis’ or ‘degenerative joint disease’.

The cardinal features of spondylosis are said to be the development of osteophytes (bony spurs) along the junction of vertebral bodies and their intervertebral discs.⁷⁰^–⁷² However, when viewed in the context of other changes that occur with ageing, it is evident that the features of spondylosis are not those of some aggressive disease that seemingly attacks the body, but are the natural consequences of the stresses applied to the spine throughout life. Whether they should be called ‘degenerative changes’ or ‘age changes’ may appear simply to be semantics but the development of osteophytes can be viewed as a reactive and adaptive change that seeks to compensate for biomechanical aberrations. The process is active and purposeful, and does not warrant the description as a degenerative process.

As the nucleus pulposus dries out, the intervertebral disc becomes less resilient and stiffer, and the anulus fibrosus bears more of the loads applied to the disc. To sustain greater loads, the disc and the vertebral bodies adapt; the pattern of adaptation depends on the nature and direction of the particular stress being compensated.

Excessive compression can result in the ossification of the terminal ends of the collagen fibres of the anulus fibrosus. This can occur focally, along the anterior and posterior margins of the disc where compressive strains are concentrated during extension and flexion movements and postures. A more prolific development of osteophytes can occur around the entire margin of the vertebral body in response to excessive vertical load-bearing. This phenomenon can be viewed as if the vertebral body is trying to expand its articular surface area. By distributing axial loads over a wider area, the vertebral body lessens the stress applied to the anulus fibrosus during weight-bearing.

Interpreted in this way, the development of osteophytes is only a natural response to the altered mechanics of the lumbar spine in turn due to more fundamental biochemical changes in the intervertebral disc. Consequently, spondylosis should not be viewed as a disease but as an expected morphological change with age.

Perhaps the most crucial argument against viewing spondylosis and spinal osteoarthrosis as diseases is that they are so irregularly (if not infrequently) associated with symptoms and disability. The incidence of spondylosis and osteoarthrosis is just as great in patients with symptoms as in patients without symptoms.⁷²^–⁷⁴

This raises the great paradox in the field of spinal pain, namely that while some patients with spondylosis or osteoarthrosis may present with pain, there are others with the same age changes who do not have pain, and many patients with pain do not have a trace of spondylosis or osteoarthrosis. Consequently, spondylosis or osteoarthrosis cannot legitimately be viewed as a pathological diagnosis. Some other, or additional, factor must be the cause of pain, and the resolution of this problem is addressed in Chapter 15.

References

1 Scott JE, Bosworth TR, Cribb AM, et al. The chemical morphology of age-related changes in human intervertebral disc glycosaminoglycans from cervical, thoracic and lumbar nucleus pulposus and annulus fibrosus. J Anat. 1994;184:73-82.

2 Taylor JR, Scott JE, Cribb AM, et al. Human intervertebral disc acid glycosaminoglycans. J Anat. 1992;180:137-141.

3 Johnstone B, Bayliss MT. The large proteoglycans of the human intervertebral disc. Spine. 1995;20:674-684.

4 Beard HK, Stevens RL. Biochemical changes in the intervertebral disc. In: Jayson MIV, editor. The Lumbar Spine and Backache. 2nd ed. London: Pitman; 1980:407-436. Ch. 14

5 Buckwalter JA. Spine update. Aging and degeneration of the human intervertebral disc. Spine. 1995;20:1307-1314.

6 Gower WE, Pedrini V. Age-related variation in protein polysaccharides from human nucleus pulposus, annulus fibrosus and costal cartilage. J Bone Joint Surg. 1969;51A:1154-1162.