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

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