Conclusiones

EFFECTS ON VERTEBRAL BODY

Aging results in progressive bone loss, which begins at 30 to 40 years of age and continues for the remainder of a person’s life. This process accelerates considerably in women for 8 to 10 years following menopause. It mainly affects trabecular bones, especially the vertebral bodies. Bone loss is 1 to 2% per year and can reach 12%

2 years following oophorectomy (Genant, Riggs). This loss of bone mass, or osteopenia, results in compression fractures, often spontaneous or following trivial trauma.

EFFECTS ON INTERVERTEBRAL DISK With age, the intervertebral disk dehydrates and the physicochemical state of the ground substance is altered.

The result is that the collagen fibers, which are few and slender at the beginning of life, become tight, thicken, and tend to group together with age, in almost parallel direc-tion, and form fibrous bundles. This can be seen on mac-roscopic sections of the aged disk. The process is called the “maturation of collagen,” and it increases notably in the second part of life, after about age 40. The rate of mucopolysaccharide production increases briefly, and then progressively diminishes for the duration of life.

Nucleus Pulposus

Little by little, the nucleus pulposus loses its gelatinous homogeneous character, the very quality that makes it a remarkable shock absorber. While this is occurring, the biaxial alignment of the fibers of the annulus fibrosus changes; they become unidirectional bundles, resulting in a significant loss of elasticity. They become less hydro-philic as the years go by, with water occupying a smaller proportion of the disk (79% in young children to 70% at 70 years of age). As we previously remarked, this process of aging also affects the cartilaginous endplates, reducing

possible sources of nutrition for the nucleus, which gets its nutrition from the apertures of the endplates. The more this osmotic exchange decreases, the more rapidly a disk deteriorates. Fortunately, this process occurs without clini-cal manifestations. At the same time that a disk ages, the ligaments stiffen and progressively limit spinal motion.

As humans age, however, they progressively reduce their activities, and therefore an equilibrium can often be estab-lished between a fragile disk and reduced disk mobility (de Séze) (Fig. 13.1).

For various reasons (e.g., trauma), some disks degen-erate earlier than others. A disk can become old in a young subject. When a disk becomes vulnerable, it is generally the posterior annulus fibrosus that is most affected. This is the part that is subject to most of the compressive loading and thus fails; it is either compressed, forced back, or torn, resulting in a posterior or posterolateral disk her-niation.

Formation of Osteophytes

De Séze states, “In other cases, under the isolated or combined influence of aging, professional activities, and constitutional weakness, while the central nucleus pulpo-sus degenerates, the annulus fibropulpo-sus is progressively driven anteriorly toward the periphery, where it comes in contact with the anterior longitudinal ligament. At this point a process of subligamentous ossification will occur, resulting in the formation of an osteophytic ring around the degenerated disk” (Fig. 13.2 and Fig. 13.3).

This osteophyte originates at the vertebral body in the subligamentous zone found between the anterior longitu-dinal ligament (which, as we noted previously, adheres loosely to the disk but firmly to the vertebral body on the side of the endplate) and the attachment of the annulus fibrosus. It is molded on that ligament, which, due to disk degeneration, will bulge more and more. This explains the tendency for osteophytes to form horizontally when a very deteriorated disk is flattened; their orientation is more vertical when a disk is less flattened (Fig. 13.3).

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EFFECTS ON FACET JOINTS

Prior to stiffening of the ligamentous system, loss of disk height creates instability of the intervertebral joint and, in some cases, joint hypermobility (Junghanns). The degenerating disk will also affect other elements of a mobile segment: facet joints (Fig. 13.4 and Fig. 13.5) that become arthrotic and interspinous ligaments. In hyperlor-dosis, two spinal segments can come into contact in the lumbar region. This is known as the “kissing spine” or, if it has progressed by one more degree, becomes a true arthrosis with molding of the spine at contact (syndrome of Baastrup; see L2, L3, and L4 on Fig. 13.6).

In 30 postmortem examinations of subjects 30 to 70 years of age, Rissanen showed that there were an equal percentage and parallelism between the degeneration of the disk and the degeneration of the interspinous ligament.

Trophostatic Syndrome of Menopause All the consequences of intervertebral disk degenera-tion of maximum intensity can be seen in what de Séze and Caroit have called the “trophostatic syndrome of the menopausal woman.” Heaviness and loosening of the abdomen, together with postural collapse and compression of the vertebral column produce the following deforma-tions. Hyperlordosis occurs, which results in increased stress on the lower lumbar facet joints. This increased stress results in increased shearing and a tendency toward anterolisthesis. As a consequence of the same stress,

Figure 13.1 a. Normal intervertebral disk. b. Degenerative disk including deterioration of the annulus fibrosus and nucleus pulposus.

Figure 13.2 Formation of an anterior osteophyte (in section).

Figure 13.3 Lateral view. The osteophyte has formed a ring.

CHAPTER 13 THE AGING SPINE 71

retrolisthesis of the vertebrae of the superior lumbar region can occur, which results in the vertebrae resting in a pos-terior position on the subjacent vertebra, producing shear-ing of the facet joints. As a result of the deformation, the spinous processes come into contact with each other to produce an arthrosis.

Intervertebral Foramen

The intervertebral foramen also undergoes changes as a result of the proliferation of osteophytes and disk degen-eration. This occurs particularly at the level of the cervical spine because of the existence of the uncinate process and the formation of disco-osteophytic nodules (Fig. 13.7) and because of the frequency of spondylosis of the facet joints.

The latter causes a narrowing of the posterior neurofo-ramina and is most commonly seen at its superior aspect.

The inferior aspect is affected only in the advanced stage of the spondylosis. At the cervical level, posterior spondy-losis can exist without a concomitant discal lesion (Hirsch, Payne et al., Friedenberg et al.).

The evolutionary formation of the disco-osteophytic nodule is debated. For some, there is an uncovertebral articulation with an articular cavity and a synovial mem-brane. This articulation could become arthrotic. When a fragment of the nucleus of the degenerated disk bulges into the articulations, it creates a “hard herniated disk”

called a disco-osteophytic nodule (Fig. 13.8).

Figure 13.4 With further disk deterioration, there is increased stress on the facet joints, resulting in posterior element arthrosis.

Figure 13.5 Lateral view of a segment with complete disk degeneration and arthrosis of the facet joint.

Figure 13.6 Postmenopausal syndrome of de Séze and Caroit.

Figure 13.7 Osteophytic nodule (N) at cervical level.

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According to Töndury, there is no uncovertebral artic-ulation (Fig. 13.9). He believed that after age 10, fibrous fissures form in the annulus at the periphery, gradually extending toward the center. When they reach the annulus, the discal jelly reaches the periphery, forming a hard her-niated disk (Fig. 13.8 and Fig. 5.4).

At the level of the cervical spine, these formations affect not only the elements going through the foramen

intervertebrale, but also the vertebral artery that extends into the transverse openings. This was demonstrated on arteriograms, but it could not be definitely affirmed that these formations, like those seen in spondylosis, play a direct pathologic role because images of sinus arteries are seen in asymptomatic patients. In spite of this, the success of uncinate processectomies has been demonstrated in some cases (Jung).

Figure 13.8 Formation of the osteophytic nodule: classic theory. a. There is an uncovertebral articulation with an artic-ular cavity and synovial tissue. This articulation can thus undergo arthritic degeneration. b. The disk degeneration pro-duces fissures in the annulus in the region of the nucleus pulposus. This can cause enlargement and reach the periph-ery. As a result, a fragment of the nucleus pulposus can then slip out into the arthrotic articulation and create a hard discal herniation known as a discal osteophyte.

Figure 13.9 Formation of the osteophytic nodules: Töndury theory. a. There is no uncovertebral articulation. b. After the age of 10, there is fissuring of the annulus fibrosus, which allows a progressive movement of the nucleus pulposus out-ward. As this happens, the material of the nucleus pulposus hardens in the fissures and, on gaining entry into the periph-ery, forms the osteophytic nodules.

III

PAIN OF SPINAL