4.1 The Demographics of Aging

A deterioration of bone quality over time is inevitable. Osteoporosis is a relentlessly progressive process. However, it does not manifest until midlife. It should be kept in mind that in millennia gone by, life expectancy was in the middle 30s to early 40s. Today, this age range equates with early life to midlife. Homo sapiens today, then, are essentially living on borrowed time. It is during this borrowed-time phase of our lives that bone quality progressively and exponentially degrades. Interestingly, the health of aging Homo sapiens is improving, and life expectancy increasing. Today, more than 20% of all Americans are older than 65 years of age (approximately 40 million people). More than 15% are older than 85 years. In fact, by 2020, it expected that there will be 55 million people older than 65 years, and that by 2030, this number will reach 72 million.

Our population is aging, and aging at a relatively alarming rate. A 65-year-old can reasonably expect to live another 20 or even another 30 or more years. General health in the aged does not correlate with bone health. Bone health in this age group diminishes at a faster rate than general health. Fixation strength in the osteopenic spine is one-fourth that of normal bone.¹ In an osteoporotic spine, fixation strength is expected to be much worse.

4.2 The Aging Intervertebral Disc

A discussion of bone and bone quality should begin with mention of intervertebral disc aging: In youth, the intervertebral disc is composed of a tough, fibrous annulus fibrosus that surrounds and contains a gelatinous nucleus pulposus (Fig. 4.1a). Over time, during the aging process, the nucleus pulposus dessicates, and the annulus fibrosus degrades into a fibrocartilaginous-like scar with suboptimal resilience. This transformation involves a change in the loading pattern of the disc. In youth, the disc is loaded centrally, with the nucleus pulposus pressurized during axial loading. This results in a distribution of pressure to the rostral and caudal endplates and annulus fibrosus circumferentially (Fig. 4.2b).

As the spine ages, axial loads are borne more laterally because the more central nucleus pulposus can no longer bear loads as a consequence of its dessication. As a result, the load is increasingly borne by the peripheral fibrocartilaginous scar equivalent of the annulus fibrosus.

The intervertebral disc degenerative process, as outlined, is associated with pressure changes within the disc interspace, as has been documented in humans. Such is depicted in (Fig. 4.2a–c). In youth, the pressures within the central portion of the intervertebral disc are relatively high and uniform during axial loading. As the aging process transpires, this high central pressure diminishes and can fall below zero in some conditions. The latter situation may be associated with the vacuum phenomenon (Fig. 4.2d).

The last phase of the degenerative process is associated with restabilization of the spine, à la Kirkaldy-Willis. During this phase, osteophytes form, disc interspace height diminishes, and the mobility of the intervertebral joint declines. Many intervertebral joints do not reach this phase before symptoms of compression or instability arise. These are the patients we often consider for surgery. Once the spine stabilizes, though, the rate of progression of spine deformation and the degenerative process itself declines.

4.3 Aging Bone

As the intervertebral joint degenerates with time, bone changes in structure in order to adapt to the loading conditions to which the spine is exposed. Bone structure forms and matures in response to loading to provide maximum strength with minimum mass. For example, trabecular bone in the vertebral body is aligned in a vertical direction. Such trabeculation supports the spine as pillars may support a building (Fig. 4.3). So, at least in early life and midlife, the intervertebral disc degenerates, while bone adapts to the loads applied. This is all in keeping with Wolff’s law, which is paraphrased as follows:

“Bone is laid down where stresses require its presence, and bone is absorbed where stresses do not require it.”

So, why is it that bone bolsters itself in response to loading yet osteoporosis ravages the aging spine from a spine competence perspective? As already stated, bone structure forms in response to loading. This provides maximum strength with minimum mass. The problem associated with aging, however, is related to the progressive loss of mass. Hence, these factors essentially compete—with one augmenting bone structural integrity and the other degrading structural integrity.

4.4 Aging-Associated Subsidence and Spine Deformation

As we age, particularly in midlife and beyond, we become shorter. Most of the shortening occurs at the level of the axial spine. Vertebral collapse and spine deformation progress. Both contribute to the aforementioned shortening. This loss of height from both causes is clearly typified in Fig. 4.4, in which degenerative rotatory kyphoscoliosis is present. Of note, once spine deformation begins, for whatever reason, it tends to progress. “Deformity begets deformity.”

It is this aging-associated subsidence and spine deformation that often progresses to such an extent that surgical intervention is considered. The remainder of this chapter focuses on the surgical treatment of such pathologies and the effect of diminished bone quality on the operative decision-making process. The focus is on bone quality as it affects bony fixation via spinal implant anchors in osteoporotic bone.

4.5 The Optimization of Bone Quality

Osteoporosis can be altered (treated) to some degree. The extent of bone demineralization is quantifiable via bone mineral density studies and bone mineral density scores. Such assessments provide valuable information regarding the patient’s bone health and a “report card” of sorts that can be used to both guide and monitor treatment. Low bone mineral density correlates with a higher incidence of fractures. Medical management strategies that are used to manage and prevent osteoporosis include calcium intake, vitamins D and K supplementation, weight-bearing exercises, lifestyle changes, and the use of antiresorptive agents and agents to stimulate bone formation. It behooves the treating physician to become familiar with all of these strategies because each may play a role, depending on the case.² One should also be cognizant of the complications associated with treatment. The observation of a correlation between bisphosphonates and femoral shaft fractures exemplifies this point.³