Introduction

Back pain is one of the most common reasons for office visits to a physician. It accounts for 2% of all visits, surpassed only by routine examinations, diabetes, and hypertension.¹ Back pain is a condition that predominantly affects the older population. Increased survival rates, better health care outcomes, and improved economic status will increase the number of older people in our society. At present, persons older than 65 years constitute 13% of our population. In 30 years, they will constitute 30% of the United States population, and by the year 2050 they will makeup 60% of the population.² It is of paramount importance to recognize this trend of aging in the population and plan how best to fulfill the health needs of this growing part of our society.

Aging is a natural, inevitable, physiological change that leads to compromises in physical, mental, and functional abilities. At a cellular level, it represents decreased regeneration and repair, and increased catabolic changes that gradual deterioration in function. The spine, composed of the framework of vertebral columns and intervertebral disks encasing the spinal cord, is not insensitive to the onslaught of changes that occur during aging. The aging of the spinal cord results in decreased strength and agility and increased reflex times. However, the predominant effects of aging in the spine involve the mechanical components of the spine. Histologically, they can be classified as aging of the disks, the vertebral bodies, the facet joints, and the muscles and ligaments.

Intervertebral Disk

The intervertebral disks are remnants of the notochord and are interspersed between adjacent vertebral bodies of the spine except between the fused bodies of the sacrum and the coccyx. The intervertebral disks are composed of a circular ring of more resilient annulus fibrosus, which holds a central core of gelatinous material called the nucleus pulposus (Figure 3-1). Biochemically, both the annulus fibrosus and the nucleus pulposus contain proteoglycans in addition to water. The amount of water varies and is responsible for their varied characteristics and, consequently, their functions. The intervertebral disks derive their nutrition by diffusion across vertebral endplates. As the rate of permeability decreases with aging, the health of the disk is threatened.

FIGURE 3-1 Intervertebral disk. Outer annulus fibrosus surrounding inner nucleus pulposus.

(Courtesy of Wolfgang Rauschning, MD.)

The intervertebral disks are primarily shock absorbers and are resistant to compressive forces. During the process of aging, the daily wear and tear damage of years of mechanical stress compounded by decreased nutrition and water predispose the disks to degeneration. Associated with these local changes, systemic changes of aging such as decreased structural protein synthesis, impaired water metabolism, and decreased physical activity serve as additional insults to the fragile microenviroment of the aging disks.

The pathophysiology of disk degeneration involves a multitude of cellular and biochemical changes. Proteoglycans, responsible for the osmotic gradient and thus the hydration of the disk, are lost. There is overall fragmentation of type I and type II collagen within the disk, with an increase in the ratio of type I to type II collagen fibers. Furthermore, there is an increase in degradative enzymatic activity including cathepsins and matrix metalloproteinases (MMPs). As a result, there is a decrease in the biomechanical and load-sharing ability of the disk.

Due to decreased turgor and nutrition of the disks, radial and concentric fissures appear in the initial phases of degeneration. The normal avascular disks may develop microvascular capillaries at the periphery of the annulus fibrosus as a compensatory mechanism for decreased nutrition (Figure 3-2). However, this impaired neovascularization is detrimental, contributes to microedema, and exposes the disks to the body’s immune cells for the first time in adult life. Also, there is dissection of the microstructural organization of the annulus fibrosus. The radial fissures eventually enlarge and follow the path of least resistance posterolaterally in relation to the vertebral bodies and overlying the intervertebral foramina. In the late stages of disk degeneration, the nucleus pulposus tracks out over the intervertebral foramina and can compress the exiting spinal nerve, potentially causing symptoms of radiculopathy.

FIGURE 3-2 Neovascularization at periphery of an annular tear.

(Courtesy of Wolfgang Rauschning, MD.)