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Living with Back Pain? Is back pain interfering with your daily activity?

Please join us for the following health lecture to learn about options for relieving pain and restoring mobility.

Dispelling Myths about Low Back Pain and Disc Degeneration
Janet Limke, MD
NEBH Spine Center

Wednesday, May 6, 2010
6 - 7 pm
New England Baptist Hospital

You'll be able to ask questions and learn about options for relieving low back pain and restoring mobility.

Space is limited at this free event. Register today by calling 617-754-5477 or 1-800-370-6325.

Free parking - Light refreshments will be served.

It is common for people with persistent and severe spinal pain to undergoing diagnostic imaging utilizing X-rays, MRI, or CAT scans. The results may show that the spine is degenerating, and that discs are collapsing, dehydrated, bulging, protruding, herniated or ruptured; the facet joints are arthritic; and the vertebrae are aligned in an abnormal way, have bone spurs, or other problems. Over the last few decades we have learned that degeneration of the spine is a result of loss of cell function, or part of the aging process, and not a result of wear and tear. These finding have important implications for everyone who has spinal pain or has had imaging studies that revealed spinal degeneration. A basic understanding of these common processes helps to put news about spinal degeneration in perspective, and helps to avoid unnecessary concern and lifestyle changes.

The Spine is a Living Structure

All parts of the body are produced and maintained by living cells, and the continued function of every part of the body is dependent on proper cellular function. The spine is no exception.

Bone Cells and Bone Changes with Aging

The strength of all bones including vertebrae is dependent on correct function of the bone cells. The most important are osteoblasts or bone building cells, osteoclasts or bone destroying cells, and osteocytes or bone maintaining cells. Osteoblasts and osteoclasts continuously balance each other to turnover or remodel our bones. A variety of hormones produced by the human body regulate the remodeling activities of the osteoblasts and osteoclasts.

Did You Know? Bone turnover is influenced mainly by parathyroid hormone, Vitamin D, calcitonin, and the sex hormones estrogen and testosterone. With advancing age, reduction of sex hormones, especially in women after menopause, results in an increase in osteoclasts or bone destroyer cell activities, with resulting loss in bone density. The bones themselves can produce powerful chemicals that influence osteoblasts and osteoclasts activities. Scientists has recently developed copies of one group of bone chemical called bone morphogenic proteins (BMP) that stimulate osteoblast bone formation and improve bone growth and healing. BMP is sometimes used in spine surgery to assist bone growth following spine fusion procedures. (For more information see The National Institute of Arthritis and Muskuloskeletal and Skin Diseases.)

The balance of bone turnover is also influenced by heredity, body build and nutrition. Tobacco use, excessive alcohol intake and frequent steroid use are several factors that increase bone loss, while good nutrition and weight bearing activities minimize bone loss.

With advancing age, bone turnover slowly shifts towards greater loss than production. This results in a gradual reduction of bone strength in everyone over age 65. When bone loss reaches a moderate level it is called osteopenia and when severe, it is called osteoporosis. These changes lead to an increase risk of bone fractures in the elderly and in others with more significant risk factors.

Regular physical stress on the bones such as occurs with physical activities and exercise has a positive influence on bone formation, and can help to slow or reverse bone loss caused by other factors. Abnormal stresses on bone can also increase bone formation.

Did You Know? In the face of degeneration of joint surfaces from arthritis, abnormal or uneven stresses can be placed on the surrounding bone and ligaments. This type of stress can result in an increased bone production next to arthritic joints (bone sclerosis) including an extension of bone into the surrounding ligaments (bone spurs). In the spine these bone changes can appear in the bone next to the discs (vertebral end plates) and the bone in the neural arch next to the facet joints.

Disc Cells and Disc Degeneration

The intervertebral discs are dependent on living cells for correct function. The gel-like material that comprises the nucleus pulposus at the center of the disc is maintained by specialized cells called nucleus cells (also called nucleus pulposus cells). These cells continuously turn over the nucleus pulposus, ensuring its proper consistency and water content. Nutrition and oxygen supply for these cells slowly diffuses into the discs through the vertebral end plates.

Surprisingly, nuclear cell function has been found to decrease early in life, resulting in gradual deterioration of the nucleus pulposus, with observed increase in fibrous content and decrease in water content starting in childhood and continuing throughout life. Ultimately, the loss of cell function results in disc dehydration (the water content of the disc no longer higher than the surrounding tissues), loss of disc volume and disc height, and splitting or fragmenting of the nucleus pulposus. These changes in the nucleus pulposus show up on MRI scans as loss of the height of the discs and as a reduction in the brightness of the discs, often reported as "reduced disc signal intensity," "disc desiccation," or "disc dehydration."

The anulus fibrosis is maintained by cells called anular cells (also called anulus fibrosis cells). Anular cells are related to fibroblast, or cells that take care of the fibers that hold the body together, and are thus responsible for maintaining the strong rings of the anulus fibrosis. It has been found that the function of these cells diminishes with age, with the onset of deteriorating function closely related in time to the loss of function of the nuclear cells and degeneration of the nucleus pulposus.

As we lose the anular cells, the collagen fibers of the anular rings begin to fray, split and disappear, which results in a general deterioration of the anulus fibrosis. Apparently, as the rings of the anulus fibrosis deteriorate, they slowly lose their ability to maintain tension in response to the compression forces on the disc, and the rings begin to fail and tear. These tears (called anular tears) never heal because inadequate numbers of cells are available to produce any meaningful repair. Over time, anular tears tend to increase in size as more and more rings fail. These tears have several patterns, some beginning in the inner layers of the anulus fibrosis and extending towards the outer edge of the disc (radial tears), and others splitting rings apart and following the circumference of the disc (concentric tears). Surprisingly, anular tears begin to appear in teenage years and gradually progress in number and size over time. These tears are so common, that 3 out of 4 people have radial tears and everyone has concentric tears in their lower lumbar discs by the age of thirty.

Did You Know? Most anular tears are not well visualized by MRI scans, though some appear as bright MRI signal in the anulus fibrosis called high intensity zones. Anular tears are well visualized using a special procedure called a discogram which involve injecting special dye into the disc and then imaging the disc with x-rays and CT scans.

Though anular tears occur in everyone, most do not produce any symptoms.

As anular tears progress through the anulus fibrosis, the outer edge of the disc wall may begin to deform. As deformities of the disc wall increases, they are called progressively disc bulges, disc protrusions and disc herniation. These terms simple mean that the disc wall extends beyond its normal anatomic boundaries, and these changes are commonly visualized by MRI and CT imaging studies. These deformities in the disc wall can extend into the vertebral canal and neural foramina, diminishing the space available for the spinal cord and nerve roots, and in some cases may actual displace or compress these structures. These changes are also common in people without any symptoms.

Anular tears can extend completely through the wall of the disc, resulting in a defect that extends from deep within the disc all the way to the epidural space of the spinal canal and neural foramen. Fragments of degenerated nucleus pulposus and inner anulus fibrosis can potentially separate from the surrounding disc material and pass through full thickness anular tears into the epidural space, potentially displacing or compressing the spinal cord or nerve roots. These fragments of disc material are referred to as disc extrusions or sequestrations, and often given the lay term "ruptured discs." These findings are uncommon in people without any symptoms, but are still noted on imaging studies in about one in every one hundred people who do not have any spine or leg complaints. It is important to remember that all of these abnormalities of the disc are the direct result of anular tears, and that anular tears results from degeneration of the anulus fibrosis as a consequence of dysfunction and progressive loss of anular cells.

The progression of disc degeneration actually occurs very slowly in most people's spines. However with advancing age, degeneration often results in a complete loss of the nucleus pulposus, development of small gas-filled cavities within the discs, and a reduction of overall disc height.

Did You Know? Several epidemiological studies have repeatedly imaged the spines of large groups of people using MRI scans and observed that loss of the height of discs and bulges of the disc walls progress very slowly, averaging about 1% per year.

The driving mechanism for disc degeneration is clearly loss of the nuclear and anular cells. The cause of this cell loss is only partially understood, but appears to be largely due to a process called apoptosis or genetically-programmed cell death. The process of apoptosis is extremely powerful, and appears to be unstoppable. Indeed, it is the process responsible for most of the changes that people notice with aging, with other examples being changes in our skin, hair, and vision. For any individual, it appears that the tendency to develop disc degeneration and other processes of aging are pre-programmed in their genetic code. Indeed in large studies of twins, it has been found that identical twins have remarkably similar degrees of disc degeneration on MRI scans.

Other factors can also influence cell loss and degeneration of the nucleus pulposus, but to a minor degree compared to genetics. These include degeneration of the cartilaginous surfaces of the vertebral end plates (also caused by apoptosis) which results in altered disc nutrition, and also smoking tobacco (which is generally harmful to all living cells). Surprisingly, daily stresses on the spine from work, physical activities and exercise have a very minor influence on disc degeneration.

Degeneration of the Facet Joints

By age 50, almost everyone has some degree of facet joint osteoarthritis (facet joint arthritis, facet joint degeneration). This is characterized by loss of the cartilage surfaces of the facet joints, thickening of the joint capsules and thickening and spurs forming in the bone around the joints called osteophytes. These degenerative changes begin to appear before age thirty, and gradually progress throughout life. The cause of facet osteoarthritis appears to be mainly age related loss of function of the cells that maintain the cartilage surfaces of the facet joints. To date, there is no evidence to suggest that other factors including physical activities or trauma accelerate this problem.

As discussed earlier (see facet joints), the facet joints act to control the degree of movement between vertebrae. As the facet joints degeneration, movement between vertebrae can be restricted, resulting in some people experience a reduction in overall mobility of the spine. For example, in the elderly facet degeneration in the cervical spine can reduce rotation and extension of the neck, which can result in limited ability to look straight up or rotate the head to the right and left.

With facet degeneration, these joints can lose their ability to control the position of the vertebrae, resulting in changes in vertebral alignment. The most common alignment change caused by facet degeneration is a forward slippage of the L3 or L4 vertebra called degenerative spondylolisthesis. This finding is commonly noted in imaging studies of people after the age of 50, and is present in about twenty percent of people over the age of 70. Degenerative spondylolisthesis is usually well tolerated and may be present for decades before it is discovered. It usually results in some degree of reduction of the dimensions of the vertebral canal, and may contribute to the development of lumbar spinal stenosis.

Degeneration of the Ligamentum Flavum

With advancing age, the ligamentum flavum also undergoes degenerative changes. The ligamentum flavum is normally very elastic. With bending forward and backward the distance between the laminae of adjacent vertebrae changes dramatically. The elastic properties of the ligamentum flavum allow it to change its length during these motions. Without this elastic ability, the ligament would fold in on itself during these movements, and potentially diminish the dimensions of the spinal canal. With aging, the elastic properties of the ligamentum flavum decrease, as the elastic fibers are lost and our production of stiffer collagen fibers increases.