November 2, 2010, researchers from the Veterans Affairs Medical Center at the University of California, San Francisco, published a study in the Annals of Internal Medicine titled (1):
The Epidemiology of Pain During the Last 2 Years of Life
The study included 4,703 older adults with mean age of 75.7 years at the time of their deaths. These subjects were evaluated for the presence of clinically significant pain, as indicated by a report that the participant was “often troubled” by pain of at least moderate severity. Their records showed that the prevalence of such pain 24 months before death was 26%. The pain prevalence remained flat until 4 months before death, then the pain increased, reaching 46% in the last month of life.
Importantly, the prevalence of pain in the last month of life was 60% among patients with arthritis versus 26% among patients without arthritis and did not differ by terminal diagnosis category (cancer, heart disease, frailty, sudden death, or other causes).
The authors concluded:
“Although the prevalence of pain increases in the last 4 months of life, pain is present in more than one quarter of elderly persons during the last 2 years of life.”
“Arthritis is strongly associated with pain at the end of life.”
This study indicates that a non-fatal condition, arthritis, significantly affects the quality of life in the elderly.
A number of well-respected reference texts indicate that the incidence of osteoarthritis is strongly associated with single event macro-trauma, repeated micro-trauma, alignment problems, and age. Such texts include:
A 1993 study published in the journal Injury (7) showed strong evidence that a single motor vehicle collision accelerates the process of disc degenerative disease of the cervical spine.
A 1997 study published in the Journal of Orthopedic Medicine (8) showed that a single motor vehicle collision accelerated degenerative changes in the cervical spine by about 10 years earlier compared to the control group.
A 2004 study published in the European Spine Journal (9) showed that the repetitive heading of soccer balls accelerates degenerative changes in the cervical spine by 10–20 years earlier than that of the normal population.
A 2009 study published in the Journal of Physical Activity and Health (10) showed that knee and hip arthritis is over 3 times more prevalent in retired NFL players than in the general U.S. population of the same age.
An excellent discussion of the pathophysiological process leading to spinal osteoarthritis is presented by the late (d. 2006) William H Kirkaldy-Willis, MD. Dr. Kirkaldy-Willis was Emeritus Professor, Department of Orthopaedic Surgery, University Hospital, University of Saskatchewan College of Medicine. In his 1988 (second edition) book Managing Low Back Pain, there are 19 international multidisciplinary distinguished contributing authors (5). Dr. Kirkaldy-Willis authored a chapter in the book titled:
“The Three Phases of the Spectrum of Degenerative Disease”
Dr. Kirkaldy-Willis describes how spinal segments are comprised of a three-joint complex: the two posterior facet joints and the intervertebral disc. He notes that the three joints always work together. Consequently, injury or stress to any single component of the three-joint complex will mechanically affect the other two components. His breakdown of the three phases of spinal degenerative disease is as follows:
First Phase of Spondylosis
In the first phase, the normal function of the three-joint complex is interrupted as a consequence of injury or chronic stress. This causes the posterior musculature of the involved segment to go into a state of hypertonic contraction. This restricts normal movement. The hypertonic contraction of the muscles also causes muscle ischemia, causing pain. The muscle hypertonicity also causes a slight misalignment of the posterior facet joints, which is known as a “subluxation.” Eventually tissue fibrosis begins to appear.
Second Phase of Spondylosis
If the first phase is allowed to persist, the second phase will eventually ensue. In the second phase, there is abnormal increased movement. Laxity of the posterior joint capsule and of the annulus fibrosus is seen in anatomical sections. Local fibrosis is problematic because “the collagen of scar tissue is not as strong as normal collagen.” Therefore, there is an increased propensity for additional injury, inflammation, pain, and muscle hypertonicity.
Third Phase of Spondylosis
If the second phase is allowed to persist, the third phase will eventually ensue. In the third phase, degenerative changes begin to appear. As the degenerative changes advance, the unstable segment regains its stability because of fibrosis and osteophytes form around the posterior joints and within and around the disc. In this stabilization phase, the facet joints will progress through the following sequence:
Degeneration of Articular Hyaline Cartilage
Development of Intra-articular Adhesions
Increasing Capsular Laxity
Subluxation of the Joint Surfaces
Formation of Subperiosteal Osteophytes
Enlargement of Both Inferior and Superior Facets
Ultimately Greatly Reduced Movement
Simultaneous with this sequence of changes in the facet joints, there are parallel changes in the intervertebral disc. These changes follow this sequence:
The Development of Small Circumferential Tears in the Annulus Fibrosis
The Circumferential Tears in the Annulus Become Larger and Coalesce to form Radial Tears that Pass From the Annulus to the Nucleus Pulposus
Eventual Internal Disruption of the Disc
Disc Degeneration with Disc Resorption
Peripheral Osteophytes Around the Circumference of the Disc
Ultimately Greatly Reduced Movement
Dr. Kirkaldy-Willis notes that the “greatly reduced motion” associated with spinal degenerative disease opens Melzack’s and Wall’s “pain gate,” accounting for the increased pain that is often associated with osteoarthritis (12).
A more recent comprehensive review of osteoarthritis appeared in the American Journal of Physical Medicine and Rehabilitation in 2006, titled (11):
Epidemiology, Risk Factors, and Pathophysiology
The authors, Susan V Garstand, MD and Todd P Stitik, MD, are from the University of Medicine and Dentistry of New Jersey. In this article, Drs. Garstand and Stitik note that osteoarthritis is “the clinical and pathologic outcome of a range of disorders that results in structural and functional failure of synovial joints. Osteoarthritis occurs when the dynamic equilibrium between the breakdown and repair of joint tissues is overwhelmed.”
Drs. Garstand and Stitik note that osteoarthritis is the most prevalent form of arthritis and a major cause of disability in people aged 65 and older. Osteoarthritis affects the majority of adults over age 55.
Garstand and Stitik note that the incidence of osteoarthritis is influenced by both systemic and local factors:
• Age: “The presence of radiographic osteoarthritis rises with age at all joint sites.”
• Hormonal Status
• Genetic Factors; osteoarthritis has a major genetic component
• Bone Density
• Nutritional Factors:
There is evidence that osteoarthritis is linked to free radicals, and that high dietary antioxidants (especially vitamins C and D) are protective against the development of osteoarthritis. “Chondrocyte senescence is thought to be the result of chronic oxidative stress.”
Local Factors: Local factors “result in abnormal biomechanical loading of
• “Altered joint biomechanics”
• ligamentous laxity
• impaired proprioception. With aging, there is a decline in proprioception, causing
decreased neurologic responses, impairing proprioceptive joint-protective
mechanisms. Consequently, reduced proprioception advances osteoarthritis.
• muscle weakness
• Prior joint injuries
• Occupational Factors
• Effects of sports and physical activities
• Developmental abnormalities
Garstand and Stitik note that if systemic factors are present, the joints are vulnerable, and thus local biomechanical factors will have more of an impact on joint degeneration and osteoarthritis.
Essential Fatty Acid Connection
In his 2008 book Toxic Fat, biochemist Barry Sears (13) describes how the omega-6 fatty acid arachidonic acid is biochemically converted into the pro-inflammatory eicosanoid hormone prostaglandin E2 (PGE2).
Cyclo-oxygenase (COX)/Lipo-oxygenase (LOX) Pathways
The conversion of the omega-6 fatty acid arachidonic acid is biochemically converted into the pro-inflammatory eicosanoid hormone prostaglandin E2 (PGE2) and is important in a discussion of osteoarthritis because a number of studies have implicated prostaglandin E2 in the accelerated degradation of cartilage. For example, in 2002 the journal Neurosurgery Focus published a study linking disc degeneration to prostaglandin E2 (14). Later in 2002, the journal Spine published a study linking intervertebral disc herniation to the enzyme cyclo-oxygenase-2, which converts the toxic fat arachidonic acid to prostaglandin E2 (15).
Also in 2002, the journal Arthritis & Rheumatism (16) published a study showing that the pathologic indicators manifested in human osteoarthritic cartilage could be significantly abrogated by exposure of the cartilage to omega-3 fatty acids. This is important because omega-3 fatty acids, especially the omega-3 eicosapentaenoic acid (EPA), is known to inhibit the conversion of arachidonic acid into prostaglandin E2. Neither omega-6 nor omega-9 (such as olive oil) could stop the cartilage breakdown biomarkers. These authors concluded that omega-3 fatty acids play a role in halting or slowing degradative and inflammatory factors that contribute to the progression of osteoarthritis. Specifically, they state:
“Dietary supplementation with n-3 PUFA may prove useful in both quiescent and active arthritis.”
“Our findings support the results of epidemiologic and clinical studies that have demonstrated dietary supplementation with omega-3 fatty acids to be beneficial in reducing pain and inflammation in human arthritic diseases.”
“It has long been recognized that dietary supplementation with fish oils that are enriched with n-3 PUFAs can provide benefit in the treatment of arthritis.”
In 2006, Leslie Cleland and colleagues published a study pertaining to the ut