Posttraumatic Osteoarthritis
Medical research clearly shows that soldiers are especially susceptible to osteoarthritis after discharge from the service, and that osteoarthritis may manifest itself many years after the initial injury. In addition, due to gait issues, an affected limb can result in the development of osteoarthritis in proximal joints.
Scientists from the San Antonio Military Medical Center and the United States Army Institute of surgical research have recently reviewed the incidence and severity of osteoarthritis in veterans serving in Iraq and Afghanistan, Posttraumatic Osteoarthritis Caused by Battlefield Injuries: The Primary Source of Disability in Warriors. Arthritis was recognized as a disabling condition an average of 19 ± 10 months after injury.
Brown et al. estimated that 12% of symptomatic OA is attributable to posttraumatic osteoarthritis (PTOA) of the hip, knee, or ankle. OA is the most common cause of disability among service members who are medically separated from active duty. Among those with osteoarthritis as an unfitting condition, injuries to the spine and shoulder occurred most commonly. The rate of arthritis by injured anatomic region varied considerably. Injuries to the knee resulted in OA in all cases, and the elbow and ankle joints became arthritic following injury in greater than 90% of cases. Traumatic injury was the cause of 94.4% of all cases of joint OA and 75% of cases of spine OA.
PTOA is a common and disabling condition in combat-wounded warriors. The prevalence of OA was 28% in the veteran study population, compared with 12% in the civilian trauma population. In veterans, the permanent disability resulting from combat-related traumatic arthritis is substantial. The diagnosis of arthritis is accelerated in this group, with an average time of <2 years from injury to determination of disability as a result of arthritis. PTOA affects not only the appendicular joints but is disabling following injury to the spine, as well.
Dominick et al. reported that U.S. veterans experience a higher frequency of OA, chronic joint symptoms, and activity limitations than do persons in the general population. The study shows that osteoarthritis in veterans is a result of wear and tear caused by excessive trauma to joints in the process of active military training and combat. The study is limited by the lack of follow-up, as the focus was solely on veterans of the recent conflict in the Middle East. Studies of veterans of the Vietnam and Korean conflicts clearly show that osteoarthritis occurs many years after discharge from the military service.
In a study published at the MSMR, a publication of the Armed Forces Health Surveillance Center (Volume 17, Number 12, December 2010), the investigators found that over the last 10 years 68,449 incident diagnosis of osteoarthritis and 43,254 incident diagnoses of spondylosis were identified. The incidence rate of osteoarthritis increased dramatically, by 65% from 2001 to 2006. The scientists concluded that military training and operational service activities are often physically demanding and sometimes traumatic, e.g. heavy load bearing, and hand-to-hand combat training. Musculoskeletal disorders including osteoarthritis have been associated with specific occupations and some military occupations are inherently stressful to bones and joints, including pilots and paratroopers.
The recent study from the Department of Veterans’ Affairs explains why osteoarthritis appears many years after trauma to the joints, challenging long-held notions that osteoarthritis is a result mainly of wear and tear on the joints. Researchers led by Dr. William H. Robinson of the Department of Veterans’ Affairs Palo Alto Health Care System and Stanford University have provided new insights into the immune-system changes that may trigger cartilage breakdown. Their report appears in the Nov. 6, 2011 online edition of Nature Medicine. “This research can lead to a better quality of life for Veterans and others with osteoarthritis,” said Secretary of Veterans Affairs Eric K. Shinseki. “This is an example of how VA’s research program can lead to many significant breakthroughs in health care.” The researchers discovered that one component of the complement system, called the membrane attack complex, or MAC, is formed and activated in the joints of both humans and mice affected by osteoarthritis. They believe that when the MAC is aberrantly activated in the joints (a phenomenon called “dysregulation”), it induces low-grade inflammation and the production of enzymes that break down cartilage and result in the development of osteoarthritis.
This new study showed that initial damage to the joint sets in motion a chain of molecular events that escalates into an attack upon the damaged joint by one of the body’s key defense systems against bacterial and viral infections, the so-called complement system. This sequence of events involves activation of a chain reaction called the “complement cascade,” and begins early in the development of osteoarthritis. The complement system consists of an orchestra of proteins present in blood. Upon activation of the complement cascade — typically, in response to the presence of bacterial or viral infection — these proteins engage in a complex interplay, variously enhancing or inhibiting one another’s actions at certain points and culminating in the activation of a protein cluster called the MAC (for “membrane attack complex”). By punching holes in the membranes of bacterial or virally infected human cells, the MAC helps to clear the body of infections.
Osteoarthritis is a degenerative disease of the discs and joints that affects millions of people worldwide. A third of people ages 60 and above suffer from the disease that causes pain and stiffness in hands, necks, knees and other joints. The VA estimates that more than 6 million World War II and Korean War Veterans are still living and could be affected. The finding may offer new insight into potential treatment. “Right now,” Robinson says, “we don’t have anything to offer osteoarthritis patients to treat their underlying disease. It would be incredible to find a way to slow it down.”
The scientific literature also supports the finding that injury to one limb will result in osteoarthritis of proximal joints. Adriacchi hypothesized that individuals with a joint pathology adopt a gait reprogramming their movement patterns. Bhargava et al. found that following hip joint replacement patients’ Copyright © Indian Journal of OrthopaedicsThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.walking ability is reduced, even after successful hip replacement surgery. Studies of gait function show that although hip movements are pain-free in postreplacement cases they are not normalized according to their age group. Symmetry of left to right foot parameters is not maintained because both hips do not equally share weight-bearing.
Dynamic loading is believed to play a significant role in the progression of knee OA. Morgenroth et al. found that the rate of dynamic loading at the knee was associated with increased medial tibiofemoral joint degenerative changes on MRI.
There have been numerous in vitro studies and in vivo animal studies suggesting the importance of the rate of loading in relation to the development of OA. Articular cartilage and underlying subchondral bone are viscoelastic structures that become less deformable when subjected to faster loading rates (Radin and Paul, 1971).
When articular cartilage is rapidly loaded, internal stresses can become quite large due to lack of fluid flow, and this can lead to fracture of the collagen matrix (Radin et al., 1991a). Subchondral bone can sustain microscopic damage with repetitive impulsive loads, which accumulate and can lead to subchondral stiffening (Radin et al., 1978, Radin and Rose, 1986), increasing shear stresses within articular cartilage thus leading to further degenerative changes (Anderson et al., 1993, Radin et al., 1991a).
Rapidly applied repetitive loading has been shown to cause joint damage as shown in vitro (Lukoschek et al., 1988) and in vivo animal models (Radin et al., 1984), even when load amplitude is within physiologic limits. For instance, when tested in rabbits in vivo, higher rate of loading led to cartilage degeneration more often than in animals with lower loading rate even though the latter had higher magnitudes of load (Yang, 1989).