Osteoarthritis

Osteoarthritis is by far the most common form of arthritis. Osteoarthritis is known as the wear and tear type of joint disease and will effect most of us at some point in our lives. In our discussion on osteoarthritis, please refer to the nomenclature and anatomy sections below for definitions of the terms that my be unfamiliar to you.

When I think of osteoarthritis (OA), I think of my grandmother's hands. Those hands had done a lot of work in their day and had a bit of arthritis to show for it. The fingers, crooked and bumpy showed many of the changes brought on by osteoarthritis. The familiar bumps on the fingers brought on by OA are called Heberden's Nodes. Heberden's Nodes are a very obvious example of how osteoarthritis occurs. If you've ever known anyone whose experienced the symptoms of OA, they'll tell you that a joint will flare for a period of several weeks to months. OA pain varies from mild to severe. And then suddenly, just as quickly as it started, the pain subsides and is disappears. Morning stiffness that lasted for 30 minutes or so was not unusual for grandma.

At first glance, OA would seem to be due to simple degeneration of cartilage. But the disease we call OA is far more complex. The pain associated with OA is the result of a series of small micro-fractures that occur in the subchondral bone (just beneath the cartilage). This bone, called cancellous bone, normally acts as a shock absorber for loads applied to the joint. In cases of osteoarthritis, the cancellous bone becomes very brittle and fragile. When load is applied to this fragile bone, it breaks. The more the joint is used, the more the bone breaks down. The repetitive breakdown and repair of the bone results in hypertrophy of the joint margins or what we've called Heberden's Nodes.

Over time, as the bone undergoes a series of flare ups, the ability of the bone to support the cartilage becomes unstable. The subchondral bone creates an unstable supporting surface for the cartilage. When the joint tries to complete its' normal range of motion, the cartilage is irregular and progressively erodes. This moves us into the second phase of OA pain, and that's when we have joint range of motion that is bone on bone. Cartilage has no nerve endings to sense pain, but bone, on the other hand, is filled with nerve endings. As the joint moves and the bone is eroded, significant pain can be experienced. 

Other clinical findings in OA include atrophy of the joint lining called the synovium.  Synovium produces the lubrication of the joint called synovial fluid.  In cases of OA, the character of synovial fluid changes becoming less viscous.  And finally, advanced OA will contribute to instability of the joint.  A normal healthy joint will have a very tight external envelop consisting of ligaments, tendons and joint capsule.  As OA progresses, this envelope will become slack and contribute to instability of the joint.  And joint instability will, in turn, result in physical damage to the joint.

The erosion of the joints seen in OA seems to occur at different rates in different individuals. In fact, every joint seems to undergo the changes of OA at a different rate. The rate of change does seem to be effected by a history of damage to the joint. In fact the classifications used to describe OA include Primary (idiopathic or no known cause) and Secondary (some known cause for the disease such as trauma). Past injuries seem to accelerate the rate of OA in most joints. We all know someone with that old football injury who develops OA early in their life.

The underlying cause of OA is unknown but it seems to have both a genetic predisposition and a relationship to joint trauma. Many authors have speculated that the cause may be mechanical as described above, but others have described changes such as biologic, biochemical or enzymatic, or even a combination of each of these.

The symptoms of OA in the foot and ankle are numerous. A very common symptom of OA is midfoot pain. The midfoot is a jigsaw puzzle of pieces that are difficult to manage when effected by a systemic disease such as OA. Other symptoms of OA in the foot include atrophy (loss) of the plantar fat pad of the forefoot and heel. The big toe joint is often affected by the changes of OA. Bunions and hallux limitus are common complaints in OA patients.

Treatment of OA begins with making the foot more efficient through the use of shoes and braces. The less work the foot performs, the more we can control the symptoms of OA. Treatment may include;

Oxford shoes with a rigid shank and stiff, laced uppers.

Carbon plates to stiffen the shank or stiffen the forefoot.

Bracing with an Arizona Brace or Ritchie Brace.

OA can also be addressed with the use of oral or topical anti-inflammatories. Non-steroidal anti-inflammatories (NSAID's) are commonly used to treat the inflammation of OA. These medication include Celebrex, Naprosyn, Motrin, etc. Topical pain relievers such as Biofreeze are helpful.

Treatment of OA of the foot and ankle with injectable hylan G-F 20 (Synvisc), or what is called viscosupplementation, is becoming increasing more popular. Although still considered an 'off-label' use of Synvisc, studies have shown that the symptoms of OA can be temporarily reduced for a period of 3-12 months following injection. Injection of Synvisc is often used in conjunction with arthroscopic debridement of the ankle.

Surgical treatment of OA of the foot may be required if bracing and medical treatment proves ineffective. Surgical care consists of joint debridement, fusion, or replacement with implants. The choice of each procedure depends upon the location of the OA and the general health of the patient.

Surgical treatment of OA of the ankle is a field of study that is undergoing rapid change. A new technique called arthrodiastasis is being used in the ankle. Arthrodiastasis involves off loading the ankle with the use of a distraction fixator. The fixator is surgically attached to the foot and leg with pins. The pins are then mechanically separated to 'off-load' the ankle. The theory behind arthrodiastasis is that off loading the joint allows the joint to regenerate cartilage. Arthrodiastasis requires 12-22 weeks of non-weight bearing in the distractor. Arthrodiastasis with Gratjacket interposition in the ankle has recently been advocated by Daniel Lee, DPM. The advantage of this procedure is that the Graftjacket acts as a scaffold for cartilaginous ingrowth. In Dr. Lee's early studies, non-weight bearing has been reduced to only 4 weeks. Long term outcome and analysis of arthrodiastasis, both with and without soft tissue interposition, are pending.

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a very complex and debilitating disease that affects approximately 1% of the general population. Women are 2-3 times more prone to develop RA. RA is an autoimmune disease. An autoimmune disease occurs when the body's immune system attacks itself. In the case of RA, the immune system attacks the cells lining the joint capsule called the synovium. The end result is thickening and fibrosis of the joint with destruction of the cartilage.

Symptoms of RA include an abrupt onset of inflammation and swelling. The swelling associated with RA may be isolated to one joint or affect several joints. Symmetrical involvement is typical with both hands or both feet being affected. In comparison to OA, morning stiffness seen in RA may last more than 30 minutes.

The onset of RA in the foot often progresses to subluxation of the joints, particularly the metatarsal phalangeal joints. Atrophy of the plantar fat pad is common.

Treatment of RA can be quite complex and depends upon the individual patient's response to medications. For a review of medications visit The Arthritis Foundations page on RA. Although treatment of the immune response is the primary goal in RA, bracing and joint support is critical in RA. Surgical revision of joints effected by RA is common.

Psoriatic Arthritis

Psoriatic arthritis (PA) is an interesting form of sero-negative arthritis. PA is associated with psoriasis in many cases, but it is not unusual to find the symptoms of PA in a patient with no previous history of psoriasis of the skin or nail.

The symptoms of PA in the foot include focal swelling of the interphalangeal joint (the toes). The toe will become swollen and painful with no history of injury. X-rays may show slow erosive changes that are called a pencil and cup deformity. This finding is seen in the metatarsal phalangeal joint where the metatarsal head resembles the point of the pencil and the base of the proximal phalanx (toe) is the receiving cup.

Treatment of PA is mostly supportive. Most cases subside within a few months of onset. Severe cases respond to immune therapy similar to treatment of RA.

Reiter's Syndrome

Reiter's Syndrome (RS) is an unusual form of arthritis that is usually found in men.. RS is often described as a sexually transmitted disease due to the history of the disease occurring following sexual intercourse which resulted in a chlamydial infection. It is suggested to treat those with RS, and their sexual partners, for C. trachomatis infections.

The symptoms of RS include burning upon urination (urethitis), dry eyes and joint pain. Joint pain in the back and feet are common. These symptoms occur 7-14 days following sexual intercourse and subside over a period of several months to years. Recurrence of pain is not unusual.