Arthritis
is the term used to describe a number of related diseases that cause
inflammation of joints. This inflammation of the joint and the
surrounding soft tissue structures may result in progressive destruction of
the joint. Arthritis is actually a collection of many different joint
diseases that effect the body and the foot in many different ways. In this
article, let's talk a bit about arthritis and how it effects the foot.
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.
