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Osteoarthritis:
Understanding the Pain by Joseph F. Fetto, MD
Vol 2
No 10 November 2000
Learning how
to cope with the inevitable effects of wear and tear on the body.
Arthritis is a very democratic disease.
Eventually every joint in every person is vulnerable to arthritis. It
can affect people of all walks of life, any sex, any age, or any ethnic
origin. It is not only a disease of the elderly.
Arthritis is a compound word. The first part means "joint"(from the
Latin word arthro) and its suffix, "itis," means inflammation. The most
common form of arthritis is "osteoarthrosis" (osteo-bone, arthro-joint,
osis-damage). It is simply a mechanical process that results from the
everyday wear and tear of life.
The degree of damage varies extensively between people. It is
dependent upon a myriad of factors: the inherent bony structural
stability of a joint; the stability provided by soft tissue structures,
both ligamentous and muscular; the amount of force per unit area to
which the joint is subjected; the number of times a load is applied; and
the possibility of illnesses or conditions that may compromise the
stabilizing structures or architecture of the joint.
To understand arthritis, it is important to understand what parts of
the body this disease damages, and also what exactly this damage is.
With a basic explanation of how the body is constructed and how it
works, it is a simple matter to help patients understand, first, what is
happening to their bodies; second, what treatment(s) may make the most
sense for their specific needs; and, most important, third, what they
can do to reduce the possibility of or prevent further damage.
Inflammation is the body’s response to an insult. This insult may be
in the form of an injury, disease (ie, rheumatoid disease), metabolic
conditions (ie, gout), or a nutritional problem. Pain, swelling,
limitation of movement, and functional impairment highlight the results
of an inflammatory reaction.
The Key to Prevention
The final outcome of these insults is the eventual destruction of the
surfaces of articulations. This destruction is called "arthrosis.” A key
to controlling arthritis is the prevention of damage to the joint
surface. Each joint of the body represents a point where two or more
bones meet. The purpose of a joint is to permit near-frictionless
movement of these bones on each other. To accomplish this low-friction
movement, the end of each bone is covered by a smooth, firm, white cap
of articular cartilage. In addition to providing a frictionless surface,
the articular cartilage acts as a shock absorber, reducing impact damage
to the underlying bone. The key to preventing arthritis and treating it
is understanding the ultrastructure of articular cartilage. This
articular cartilage is a very intricate structure. It is composed of
cells (chondrocytes) resting within a matrix of a ground substance
called proteoglycan. This ground substance is composed of water and
hyaluronic acid. The ground substance and the imbedded cells are
surrounded by a protein surface layer composed of collagen.
Hyaluronic acid is a complex molecule that can be imagined to look
like a long, wavy bristle brush, from which smaller bristle brushes are
protruding perpendicularly from its core. The side chains are composed
of protein cores with sulfate radicals extending to either side. The
sulfate radicals create a highly charged electronegative surface, which
has a very strong hydrophilic attraction for water. As such, the ground
substance will absorb water from the joint space through small pores on
the collagenous surface of the articular surface.
The Necessity of Collagen
Collagen is a long, linear molecule usually associated with areas of
tension loading within the body, such as tendons and ligaments.
Paradoxically, collagen is critically necessary to the proper
functioning of articular cartilage in managing compressive loads. An
explanation of this seeming paradox is as follows. As fluid enters
through the porous articular surface, the material beneath fills the
space like the stuffing of a pillow, expanding and pushing outward
against the collagenous skin. The skin is anchored to the subchondral
bone by long, thin filaments of collagen molecules extending
perpendicular from the subchondral bone, arching outward and eventually
lying transversely parallel to the articular surface. As weight is
applied to a lower extremity articulation, water that has been pulled
into the ground substance is forced out through the surface pores,
creating an extremely efficient, frictionless, hydrostatic bearing
between the articular surfaces. When weight is removed, such as lifting
the foot off the ground to take the next step, water is again sucked
into the ground substance matrix, once more plumping up and creating a
firm articular surface protecting the underlying bone. It is easy to
understand, therefore, that anything that damages the integrity of the
articular surface will enlarge the holes through which the "stuffing”
underneath will escape.
The stuffed pillow analogy easily can be extended to understand how
the articular cartilage will then lose its resilience and become
irregular, and a noncongruous surface will be presented to the
reciprocal side of the joint. This results in increased friction between
the articular surfaces, further eroding the articular material from the
end of the bone. Ultimately, there will be loss of the protective
covering. This then exposes the underlying bone to direct pressure from
the other side of the joint. Pain results from excessive point loading
of the subchondral bone due to the loss of the overlying articular
cartilage.
It is easy to understand the mechanism by which disease processes
other than trauma can cause the same final pathway of destruction for
the articular cartilage. For example, rheumatoid arthritis, which
involves an expansion and proliferation of the synovial tissues in an
exuberant inflammatory response to a yet-to-be-recognized cause, expands
the synovium to cover the articular cartilage, interfering with proper
nutrition, which causes excessive production of proteolytic enzymes that
begins to degrade the surface collagen. Both the nutritional
interference and the direct articular damage allow for the escape of the
underlying hyaluronic matrix material, thereby leading to eventual
secondary osteoarthrotic destruction of the joint.
Similarly, gout is the metabolic condition
in which excessive uric acid is deposited within the tissues. When
small, needle-like uric acid crystals are precipitated in the synovium,
the exquisite inflammatory response that results mimics, in a lesser
degree, the process by which rheumatoid disease damages articular
cartilage.
Infections caused by bacteria producing proteolytic enzymes will
cause rapid dissolution and destruction of joint surfaces. Bacterial
infections, such as gonococcus, which do not produce proteolytic
enzymes, will cause a secondary synovitis and hence will damage
articular surfaces, but at a much less rapid pace than will the
aggressive proteolytic enzyme-producing staphylococcus. Tubercular
infections of the joints cause secondary arthrosis, not by direct attack
on the synovium or the articular cartilage, but by the creation of
granulomas and cavitary defects in the subchondral bone. This loss of
support of the articular cartilage creates incongruities in the
articular surfaces, resulting in increased frictional loads and
secondary mechanical erosion of the joint surface.
In similar fashion, conditions that compromise blood supply to the
subchondral bone, such as avascular necrosis due to steroid or alcohol
abuse, cause loss of articular support to the articular cartilage and,
just as in the collapse due to tubercular granulomas, will create an
incongruity due to the loss of subchondral support of the articular
cartilage and, hence, secondary osteoarthrosis.
Excessive Point Pressures
Mechanically, conditions not related directly to trauma involving the
articular surface, but changes in the mechanics or mechanical loading of
the joint, will cause excessive point pressures that will lead also to
the mechanical erosion of the articular cartilage. These would be
conditions such as slipped epiphysis of the proximal femur, dysplasias
of the joint (whether congenital or secondary to metabolic disorders),
or mechanical misalignments, such as improper tracking in the
patellofemoral mechanism. Mechanical derangements secondary to loss of
ligament supports will also lead to mechanical erosion secondary to
increased shear and point stresses on articular cartilage. This is
evident in the case of the knee following loss of the anterior cruciate
ligament, or in the ankle, where hyperdorsiflexion injuries cause
widening of the ankle mortise and instability in the unusually stable,
and seemingly immune to arthritis, ankle joint.
Once understood, the process of arthritis can be dealt with in a very
logical and systemic manner. To demonstrate this, we can consider the
hip joint. It is not difficult to imagine how a normal hip, which is
exposed to more than a million steps per year during daily activities,
can become worn over a lifetime of use. Arthritis of the hip, like that
of other joints, is a painful inflammation and results from the erosion
of the smooth surfaces that cap the proximal end of the femur. This
wearing-out process may be the result of chronic use (aging), repetitive
overuse (jogging), trauma (fracture, dislocation), infection,
inflammatory disease (rheumatoid), congenital deformity, or damage to
supporting bone by chemical agents such as steroids, alcohol, or a
variety of metabolic conditions. Regardless of the cause, each condition
inevitably leads to the same endpoint, categorized by painful limp,
stiffness, limited range of motion, and decreased function in activities
of daily living.
The normal hip is composed of a large, white, spherical knob at the
top of the femur. This knob is approximately two inches in diameter and
appears much like a billiard ball. It is seated in a hemispherical
socket within the lateral aspect of the pelvis. In the arthritic hip,
the usual ball-and-socket architecture becomes disfigured. This
resultant deformation causes a restriction in movement and stretching of
soft tissues. This results in pain, as the deformed ball attempts to
rotate within its socket.
The hip pain is further aggravated by the inflammatory response of
the body. The inflammatory response is characterized by both chemical
and cellular factors, both of which serve to stimulate nerves and create
pain. The purpose of the pain is strictly to force recognition of the
damaged area and to protect it from further loading. Therefore, hip pain
due to arthritis is typically aggravated by activity and relieved by
rest, and therefore is usually described by the patient as emanating
from deep within the thigh, radiating to points down the front and inner
aspects of the thigh and along the inner side of the knee.
The treatment of hip arthritis, like that of other arthritic joints,
can be divided into two general categories: nonoperative (conservative)
and surgical. The primary goals of each form of treatment are to reduce
pain and restore function.
Nonoperative Treatments
Nonoperative treatments can be broken down into two categories:
mechanical and pharmacologic.
Mechanical treatment modalities include assistive devices that will
help to reduce the pressure on the affected joint. These may be braces,
crutches, splints, canes, or wheelchairs, and are used in concert with
modification of activities and reduction in amount of time standing,
climbing, bending, stooping, or other strenuous activities that would
place excessive or unacceptable load on the damaged surface. A critical
mechanical adjunct is that of weight reduction. Reducing the amount of
body mass greatly minimizes stress at the hip joint. This can even be
greater at affecting joints more distal along the lower extremity. Also,
changes in environment can have significant relief on the inflammatory
process. Using cushioned innersoles, walking on softer surfaces, sitting
in higher chairs, and using other seating modifications serve to reduce
the amount of stress and movement the damaged articular surface must
withstand.
Pharmacologic Treatments
Pharmacologic treatment of arthritis stems primarily from treatment
of the secondary inflammatory response of the body. Nonprescription
nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or
ibuprofen are excellent, safe initial courses of treatment. Prescription
non-steroidal medications are utilized when milder forms of medication
are insufficient to control symptoms. However, as strength of medication
increases, so too do the collateral complications and morbidities, such
as gastrointestinal (GI) upset, GI bleeds, salt and water retention,
increased hypertension, and secondary renal dysfunction. Steroid
medications, whether oral or parenteral, such as cortisone, into the
joint on an occasional or rare basis, may provide substantial relief and
temporize against inevitable surgery. Analgesics, although necessary in
relieving some extreme painful conditions, may give a false sense of
well-being to patients, thereby causing them more harm by removing their
awareness of the underlying inflammation in the joint.
Nonsurgical options, however, are not for everyone. Some people are
not able to tolerate these medications. Most important, it is necessary
to recognize that nonsurgical measures do not prevent the progression of
arthritis, and more important, cannot reverse damage that is already
present. As of today, there is no known pharmacologic "cure” for
arthritis. The only purpose for nonsurgical remedies is to make the
condition less debilitating. At best, it slows the inevitable course of
deterioration. Arthritis is not a life-hreatening condition, and
therefore there is never an absolute need for an individual to undergo
an operation. However, at some point, the pain and disability of a
severely arthritic joint may force the patient to explore surgical
treatment options.
When Surgery Is Needed
Surgical treatment of an arthritic joint is based on the amount of
damage present in the articular cartilage and the functional needs and
medical status of a patient. Indirect surgical treatment of arthritis is
termed "debridement." A debridement is a temporizing procedure that does
not change the inevitable course of arthritis. It is intended only to
improve movement by removing calcium deposits and bony "barnacles" that
restrict normal motion of the articular surfaces. It also includes the
removal of hypertrophic or exuberant soft tissues that have formed in
response to the arthritic process. Debridements usually require an open
operation. They may sometimes be performed in a minimally invasive
fashion through the use of an arthroscope.
At the other extreme from debridement is fusion, or arthrodesis. An
arthrodesis is an operation in which the articular surfaces are
completely denuded down to the underlying bone. The bony surfaces are
then approximated and held rigidly in place either by internal fixation
or by external immobilization. If successful union has been achieved
between the bony surfaces, an arthrodesis provides permanent relief of
pain. However, it eliminates all possibility of movement between the
bony surfaces. Therefore, an arthrodesis creates significant load on
joints proximal and distal to the surgical site. In the case of the hip,
this means that the lower lumbar segments and knee must compensate for
loss of hip mobility. This is a major disadvantage of a hip fusion,
because over time, although the arthritic hip is no longer a painful
limitation to the patient, there will be increased loads at lumbar and
knee articulations, ultimately causing degeneration and arthrosis at
those sites.
An alternative to the permanency of arthrodesis is joint replacement.
A replacement of a joint ideally should be one in which there is a
recreation of a new articular surface. In the ideal, a joint replacement
should involve the replacement of the worn articular cartilages with a
resurfacing of the bones by an artificial material. This material must
be well fixed to provide a stable articulating surface, durable so as
not to rapidly wear under normal use, and nonreactive so as to not cause
reaction within the surrounding soft tissues and rejection by the body.
The way in which this is achieved varies based on the architecture of
each specific joint. In the case of the knee, it can be carried out as
truly a surface replacement. In the hip, however, greater success has
been achieved by stabilizing the femoral component in some way within
the intermedullary cavity of the proximal femur. In other cases, such as
the basal joint of the thumb, a third option, that of interposing a soft
tissue and creating a pseudarthrosis, has been found to be a reasonably
successful solution for the relief of arthritic pain and dysfunction in
that joint.
Ultimately, however, joint replacements suffer from the limitation of
available technology. There are no materials available today that can
provide as frictionless a surface as that of natural articular
cartilage. There is also no material available today that has the
durability and resiliency as to provide nearly 90 years of useful
function as do normal articular cartilages.
To this end, although dramatic in the relief of pain and restoration
of function, joint replacements are not permanent solutions to the
problem of arthritis. Therefore, before considering surgical
intervention as treatment of an arthritic joint by means of replacement,
it is necessary to examine the materials to be used, the means of
fixation to be relied upon, and the types of bearing surfaces that will
be inserted, all of which will have a direct impact on the longevity of
the reconstructed joint. Also, it should be recognized that a joint
replacement is a surgical procedure, and therefore requires anesthesia
and violation of the skin, exposing the patient to risk not only of
anesthesia medications, but also that of infection. Therefore, planning
for total joint replacement is of critical import and should include a
full medical examination, proper patient education, consideration of
pharmacologic agents to help minimize possible complications such as
thromboembolic phenomena or infection, and consideration of a patient's
home and work environments and functional needs.
Controlling the Inevitable
In conclusion, arthritis is a disease that represents the inevitable
wear and tear of the joints of the body. It is a process that can be
accelerated and aggravated by a myriad of factors, some of which can be
controlled and modified, such as jogging or traumas, or others that are
out of a patient's control, such as illnesses or congenital conditions.
It can, however, be modified in its progression by both nonoperative
mechanical and pharmacologic treatments. It can be delayed by
appropriate nutritional management and functional considerations, but
when it has occurred and has resulted in painful, debilitating
compromise of a patient's function, it can be managed surgically by a
reconstruction. In any event, no matter which course of management is
chosen, the most critical factor for the successful treatment of an
arthritic joint is patient education and understanding.
Joseph F. Fetto, MD, is clinical associate professor of orthopedic
surgery at New York University Medical Center, New York; associate
professor of orthopedic surgery at the Hospital for Joint Diseases, New
York; and director of orthopedic surgery at Manhattan Veterans Affairs
Medical Center, New York.
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