Copyright © 2006 by The Journal of Bone and Joint Surgery, Inc.
Commentary & Perspective
Commentary & Perspective by
Thomas J. Gill, MD*,
Department of Orthopaedic Surgery, Massachusetts General Hospital, Boston, Massachusetts
Posted November 2006
The long-term effect of bone bruises and acute osteochondral
injury in the knee remains a topic of much debate in the field of sports medicine.
With the advent of magnetic resonance imaging, the incidence and prevalence of
bone bruises seen in conjunction with ligamentous injury, particularly anterior
cruciate ligament tears, have become better
understood. Bone bruises have been reported in up to 80% of patients with
anterior cruciate ligament tears alone. Initially, the relative importance (or
lack thereof) of these occult osteochondral injuries was believed to be benign—nothing
more than incidental radiographic findings. More recently, clinicians caring
for patients with these injuries have noted that not all injuries have such a
benign clinical course. Typically, patients with substantial bone bruises seem
to have more pain and often a more prolonged clinical course than those without
such radiographic findings.
A key issue in the management of patients with acute osteochondral
injuries pertains to the natural history of bone bruises. There have been
studies in which a relatively "benign" natural history has been reported.
Typically, magnetic resonance imaging is used to follow the progression or recession
of the bone bruises, with resolution occurring at an average of six months for
isolated injuries. Conversely, bone bruises that are associated with injury to
the anterior cruciate ligament have been reported to persist for extended
periods, often well over a year. The question must then be asked whether the
initial occult osteochondral injury is responsible for the articular cartilage
defects that are often seen in these patients, especially those who undergo
anterior cruciate ligament reconstruction, or whether these chondral defects
are due to some other factor, such as the ligament reconstruction itself,
altered kinematics of the joint, or the production of inflammatory mediators
and degradative enzymes.
Regardless of what one believes is the natural history of a
bone bruise, there seems to be little doubt that patients with acute
osteochondral injury have more pain, and often more stiffness, than patients
without such injury. This clinical observation may be a result of the degree of
the initial trauma, in which higher blunt-impact forces result in bone bruises,
while lower-force injuries do not. The higher the level of
trauma, the higher the expected degree of inflammatory mediator production and
associated enzymes. Such mediators include the expression of tumor
necrosis factor-alpha, nitric oxide, interleukin-10,
matrix metalloproteinases, and neutrophils. It stands to reason that optimizing
the biochemical milieu of the joint will provide the best opportunity to
minimize the long-term morbidity following acute osteochondral injury.
From a clinical perspective, the question remains how best
to balance the goal of accelerated rehabilitation and rapid return to premorbid
level of activity with the need to protect the underlying biology of the joint
and prevent long-term damage to the articular cartilage. Many clinicians prefer
immediate weight-bearing and range of motion in an effort to prevent joint
stiffness and permit an earlier return to sport or work. In support of this
approach is the fact that there are ample data to support the use of early
protected weight-bearing and motion on the healing of articular cartilage
injuries. However, the current paper by Green et al. highlights the potential
benefits of limited weight-bearing with gradual progression to full weight-bearing
over a period of four weeks. By restricting the degree of initial weight-bearing,
the production of deleterious inflammatory mediators and degradative enzymes is
apparently minimized, with theoretic biologic protection of the joint itself. Accelerated rehabilitation may therefore not be synonymous with accelerated
biologic recovery and may in fact be detrimental to the long-term outcome of
the patient who has sustained an acute osteochondral injury.
So how should the patient with an acute
osteochondral injury be managed? There is no absolute answer at this
time. However, studies such as that of Green et al. should make the reader take
a step back and reconsider the biology of the injury, rather than simply follow
a "cookbook" approach. Clinicians treating such injuries must remember, for
example, that not all anterior cruciate ligament tears are the same; the
presence of associated bone bruises may influence the eventual function and
activity level of the patient. Currently, my approach to such patients is to
individualize treatment and let each patient determine when he or she is ready
to progress in terms of recovery. Although it may not be possible to assess the
biochemical status of the joint, pain itself can be used as a surrogate for
biochemical markers of joint health. Thus, I typically recommend an initial
period of protected weight-bearing. Once the patient is able to bear weight
without pain, and once a more normal gait pattern is established, the patient is
able to resume full weight-bearing.
It is likely, although not proven, that clinical symptoms
tend to improve as the inflammatory mediators within the joint begin to
diminish. The exact course of time for this progression remains variable and is
dependent on the degree of the initial trauma, the extent of the osteochondral
injury, and the presence of associated ligamentous, osseous, or meniscal
injury. Future research will undoubtedly be focused on whether we can alter the
acute biochemical environment of the joint and on whether such biochemical
engineering can alter the long-term function and biology of the joint itself after
injury.
*The author did not receive any outside funding or grants in
support of his research for or preparation of this work. Neither he nor a
member of his immediate family received payments or other benefits or a
commitment or agreement to provide such benefits from a commercial entity. No
commercial entity paid or directed, or agreed to pay or direct, any benefits to
any research fund, foundation, division, center, clinical practice, or other
charitable or nonprofit organization with which the author, or a member of his
immediate family, is affiliated or associated.
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