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The acute neuropathic joint.

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Neuropathic osteoarthropathy is a dramatic arthropathy that is both easily diagnosed and easily
misdiagnosed. Radiographically, the neuropathic joint
presents a spectrum of changes, from excessive bone
production to extensive bone resorption (1). The joint
with excessive bone production, or hypertrophic joint,
is easily diagnosed. Its hallmarks are complete dissolution of the normal joint, excessive juxtaarticular new
bone formation, massive osteophytes, fragmentation,
and osseous debris (Figure 1). The extensively resorbed, or atrophic, joint usually presents a diagnostic
dilemma. The radiographic appearance is often mistaken for a rampant infection or aggressive bone tumor (2).
The resorbed or atrophic joint usually evolves
from a normal-appearing joint, within a period of 2-4
weeks (3). It is therefore more appropriate to use the
term “acute neuropathic joint” in reference to this
condition. This “acute” joint is most commonly observed in non-weight-bearing joints, predominantly
the shoulder and the elbow. However, it is also seen in
weight-bearing joints-the hip and the knee.
Patients usually present with pain in the inThe opinions and assertions expressed herein are those of
the author and are not to be construed as reflecting the views of the
Department of Defense or the Uniformed Services University of the
Health Sciences.
From the Department of Radiology/Nuclear Medicine, Uniformed Services University of the Health Sciences, F. Edward
Hkbert School of Medicine, Bethesda, Maryland.
Anne C. Brower, MD.
Address reprint requests to Anne C. Brower, MD, Department of Radiology/Nuclear Medicine, Uniformed Services University of the Health Sciences, F. Edward Hkbert School of Medicine,
4301 Jones Bridge Road, Bethesda, MD 20814-4799.
Submitted for publication June 6 , 1988; accepted July 5 ,
Arthritis and Rheumatism, Vol. 31, No. 12 (December 1988)
volved joint, and swelling and deformity are often
present. Demonstrable neurologic abnormalities may
or may not be present (4).The appropriate diagnosis in
the patient presenting with pain and no neurologic
change may be made by radiography of the involved
joint, if the radiograph(s) is interpreted correctly.
The radiographic changes in the acute neuropathic joint are very specific (Figure 2). Various degrees of bone resorption are present. The diagnostic
clue to the cause of this bone resorption is found at the
edge of the resorption. The edge, or transition zone,
between the resorbed bone and the remaining bone is
extremely sharp, resembling surgical amputation.
Normal mineralization is present in the remaining
bone. There is a notable absence of bone repair. Soft
tissue swelling, with bone debris in this soft tissue, is
These radiographic changes are most commonly misdiagnosed as a rampant infection or as an
aggressive bone tumor. The acute neuropathic joint
produces resorptive changes on both sides of the joint.
An aggressive bone tumor, regardless of the pathophysiology, will almost never violate cartilage. The
aggressive resorption caused by a tumor, therefore,
will be limited to one side of the joint. A rampant
infection will involve both sides of the joint. With this
amount of resorption, however, the adjacent, surrounding bone will be osteoporotic. The sharp surgical-like
edge seen in the neuropathic joint will be ill-defined
and ragged in a septic process.
The acute neuropathic joint will evolve with
time, and the radiographic abnormalities will more
easily be recognized as those of a neuropathic joint. If
the evolving joint is a weight-bearing joint (i.e., hip,
knee, or ankle), bone repair will occur in the remaining
radiographic changes seen in the acute or atrophic
joint. Other possible causes must be considered. The
possibility of a neurovascular origin, in which injury to
the sympathetic nervous system leads to increased
bone blood flow in a limited region, with secondary
bone resorption, has been presented in the literature
(5). Pathologic findings in some bone specimens support this theory (6). Whatever the pathophysiology,
repetitive trauma must not be considered the only
possible cause. As long as trauma is believed to be the
primary cause, the acute neuropathic joint will continue to be misdiagnosed as an infectious process or as
a tumor.
In summary, the radiographic changes in neuropathic osteoarthropathy cover the spectrum of bone
Figure 1. Anteroposterior view of a neuropathic knee, showing
chronic hypertrophic changes. There is complete dissolution of the
joint space, with lateral subluxation of the tibia, massive subchondral sclerosis, and fragmentation. (Reproduced, with permission,
from Radiologic Clinics of North America [ 6 ] . )
surrounding bones. Remodeling, massive new bone
formation, osteophytosis, and fragmentation will
eventually occur. In other words, with weight-bearing,
the acute atrophic joint will evolve into the chronic
hypertrophic joint. If the joint is a non- weight-bearing
joint, however, the hypertrophic reparative changes
will not occur. Instead, cortical borders will form at
the surgical edges of the resorbed bone and cortical
borders will form around the osseous fragments
(Figure 3).
This sequence of changes raises questions as to
the pathogenesis of a neuropathic joint. Although
chronic repetitive trauma to an insensitive joint could
create the changes seen radiographically in the chronic
or hypertrophic joint, it could not be the cause of the
Figure 2. Anteroposterior view of a neuropathic shoulder, demonstrating acute, or atrophic, changes. The humeral head and proximal
humeral shaft have been resorbed. There is a sharp edge, resembling
surgical amputation, at the proximal end of the remaining humerus,
which is normally mineralized. There is soft tissue swelling in the
shoulder, with extensive osseous debris present within the soft
tissue. The glenoid appears shallow. (Reproduced, with permission,
from Brower AC, Allman RM: The pathogenesis of the neurotrophic
joint: neurotraumatic vs. neurovascular. Radiology 139:349-354,
Figure 3. A, Anteroposterior (AP) view of an acute neuropathic hip. Note the complete resorption of the femoral head and most of the femoral
neck. Bone mineralization is normal. There is a sharp surgical-like edge to the proximal femur. There is some resorption and shallowing-out
of the acetabulum, and the femur is subluxed laterally and superiorly to the acetabulum. B, AP view of the same hip 3 years later. The femoral
head and neck are absent, and the remaining femoral shaft and adjacent acetabulum are well corticated. Bone fragments within the joint have
become well corticated. There is absence of massive subchondral sclerosis and osteophytosis. (Reproduced, with permission, from Radiology:
Diognosisllmagingllntervention. Vol. 5. Edited by JM Traveras, JT Ferruci. Philadelphia, JB Lippincott, 1986.)
change, from excessive repair to extensive resorption.
The hypertrophic or productive joint presents no diagnostic problem. The acute or atrophic joint is often
mistaken for an infectious process or a tumor. Knowledge about and careful observation of specific radiographic changes, as well as a clear understanding of
the pathophysiology of the changes, will help in making the correct diagnosis.
1. Brower A: Neuropathic osteoarthropathy, Arthritis in
Black and White. Philadelphia, WB Saunders, 1988
2. Feldman F: Neuropathic osteoarthropathy, Diagnostic
Radiology. Edited by AR Margulis, CA Gooding. San
Francisco, University of California Press, 1977
3. Norman A, Robbins H, Milgram JE: The acute neuropathic arthropathy-a rapid, severely disorganizing form
of arthritis. Radiology 90: 1159-1 164, 1968
4. Katz I, Rabinowitz JG, Dziadiw R: Early changes in
Charcot’s joints. AJR 86:965-974, 1961
5. Johnson LC: Circulation and bone (Charcot’s disease and
trophic change), Bone Biodynamics. Edited by HM
Frost. Boston, Little, Brown & Company, 1964
6. Brower A, Allman RM: The neuropathic joint: a neurovascular bone disorder. Radio1 Clin North Am 19571580, 1981
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