Loose bodies, or osteochondral fragments, are commonly found in human
joints. They are presumed to arise from trauma, joint disintegration (for
example, degenerative changes), or synovial
proliferation1. The
natural history of loose bodies in synovial joints is slow enlargement with
deposition of additional surface layers. However, if the loose body becomes
trapped and reattaches to the synovium, it is then generally reabsorbed.
Neuropathic or degenerative joints with hyperemic or inflamed synovium are
particularly prone to the development of loose bodies, but they also tend to
rapidly reabsorb
them2. Histological
studies have generally demonstrated varying amounts of osseous, cartilaginous,
and fibrous tissue with living and dead osteocytes, chondrocytes, osteoclasts,
and osteoblasts found in the tissue layers. No blood supply nourishes these
loose bodies; therefore, they derive sustenance from the synovial fluid
alone3.
We report the case of a patient with an asymptomatic, osseous loose body
lying in the spine canal. To our knowledge, this is the first time this
condition has been reported in the literature.
An eighty-seven-year-old female restrained driver was involved in a
low-speed motor-vehicle accident and sustained an open left tibiotalar
fracture-dislocation. She had no loss of consciousness and had no pain,
numbness, or weakness in the neck and/or the upper extremities. She reported
no previous history of neck pain or upper-extremity radicular symptoms.
Examination revealed no tenderness of the paraspinal tissues or the spinous
processes; neurological examination of all four limbs was normal. There was
full painless range of motion of the cervical spine, with no Hoffmann sign.
The left ankle wound was irrigated, the fracture-dislocation was reduced, and
the ankle was placed in a splint in the emergency department.
Routine trauma radiographs, including radiographs of the cervical spine,
were made. The lateral radiograph of the cervical spine demonstrated severe
cervical spondylosis (Fig. 1).
Computed tomography scans revealed marked spondylosis throughout the cervical
spine, calcification of the ligamentum flavum, and one large, oval,
osteochondral fragment lying within the cervical spinal canal at the level of
C6 to C7. The fragment had the same average density (mean, 350-400 HU
[Hounsfield units]) as the vertebrae (Figs.
2-A and 2-B). The diameters of
the loose body were 1.58 × 1.34 × 0.57 cm, and the loose body
occupied a considerable portion of the spinal canal on the axial cross
section. This fragment had no apparent donor site and had smooth surfaces. A
number of osteophytes at multiple other levels were identified as the cause of
mild stenosis. The patient was placed in a cervical collar and underwent
emergent surgery for the purpose of irrigation, débridement, and
provisional fixation of the ankle fracture-dislocation.
Magnetic resonance imaging of the cervical spine was performed during the
hospital stay. The spinal cord was found to be mildly compressed and deformed
at the C6-C7 level, but there was no sign of myelomalacia. Use of the cervical
collar was discontinued.
The patient underwent surgery a second time for definitive fixation of the
ankle fracture, and she was subsequently discharged to a skilled nursing
facility.
Although loose bodies in synovial joints have been extensively recorded and
studied since the 17th century, we are aware of only a single published report
regarding a similar osteochondral loose body in the spinal
canal4. In that
case, a sixty-eight-year-old man presented with decreased walking tolerance
and neurogenic claudication with weakness and numbness in the L5-S1
dermatomes. That patient had a fairly acute, progressive lumbar stenosis,
which was found intraoperatively to result from a loose body, 9 × 5
× 2 mm in size. No donor site for the fragment was apparent either
radiographically or intraoperatively, and the surfaces of the loose body were
quite smooth. The subject had no history of previous trauma. Tambe et
al.4 speculated that
the loose body had recently migrated from another location where it had
resided asymptomatically for years. The posterior compression and stenosis had
been attributed preoperatively to infolding of the ligamentum flavum. The
loose body in our study was larger than the one in this previous report and
yet it was asymptomatic.
We hypothesize that the loose body in our patient originated from an
adjacent synovial joint. The fragment was asymptomatic, even though it
occupied a considerable space within the spinal canal. We believe it most
likely that the fragment slowly increased in size over a long period, allowing
the spinal cord to adapt. Other features of the mass included round edges and
a density that was consistent with bone. Loose bodies in synovial joints may
have round edges due to a layering phenomenon as described by
Milgram3, and they
may also undergo calcification. Synovial fluid provides nutrition, thus
allowing a loose body to enlarge at an extremely slow pace as a result of the
layering
mechanism1,3,5.
A detached osteophyte may have provided the primary nidus for this loose
body.
Other reports have described calcified ligamentum flavum or nodules in the
cervical canal as a cause for stenosis, radicular symptoms, or myelopathy
principally in elderly, female, and Asian
subjects6-13.
These lesions are most commonly attributed to the calcium pyrophosphate
dihydrate crystals that form in patients with calcium pyrophosphate deposition
disease (also known as pseudogout), although hydroxyapatite crystals have also
been
implicated14,15.
Calcium pyrophosphate deposition disease is occasionally associated with
inflammatory or metabolic disorders such as hemochromatosis, diabetes
mellitus, hyperparathyroidism, Wilson disease, hypophosphatasia, and
rheumatoid
arthritis11.
Calcium pyrophosphate dihydrate crystal deposition can occur in spinal
structures, such as intervertebral discs, ligaments, articular cartilage,
synovium, and joint
capsules16. The
calcified ligamentum flavum can be difficult to visualize on magnetic
resonance imaging, as it was in the case of our patient, but it can be seen
well on a computed tomography scan (Fig.
2-C)14,15.
Our patient had no previous trauma, no diagnosed history of metabolic
disease, and was not of Asian descent. She was, however, an elderly woman who
appeared to have radiographic evidence of calcium pyrophosphate deposition
disease in other joints as well as a calcified ligamentum flavum and
moderately severe spondyloarthropathy. It is also possible that the nidus of
the osteochondral loose body was a completely detached portion of calcified
ligamentum flavum. In this case, however, the presence of smooth edges and the
basis for gradual growth cannot be explained.
The adaptive mechanism by which the spinal cord remained asymptomatic is
unclear, although such tolerance has also been demonstrated in patients with
cervical spinal
stenosis17. A high
association between sagittal diameter of the cervical spinal canal in cervical
spondylosis and the development of myelopathy has been
demonstrated18.
This may partially explain the absence of symptoms in our patient due to the
position of the loose body in the lateral side of the canal. A normal-size
spinal cord occupies approximately 75% of the cervical canal at the levels of
C4 to C717, yet the
spinal cord occupied less than 50% of the canal at the level of C6-C7 in our
patient, which is another unique aspect of this case.
To our knowledge, this is the first case of an asymptomatic osseous loose
body of the spinal canal to be published in the literature. This case also
demonstrates the remarkable ability of the spinal canal to adapt to a slowly
enlarging loose body lying within a small cervical spinal canal. ?
Note: We gratefully acknowledge the editorial assistance of
Kristi Overgaard during the preparation of this manuscript.