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False-positive findings in the atlantoaxial facet joints using the open-mouth view of the odontoid.

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125
LETTERS
hour versus one of 35 mm/hour, or a thrombocyte count of
108 x lo9 liter versus one of 375 x 109/liter. In practice, they
learn quickly and these abstract numbers become concrete.
For clinicians, it is even easier to learn the meaning of a new
measurement such as a composite index, because of their
familiarity with the composing elements. Especially in the
beginning, the new composite index can be used together
with more familiar measurements. In fact, the Ritchie score
is a widely used composite index. It is a combination of the
number and the intensity (grade) of pain in single joints and
groups of joints. Therefore, we think that the problem of
clinicians’ difficulty with interpretation can be overcome,
especially if they can be convinced of the benefit of a single
outcome measure. Our conclusion is to use a validated,
sensitive composite index of disease activity as an endpoint
measure in clinical trials. The acceptance of such an index in
clinical practice will be the next step.
Desiree M . F. M. van der Heijde, MD
Piet L. C. M. van Riel, MD
Martin A. van ’t Hof, PhD
Levinus B. A. van de Putte, MD
University Hospital Nijmegen
Nijmegen, The Netherlands
False-positive findings in the atlantoaxial facet joints
using the open-mouth view of the odontoid
To the Editor:
I read with interest the article by Halla et a1 (Halla
JT, Hardin JG Jr: The spectrum of atlantoaxial facet joint
involvement in rheumatoid arthritis. Arthritis Rheum 33:
325-329, 1990) on the spectrum of atlantoaxial facet joint
involvement in rheumatoid arthritis. In that study, the openmouth view of the odontoid was used to evaluate, among
other things, Cl-C2 cartilage loss, articular process height,
and subchondral sclerosis. It was stated that multiplanar
tomography of the Cl-C2 region was performed when routine views were inadequate in showing these facet joints.
“Inadequate” was not defined, and the percentage of “positive” cases where polytomography was used is not stated.
The open-mouth view of the odontoid may not be
reliable in the routine evaluation of the Cl-C2 cartilage
spaces, articular process height, or subchondral sclerosis in
many patients with arthritis. These patients often have
abnormal cervical posture, particularly increased lordosis,
such that the atlantoaxial cartilage spaces are not well seen
on the open-mouth view, and superimposition of the lateral
masses of C1 on the articular processes of C2 can create the
Figure 1. A, Apparent marked cartilage loss and subchondral sclerosis (eburnation) of the atlantoaxial joints.
B, The same atlantoaxial apophyseal joints on the same day, using the overpenetrated anteroposterior
vertebral arch view. The cartilage spaces are normal and there is no eburnation.
LETTERS
126
appearance of subchondral sclerosis, even when there is
none (Figure 1A).
The atlantoaxial apophyseal joints are generally best
seen in the anteroposterior vertebral arch projection with
overpenetration of the x-ray beam (Figure IB). The openmouth odontoid view is obtained with the patient in the
supine position and the central beam perpendicular to the
tabletop and centered on the middle of the patient’s open
mouth. In the anteroposterior vertebral arch view, the
patient is in the supine position with the central beam angled
25” to 30” from the horizontal and toward the feet (centered
at the suprasternal notch). Overpenetration is obtained by
increasing the exposure time by 50%. Unless this view or
polytomography is used in every “abnormal” case, falsepositive results are possible.
William W. Daniel, MD
The University of Alabama at Birmingham
Absence of reverse transcriptase activity in cultured
peripheral blood mononuclear cells from patients with
systemic-onset juvenile rheumatoid arthritis
To the Editor:
Systemic-onset juvenile rheumatoid arthritis (JRA),
of all the childhood rheumatic diseases, seems the most
likely to have an infectious etiology. Still (I), in his original
description in 1896, speculated that this disease was “infective in nature.” The prominent features of high fever, rash,
lymphadenopathy, and polyserositis suggest a viral illness.
Epidemiologic data indicate a seasonal pattern with a peak in
spring or summer (2).
One class of agents that has not been studied as a
potential cause of systemic-onset JRA is the retroviruses. In
sheep and goats, caprine arthritis encephalitis virus, a member of the lentiviruses, causes a chronic, progressive arthritis
similar to chronic S-JRA (3). We undertook this study to
determine if retrovirus-associated reverse transcriptase activity could be detected in cultured peripheral blood mononuclear cells from patients with systemic-onset JRA.
Peripheral blood mononuclear cells (PBMC) were
obtained from 7 patients with chronic systemic-onset JRA
and from 5 control subjects. Of the 7 systemic-onset JRA
patients, only 2 had active disease at the time of study, as
defined by the presence of fever, rash, leukocytosis, and
elevated sedimentation rate, in addition to arthritis. The 5
control subjects included 2 healthy adults and 3 children with
fever of unknown origin, dermatomyositis, and polyarticular
JRA, respectively. Cultures were coded and the investigator
performing the reverse transcriptase assays was blinded as
to whether the culture was from a study patient or a control.
PBMC were separated by Ficoll-Hypaque density
gradient centrifugation, cultured in RPMI 1640 (Gibco,
Grand Island, NY) supplemented with 10% fetal calF serum
(Whittaker, Walkersville, MD) and 1 mM glutamine (Gibco),
and stimulated with phytohemagglutinin and 3% recombinant interleukin-2 (Cellular Products, Buffalo, NY). Cultures
were maintained at a density of 0.5-2.0 x lo6 cells/ml for 3
weeks. Cells were examined every 3-4 days for evidence of
cytopathic effects, and supernatant samples were harvested
at these times.
Aliquots of culture supernatants (5 ml) were filtered
(0.45-pm filter) and centrifuged at 190,OOOg for 30 minutes.
The pellet was resuspended in 50 mM Tris HC1, pH 8.0, 1
mM dithiothreitol (DTT), 500 mM KC1, and 0.25% (volume/
volume) glycerol. Reverse transcriptase was assayed by
incubation of the sample with a reaction mixture containing
0.125 pCi 32P-dTTP (specific activity 600-800 Ci/mmole;
Arnersham, Arlington Heights, IL), 60 mM Tris HCI, pH
8 . 0 , 6 mM DTT, 0.6% Triton X-100, 12.5 p M dTTP, 12.5 pM
dATP (Boerhinger Mannheim, Indianapolis, IN), 0.073 pg/pl
poly(rA):oligo(dT) (Sigma, St. Louis, MO), and 7.5 mM
MgCl,. Positive control supernatants were derived from the
human T cell leukemia I (HTLV-I)-infected cell line HUT102 (kindly provided by Dr. Myron Essex, Harvard School
of Public Health, Boston, MA) and treated identically to the
patient supernatants. Incorporated 32P-dTMP was measured
by trichloroacetic acid precipitation and counted in liquid
scintillant (Biofluor; New England Nuclear, Cambridge,
MA). Picomoles of dTMP incorporated were calculated from
the specific activity of 300-850 counts per minute/pmole.
Background incorporation for each assay (with buffer alone)
was subtracted from all results.
No difference was seen in the picomoles of dTMP
incorporated by the particulate fraction of supernatants in
systemic-onset JRA patient cell cultures and control cell
cultures (mean SEM peak incorporation 3.7 0.4 pmoles
in patients versus 3.8
0.4 in controls; HTLV-I-positive
control 40.5 2 5.3 pmoles). No increase in incorporation was
observed in the supernatants of systemic-onset JRA patient
cultures during the second week after initiation of the
cultures, as has been reported in studies of cultured PBMC
from patients with other conditions (4). No cytopathic
changes were noted on serial examinations.
We were thus unable to detect either the presence of
reverse transcriptase or cytopathic changes in PBMC cultures from 7 patients with systemic-onset JRA. Previous
studies of patients with adult rheumatoid arthritis have failed
to detect a retrovirus using similar methodology (5). This
approach would be expected to detect retroviral infection
only if relatively large numbers of circulating PBMC harbor
the agent in the chronic phase of the disease. Additional
culture studies of patients with systemic-onset JRA of short
duration, cultures of synovial lymphocytes, monocytes, and
macrophages, and gene amplification of systemic-onset JRA
DNA with the polymerase chain reaction using retroviral
primers from highly conserved regions of the genome (6)
should be considered before retroviruses are excluded as
causative agents in systemic-onset JRA.
Nadina Rubio, MD
Susan Hoch, MD
Jane C. Burns, MD
Harvard Medical School
Boston, MA
*
*
*
1 . Still GF: A form of chronic joint disease in children. Br Med J
2:1446-1447, 1896
2. Lindsley CB: Seasonal variation in systemic onset juvenile
rheumatoid arthritis (letter). Arthritis Rheum 30:838439, 1987
3. Narayan 0, Cork LC: Lentiviral diseases of sheep and goats:
chronic pneumonia, leukoencephalomyelitis and arthritis. Rev
Infect Disease 729-98, 1985
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