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Synovial fluid pH lactate oxygen and carbon dioxide partial pressure in various joint diseases.

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Synovial Fluid pH, Lactate, Oxygen and Carbon Dioxide
Partial Pressure in Various Joint Diseases
Paul S. Treuhaft and Daniel J. McCarty
Fifty-five samples from knee joints of 44 patients with a wide variety of joint diseases were analyzed by routine gross and microscopic examination, and for pH,
pOz and pC0,; 18 fluids were analyzed for lactate. PO, values ranged from 8-78
mm Hg. Lower values were found generally i n fluids of the inflammatory type.
pH values ranged between 6.6 and 7.41 units and correlated poorly with PO,.
pCOz ranged between 34 and 150 mm Hg. PO, correlated poorly with pC0, (r =
-0.22) but better with lactate (r = -0.67). In the same 18 samples, lactate
correlated better with pH ( r = -0.9) than did pC0, (r = -0.38). No single
entity could be identified with a given degree of physiologic abnormality. These
changes appear to be nonspecific. The good correlation between lactate and both
pH and pOz suggests that anaerobic.glycolysis by an anoxic synovium may be
the most important underlying factor.
T h e availability of the Clark electrode
and microsampling technics has provided
the means for determining oxygen partial
pressure (PO,), carbon dioxide partial
pressure (pCO2) and p H in biologic fluids,
using relatively small volumes. When this
study was begun, there were no reported
data on pOz in synovial fluid, although
previous workers had studied pCO,, p H
and lactate concentrations (1-3). Subsequently two papers have appeared that
show diminished PO, in effusions from
rheumatoid arthritis (4, 5). Although this
From the Section of Arthritis and Metabolism,
Department of Medicine, Division of Biological
Sciences, University of Chicago, 950 East 59th Street,
Chicago, I11 60637.
PAUL s. TREUHAF~. MD: Formerly Fellow in Rheumatology; presently Captain USAFR, Dyes AFB,
Abilene, Tex. DANIEL J . MCCARTY, MD: Professor of
Medicine. University of Chicago, School of Medicine,
Chicago, Ill.
Reprint request should be addressed to Dr. McCarty.
Submitted for publication Oct 19, 1970: accepted
Dec
10, 1970.
Arthritis and Rheumatism, Vol. 14, No. 4 (July-Aupust 1971)
report is, in general, confirmatory, two important additional findings emerged from
an analysis of our data: (a) lowered synovia1 fluid PO, is not specific for rheumatoid
arthritis, as might be inferred from previous reports (4,5) and, (b) p H changes correlated much better with lactate concentration than with pCOz.
MATERIALS AND METHODS
Fifty-five samples of joint
fluid were obtained from one or both knees of 44
patients with a variety of joint diseases. Clinical
data relative to individual patients are given in
Table 1. Standard criteria were used for diagnosis.
Criteria for the diagnosis of rheumatoid arthritis
were those of the American Rheumatism Association (6).
Potlont roloctlon.
Sample coll~ctlon. All samples were collected in
glass Luerlock syringes lubricated with silicone
stopcock lubricant. and rinsed in heparin (l0,OOO
units/ml) . Analyses were performed immediately or
after storage anaerobically at 4O C for up to 4
~DOW
Corning Co, Midland, Mich.
475
TREUHAFT & MCCARTT
Table 1. Clinical Data
Fluid PaNo. tient
Age
Sex Race*
Diagnosist
Mucin
Knee Group clot
WBC/
cumm
X1P
Comments
~
L
L
I1
I1
Poor
Poor
2.75
4.0
R
I
Poor
1.7
L
I1
Fair
4.0
C
N
N
JRA (neg)
Granulomatous
colitis
internal derangement
Ankylosing
spondylitis
RA (128)
Reiter's
Gout
L
R
R
II
II
II
NAS
Poor
NA
11.0
14.0
20.0
M
F
F
M
F
C
N
C
N
C
Psoriasis
Unknown
RA (256)
RA (256)
Psoriasis
"
"
L
R
L
L
R
R
R
R
L
R
R
R
L
R
I
II
II
II
II
II
I
I
I
I
II
II
II
II
Good
Fair
Poor
NA
Fair
Poor
NA
NA
NA
NA
Poor
Poor
Poor
Poor
0.6
11.5
15.7
11.3
100.5
87.0
0.7
1
2
PR
LC
13
30
M
M
C
N
3
MW
56
F
N
4
JR
18
M
N
5
6
7
sw
30
31
39
F
M
M
8
9
10.
11
12
13
14
15
16
17
18
19
20
21
GR
50
44
36
68
41
II
LD
DJ
sc
DP
LJ
DB
BT
EW
WS
MT
CP
NM
AD
22
I'
23
'I
24
25
26
27
28
29
30
31
32
33
34
476
U
SMcF
"
u
DS
BR
VC
'I
57
F
62
M
9 0 M
C
N
N
1'
Trauma
OA
Unknown
"
u
57
25
65
40
F
M
F
F
C
C
C
C
'I
"
"
U
R
II
Poor
37.0
I'
u
"
"
R
II
Poor
80.5
16
I'
I'
"
L
II
Poor
64.0
42
F
N
L
I1
Poor
45.0
u
"
Y
"
L
II
Poor
29.0
u
u
R
R
L
L
II
Fair
Good
Good
Good
6.0
7.3
NA
NA
Good
Excellent
Fair
NA
NA
0.1
35
F
5 4 F
71
F
U
MR
4
OR
BH
48
33
U
4
F
M
M
Psoriasis
Re iter's
RA (1024)
Psoriasis, hypoparathyroidism
Gonococcal
arthritis
'
u
'I
C
C
C
RA (8)
OA
Leg edema;
electrolyte imbalance
Y
"
II
I
I
N
OA
L
R
I
I
N
N
Unknown
Gout
L
R
II
II
Acute attack, urate
crystals found
Severely inflamed
One day later
0.25
0.40
29.8
15.4
13.1
12.0
u
II
Huge effusion tense
21.0
3.1
During flare-up 14
days later
Height of flare 17
days later
Opposite knee also
flared
Severe pain
48 hours later (improving)
Mild symptoms
Never had joint
symptoms
12 days later
Nearly normal fluid
Subsiding acute attack; urate crystals
found
Arthritis and Rheumatism, Vol. 14, No. 4 (July-August 1971)
SYNOVIAL FLUID ANALYSES
Table 1.-Continued
Fluid
No.
Patient
Age
Sex Race*
Diagnosist
Vascul itis
Much
Knee Group clot
WBC/
cumm
Xl&*
iI
NA
NA
Poor
NA
NA
37.0
R
II
Poor
31.0
Gout
L
II
NA
39.0
C
OA
L
I
NA
F
F
F
F
F
M
M
M
N
C
C
C
C
C
C
N
RA (1024)
Psoriasis
RA (neg)
OA
SLE
Psoriasis
RA (8192)
Reiter's (128)
R
R
L
"
"
U
II
II
II
I
I
II
II
I
I
Excellent
Poor
Fair
Fair
NA
NA
Good
Fair
Fair
Good
22
56
60
64
58
M
F
M
M
F
C
C
N
C
C
Reiter's
OA
Trauma
Psoriasis
Gout
L
L
L
R
L
II
NA
NA
II
54
JE
AM
PC
MM
AM
II
Poor
NA
NA
Poor
Fair
55
JS
55
M
C
Gout
R
I
Good
48
M
N
u
"
u
u
RC
46
M
C
RA (5125)
38
''
'1
U
'1
39
BB
57
M
N
40
AK
61
F
41
42
43
44
45
46
47
48
49
EH
SW
HG
LL
JC
FF
HL
JM
42
26
54
44
29
70
62
60
50
51
52
53
35
36
37
GM
(I
ti
11
11
L
L
R
R
R
R
L
L
R
Comments
Acute flare, couldn't
walk
5 days later subsiding
Acute attack; urate
crystals found
Nearly normal fluid
11.1
4.1
9.2
1.3
12.0
15.4
5.8
0.6
Tender, warm knee
Nontender, cool
knee
31.5
40.0
21.0
Subacute attack;
urate crystals seen
1.05 Asymptomatic-cool
knee; no crystals
found
C = Caucasian; N = Negro
RA = rheumatoid arthritis; reciprocal of anti-lgG titer given i n parentheses (sensitized sheep
cell-normal = 8)
OA = osteoarthritis
Groups according to classification of Ropes and Bauer (2); mucin clot as described by same authors
t NA = not available
t
hours. Eighteen samples were further analyzed for
pyruvate and lactate. Aliquots of many fluids were
subjected to both gross and microscopic synovianalysis (7).
PO,, f l O a , and pn. Each determination was
performed in duplicate with a Radiometer model
P27b p H meter. a model pH.4 927b gas monitor
and E5021 microelectrode unit, using a constant
temperature water bath. Calibration of each elec-
trode with appropriate standards was carried out
both before and after each determination. Membranes on the oxygen and carbon dioxide electrodes
were changed as often as necessary to keep the unit
response time within the manufacturer's stated
tolerances. This was necessary much oftener than is
required with blood samples (often after every
third sample) . Duplicate determinations agreed
1 mmHg pCO,, f 1.5 mmHg PO,, and
.005
pH unit.
Arthritis and Rheumatism, Vol. 14, No. 4 (July-August 1971)
477
*
*
TREUHAFT 8 MCCARTV
berate. Lactate was measured i n 18 consecutive samples by an enzymatic spectrophotometric
method, using materials obtained from thc
Boehringer Mannheim C0rp.t T h e method is based
on that descrisbed by Horn and Bruns (8). In
essence, 1 ml of fresh joint fluid was mixed with 1
ml of 3.5% perchloric acid, using a vortex genie,
and the supernatant recovered by centrifugation;
0.1 ml,was then added to 2.0 ml of 0.08 M glycine
buffer, p H 9.0, containing 0.065 M hydrazine, 0.03
ml of a suspension of lactic acid dehydrogenase
containing 2 mg of the enzyme/ml, and 0.2 ml of 3.4
mM diphosphopyridinenucleotide (DPN) . A blank
was prepared for each series of determinations. Test
samples were run in duplicate. T h e optical densities
were read against air after 60-minute incubation at
25" C at 366 mm using a Beckman DU spectrophotometer with a Gilford attachment. Lactate concentration was calculated by reference to a standard
curve prepared using known concentrations of
L-lactate. This curve corresponded exactly to the
theoretical curve predicted on the basis of the
molar extinction coefficient for DP.NH. As an additional check, internal standards and known standards were run in duplicate with each set of samples.
T h e mean and standard error in 24 determinations on a standard solution of lactate containing 78
mg % was 78.07
0.1. T h e coefficient of variation
was 2.9%. Results on a standard solution containing
SE = 38.8
0.15,
39 mg % were: N = 10, mean
coefficient of variation = 3.5y0,. T h e variance and
standard deviation in the 18 samples analyzed in
duplicate were 0.64 and 0.8 mg respectively.$
*
*
*
Pyruvore. Pyruvate was estimated in duplicate
using test kit reagents.§ Duplicate determinations
showed a n agreement of 2 0.02 mg/100 ml.
RESULTS
Oxygen (PO,) and carbon dioxide
(pC0,) partial pressures, hydrogen ion
concentration (pH), lactate and pyruvate
levels are listed in Table 2. PO, values
ranged from a high of 78 to a low of 8
mmHg. I n general, lower values were
found in fluids of the inflammatory type,
although occasional exceptions were noted.
Fluids 33 and 49, from clinically noninflamed knees had PO, of 27 and 20
mmHg, for example. PO, values are
plotted against pH, pCO,, and lactate Fig
lA, B and C respectively. T h e correlation
between PO, and p H was poor but significant (r = 0.23 P < 0.05); many fluids with a
low PO, had a p H of 7.32 o r above. Fluids
from markedly inflamed joints tended to
have a low PO,, low pH and high pC0,.
All fluids with a p H of 7.12 or less had a
PO, of less than 25 mmHg. In this group,
none, except Patient 1, could bear weight
on the affected limb because of the severity
of the inflammation.
Patient 1, a young boy with juvenile
rheumatoid arthritis, had extraordinarily
tense effusions in both knees, but was nearly asymptomatic otherwise, leading a nearnormal existence.
PO, correlated poorly with pC0, (r =
-0.22 P = ns). If values of PO, below 30
only were considered, the correlation was
somewhat better (r = -0.43 P < O.Ol).ll A
much better correlation was found between
PO, and synovial fluid lactate concentration
(r = -0.67 P < .0025).
As can be readily appreciated from Table 1 and 2, there was no single disease
entity that correlated with a given degree
of physiologic abnormality. Diagnosis in
the most abnormal group included 1 patient with Reiter's syndrome, 2 with psoriatic arthritis, 1 with gonococcal arthritis, 2
with adult and 1 with juvenile rheumatoid
arthritis and 1 patient in whom no diagnosis could be made. With the exception of
t219 East 44 Street, New York. NY.
$Holman HH: Estimation of error by duplicate
measurements, Biological Research Method. New
York, Hafner Publishing Co, 1962, p 75
§Provided by the Boehringer Mannheim Corp,
219 East 44 Street, New York, NY.
IlElimination of 4 values for pC0, in Fig 1B that
appeared to be erroneous because they were so low,
provided a nearly vertical regression line when PO,
values over 30 mmHg were considered. But the p H
values corresponding to these low pC0, values were
not particularly high (Table Z), suggesting the presence of buffers more significant than bicarbonate.
478
Arthritis and Rheumatism, Vol. 14, No. 4 (July-August 1971)
SYNOVIAL FLUID ANALYSES
Table 2.
P o 2 PCOI
Fluid (rnrn (rnrn
No. Hg) Hg)
Laboratory Data
pH
Table 2.-Continued
Lactate
(mgl
100rnl)
Pyruvate
(mgl
100 rnl)
~~
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
21
28
29
30
31
32
33
34
35
36
31
38
39
40
41
42
43
44
45
46
41
48
15
58
78
60
18
24
30
58
55
42
38
34
15
31
65
69
70
15
21
10
40
26
6
10
10
10
26
9
38
45
34
40
21
45
8
14
8
16
24
44
10
12
28
67
16
47
15
20
60
35
45
46
42
54
40
43
46
52
46
38
34
45
42
44
44
82
68
58
31
48
78
70
70
12
42
54
50
40
25
22
54
15
50
64
68
16
40
24
50
60
56
40
44
46
60
48
1.02
7.35
7.32
7.33
1.15
7.26
1.25
1.35
7.38
1.195
1.31
7.145
1.238
7.34
1.32
1.34
1.34
1.143
1.195
7.41
7.77(?)
1.28
1.12
1.08
7.12
1.16
1.32
1.45
1.39
7.28
1.28
7.34
7.22
7.32
7.27
7.40
6.92
6.99
1.10
1.30
1.21
7.33
1.28
1.35
1.24
7.36
1.09
1.32
55.9
15.1
15.8
15.0
33.1
22.0
23.3
17.8
12.5
39.5
24.3
1.52
1.44
1.41
1.06
1.18
1.43
1.31
1.64
1.05
1.25
1.23
18.1
23.1
12.1
14.5
46.1
31.6
25.7
1.42
1.26
1.13
1.13
1.21
1.28
2.08
-
-
-
-
-
-
-
-
-
Mhritlr and Rheumatism, Vol. 14, No. 4 (July-Au~d1971)
Lactate
PO2 PCO?
Fluid (rnm (mm
No. Hg) Hg)
~-
PH
20
16
29
17
5
18
74
1.25
6.95
1.35
1.36
6.60
1.29
1.31
49
50
51
52
53
54
55
50
88
52
52
150
16
58
ms/
100 ml)
Pyruvate
(mgl
100 rnl)
Patient 1, the arthritis was of recent onset
or represented a severe flareup of a previously existing condition.
Correlation between PO,, and synovial
fluid leukocyte count was poor (r = -0.43),
although, as expected, the leukocyte count
generally paralleled the severity of the
inflammation. p H was correlated much
more strongly with lactate (r = -0.9 P <
0.0005) than with pC0, in the same 18
samples (r = -0.38 P = NS) Fig 2a and b.
But when regression analysis was carried
out using values from all 55 samples, $0,
correlated better with pH (r = -0.68 P <
.001) (Fig 3).
Joint fluid pyruvate values were not
helpful. They failed to correlate with any
other parameter that we measured.
DISCUSSION
The data presented here in general
confirm the findings of Falchuk, Goetzl and
Kulka who studied PO,, pCO,, pH and
lactate concentration in joint fluids of 30
hospitalized patients (4). Twenty-two of
their patients had rheumatoid arthritis.
These workers found a p 0 2 of less than 27
mmHg only in severe rheumatoid arthritis.
They interpreted their data as showing a
sharp rise in pC0, and lactate and a fall in
pH when PO, fell below 27 mmHg. They
presumed that the low oxygen tension ob479
0
n
N
\s
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20
10 '
20 '
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10-
-
30
40-
50-
60 -
70
80 -
90
.
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a
.
*.\
-. .
. . .
r'
*
.
*
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.
..
.
.
8
*.
$
0"n
&
-3
10
20
30
40
50
60
70
LACTATE(mg/loo mi)
Fig 1A. Values of PO, in 55 joint fluids are shown plotted against
the values for pH in the same fluids (correlation is poor (r = 0.23)).
In general, fluids from patients with severe inflammation showed
both a low PH and a low PO,, although frequent exceptions were
noted). B. Values of PO, in 55 joint fluids are plotted against
values for pC0, in the same fluids (overall correlation is poor (r =
-0.22)). The four values of pC0, below 30 mmHg are excluded from
statistical calculations as erroneous. I f values of PO, above and
below 30 mmHg were considered separately, pC0, and PO, varied
independently when PO, was above 30 mmHg (1 = +0.07), whereas
at PO, below 30 mrnHg, a negative correlation obtained (r =
-0.43).
C. Values for PO, in 18 joint fluids are plotted against
the values for lactate in the same fluids (correlation is good (r =
-0.67)).
SYNOVIAL FLUID ANALYSES
served was due to an imbalance between
the arterial blood supply to the joint and
the increased metabolic demand of the
inflamed tissues. Synovial membranes, biopsied in 24 cases, showed more histologic
evidence of fibrinoid necrosis, focal cellular
to vascular imbalance, obliterative microangiopathy, leukocytic infiltration and
fixed cellular hyperplasia in those instances
where the synovial fluid physiologic alter-
Fig 2A (top). Values for lactate
in 18 joint fluids are plotted against
the pH values of the same fluids
(correlation is excellent (r = -0.9)).
B (bottom). Values for pC0, in the
same 18 joint fluids are plotted
against the pH values of the same
fluids (correlation is poor (r =
-0.38)).
Arthritis and Rheumatism, Vol. 14, No. 4 (July-August 1971)
481
TREUHAFl & MCCARTY
Our data show a much better correlation
between p H and lactate than between p H
and pCO,, supporting the notion that the
elevated pC0, may be, at least in part,
secondary to the lactic acid production. It
should be pointed out that in the data
presented by Falchuk et a1 (4) both lactate
and pC0, correlated strongly with pH (r =
-0.92 and r = -0.95 respectively). T h e
reason for the difference between their
pC0, data a n d our own is not apparent.
Our material included many more patients
with inflammatory arthritis other than rheumatoid, and most of our patients were
ambulatory.
More recently, Lund-Oleson has reported PO,, pC0, and p H studies on 103 joint
fluids from 40 patients (5). He found a
correlation between PO, and p H (I =
0.34), and between PO, and pCO, (r =
-0.31) and between pC0, and p H (no
correlation coefficient given). He found
considerable variations in pOz values in 85
fluids from patients with rheumatoid arthritis: mean f SD = 26.5 -t 19.3. These were
generally lower than in osteoarthritis
(mean f SD = 42.9
15.1), and in traumatic effusions (mean f SD = 63 -c 19.2).
He stated that the lowest PO, were from
patients with severe R A but admitted that
this was a retrospective opinion. He presented data contrasting PO, in the right and
left knee o f 14 subjects and found that they
varied concomitantly, although discrepancies of over 50mmHg were noted in 2 instances. Four rheumatoid patients were subjected to active exercise for one hour after
fluid first had been withdrawn for study.
p 0 2 fell in 3 of the subjects and rose in the
fourth. But p H rose in three of the 4 and
p C 0 2 fell in the same three fluids. Thus,
the physiologic disturbance was not obviously worse after exercise, and might even
have improved. More extensive studies of
this sort might resolve the question of the
effect of exercise on joint fluid gases.
Serial observations of gas tensions and
p H were made in relatively few of our
patients. In general, the degree of physiologic abnormality noted in serial studies
paralleled the degree of inflammation noted
clinically. Fluids 21-24 from patient AD,
25-27 from patient SMcF, 37-38 from patient RC demonstrate this. Careful serial
observations of selected patients over a
long period of time may answer the question of the possible deleterious effects of
prolonged anoxia on joint function-ie, is
prolonged anoxia correlated with the development of cartilage damage, erosions
and joint instability? Is anoxia related to
the quality and quantity of local immune
482
Arthritis and Rheumatiun, Vol. 14, No. 4 (July-August 1971)
*
6.6
6.7
6.8
6.9
7.0
7.1
7.2
7.3 7.4
7.5
PH
mg 3. Values for pC0, in 55 joint fluids are plotted
against the pH values of the same fluids.
ations were most profound. T h e rise in
lactate was believed due to the anoxic
synovial tissue utilizing anaerobic glycolysis. T h e increase in pC0, was thought to
be due to the buffering of lactic acid by
bicarbonate in accordance with the following equation:
[H+]
+ [HCOa-]@
[H&Oa]*
COz
+ HzO
SYNOVIAL FLUID ANALYSES
complex production? What are the factors
leading to lowered PO, and lactate production in the first place? Can the hypothesis
of circulatory-metabolic imbalance be substantiated? Alternatively, how much of the
observed changes are a result of “synovialcapillary” block-secondary
perhaps to
fibrin deposition, to tissue edema, or to the
functional microcirculatory effects of increased hydrodynamic synovial fluid pressure. T h e answers to such questions await
the development of new technics and well
planned investigation.
It seems fair to state that the study of
joint physiology is in its infancy. Interest in
immunology and connective tissue biochemistry preoccupies most academic rheumatologists, and little research, using modern technics, has been done on the organ
physiology of the joint. This approach
seems important, however, as physiologic
understanding is the basis of rational treatment. The concept of a circulatorymetabolic imbalance, elaborated by Falchuk, Goetzl and Kulka, for example, may
be invoked to explain the marked therapeutic effect of joing splinting (S), for if
demand for oxygen is reduced and blood
flow remains unchanged, tissue healing
may be promoted.
fluids with a low pOz showed a pH of 7.32
or above. All with a pH < 7.12 had PO, <
25 mmHg; 7 of 8 patients with such fluids
could not bear weight on. the affected limb
due to the clinical severity of the inflammation. pC0, ranged between 34 and 150
mmHg. PO, correlated poorly with pCOz
(r = -0.22) but better with lactate ( r =
-.67). In the same 18 samples, lactate correlated better with pH ( r = -0.9) than was
the case with pC0, (r = -0.38). Correlation bctween PO, and synovial fluid leukocyte was poor (r = 0.43). No single
disease entity could be identified with a
given degree of physiologic abnormality.
Diagnosis in the most abnormal group included 1 patient with Reiter’s syndrome, 2
with psoriatic arthritis, 1 with gonococcal
arthritis, 2 with adult and 1 with juvenile
rheumatoid arthritis, and 1 patient in
whom no diagnosis could be made.
We conclude that these changes are nonspecific and may be a result of a variety of
unknown factors. The strong correlation
between lactate and both pH and pOz
suggests than anaerobic glycolysis, by an
anoxic synovium, is the final common result of these undefined antecedent factors.
SUMMARY
1 . Kling DH: The synovial membrane and the
Fifty-five samples from knee joints of 44
patients with a wide variety of joint d i s
eases were analyzed by routine gross and
microscopic examination, and for p H (2
0.005 unit), PO, (2 1.5 mmHg). pC0, (2
1 mmHg); 18 consecutive fluids were analyzed for lactate (& 0.8 mg/100 ml). PO,
values ranged from 8 to 78 mmHg. In
general, lower values were found in fluids
of the inflammatory type, with frequent
exceptions. pH values ranged between 6.6
and 7.41 units. The correlation between
PO, and p H was poor (r = 0.23). Many
Althritis a d Rhdumlfjsm, Vol. 14, No. 4 ( J u l y - A u ~1971)
REFERENCES
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Ropes MW, Bauer W: Synovial Fluid
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Cummings NA, Nordby G L Measurement
of synovial fluid pH in normal and arthritic knees. Arthritis Rheum 9:47. 1966
Falchuk KH, Goetzl EJ. Kulka JP: Respiratory gases of synovial fluids. Amer J Med
49223-231, 1970
Lund-Oleson K: Oxygen tensions in syn463
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6. Ropes MW, Bennett GA, Cobb S, et al:
1958 revision of diagnostic criteria for rheumatoid arthritis. Bull Rheum Dis 9:175.
1958
7. Hollander JL, Jessar- RA, McCarty DJ:
Synovianalysis. Bull Rheum Dis 12:263-264,
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8. Horn HD, Bruns FH: Quantitative deter-
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9. Gault SJ, Spyker JM: Beneficial effect of immobilization of joints in rheumatoid and
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lVth INTERNATIONAL OSTEOLOGICAL SYMPOSIUM
T h e symposium will be held i n Prague, Czechoslovakia, Sep
tember 28-30, 1972. I t will be organized by the Europalache
Arbeitegemeinschaft fiir Osteo-Arthrologie, the Czech Rheumatology Society and the Czechoslovak Medical Society as a presymposium to the IIIrd Czechoslovak Congress on Rheumatology.
For further information write to:
Stanislav Havelka, MD
General Secretary
PRAHA 2-Sokolski 3 1/ Czechoslovakia
Arthritis and Rheumrtkm, Vol. 14, No. 4 (July-August 1971)
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dioxide, joint, pressure, disease, partial, lactate, synovial, oxygen, carbon, fluid, various
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