The document discusses spinal involvement in crystal-related diseases, focusing on gout. Spine involvement in gout is uncommon but can occur in cases of severe tophaceous gout. Symptoms may be asymptomatic initially or include acute or chronic back pain and nerve compression. Diagnosis is made through identification of urate crystals via aspiration or biopsy of spinal lesions. Imaging such as CT, MRI can show erosions, tophi, and lesions affecting various spinal structures including intervertebral discs, facet joints, and ligaments. Spinal cord or cauda equina compression may occur due to large tophi. While back pain is present in about half of cases, spinal involvement in gout is often missed likely due to

1. Spine
involvement
in
Crystal
diseases
JFIM
Hanoï
2015
Pr
Jean
Denis
LAREDO
Hôpital
Lariboisière
-­‐
Paris

2. Spinal
Crystal
diseases
§ Urate monosodium : Gout
§ Calcium crystals
– Calcium phosphate « Apatite disease »
– Calcium pyrophosphates « CPPD disease »
– Calcium oxalate

3. Spinal
Crystal
diseases
§ Urate monosodium : Gout
§ Calcium crystals
– Calcium phosphate « Apatite disease »
– Calcium pyrophosphates « CPPD disease »
– Calcium oxalate

4. Gout

5. Gout

8. Spine Gout
§ Very uncommon
§ Severe tophaceous gout
§ Symptoms
Asymptomatic at an early stage
Acute and chronic back pain
Nerve compression +++
§ Diagnosis: urate crystals
Aspiration or biopsy
DECT ?
Kersley, 1950

9. S Semlali et al. Tophus goutteux du rachis lomba
spondylodiscite : asp
thogénie
sultats d
la suite d
destruct
bre cervi
sub-luxa
Le dépô
fait le plu
tions et l
riphériq
le squele
est due à
le disqu
bral, le l
tervertéb
dégénéra
comme
d’urate,
l’atteinte
atteinte v
estimée,
S Semlali et al.
Fig. 2 : Tomodensitométrie lombaire.
a Coupe axiale passant par L2, fenêtre osseuse.
b Reconstructions sagittales, en fenêtre osseuse
teaux vertébraux de L1 et L2. Noter les érosion
rieures de L1 (flèche).
a
c
b
Semlali
J
Radiol
2008;89:904-­‐6
152 DUPREZ AJNR: 17, January 1996
Duprez
et
al.
AJNR
1996;17:151-­‐3
Haush
et
al.
J
Clin
Rheumatol
1999;6:335-­‐41
• Gout
:
joint
deposits
ü Intervertebral
disc

10. patients had laboratory markers for systemic inflammation.
Magnetic resonance imaging (MRI) and computed tomography
(CT) showed discovertebral lesions in three patients (at the cer-
vical spine in two [Fig. 1] and lumbar spine in one [Fig. 2]) and
lumbar facet joint lesions in two patients (Fig. 3). Specimens of the
spinal lesions were obtained in three patients: in each of the two
patients with facet joint involvement, the surgical biopsy recov-
ered a tophus and the needle aspirate contained monosodium urate
crystals; and in the patient with lumbar discitis, the biopsy con-
tained an inflammatory granuloma and the needle aspirate was
positive for monosodium urate crystals. In the two patients with
cervical lesions, the diagnosis relied on a history of gout attacks
and a rapid response to colchicine with resolution of the clinical
manifestations and decreases in the serum uric acid and/or CRP
levels. The outcome was rapidly favorable with colchicine therapy
alone in four of the five patients. Surgical resection of the affected
facet joint was performed in the remaining patient.

11. M
42,
Gout
for
15
years.
Tophus
of
the
extremiQes
for
1
year.
IntermiRent
back
pain

14.
T1-­‐WI
Gad-­‐enhanced
T1-­‐WI

15. éatininémie, mais le patient avait été perdu de
une était originaire d’Amérique du Sud et tra-
rme laitière.
ysique, le patient était apyrétique et ses fonc-
t normales. La seule anomalie consistait en une
leur de nombreuses articulations. Les examens
x montraient une créatininémie à 700 ␮mol/L,
2 ␮mol/L et une leucocytose à 13 500/mm3. La
gène HLA B27 était négative. L’analyse du liquide
par ponction du genou droit révélait des cristaux
Les sérologies infectieuses étaient négatives, de
uberculinique, les hémocultures, les cultures des
articulaire. L’échographie rénale était en faveur
e chronique.
métrie (TDM) abdominopelvienne mettait en
ons articulaires érosives, bien limitées, sans
nodules tissulaires siégeant aux articulations
roites de T9 et T10, à l’articulation costoverté-
12 (Fig. 1), aux articulation interapophysaires
te en L3-L4 et L4-L5, et à gauche en L5-S1. Il exis-
atteinte érosive de l’articulation sacro-iliaque
de sacroiliite (Fig. 2). Les diagnostics envisagés
: goutte, brucellose, tuberculose, amylose, ainsi
thrite sous-jacente.
enne, on observait de nombreuses lésions bien
rées sur les articulations, en hyposignal T1 et
crètement hétérogène en T2. Il existait des éro-
aque gauche.
rs, sous contrôle TDM, une biopsie percutanée
rc postérieur de L5 à gauche. L’analyse mettait
patients âgés de moins de 45 ans. Dans la littérature, il en
rapporté trois cas atteignant le rachis lombaire (âge des patie
17, 27 et 29 ans), un cas atteignant le rachis thoracique (28 an
un cas atteignant le rachis cervical (29 ans) [4–8]. Les mécani
physiopathologiques incriminés sont une longue évolution
maladie goutteuse, une atteinte rachidienne dégénérative asso
et une transplantation rénale.
Dans les cas de goutte rachidienne, la TDM peut m
trer des érosions intra-articulaires et juxta-articulaires
• Gout
:
joint
deposits
ü Intervertebral
disc
ü Costo-­‐vertebral
joint
ü Facet
joint

16. Interspinous
gout
bursi2s

17. Tophus
in
ligaments

18. Spinal
cord
compression
due
to
tophus
Dharmadhikari et al., A rare cause of spinal cord compression, Skeletal Radiol(2006)35:

19. Dharmadhikari et al., A rare cause of spinal cord compression, Skeletal Radiol(2006)35:

20. Fig 2. A, T2-weighted sagittal image (TR/TE, 4550/110) shows predominantly hypointense mass lesions replacing the posterior elements of T4 through T7. B, T1-weighted sagittal image
(516/12) demonstrates hypointensity of the same lesions. C, T1-weighted fat saturation images with gadolinium (816/12) with avid enhancement of the lesions.
Fig 2. A, T2-weighted sagittal image (TR/TE, 4550/110) shows predominantly hypointense mass lesions replacing the posterior elements of T4 through T7. B, T1-weighted sagittal image
(516/12) demonstrates hypointensity of the same lesions. C, T1-weighted fat saturation images with gadolinium (816/12) with avid enhancement of the lesions.
Fig 3. A, T1-weighted axial image (TR/TE, 617/10); B, T1-weighted axial image with 20 mL gadolinium (550/12) and C, T2-weighted axial image (6350/80) demonstrate extradural lesions
Spinal
cord
compression
due
to
tophus
Popovitch
et
al
AJNR
2006
27:1201-­‐3

21. T1
T2
T1
G
Cauda
equina
compression
due
to
tophus

22. Odontoid
fractures
emained sterile.
De
Parisot
et
al
Joint
Bone
Spine.
2013;38:550-­‐1
Fig. 2. Multimodal
between CT scan a
jection of inflamma
lesions.
Cervical spin
vial hypertroph
(Fig. 1). Comput
base of the odo
luxation (Fig. 1D
views highlight
trophy at C1-C2
instability and m
performed usin
to colchicine, fe
CRP and SUA ha
[−33%], respect

23. in the study.
d by the clin-
n patient; the
tive patient’s
mation of the
of axial gout
ses included
h the clinical,
frequency of
on of gout in
ears in those
rd deviations
r varied from
the estimated
phic and clin-
tinuous vari-
and by axial
were used to
oups, respec-
y significant.
y, NC, USA).
stics of the
Clinical tophi present, % 46
Back pain present, % 50
Peripheral radiographic erosions, n (%) 21/47 (45)
Axial gout erosions and/or tophi, n (%) 17/48 (35)
Axial tophi, n (%) 7/48 (15)
Table 2. Features of subjects with and without axial gout.
Characteristic Axial Gout, No Axial Gout, p
n = 17 n = 31
Mean age (SD), yrs 65 (10.8) 59 (13.5) 0.16
Duration of gout > 10 years,
n (%) 11 (65) 15 (48) 0.37
Mean serum uric acid level (SD),
mg/dl 7.5 (2.7) 7.9 (2.5) 0.39
Back pain, n (%) 10 (59) 14 (45) 0.55
Peripheral clinical tophi, n (%) 11 (65) 11 (35) 0.07
Hypertension, % 94 81 0.40
Body mass index > 25, % 62 67 0.10
Creatinine clearance < 60 ml/min, % 93 62 0.07
Current allopurinol therapy, % 41 42 1.0
Diabetes mellitus, % 65 32 0.04
Peripheral radiographic erosions,
n (%) 13 (81) 8 (26) < 0.001
Correlates of Axial Gout: A Cross-sectional Study
RUKMINI M. KONATALAPALLI, ELENA LUMEZANU, JAMES S. JELINEK, MARK D. MURPHEY, HONG WANG,
and ARTHUR WEINSTEIN
ABSTRACT. Objective. A cross-sectional study was undertaken to determine the prevalence of axial gout in
patients with established gouty arthritis and to analyze clinical, laboratory, and radiological
correlations.
Methods. Forty-eight subjects with a history of gouty arthritis (American College of Rheumatology
criteria) for ≥ 3 years under poor control were included. Subjects underwent history, physical exam-
ination, laboratory testing, and imaging studies, including radiographs of the hands and feet and
computerized tomography (CT) of the cervical and lumbar spines and sacroiliac joints (SIJ). Patients
with characteristic erosions and/or tophi in the spine or SIJ were considered to have axial or spinal
gout.
Results. Seventeen patients (35%) had CT evidence of spinal erosions and/or tophi, with tophi iden-
tified in 7 of the 48 subjects (15%). The spinal location of axial gout was cervical in 7 patients
(15%), lumbar in 16 (94%), SIJ in 1 (6%), and more than 1 location in 14 (82%). Duration of gout,
presence of back pain, and serum uric acid levels did not correlate with axial gout. Extremity radio-
graphs characteristic of gouty arthropathy found in 21 patients (45%) were strongly correlated with
CT evidence of axial gout (p < 0.001). All patients with tophi in the spine had abnormal hand or feet
radiographs (p = 0.005).
Conclusion. Axial gout may be a common feature of chronic gouty arthritis. The lack of correlation
with back pain, the infrequent use of CT imaging in patients with back pain, and the lack of recog-
nition of the problem of spinal involvement in gouty arthritis suggest that this diagnosis is often
missed. (First Release April 15 2012; J Rheumatol 2012;39:1445–9; doi:10.3899/rheum.111517)
Key Indexing Terms:
GOUT SPINE TOPHI EROSIONS COMPUTERIZED TOMOGRAPHY BACK PAIN
From the Division of Rheumatology, Department of Medicine, and
Department of Radiology, Washington Hospital Center, Washington, DC;
and Department of Biostatistics and Epidemiology, MedStar Health
Research Institute, Hyattsville, Maryland, USA.
Supported in part by a research grant from Savient Pharmaceuticals, Inc.
and by a Fellowship Training Award from the Research and Education
Foundation, American College of Rheumatology.
Axial gout is recognized as a known feature of chronic
gout1. With the increasing prevalence of hyperuricemia and
gout, it is likely that axial gout would be recognized more
frequently2. Although literature reviews have described
many cases3,4, its prevalence and clinical correlations remain
uncertain, as no large, prospective studies have been pub-
lished. In an earlier analysis of patients with gout who had
spinal computerized tomography (CT) available for evalua-
tion, the prevalence of axial gout was 14%1. However,
because of its retrospective design, we were not able to
derive definitive data on the possible association of axial
gout with important clinical and laboratory features includ-
ing duration of peripheral gouty arthritis; serum urate levels;
and presence of clinical or radiological tophi, symptomatic
back pain, and comorbidities such as hypertension (HTN),
diabetes mellitus (DM), and chronic renal insufficiency.
This cross-sectional study was undertaken to obtain a
more accurate estimation of the prevalence of axial gout and
to explore its clinical, laboratory, and radiologic correlates.
Similarly to our prior study, CT was utilized as the imag-
5
CT evidence of axial gout (p < 0.001). All patients with tophi in the spine had abnormal hand or feet
radiographs (p = 0.005).
Conclusion. Axial gout may be a common feature of chronic gouty arthritis. The lack of correlation
with back pain, the infrequent use of CT imaging in patients with back pain, and the lack of recog-
nition of the problem of spinal involvement in gouty arthritis suggest that this diagnosis is often
missed. (First Release April 15 2012; J Rheumatol 2012;39:1445–9; doi:10.3899/rheum.111517)
Key Indexing Terms:
GOUT SPINE TOPHI EROSIONS COMPUTERIZED TOMOGRAPHY BACK PAIN
sion of Rheumatology, Department of Medicine, and
f Radiology, Washington Hospital Center, Washington, DC;
ent of Biostatistics and Epidemiology, MedStar Health
tute, Hyattsville, Maryland, USA.
part by a research grant from Savient Pharmaceuticals, Inc.
owship Training Award from the Research and Education
American College of Rheumatology.
apalli, MD, Former Fellow; E. Lumezanu, MD, Fellow,
heumatology; J.S. Jelinek, MD, FACR, Chair, Department of
ashington Hospital Center; M.D. Murphey, MD, FACR,
Chief, American Institute for Radiologic Pathology, Silver
and, and Professor of Radiology, Uniformed Services
the Health Sciences, Bethesda, Maryland; H. Wang, MD,
an, Department of Biostatistics and Epidemiology, MedStar
rch Institute, the Georgetown and Howard Universities
nical and Translational Sciences, Georgetown; A. Weinstein,
RCP, MACR, Professor of Medicine, Georgetown University
er; Chief, Division of Rheumatology, Washington Hospital
is recognized as a known feature of chronic
h the increasing prevalence of hyperuricemia and
ikely that axial gout would be recognized more
. Although literature reviews have described
3,4, its prevalence and clinical correlations remain
as no large, prospective studies have been pub-
n earlier analysis of patients with gout who had
spinal computerized tomography (CT) available for evalua-
tion, the prevalence of axial gout was 14%1. However,
because of its retrospective design, we were not able to
derive definitive data on the possible association of axial
gout with important clinical and laboratory features includ-
ing duration of peripheral gouty arthritis; serum urate levels;
and presence of clinical or radiological tophi, symptomatic
back pain, and comorbidities such as hypertension (HTN),
diabetes mellitus (DM), and chronic renal insufficiency.
This cross-sectional study was undertaken to obtain a
more accurate estimation of the prevalence of axial gout and
to explore its clinical, laboratory, and radiologic correlates.
Similarly to our prior study, CT was utilized as the imag-
ing modality to identify axial gout5. CT reveals characteris-
tic changes of axial gout: intraarticular and juxtaarticular
erosions with sclerotic margins and an attenuation or densi-
ty greater than the surrounding muscle due to deposition of
sodium urate crystals. Multiple anatomic sites within the
vertebral column can be involved, including the epidural
space, intradural space, ligamentum flavum, discovertebral
junction, the pedicles, facet joints, spinous processes, filum
terminale, and neural foramina5. Other reports have shown
biopsy-proven urate crystals in the spine in the presence of
Correlates of Axial Gout: A Cross-sectional Study
RUKMINI M. KONATALAPALLI, ELENA LUMEZANU, JAMES S. JELINEK, MARK D. MURPHEY, HONG WANG,
and ARTHUR WEINSTEIN
ABSTRACT. Objective. A cross-sectional study was undertaken to determine the prevalence of axial gout in
patients with established gouty arthritis and to analyze clinical, laboratory, and radiological
correlations.
Methods. Forty-eight subjects with a history of gouty arthritis (American College of Rheumatology
criteria) for ≥ 3 years under poor control were included. Subjects underwent history, physical exam-
ination, laboratory testing, and imaging studies, including radiographs of the hands and feet and
computerized tomography (CT) of the cervical and lumbar spines and sacroiliac joints (SIJ). Patients
with characteristic erosions and/or tophi in the spine or SIJ were considered to have axial or spinal
gout.
Results. Seventeen patients (35%) had CT evidence of spinal erosions and/or tophi, with tophi iden-
tified in 7 of the 48 subjects (15%). The spinal location of axial gout was cervical in 7 patients
(15%), lumbar in 16 (94%), SIJ in 1 (6%), and more than 1 location in 14 (82%). Duration of gout,
presence of back pain, and serum uric acid levels did not correlate with axial gout. Extremity radio-
graphs characteristic of gouty arthropathy found in 21 patients (45%) were strongly correlated with
CT evidence of axial gout (p < 0.001). All patients with tophi in the spine had abnormal hand or feet
radiographs (p = 0.005).
Conclusion. Axial gout may be a common feature of chronic gouty arthritis. The lack of correlation
with back pain, the infrequent use of CT imaging in patients with back pain, and the lack of recog-
nition of the problem of spinal involvement in gouty arthritis suggest that this diagnosis is often
missed. (First Release April 15 2012; J Rheumatol 2012;39:1445–9; doi:10.3899/rheum.111517)
Key Indexing Terms:
GOUT SPINE TOPHI EROSIONS COMPUTERIZED TOMOGRAPHY BACK PAIN
From the Division of Rheumatology, Department of Medicine, and
Department of Radiology, Washington Hospital Center, Washington, DC;
and Department of Biostatistics and Epidemiology, MedStar Health
Research Institute, Hyattsville, Maryland, USA.
Supported in part by a research grant from Savient Pharmaceuticals, Inc.
and by a Fellowship Training Award from the Research and Education
Foundation, American College of Rheumatology.
R.M. Konatalapalli, MD, Former Fellow; E. Lumezanu, MD, Fellow,
Axial gout is recognized as a known feature of chronic
gout1. With the increasing prevalence of hyperuricemia and
gout, it is likely that axial gout would be recognized more
frequently2. Although literature reviews have described
many cases3,4, its prevalence and clinical correlations remain
uncertain, as no large, prospective studies have been pub-
lished. In an earlier analysis of patients with gout who had
spinal computerized tomography (CT) available for evalua-
tion, the prevalence of axial gout was 14%1. However,
because of its retrospective design, we were not able to
derive definitive data on the possible association of axial
gout with important clinical and laboratory features includ-
ing duration of peripheral gouty arthritis; serum urate levels;
and presence of clinical or radiological tophi, symptomatic
back pain, and comorbidities such as hypertension (HTN),
diabetes mellitus (DM), and chronic renal insufficiency.
This cross-sectional study was undertaken to obtain a
more accurate estimation of the prevalence of axial gout and
to explore its clinical, laboratory, and radiologic correlates.
Similarly to our prior study, CT was utilized as the imag-
ing modality to identify axial gout5. CT reveals characteris-
48
paQents,
gout
>
3y;
lumbar
&
cervical
CT-­‐scan;
hands
and
feet
radiographs

24. Oxalate de calcium et rachis
Oxalose primitive
Condensation osseuse
Fragilité osseuse, tassements vertébraux

25. Spinal
Crystal
diseases
§ Urate monosodium : Gout
§ Calcium crystals
– Calcium phosphate « Apatite disease »
– Calcium pyrophosphates « CPPD disease »
– Calcium oxalate

26. Intervertebral disc apatite
(phosphocalcic bruschite) deposits
«
ApaQte
rheumaQsm
»
§ Hydroxyapatite deposition disease
§ Children intervertebral disc calcification
§ Intradiscal steroid injections
§ Disc ankylosis (Forestier, SPA, spine
arthrodeses…)
§ Chronic hemodialysis for renal failure
§ Ochronosis

27. «
ApaQte
rheumaQsm
»
Amor
et
al
Rev
Rhum
1977
:
45
paQents
§ Acute
back
pain:
33%
§ CalcificaQons
:
53%

28. Spine
apaQte
deposits
and
clinical
findings
§ Acute back pain and sometimes fever
§ Tensor longus capitae tendinitis
§ Crowned dens syndrome
§ Calcifyed herniated discs
ü Thoracic spine : spinal cord
compression
ü Lumbar spine : inflammatory painful
nerve root pain

29. Rev
Rhum
1982;
49:
549-­‐551

30. § 4
paQentes
avec
cervicalgie
haute
aiguë
§ 2
femmes
âgées
de
59
et
63
ans,
porteuses
de
mulQples
calcificaQons
péri-­‐arQculaires
évocatrices
de
rhumaQsme
apaQQque
§ 2
femmes
âgées
de
69
de
75
ans,
porteuses
d’une
CCA
typique
§ Dépôts
calciques
péri-­‐odontoïdiens
§ Bonne
réponse
aux
AINS
Ziza
et
al,
Rev
Rhum
1982;
49:
549-­‐551

31. Crowned
dens
syndrome
§ Occipital
pain
§ +
Arnold
pain,
ear
pain,
mandibular
or
temporo-­‐
mandibular
pain
§ Abrupt
onset,
intense
pain
§ SomeQmes
subacute
or
even
chronic
pain
§ Fever,
increased
CRP/blood
sedimentaQon
rate
§ Cervical
moQon
limitaQon

32. WU
et
al
ArthriOs
Care
Res
2005;
53:
133-­‐7

33. Mai
1981
Septembre
1981

34. § W
69y
§ Past
history
:
shoulder
calcific
tendiniQs
§ Acute
cervical
and
ear
pain
§ Impossibility
to
turn
the
head
on
the
len
§ Free
other
cervical
moQon
§ Bone
scinQgraphy
increased
uptake
§ Increased
sedimenQon
rate
§ Radiographs:
calcific
deposits
around
the
dens
§ Complete
recovery
within
4
days
with
diclofenac
(200mg/j)

35. Crowned
dens
syndrome

36. Crown
dens
syndrome
due
to
apaQte
deposits
El
Mahou
et
al
Presse
Méd
2006;
35:803-­‐4

37. Tensor longus capitae tendinitis

38. Intervertebral
disc
apaQte
deposits

40. ApaQte
disc
space
inflammaQon
mimicking
infecQon
*
*
*
*

41. Intervertebral
disc
apaQte
deposits
• Intraspinal
migraQon
of
dense
calcificaQons
of
the
nucleus
pulposus
(arrows)
through
a
rupture
of
the
annulus
fibrosus
(black
arrow).
• Interspinous
dense
and
round
calcificaQon
(arrowhead).

42. • Intraspinal
migraQon
of
disc
calcificaQon.
• Note
the
less
dense
calcificaQon
in
L1-­‐L2
compared
to
T12-­‐L1,
probably
due
to
parQal
migraQon
of
the
calcificaQon.
Intervertebral
disc
apaQte
deposits
migraQon

43. ArthriOs
Rheum
1985;
28:
1417-­‐1420

44. Syndrome
de
la
dent
couronnée
§ DiagnosQc
=
imagerie
§ Cliché
bouche
ouverte
de
la
charnière
cervico-­‐
occipitale
de
face
§ ScinQgraphie
osseuse
§ Scanner
:
opacités
entourant
le
sommet
et
les
côtés
de
l’odontoïde
en
couronne
ou
halo

45. Dépôts
coccygeal
deposits
RicheSe
P,
Maigne
JY,
Bardin
T.
Spine
2008

46. Spinal
Crystal
diseases
§ Urate monosodium : Gout
§ Calcium crystals
– Calcium phosphate « Apatite disease »
– Calcium PyroPhosphates « CPPD disease »
– Calcium oxalate

47. Intervertebral
disc
CPPD
:
Frequency
in
the
general
populaQon
§ Autopsic
studies
(Pritzker.Orthop
Clin
North
Am
1977;8:65-­‐77,
Feinberg
Clin
Orthop1990;254:303-­‐10)
ü
6
à
20
%
ü Increases
with
age
§ Discectomy
samples
(Andres
Arch
Pathol
Lab
Med
1980;104:269-­‐71;
Lagefoged
Ann
Rheum
Dis
1986
Ann
Rheum
Dis
1986;45:239-­‐43;
Markiewitz
Spine;21:506-­‐11)
ü
10-­‐26
%
ü
AsymptomaQc

48. Intervertebral
disc
CPPD:
Radiologic
appearance
§ Lines
or
minispots,
someQmes
aggregates
§ Annulus
fibrosis
>
nucleus
pulposus
:
verQcal
lines
§ CarQlage
endplate
:
horizontal
lines
parallel
to
the
endplate

50. Resnick & Niwayama
CPPD
Intervertebral disc

53. CPPD:
Disc
deposits

55. Resnik & Niwayama
Facet joints and posterior ligaments CPPD deposits

56. Facet
joint
Ligamentum
flava
CPPD

57. Resnik & Niwayama

58. CPPD
Transverse
ligament
§ Frequent
at
CT-­‐scan:
• ConstanQn
et
al:
14/21
(Ann
Rheum
Dis
1996;
55:
137-­‐9)
• Finkh
et
al
:
24/35
vs
4/11
chez
les
contrôles
(J
Rheumatol
2004;31:544-­‐51)
§ Usually
asymptomaQc
Kakitsubata.
Radiology
2000;
216:
213-­‐219

59. CPPD
Transverse
ligament
calcificaQon

60. CPPD
Crowned dens syndrome
Acute cervical and occipital pain, fever, loss of motion (rotations +++)
Traitement:
pain killers
oral steroids
immobilisation
C1-C2 lateral joint steroid injection (Frey et al PM&R 2009;1:379-82)

61. CPPD
vs
apaQte
deposits
around
the
dens
Differences
in
distribuQon
and
appearance
Round
and
dense
calcificaQons
bone
erosions
Concentric,
linear
calcificaQons
«crowned
dens
»
CPPD
ApaQteE
Periodontoid
deposits

62. CPPD
Frequency of atlanto-axial deposits at CT-scan
This is highlighted by the fact that we
had many more men (354 patients) than
women (159 patients) and that there
were disproportionately higher numbers
of men aged 20–30 years and elderly
women. However, ethical concerns with
the delivery of ionizing radiation pre-
clude the evaluation of consecutive pa-
tients in the general population. In addi-
tion, although CT is generally regarded
as sensitive for the detection of small
calcifications, it is certainly less sensitive
than histologic examination (17), which
may result in underestimation of the
true prevalence. Furthermore, not all
CT-evident calcifications relate to CPPD
crystal deposition at histologic examina-
tion, although histologic analysis is gen-
erally not performed in the clinical set-
ting and characteristic calcifications are
generally assumed to be due to CPPD
crystal deposition (22,28). With regard
to retro-odontoid soft-tissue thickness,
Figure 4
Figure 4: Bar chart shows prevalence of atlantoaxial CPPD deposition ac-
cording to age group. Prevalence increases with advancing age for both male
(blue) and female (red) patients (P , .0001, logistic regression coefficient).
Scatter plot of age versus retro-odontoid soft-tissue thickness in (a) male (blue) and female (red) patients and (b) patients without CPPD crystal depo-
and those with CPPD crystal deposition (red). There is significant positive correlation (r = 0.48, P , .0001) between age and retro-odontoid soft-tissue
entire population.
Chang et al. Radiology 2013; 269:519-24
CPPD crystal deposition = 0.0067, P =
.004, multiple R2
= 0.35). There was no
significant difference between the retro-
odontoid soft-tissue thickness in men ver-
sus that in women (mean, 2.4 mm vs 2.3
mm, respectively; P = .2574, t test). The
mean retro-odontoid soft-tissue thickness
in patients with CPPD crystal deposition
was greater than that in patients without
CPPD crystal deposition (3.4 mm vs 2.2
mm, respectively; P , .0001; Fig 5b).
Discussion
In this study, we demonstrated that
atlantoaxial CPPD crystal deposition
is more common than previously rec-
ognized. In fact, nearly half of our
patients aged 80 years and older had
atlantoaxial CPPD crystal deposition at
CT. We have confirmed that there is an
increasing prevalence of such deposi-
tion with advancing age (4–7,24,25). In
Figure 3
Figure 3: Bar charts show age distribution of (a) male and (b) female patients. There were 354 male patients and 159 female patients (P , .0001, x2
test).
Of note, female patients were disproportionately older than male patients (mean age, 62 years vs 48 years, respectively; P , .0001, t test).
Summary of Demographic Characteristics
Age (y) No. of Male Patients No. of Female Patients No. of Patients with Calcification*
,20 (n = 14) 10 4 0 (0)
20–29 (n = 85) 68 17 0 (0)
30–39 (n = 62) 45 17 0 (0)
40–49 (n = 83) 65 18 2 (2.4)
50–59 (n = 99) 83 16 4 (4.0)
60–69 (n = 42) 31 11 4 (9.5)
70–79 (n = 53) 28 25 17 (32)
80–89 (n = 54) 19 35 21 (39)
90–99 (n = 21) 5 16 16 (76)
* Numbers in parentheses are percentages.
sensitive to soft-tissue calcifications re-
lated to the superimposition of adjacent
structures (17). To our knowledge, the
only study to date in which CT was used
to determine the prevalence of CPPD
crystal deposition in the cervical spine
in the diagnosis of crowned dens
syndrome, which is seen in patients
who present with severe neck pain due
to calcium deposits about the odontoid
process (22). As expected, a major di-
agnostic criterion is the finding of peri-
513 consecutive patients CT-scan for trauma
Overall prevalence :12,5 %
Increase with age

63. Calcium pyrophosphate deposits (CPPD)
involving the spine
§ Intervertebral discs, facet joints, ligaments
§ Cervical and lumbar spine
§ Clinical findings
– Asymptomatic
– Acute pain and fever
– Subacute pain
– Disc inflammation mimicking infection
– Nerve compression

64. Acute
arthriQs
F
70.
T12
fracture
aner
a
fall.
Inflammatory
low
back
pain

69. Rachis
cervical
haut
et
dépôts
de
CPP
§ Dépôts
péri-­‐odontoïdiens
Syndrome
de
la
dent
couronnée
Arthrites
aiguës
C1-­‐C2
latérales
Érosions
de
l’odontoïde;
fractures
de
type
2
Compressions
bulbo-­‐médullaires
(foramen
magnum)
§ Arthropathies
C1-­‐C2
latérales

70. CPPD
Erosive
changes

71. CPP atlanto-axial deposits
erosions of the dens

72. CPP atlanto-axial deposits
Fractures of the dens
Kakitsubata. Radiology 2000;216:213-9 : 9 cas de fractures de l’odontoïde (type 2)
b. c.

73. CPPD
Atlanto-axial lateral joint acute arthritis
Tobyashi
et
al.
The
Spine
Journal
2014
§ 27
paQents,
56
to
90y
(mean
76)
§ Acute
(VAS>7)
upper
cervical
pain
for
2-­‐3
days
§ Head
rotaQon
<
20°
§ Increased
CRP
§ Radiographs:
normal
or
mild
erosive
changes
§ CT-­‐Scan:
Transverse
ligament
calcificaQon:
81
%,
§ PoncQon
C1-­‐C2
latéral
joint
aspiraQon:
5,000-­‐14,000
WBC/mm3
PPC
crystals
:
10
pts
Pain
improvement
with
aspiraQon:
VAS
decreasing
from
82
to
35,5
within
30
mn
The Spine Journal
The Spine Journal
M
ANUS
CEPTED
NUSCRIPT
ACCEPTED MANUSCRIPT

74. Pseudotumoral
interspinous
CPP
deposit
and
acute
upper
cervical
pain
GEORGE LINDBECK• EXTRA-ARTICULARCPPD 583
FIGURE 1. Cervical spine radiograph shows calcified mass
between C1 and C2.
Calcium pyrophosphate dihydrate deposition (CPPD)
disease is characterized by the deposition of calcium pyro-
phosphate crystals in tissue, most commonly articular carti-
lage. Chondrocalcinosis (CC), manifest by deposition of
calcium pyrophosphate crystals in hyaline and fibrocartilage
and in the synovial space, is the most common form of
CPPD and has been estimated to occur in 5% to 10% of the
adult population? The prevalence of CPPD increases with
age to as high as 30% in those older than 75 years of age, and
there is probably a female preponderance with an estimated
relative risk of 1.33.2 CPPD has been noted to occur as a
sporadic or idiopathic disease, related to underlying diseases
that affect calcium and phosphate metabolism such as
hyperthyroidism, hemochromatosis, hypomagnesemia, and
in a familial pattern.3
The mechanism of calcium pyrophosphate crystal deposi-
tion is not well understood, and theories have generally
focused on abnormalities of the cartilage matrix, including
mechanical damage, that promote crystal deposition, or
biochemical abnormalities that lead to elevated serum and
synovial fluid levels of calcium or inorganic pyrophos-
phate.3 Pyrophosphate is a product of many enzymatic
reactions, and conditions causing elevations in calcium (eg,
hyperparathyroidism) or pyrophosphate (eg, hypophosphata-
sia) concentrations could increase the ionic product and thus
promote crystal formation and deposition. Crystal formation
and deposition are promoted by the environment in which
crystal formation occurs, and "gels" such as cartilage are
sms. The patient's
d no neurological
er resection of the
mon complaint
rvical spine are
ain is broad and
and rheumato-
of a history of
nitial concern of
meningeal focus.
s suggested by
oft tissue views
lesion through
to the operating
imary tumor of
rvical spine are
G
Lindbeck
AM
J
Emergency
Med
1996;14:582-­‐5
H
de
43
ans,
cervicalgie
aiguë,
opéré
pour
suspicion
de
tumeur:
anapath
dépôts
de
CPP

75. Dépôts cervico-occipitauxde PPi de Ca
Arthropathies C1-C2 latérales
Gerster. Osteoarthritis Cartilage 1994;2:275-9

76. • Consequence
of:
• Facet
joint
damage,
with
secondary
spondylolisthesis
• Erosive
disc
disease
• Spinal
ankylosis
CPPD
DestrucQve
arthropathy

77. Atlanto-axial CPP deposits causing
spinal cord compression
Assaker. Spine, 2001;26:1396-1400

78. Spinal
canal
ligaments
CPP
deposits
and
cervical
spinal
cord
compression
162 P. Cabre e
A B
m flavum calcification 161
Figure 1. Cervical computed tomography coupled with myelogra-
phy (case 1): axial section through C4-C5. Compression of the spinal
cord by two masses with high attenuation values similar to that of
calcium. The masses are at the level of the laminas. Calcification or
ossification of the posterior longitudinal ligament (A). Computed
tomographycoupledwithmyelography:sagittalreconstructionshow-
ing a large calcific deposit at C4-C5 forming an acute angle with the
supra- and infrajacent laminas and stopping the progression of the
contrast agent (B).
A B
Cervical ligamentum flavum calcification 16
A B
Cervical ligamentum flavum calcification 163
Cabre
et
al.
Joint
Bone
Spine
2001;68:
158-­‐65:
6
paQents
from
french
anQlles,
5
fast-­‐onset
spinal
cord
compression.
2
posterior
decompressve
surgery.
PPC
et
BPC
in
ligamentum
flava

79. Progressive
onset
tetraparesia
in
a
90
y-­‐o
man
Atlanto-axial CPP deposits causing
spinal cord compression

80. Calcium
Pyrophosphate
Dihydrate
DeposiQon
Disease
Causing
Thoracic
Cord
Compression:
Case
Report.
Muthukumar
et
al.
Neurosurgery.
2000;
46(1):
222

81. had irregular nuclei and nucleoli. Initial stained sections
revealed no polarizable material. However, birefrigent rhom-
boid crystals were found in sections made by one of us (H.D.)
and also found in additional unstained deeper sections made
by us at URMC (Fig. 4a, b). Ki-67 labeling was seen but
appeared, in part, in reactive cells. No EMA, S100, factor 13
or CD68 immunostaining was seen. A final diagnosis of
tophaceous pesudogout was made.
Upon further staining, the specimen (Fig. 3) appeared to
be an epithelioid mass with granular material, with rare
reactive chondrocytes and concentric calcifications. The
cells themselves had irregular nuclei and nucleoli with rare
mitoses and scattered Ki-67 labeling. Initial stained sections
revealed no polarizable material. However, upon further
analysis of deeper sections, and in concert with another
a Axial view of a T2-weighted non-contrast MRI demonstrat-
niation of the intervertebral disc with encroachment of the left
Fig. 2 Frozen section. Yellow arrows point to three psammoma bodies;
blue arrow points to leptomeningeal cells with hyalinzed blood vessels
(H & E, original magnification 400×)
Fig. 2 F
blue arro
748
Acta Neurochir (2012) 154:747–750
Compression
médulaire
dorsale
Srinivasan
Acta
Neurochir
2012;154:747-­‐50

82. CPPD and
intervertebral disc destructive arthropathy
§ Elderly patients
§ Variable clinical symptoms
and signs
§ Cervical and lumbar spine
§ Multiple involvement
§ Mimicking disc space
infection

83. CPPD
Chronic upper cervical pain and
Atlanto-axial lateral joint erosive arthritis

84. CPPD
Chronic upper cervical pain and
atlanto-axial lateral joint erosive arthritis

85. Fig.7

88. 81
yo
woman
diagnosed
as
vertebral
infecQon

89. IRM
T1
IRM
T1
+
gado
IRM
T2

90. CT-­‐scan
T1-­‐W.MRI
STIR
MRI
CPPD
mimicking
disc
space
infecQon
G-­‐E.T1-­‐W.MRI

91. CPPD
mimicking
disc
space
infecQon

92. T1
T1+G
T2
SQr
CT
scan

93. T1
T1
+
Gado
STIR
CPPD
mimicking
disc
space
infecQon

95. CPPD
:
microgeodes

96. CPPD
Calcifyed facet joint cysts
Namazie.
J
Orthop
Surg
2012;20:254-­‐6

97. • Spondylolisthesis
CPPD

98. Dépôts
rachidiens
de
CPP
Lésions
non-­‐spécifiques
§ Discopathie
dégénéraQve
§ Vide
discal
§ Spondylolisthesis
§ HVA

101. T1
T2
SQr

102. CPPD
and
adult
lumbar
scoliosis
§ Scoliosis
with
intervertebral
subluxaQon
in
elderly

104. Resnik & Niwayama

105. Spine involvement in crystal diseases
§ Joint and ligaments calcified deposits
§ Acute tendinitis
§ Acute arthritis (C1-2, disc space, facets, costovert. J.)
§ Erosive and destructive arthritis mimicking infection
§ Spinal cord compression
§ Dens fracture
§ Scoliosis and intervertebral subluxation
§ Inflammatory & erosive sacroiliitis

106. Erosive and destructive intervertebral disc joint
§ Infection (tuberculosis and others)
§ Spondyloarthritis
§ Crystal deposition diseases
§ Erosive osteoarthritis
§ Charcot joint
§ Amyloïdosis

107. Thank
you

108. CPPD
Erosive
and
inflammatory
sacroiliac
arthriQs

109. Scanner
T1
T1+gado
T2
CPPD:
sacroiliiQs

110. CPPD:
Sacro-­‐Iliac
ankylosis
Scanner
IRM
T1

111. T1
STIR
F
85.
Suspicion
of
sepQc
sacroiliiQs
concomitant
pyelonephriQs

112. Gadolinium-­‐enhanced
T1-­‐WI

115. M
47,
Inflammatory
polyarthralgia
STIR
STIR
T1G
T1G
T1G