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1 ll cases were screened for known features of chondrocalcinosis.
2 were included, of which 69 knees (18.5%) had chondrocalcinosis.
3  BOKS, 23 of the 265 included knees (9%) had chondrocalcinosis.
4 t, are linked to autosomal-dominant familial chondrocalcinosis.
5 r ANKH sequence variants to promote sporadic chondrocalcinosis.
6 organic pyrophosphate (PPi), which stimulate chondrocalcinosis.
7  to potential future advances in controlling chondrocalcinosis.
8 d in several kindreds affected with familial chondrocalcinosis.
9 ganic pyrophosphate (PPi) supersaturation in chondrocalcinosis.
10 n the association between hypothyroidism and chondrocalcinosis.
11 subjects had a much lower prevalence of knee chondrocalcinosis (1.8% in men, 2.7% in women) than did
12 previously linked with familial and sporadic chondrocalcinosis (+14 bp C-to-T and C-terminal GAG dele
13 f cartilage loss compared with knees without chondrocalcinosis (adjusted risk ratio [RR] 0.4, 95% con
14 n male Hartley guinea pigs, a model in which chondrocalcinosis also supervenes.
15     In humans, some dominant mutations cause chondrocalcinosis, an adult-onset disease characterized
16  not associated with the risk of OA included chondrocalcinosis and a history of hand OA.
17 en implicated in familial autosomal-dominant chondrocalcinosis and autosomal-dominant craniometaphyse
18 iation of a variety of genetic variants with chondrocalcinosis and ectopic mineralization elsewhere.
19 evels of expression of ANK in cartilage from chondrocalcinosis and osteoarthritis patients.
20    Our understanding of the causation of the chondrocalcinosis and other disorders characterized by e
21  discuss what is known about the genetics of chondrocalcinosis and what we have learned from genetic
22                                         Knee chondrocalcinosis and wrist chondrocalcinosis are far le
23 yrophosphate crystal inflammatory arthritis (chondrocalcinosis) and that SBS patients may be prone to
24 d models controlled for age, sex, hand pain, chondrocalcinosis, and hand hypermobility.
25                         A subset of sporadic chondrocalcinosis appears to be heritable via a -4-bp G-
26             Knee chondrocalcinosis and wrist chondrocalcinosis are far less common in Chinese subject
27 c and environmental factors on occurrence of chondrocalcinosis are indicated.
28               Early-onset osteoarthritis and chondrocalcinosis are linked to chromosome 8q.
29                                A syndrome of chondrocalcinosis associated with recurrent childhood se
30 ple, ANKH variants may not all predispose to chondrocalcinosis by effects on PPi transport, but may a
31 losis gene ANKH have been linked to familial chondrocalcinosis (CCAL2), craniometaphyseal dysplasia (
32 ent lack of understanding of the etiology of chondrocalcinosis, further epidemiologic studies of the
33                          In BOKS, knees with chondrocalcinosis had a lower risk of cartilage loss com
34 e pathogenesis of arterial calcification and chondrocalcinosis has become concurrently illuminated in
35 inant calcium pyrophosphate dihydrate (CPPD) chondrocalcinosis has previously been mapped to chromoso
36 equencing were screened for association with chondrocalcinosis in 128 patients with severe sporadic c
37  factor in both degenerative arthropathy and chondrocalcinosis in aging.
38                We compared the prevalence of chondrocalcinosis in Chinese subjects with that in white
39  was undertaken to compare the prevalence of chondrocalcinosis in Chinese subjects with that in white
40 cur in single locations without radiographic chondrocalcinosis in other joints.
41                                              Chondrocalcinosis is one of a family of conditions assoc
42 , respectively), but not the French familial chondrocalcinosis kindred 143-bp T-to-C mutation, increa
43 nct ANKH mutations associated with heritable chondrocalcinosis may promote disease by divergent effec
44 enerative arthropathy and directly stimulate chondrocalcinosis, may be primarily driven by chondrocyt
45                        The gene for familial chondrocalcinosis (MIM 118600; gene symbol CCAL2) has be
46  crystal inflammatory arthritis (pseudogout, chondrocalcinosis).Multidisciplinary treatment included
47                                              Chondrocalcinosis mutations retain apparently wild-type
48 herapy suggests that the combined absence of chondrocalcinosis on plain films and identifiable crysta
49 cinosis in 128 patients with severe sporadic chondrocalcinosis or pseudogout and in ethnically matche
50 sterase-1 (NPP1) activity is associated with chondrocalcinosis, osteoarthritis, and type 2 diabetes.
51  tissues that are presumably relevant to the chondrocalcinosis phenotype.
52                  The concurrence of DISH and chondrocalcinosis suggests a shared pathogenic mechanism
53 lated reaction, aminotransferases increased, chondrocalcinosis, synovitis, and interstitial nephritis
54                                     Sporadic chondrocalcinosis was associated with a G-to-A transitio
55                                 Radiographic chondrocalcinosis was defined as present in a knee or wr
56                                              Chondrocalcinosis was determined as present or absent on
57                         Concomitant DISH and chondrocalcinosis was diagnosed in 12 patients.
58 rved in 35 and 5 patients, respectively, and chondrocalcinosis was identified in 12 patients.
59            In knees with OA, the presence of chondrocalcinosis was not associated with increased cart
60                                        Wrist chondrocalcinosis was rare in elderly Chinese subjects (
61 iopathic skeletal hyperostosis (DISH) and/or chondrocalcinosis, were identified on the island of Terc
62                                              Chondrocalcinosis, which can promote joint inflammation
63  findings do not support the hypothesis that chondrocalcinosis worsens OA progression.

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