Digital imaging combined with picture archiving and communication system (PACS) access allows detailed image retrieval and magnification. Calcium pyrophosphate dihydrate (CPPD) crystals preferentially deposit in fibrocartilages, the cartilage of the acromioclavicular (AC) joint being one such structure. We sought to determine if examination of the AC joints on magnified PACS imaging of chest films would be useful in identifying chondrocalcinosis (CC). Retrospective radiographic readings and chart reviews involving 1,920 patients aged 50 or more who had routine outpatient chest radiographs over a 4-month period were performed. Knee radiographs were available for comparison in 489 patients. Medical records were reviewed to abstract demographics, chest film reports, and diagnoses. AC joint CC was identified in 1.1 % (21/1,920) of consecutive chest films. Patients with AC joint CC were 75 years of age versus 65.4 in those without CC (p < 0.0002). Four hundred eighty-nine patients had knee films. Six of these patients had AC joint CC, and of these, five also had knee CC (83 %). Of the 483 without AC joint CC, 62 (12 %) had knee CC (p = 0.002). Patients with AC joint CC were more likely to have a recorded history of CPPD crystal deposition disease than those without AC joint CC (14 versus 1 %, p = 0.0017). The prevalence of AC joint CC increases with age and is associated with knee CC. A finding of AC joint CC should heighten suspicion of pseudogout or secondary osteoarthritis in appropriate clinical settings and, in a young patient, should alert the clinician to the possibility of an associated metabolic condition.

Objective.

To study the role of different imaging modalities, ultrasonography, conventional radiography (CR) and CT, in visualization of chondrocalcinosis of the knees in patients with CPDD. Methods. Twenty-five patients (14 males and 11 females) with CPDD were enrolled in the study. Diagnosis was made according to D.J. McCarty classification criteria. All patients had arthritis of the knee and underwent aspiration of SF from the knee and microscopic investigation of SF samples. Diagnosis of CPDD was crystal proven. Three imaging methods were performed in patients: CR, CT and US of the knees.

Results.

CR of the knee confirmed cartilage calcification (CC) in 13 patients, CT in 18 patients and US in 25 patients. No difference in age or disease duration between patients with CC detected by different imaging methods was found.

Conclusion.

US appeared to be a helpful tool, possibly better than CR or CT, in revealing CC in patients with CPDD. Informativity of CT and CR in the detection of CC is almost equal.

OBJECTIVES:

To determine whether there is a systemic predisposition to chondrocalcinosis (CC) and to examine the association between CC and osteoarthritis (OA) at distant joints.

METHODS:

A cross sectional study embedded in GOAL (Genetics of Osteoarthritis and Lifestyle) database (n=3,170). All GOAL participants have had radiographs of knees, hands, and pelvis. These were scored for OA at the knee, hip, wrist, and MCPJ; for CC at the knee, hip, wrist, symphysis pubis, and for MCPJ calcification. Systemic predisposition to CC was established using cluster analysis. OR (95%CI) was used to examine the association between CC at index and distant joints; CC and OA at the same joint; and, index joint OA and distant joint CC. This was adjusted for age, gender, BMI; and for distant joint OA if required.

RESULTS:

Joints with CC clustered together. This was observed when participants with OA were excluded from the analysis. CC at each joint associated with CC at distant joints. Knee and wrist OA but not hip OA associated with CC at same joint. MCPJ OA associated with MCPJ calcification. Knee OA associated with CC at other joints, and this was independent of OA at the distant joint. There was no association between hip OA and distant joint CC.

CONCLUSIONS:

There is a systemic predisposition to the apparently sporadic CC. OA associates with CC at the same joint, and at distant joints, except hip OA which does not associate with hip CC, or with CC at distant joints. © 2013 by the American College of Rheumatology.

ABSTRACT:

With advanced age, articular calcium pyrophosphate crystal deposition (CPPD) is common. Defining who has CPPD is of growing importance, given increases in longevity in many countries and the frequent association of chondrocalcinosis with osteoarthritis. Chondrocalcinosis detected by plain radiography serves as a major screening tool, but how many and which sites to screen have not been adequately defined in the past. The work of Abhishek and colleagues in the previous issue of Arthritis Research and Therapy sheds new light on the incomplete information from knee radiographs, and helps position us to learn more about the epidemiology, pathophysiology, diagnosis, and clinical impact of CPPD.

US plays a useful role in diagnosing and monitoring therapy in microcrystalline arthritis, as it may detect both monosodium urate and calcium pyrophosphate crystal aggregates. The knowledge of some tips and tricks in the identification of these findings can play a key role in exploiting the relevant potential of US in microcrystalline arthritis, avoiding errors and misinterpretations. This review provides an in-depth description of simple technical and methodological issues to guide the rheumatologist in daily clinical practice.

ABSTRACT:

INTRODUCTION:

We aimed to describe the distribution of radiographic chondrocalcinosis (CC) and to examine whether metacarpophalangeal joint (MCPJ) calcification and CC at other joints occurs in the absence of knee involvement.

METHODS:

This was a cross-sectional study embedded in the Genetics of Osteoarthritis and Lifestyle study (GOAL). All participants (n = 3,170) had radiographs of the knees, hands, and pelvis. These were scored for radiographic changes of osteoarthritis (OA), for CC at knees, hips, symphysis pubis, and wrists, and for MCPJ calcification. The prevalence of MCPJ calcification and CC overall, at each joint, and in the presence or absence of knee involvement, was calculated.

RESULTS:

The knee was the commonest site of CC, followed by wrists, hips, and symphysis pubis. CC was more likely to be bilateral at knees and wrists but unilateral at hips. MCPJ calcification was usually bilateral, and less common than CC at knees, hips, wrists, and symphysis pubis. Unlike that previously reported, CC commonly occurred without any knee involvement; 44.4% of wrist CC, 45.9% of hip CC, 45.5% of symphysis pubis CC, and 31.3% of MCPJ calcification occurred in patients without knee CC. Those with meniscal or hyaline articular cartilage CC had comparable ages (P = 0.21), and neither preferentially associated with fibrocartilage CC at distant joints.

CONCLUSIONS:

CC visualized on a plain radiograph commonly occurs at other joints in the absence of radiographic knee CC. Therefore, knee radiographs alone are an insufficient screening test for CC. This has significant implications for clinical practice, for epidemiologic and genetic studies of CC, and for the definition of OA patients with coexistent crystal deposition.

Objective.

To evaluate the association between the purported risk factors for chondrocalcinosis and gout and the risk of pseudogout in the general population. Methods. We conducted a case-control study nested within a UK general practice database (The Health Improvement Network) by identifying incident cases of pseudogout between 1986 and 2007 and up to 10 control subjects matched to each case, based on age, sex and follow-up time. We evaluated the purported risk factors for chondrocalcinosis (i.e. OA, RA, hyperparathyroidism and diuretics) and established risk factors for gout (as comparison exposures) using conditional logistic regression analysis.

Results.

We identified 795 cases of pseudogout and 7770 matched control subjects. The risk of pseudogout was associated with hyperparathyroidism [odds ratio (OR) 4.87; 95% CI 2.10, 11.3], OA (OR 2.91; 95% CI 2.48, 3.43) and loop diuretic use (OR 1.35; 95% CI 1.09, 1.67). RA, thiazide diuretic use, BMI and other gout risk factors were not associated with the risk of pseudogout, except for chronic renal failure (OR 2.29; 95% CI 1.30, 4.01).

Conclusion.

This general population study based on physician-recorded pseudogout suggests that most of the previously observed associations with chondrocalcinosis are replicable with the risk of pseudogout, but there are notable differences, such as thiazide diuretics, RA and chronic renal failure, highlighting the need to study the clinical outcome, pseudogout. Avoiding loop diuretics may help individuals with recurrent pseudogout.

Bone destruction is a common feature of inflammatory arthritis and is mediated by osteoclasts, the only specialized cells to carry out bone resorption. Aberrant expression of receptor activator of nuclear factor kappa β ligand (RANKL), an inducer of osteoclast differentiation has been linked with bone pathology and the synovial fibroblast in rheumatoid arthritis (RA). In this manuscript, we challenge the current concept that an increase in RANKL expression governs osteoclastogenesis and bone destruction in autoimmune arthritis. We isolated human fibroblasts from RA, pyrophosphate arthropathy (PPA) and osteoarthritis (OA) patients and analyzed their RANKL/OPG expression profile and the capacity of their secreted factors to induce osteoclastogenesis. We determined a 10-fold increase of RANKL mRNA and protein in fibroblasts isolated from RA relative to PPA and OA patients. Peripheral blood mononuclear cells (PBMC) from healthy volunteers were cultured in the presence of RA, PPA and OA synovial fibroblast conditioned medium. Osteoclast differentiation was assessed by expression of tartrate-resistant acid phosphatase (TRAP), vitronectin receptor (VNR), F-actin ring formation and bone resorption assays. The formation of TRAP(+), VNR(+) multinucleated cells, capable of F-actin ring formation and lacunar resorption in synovial fibroblast conditioned medium cultures occured in the presence of osteoprotegerin (OPG) a RANKL antagonist. Osteoclasts did not form in these cultures in the absence of macrophage colony stimulating factor (M-CSF). Our data suggest that the conditioned medium of pure synovial fibroblast cultures contain inflammatory mediators that can induce osteoclast formation in human PBMC independently of RANKL. Moreover inhibition of the TNF or IL-6 pathway was not sufficient to abolish osteoclastogenic signals derived from arthritic synovial fibroblasts. Collectively, our data clearly show that alternate osteoclastogenic pathways exist in inflammatory arthritis and place the synovial fibroblast as a key regulatory cell in bone and joint destruction, which is a hallmark of autoimmune arthritis.

A 54-year-old woman with recurrent episodes of bilateral knee arthritis was admitted several times to the Department of Rheumatology. She was diagnosed to have chronic calcium pyrophosphate crystal arthritis. Interleukin 1β (IL-1β) plays a central role in the pathogenesis of inflammation induced by calcium pyrophosphate crystals, and IL-1β blockade may be an effective treatment in patients with severe chronic calcium pyrophosphate crystal arthritis. Because of the short effect of treatment with corticosteroids and the frequent attacks of arthritis, the patient was treated with the IL-1 receptor antagonist anakinra. She responded well after 1 week with normalization of inflammation. Eight months after the initiation of treatment, the patient has had no relapses, although we were unable to withdraw the anakinra.