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The calcaneal lesions that could be found in EOA are similar to those observed in NOA. The frequency of calcaneal enthesophytosis is similar in EOA, NOA, and PsA, but inflammatory lesions of calcaneal entheses and of the adjacent bursae are more frequent in RA and in PsA. In terms of heel involvement, EOA seems to be similar to NOA. US shows an excellent concordance with radiography in detecting entheseal cortical bone abnormalities.

Objective: To investigate by high frequency ultrasonography the appearance of calcium pyrophosphate dihydrate (CPPD) calcifications, in the most commonly affected sites in CPPD disease, and the relationship between ultrasonographic CPPD deposits and the presence of CPPD crystals in synovial fluid. Methods: Three ultrasonographic patterns of CPPD calcification were identified and 11 patients enrolled. A control group comprised 13 patients with no evidence of CPPD deposits. Synovial fluid was aspirated from all patients and controls and examined for identification of crystals. All patients underwent a standard radiography examination at the same sites investigated by ultrasound. Results: In all patients with ultrasonographically defined CPPD deposits, CPPD crystals were found in the synovial fluid. In two cases, standard radiographic examination did not show evidence of the calcific deposits that were identified by ultrasonography. CPPD crystals were not found in the synovial fluid of controls. In four control group patients, ultrasonography identified calcifications defined as deposits of another nature. Conclusions: The ultrasonographic pattern used in this study for the diagnosis of CPPD disease demonstrated a very high correlation with the presence of CPPD crystals in synovial fluid. Ultrasonography demonstrated a sensitivity and specificity at least equal to that of radiography in identifying CPPD crystal calcifications. U ntil now, the diagnosis of calcium pyrophosphate dihydrate (CPPD) crystal deposition disease has been based mainly on radiographic or microscopic detection of CPPD crystals.Ryan and McCarty proposed several diagnostic criteria for the diagnosis of CPPD crystal deposition disease, 1 based on the premise that CPPD crystals are the specific feature of the disease and including radiographic clues suggested by Resnick et al 2 and Martel et al. 3 According to these criteria, a case is definite if CPPD crystals are demonstrated in tissues or synovial fluid by definite means (for example, chemical analysis) or if crystals are demonstrated by compensated polarised light microscopy and typical calcifications are seen on radiographs. In this last case, if only one of these criteria is found, a probable diagnosis is made.Ultrasound (US) is a very sensitive and specific technique for detecting calcifications of soft tissues, 4 5 but only a few papers have described sonographic evidence of articular and periarticular changes caused by CPPD disease. [6][7][8][9] In this paper we tried to define the US aspect of CPPD calcifications in order to propose ultrasonographic criteria for the differentiation of CPPD deposits and hyperechoic deposits of another nature. We then tried to verify the relationship between the ultrasonographically defined presence of CPPD calcifications in cartilage and periarticular tissues and the presence of CPPD crystals in the synovial fluid and compare the US findings with the radiographic findings. PATIENTS AND METHODSWe enrolled in this study all patients with US evidence of CP...

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US and PDUS can be useful in distinguishing, at onset of disease, pure PMR from other diseases mimicking this condition.