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OBJECTIVE The coexistence of calcium pyrophosphate dihydrate (CPPD) and monosodium urate monohydrate crystals in gouty tophi has rarely been reported. We undertook this study to investigate CPPD crystal deposits in a series of surgically removed gouty tophi and to identify factors associated with these deposits. METHODS Twenty-five tophi from 22 gout patients were analyzed using polarized light microscopy, field emission scanning electron microscopy (FESEM), and μ Fourier transform infrared (μFTIR) spectroscopy. RESULTS Tophi consisted of multiple lobules separated by fibrous septa and surrounded by a foreign-body giant cell reaction. CPPD crystal aggregates were identified in 9 of 25 tophi from 6 patients. CPPD crystals were dispersed or highly compacted, localized at the edge or inside the tophus lobules, with some lobules completely filled with crystals. Both monoclinic and triclinic CPPD crystal phases were identified using FESEM and μFTIR. Compared to patients without CPPD, those with CPPD-containing tophi were older (mean 60.5 years versus 47.2 years; P = 0.009), and had longer-term gout duration (mean 17.0 years versus mean 9.0 years; P < 0.05) and tophi duration (mean 10.0 years versus mean 4.6 years; P < 0.01). None of the patients had radiographic chondrocalcinosis of the knee or wrist. CONCLUSION CPPD crystal formation seems to be a late and frequent event of tophus maturation, occurring more frequently with aging, and could contribute to the speed of tophus dissolution and the apparent persistence of tophus sometimes observed even after effective, long-lasting urate-lowering therapy.

SummaryObjectivesThe purpose of this study was to reveal the accurate prevalence and related factors to the presence of calcium pyrophosphate dihydrate (CPPD) crystal deposition in cadaveric knee joints.DesignControlled laboratory study.MethodsSix hundred and eight knees from 304 cadavers (332 male knees and 276 female knees, formalin fixed, Japanese anatomical specimens) were included in this study. The average age of the cadavers was 78.3 ± 10.7 years. Knees were macroscopically evaluated for the existence of CPPD, and the depth of cartilage degeneration of the femoro-tibial joint following the Outerbridge's classification. CPPD crystal was confirmed under Fourier transform infrared spectroscopy (FTIR) analysis using light microscopy. Statistical analysis was performed to reveal the correlation between the occurrence of CPPD deposition in the knee joint and gender, age, and the depth of cartilage degeneration of the femoro-tibial joint.ResultsThe prevalence of grossly visible CPPD crystal was 13% (79 knees). In all of these knees, CPPD crystal was confirmed under FTIR analysis. Statistical analysis showed significant correlation between the occurrence of CPPD deposition and gender (P

We sought to determine the prevalence of sternoclavicular (SC) joint calcium pyrophosphate dihydrate (CPPD) crystal deposition and its association with age, osteoarthritis, and atlantoaxial CPPD crystal deposition. In 209 consecutive patients, computed tomographic examinations of the cervical spine were retrospectively reviewed. Overall prevalence of CPPD crystal deposition in the SC joint was 17.2% (36/209), which increased with age (P

Articular calcium-containing crystals cause calcium pyrophosphate dihydrate (CPPD) deposition disease, basic calcium phosphate (BCP)-associated syndromes, and calcium oxalate arthritis. During the past year, important contributions have been made to our understanding of CPPD- and BCP-related syndromes. Clinical studies of CPPD deposition disease underscore the importance of extra-articular and spinal CPPD deposits, and question the association between hypothyroidism and chondrocalcinosis. Laboratory reports add key information to our current paradigms of CPPD crystal formation and CPPD-induced inflammation. Several interesting new therapeutic interventions may arise from this work. A case collection of BCP-related syndromes emphasizes the need for considering this diagnosis in young healthy patients with acute arthritis or periarthritis.

Pyrophosphates have their historical mode of formation embedded in their name. These condensed phosphates are commonly synthesized by the application of heat to orthophosphates.1,2 Amongst condensed phosphates, pyrophosphate (P2O7), can be considered to be the smallest structure and shortest linear polyphosphate.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease continues to be of intense clinical and basic science interest. Follow-up of studies of hereditary CPPD crystal deposition indicate differences from the common sporadic disease. The results of a prospective study of CPPD crystal deposition arthropathy confirm that clinical symptoms appear to be independent of radiologic progression. Novel clinical presentations include association with pregnancy and simulation of meningitis. CPPD crystal deposition pathology in synovium ultrastructurally resembles that in cartilage. Factors such as the presence of ATP can induce experimental calcifications in tissue culture that resemble CPPD crystal deposition. Interleukin-8 and tyrosine phosphorylation of neutrophil protons can mediate CPPD crystal deposition-associated inflammation. The control of crystal function and dissolution recently has been the subject of many general reviews. The theory outlined in these papers is important for understanding CPPD crystal deposition and basic phosphate crystal formation and dissolution.

There are a limited number of known insults which damage synovial joints. They include mechanical derangement,infective organisms, metabolic factors altering cellular metabolism, immunological stimuli and joint particles. This chapter reviews the evidence that intra-articular particles play a role in the pathogenesis of many joint diseases and explores possible mechanisms of particle-induced damage.

The number of crystalline compounds whose presence has been demonstrated in articular and periarticular structures has rapidly increased during the past 20 years thanks to progress in techniques of observation and identification. Their origin and the pathophysiological role which they play in the rheumatic disorders in which they are implicated are far from being well understood. Some effects ascribed to crystals might be only of incidental importance. This topic will be reviewed under four different headings: 1 The identification of crystals. 2 The different crystals implicated in rheumatic disorders. 3 The pathophysiological consequences of inflammation and articular degeneration. 4 The source of crystals.