Patterns of radiographic abnormalities associated with basic calcium phosphate and calcium pyrophosphate dihydrate crystal deposition in the knee.

Halverson, Paul B.; McCarty, Daniel J.

doi:10.1136/ard.45.7.603

Cited by 114 publications

(42 citation statements)

References 12 publications

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“…CPPD and basic calcium phosphate crystals frequently appear together in the Milwaukee shoulder syndrome, in osteoarthritis, and in chondrocalcinosis (22,23). In fact, 75% of CPPD crystal-contahing joint fluids also contain basic calcium phosphate crystals (22).…”

Section: Methodsmentioning

confidence: 99%

Articular Cartilage Vesicles Generate Calcium Pyrophosphate Dihydrate‐Like Crystals in Vitro

Derfus

Rachow

Mandel

et al. 1992

Arthritis & Rheumatism

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Objective. To identify the morphology of a mineral-forming fraction of adult porcine hyaline articular cartilage digest and characterize the mineral it forms.Methods. Electron microscopy, Fourier transform infrared (FTIR) spectroscopy, x-ray microanalysis, compensated polarized light microscopy, and biochemical studies including 14C-labeled UDPG pyrophosphohydrolase radiometric assay.Results. plate cartilage matrix vesicles and formed mineral after only 24 hours in physiologic salt solution containing 1 mM ATP. The mineral contained inorganic pyrophosphate, 95% of which derived from ATP, and phosphate, 93% of which derived from inorganic phosphate in the medium. The FTIR spectrum of this mineral closely resembled the spectrum of standard calcium pyrophosphate dihydrate (CPPD) crystals. Compensated polarized light microscopy showed positively birefringent, rod-shaped crystals morphologically identical to CPPD. Ca:P ratios, defined by energy-dispersive microanalysis, were also consistent with CPPD.Conclusion. The articular cartilage vesicle fraction of porcine hyaline cartilage is capable of generating mineral that strongly resembles CPPD.Calcium pyrophosphate dihydrate (CPPD) and basic calcium phosphate crystals occur in articular cartilage and synovial fluid of patients with diverse arthropathies (1-3). Both crystal types may initiate or amplify articular tissue destruction ( 4 3 , but the source of these crystals has not been precisely identified. A sedimentable fraction of adult porcine articular cartilage digest which supports ATP-enhanced calcium deposition under physiologic ionic conditions has been demonstrated (6). We sought to characterize the morphology of this fraction by electron microscopy for comparison with a similar mineralizing fraction of epiphyseal growth plate matrix vesicles (7,8). We then characterized the mineral produced by this fraction, comparing it with crystals observed in human articular diseases. We report that a vesicle-containing fraction of articular cartilage digest produces both calcium phosphate and calcium pyrophosphate mineral in

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Section: Methodsmentioning

confidence: 99%

Articular Cartilage Vesicles Generate Calcium Pyrophosphate Dihydrate‐Like Crystals in Vitro

Derfus

Rachow

Mandel

et al. 1992

Arthritis & Rheumatism

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“…The prevalence of BCP crystals in synovial fluid from patients with knee OA is between 30 and 60%, and their presence correlates strongly with radiographic evidence of cartilage degeneration (2). Larger joint effusions are seen in affected joints when compared with joint fluid from OA knees without BCP crystals (3).…”

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confidence: 97%

Molecular Mechanism of Basic Calcium Phosphate Crystal-induced Activation of Human Fibroblasts

McCarthy

Augustine

Baldwin

et al. 1998

Journal of Biological Chemistry

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Synovial fluid basic calcium phosphate (BCP) crystals are markers of severe joint degeneration in osteoarthritis. BCP crystals cause mitogenesis of articular cells and stimulate matrix metalloprotease production, thus promoting degradation of articular tissues. Previous work suggested that BCP crystal-induced cell activation required intracellular crystal dissolution, induction of proto-oncogene expression, and activation of signal transduction pathways involving protein kinase C and mitogen-activated protein kinases. Here we further elucidate the mechanisms of BCP crystal-induced cell activation as BCP crystals activate transcription factors nuclear factor B and activator protein 1 in human fibroblasts. We confirm the role of protein kinase C in BCP crystal-induced mitogenesis in human fibroblasts.In contrast, we demonstrate that BCP crystals do not activate signal transduction pathways involving protein tyrosine kinases or phosphatidylinositol 3-kinase. These data further define the mechanism of cell activation by BCP crystals and confirm its selectivity, an observation that may have therapeutic implications. Synovial fluid basic calcium phosphate (BCP)1 (hydroxyapatite, octacalcium phosphate, and tricalcium phosphate) crystals are common in osteoarthritis (OA) and are associated with severe degenerative arthropathies (1). The prevalence of BCP crystals in synovial fluid from patients with knee OA is between 30 and 60%, and their presence correlates strongly with radiographic evidence of cartilage degeneration (2). Larger joint effusions are seen in affected joints when compared with joint fluid from OA knees without BCP crystals (3).Clinical and pathological studies have demonstrated that synovial lining proliferation of varying degrees is associated with BCP crystals in osteoarthritis (4). BCP crystals themselves are at least partly responsible for such proliferation since they stimulate cell replication in vitro (5). Increased cellularity in the synovial lining enhances the capacity for secretion of cytokines, which may promote chondrolysis. Noninflammatory destruction of matrix-rich articular structures including cartilage, ligament, and tendon is also characteristic of BCP crystal deposition (1). BCP crystals promote tissue damage by induction of matrix metalloprotease (MMP) synthesis and secretion. Since there are no available drugs to inhibit deposition or affect reabsorption of these crystals, prevention of the biological consequences of the destructive processes initiated by BCP crystals is an attractive therapeutic strategy.The in vitro effects of BCP crystals emphasize their pathogenic potential. BCP crystals induce mitogenesis in cultured fibroblasts (5, 6). However, mechanisms by which BCP crystals induce mitogenesis have been incompletely studied. Endocytosis and intracellular dissolution of the crystals, producing an elevated cytoplasmic calcium concentration, are important (7). BCP crystals activate a protein kinase signal transduction pathway involving p42 and p44 mitogen-activated protein (MA...

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“…CPPD crystals and hydroxyapatite (HA) crystals are frequently present, alone or in combination, in fluid taken from OA knees. It has been suggested that CPPD crystals reflect an aging process, whereas HA crystals result from the OA process (17).…”

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confidence: 99%

“…Various concepts about the association of CC and OA can be resolved into 5 categories, as follows: 1) There is no relationship between CC and OA (2,3,9); 2) CPPD crystal deposi-tion favors the development of OA, or at least its inflammatory manifestations (10); 3) OA and, perhaps, other joint diseases facilitate the deposition of CPPD crystals (4); 4) Chondrocalcinotic arthropathy is a distinct entity that simulates OA (1 1); and 5 ) CC, even at a distance from the affected joint, is in some manner linked to rapid destruction of the OA hip (6). The methods for arriving at these conclusions have varied from histologic to clinical analysis (12,13) and from radiography of specimens (14,15) to analysis of synovial fluid (16,17). CPPD crystals and hydroxyapatite (HA) crystals are frequently present, alone or in combination, in fluid taken from OA knees.…”

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confidence: 99%

Chondrocalcinosis in surgically resected joints

Sokoloff

Varma

1988

Arthritis & Rheumatism

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To investigate the association between chondrocalcinosis (CC) and osteoarthritis (OA), 338 joint specimens were examined histologically (55 knees and 84 hips surgically resected because of idiopathic OA, 106 control knees obtained postmortem, and 93 fractured hips). The risk for CC in the OA knees was sixfold that of the ageand sex-adjusted control sections. CC occurred much less frequently in the hip than in the knee; the association with OA was less clear-cut. It was not possible to resolve by statistical analysis which of the two pathological processes was the horse and which was the cart.Many published reports address the coexistence of chondrocalcinosis (CC) and osteoarthritis (OA), but there is much controversy about the frequency and significance of the association (1-8). Determining the relationship between the two processes is complicated by the fact that each lesion occurs with a certain frequency in the absence of the other, and both are related to age. The principal calcinotic deposits found are those of calcium pyrophosphate dihydrate (CPPD) crystals. Various concepts about the association of CC and OA can be resolved into 5 categories, as follows: 1) There is no relationship between CC and OA (2,3,9); 2) CPPD crystal deposi-

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Patterns of radiographic abnormalities associated with basic calcium phosphate and calcium pyrophosphate dihydrate crystal deposition in the knee.

Cited by 114 publications

References 12 publications

Articular Cartilage Vesicles Generate Calcium Pyrophosphate Dihydrate‐Like Crystals in Vitro

Articular Cartilage Vesicles Generate Calcium Pyrophosphate Dihydrate‐Like Crystals in Vitro

Molecular Mechanism of Basic Calcium Phosphate Crystal-induced Activation of Human Fibroblasts

Chondrocalcinosis in surgically resected joints

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