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Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is characterized by the accumulation of CPPD crystal in articular and periarticular tissues, but CPPD crystal deposition along the spinal dura mater has not been previously reported. We report a 54-year-old male presenting with progressive neck pain and numbness of the extremities. CT showed diffuse dorsal epidural calcification from C3-T6 which resulted in spinal canal stenosis. On MR imaging, the lesion was hypointense on both T1 and T2 weighted images. From these findings, CPPD crystal deposition in the ligamentum flavum was suspected preoperatively. Biopsy at the level of C5-6 were performed to confirm the diagnosis. Perioperative and histopathological findings revealed that CPPD crystals were deposited along the dorsal dura mater, not in the ligamentum flavum. We firstly report the CT and MR imaging features of a possible new concept in the differential diagnosis of CPPD crystal deposition disease.

Ultrasonography has been increasingly used the last years for the identification of calcium pyrophosphate dihydrate crystal deposition (CPPD) in joints and on 2011 has been considered by the EULAR task force on CPPD as a promising tool for the diagnosis of the disease. However, it is common experience between sonographers that in daily clinical practice CPP identification by US is rather challenging as crystal deposits are not always numerous and diffuse. Furthermore, other conditions can mimic CPP deposition leading to a wrong diagnosis. The recently created OMERACT US for CPPD subtask force has created for the first time a set of criteria for identification of CPP deposition and assessed their reliability trying to address some of the issues that impede a wider use of US for CPPD diagnosis. During this section will be exposed the main US features of CPP deposition according to the new criteria as well as the principal pitfals that could mislead diagnosis. The scanning techique and some tips and tricks that could help sonographers to identify correctly CPP deposition will also be explained. Disclosure of Interest None declared

Background Identification of calcium pyrophosphate dihydrate (CPP) crystals in the synovial fluid (SF) from inflamed joints provides a definitive diagnosis of CPP deposition disease (CPPD) (1). CPP crystals may also be found in non-inflamed joints, allowing diagnosis also during asymptomatic periods (2). SF analysis and CPP crystals count could be used to evaluate disease activity during follow-up. It is more difficult than the count of monosodium urate (MSU) crystals, already tested in a previous work (3), for CPP crystals show different shapes, are often very minute and non-birefringent. Objectives To study an objective method for counting CPP crystals in the SF. Methods The SFs aspirated from the knees of 15 consecutive patients (8 men) affected by CPPD diagnosed according to the EULAR definition were analysed. Cytological evaluation included SF leukocyte and differential count. For crystal detection, a small drop of fresh SF was placed on a glass slide and examined by compensated polarized microscopy (400x). To facilitate crystal count, the slide was divided into 4 equal parts drawing a cross with a pencil. The count was performed by continuous viewing and for each field both the number of birefringent and non-birefringent crystals was noted. Two observers evaluated separately 6 SFs and repeated the count after 24 hours. SFs were divided into 4 groups: SFs with 1200 crystals. Results Mean time needed for the count was 60 minutes. Inter-reader agreement was 0.68 (0.47–0.88) for CPP crystals, 0.68 (0.50–0.85) for the birefringent ones and 0.60 (0.38–0.81) for the non-birefringent. Intra-reader agreement was 0.48 (0.17–0.78) for the first examiner and 0.30 (0.14–0.74) for the second. In 7 patient the SF was aspirated from an inflamed knee. Crystal number did not correlate with the presence of knee inflammation (r=0.41; p=0.19), the SF volume (r=0.14; p=0.61), the number of leukocytes (r=0.36; p=0.19), the % of PMN (r=0.25; p=0.37), and the presence of intracellular crystals (r=0.31, p=0.27). Actively inflamed joints had a higher SF volume [11 ml (10–20 ml) vs. 2 ml (1–10 ml), p=0.03] and a higher percentage of PMN [72% (0–94%) vs. 12% (0–68%), p=0.028]. SF with intracellular crystals showed also a higher percentage of PMN (57.1%±34.3% vs. 3%±6% p=0.006). Conclusions Our preliminary results indicate that CPP crystal count is less reliable and more time-consuming that that of MSU crystals. Non-birefringent crystals show lower inter-reader agreement than birefringent ones. References Pascual E. J Rheumatol 1996; 35:306–8. Martinez A. Arthritis Rheum 1995; 38:S 246. Montagna P. Reumatismo 2015; 67(1):29–32. Disclosure of Interest None declared

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

The finding of two different crystal species in the same synovial fluid, although unusual, has been recognized for monosodium urate monohydrate (MSU) and calcium pyrophosphate dihydrate (CPP) cryst...

Calcium pyrophosphate dihydrate crystal deposition disease of the temporomandibular joint is a rare entity that has a tendency to mimic bone tumour, leading to unnecessary surgery. This report describes a patient with calcium pyrophosphate dihydrate crystal deposition disease in the temporomandibular joint with characteristic computed tomography and histological features.

In clinical practice, the diseases caused by the deposition of microcrystals are an important reason for consultation among primary care professionals. More and more emphasis is being given to the impact of the drop in the quality of life of patients and their role as independent cardiovascular risk factor. Moreover, as both gout arthropathy of calcium pyrophosphate dihydrate crystals pose a diagnostic challenge for the professionals who are not familiar with the use of light microscopy polariazada or not have access to it in the consultation. Therefore, either the frequency or the comorbidity simulate the ease of articular processes of other different prognosis and treatment necessary knowledge about important for the diagnosis of microcrystalline arthropathies on purely clinical basis. In this chapter we emphasize the diagnostic guidelines and recommended an update in the treatment of this disease.

To investigate the association of calcium pyrophosphate dihydrate (CPPD) crystal deposition and cruciate ligament (CL) degeneration, 10 cadaveric knees were studied with 1.5-T magnetic resonance imaging and sectioned in three planes. The slices were evaluated with high-resolution Faxitron radiography. The images and specimens were evaluated by two radiologists. Histologic sections were obtained from eight that contained calcifications and from two without calcifications. Radiographs and histologic analysis demonstrated CPPD crystal deposition in 80% of specimens and 75% of CLs in these eight specimens. Degenerative changes were observed in 75% of them. Such analysis demonstrated no evidence of CPPD crystals or degeneration in the control specimens.

A variety of different diseases affect the synovium, including infection, noninfectious immunologic inflammatory conditions, degenerative arthroses, crystal deposits, trauma, and tumors. Tumors of the synovium are relatively uncommon. Any mesenchymal tumor may arise in the synovium, but most recapitulate its normal counterpart including synoviocytes, blood vessels, fat, and fibrous tissue. These tumors can arise in any synovial lined structures both within joints and in extraarticular locations. Most synovial tumors are benign. Malignant tumors are rare but important to recognize because many are aggressive and must be treated appropriately. Among common nonneoplastic conditions that affect the synovium and surrounding structures are crystal deposits such as monosodium urate crystals, calcium pyrophosphate dihydrate crystals, and hydroxyapatite crystals. These crystal deposits may be asymptomatic or cause severe pain or chronic joint destruction. Their accurate identification is important to guide appropriate therapy.

Deposition of calcium pyrophosphate dihydrate (CPPD) crystals in the articular structures affects predominantly temporomandibular, knee, hip, spine, and wrist joints, and is a rare condition, often mimicking malignancy. Sternoclavicular joint is extremely rarely involved. We present a patient with swelling of the right upper extremity, in whom on computed tomography a mass posterior to the sternoclavicular joint causing compression of the brachiocephalic vein was detected. A modified resection arthroplasty was performed, and the histopathological findings revealed massive deposits of CPPD in the articular cartilage. To our knowledge, there is only one similar case published in the literature.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease of the temporomandibular joint (TMJ) is rare. This article presents a 72-year-old man with CPPD deposition disease of TMJ. The patient's initial clinical presentation, diagnosis and treatment are discussed.

Purpose: Calcium pyrophosphate dihydrate crystal deposition disease(CPPD) is a disease of the elderly and extremely rare in young individuals. If young people develop CPPD crystal deposition disease, it may be associated with metabolic diseases, such as hemochromatosis, hyperparathyroidism, hypophosphatasia, hypomagnesemia, Wilson’s disease, hypothyroidism, and gout. Materials and Methods: Therefore, in young-onset CPPD crystal deposition disease, an investigation of any predisposing metabolic conditions is warranted. Conclusion: We report a case of a young female patient who presented with idiopathic CPPD crystal deposition disease at 25 years of age.

The so-called "crowned dens" is a peculiar manifestation of calcium crystal deposition diseases, either caused by calcium pyrophosphate dihydrate or caused by calcium hydroxiapatite crystals, characterized by the presence of calcific deposits around the odontoid, often showing a crown-like configuration on imaging. It has protean clinical and radiological pictures, and care should be taken to avoid misinterpretation and diagnostic errors. Although asymptomatic in many patients, this entity may present as a predominantly algic or febrile condition, and in some cases, signs of compression of the spinal cord may be the major complaint. The detection of calcifications in the periodontoid tissues is the key to the diagnosis, erosive osseous changes, and variably calcified soft-tissue masses being occasionally associated. Computed tomography is the most important imaging study to be performed in this setting.

Raman microspectroscopy was first used to determine the composition of a calcified plaque located at the pterygium-excision site of a 51-year-old female patient's left nasal sclera after surgery. It was unexpectedly found that the Raman spectrum of the calcified sample at 1149, 1108, 1049, 756, 517, 376 and 352/cm was similar to the Raman spectrum of monoclinic form of calcium pyrophosphate dihydrate (CPPD) crystal, but differed from the Raman spectrum of triclinic form of CPPD. An additional peak at 958/cm was also observed in the Raman spectrum of the calcified plaque, which was identical to the characteristic peak at 958/cm of hydroxyapatite (HA). This is the first study to report the spectral biodiagnosis of both monoclinic CPPD and HA co-deposited in the calcified plaque of a patient with sclera dystrophic calcification using Raman microspectroscopy.

Summary Objective Pathological mineralization is induced by unbalance between pro- and anti-mineralization factors. In calcifying osteoarthritic joints, articular chondrocytes undergo terminal differentiation similar to that in growth plate cartilage and release matrix vesicles (MVs) responsible for hydroxyapatite (HA) or calcium pyrophosphate dihydrate (CPPD) deposition. Inorganic pyrophosphate (PP i ) is a likely source of inorganic phosphate (P i ) to sustain HA formation when hydrolyzed but also a potent inhibitor preventing apatite mineral deposition and growth. Moreover, an excess of PP i can lead to CPPD formation, a marker of pathological calcification in osteoarthritic joints. It was suggested that the P i /PP i ratio during biomineralization is a turning point between physiological and pathological mineralization. The aim of this work was to determine the conditions favoring either HA or CPPD formation initiated by MVs. Methods MVs were isolated from 17-day-old chicken embryo growth plate cartilages and subjected to mineralization in the presence of various P i /PP i ratios. The mineralization kinetics and the chemical composition of minerals were determined, respectively, by light scattering and infrared spectroscopy. Results The formation of HA is optimal when the P i /PP i molar ratio is above 140, but is completely inhibited when the ratio decreases below 70. The retardation of any mineral formation is maximal at P i /PP i ratio around 30. CPPD is exclusively produced by MVs when the ratio is below 6, but it is inhibited for the ratio exceeding 25. Conclusions Our findings are consistent with the P i /PP i ratio being a determinant factor leading to pathological mineralization or its inhibition.

Both gout and calcium pyrophosphate dihydrate (CPPD) arthropathies are crystal deposit diseases; finding monosodium urate (MSU) or CPPD crystals in a synovial fluid sample, or in a tophi in the case of gout, provide a definitive, unequivocal diagnosis. Despite having such a simple and precise diagnostic test, in both crystal arthitides there is the accepted habit of approaching their diagnosis on clinical grounds (accompanied by hyperuricemia for gout, or chondrocalcinosis for the CPPD related arthropathy). Typical clinical presentations suggesting crystal arthitides may be due to other causes, and more important, less typical presentations, which are not uncommon, will pass undiagnosed unless crystals are systematically searched for in a synovial fluid sample from all undiagnosed arthropathies. Finally the precision of a clinical diagnosis made by an expert rheumatologist is higher than that of a less experienced or less specialized physician, and by approaching the diagnosis of the crystal arthritides on clinical grounds, expert rheumatologists support the inaccurate approach of other physicians with a wider margin of error.

Only few cases of acute calcium pyrophosphate dihydrate arthritis in total knee arthroplasty have been published. We report about a 63-year-old woman with an acute arthritis occurring six years after implantation of a total knee arthroplasty. The negative culture results and the identification of calcium pyrophosphate dihydrate crystals in synovial fluid and synovial tissue provided the diagnosis of pseudogout arthritis. The patient recovered under conservative treatment. Antibiotics or retrieval of the implant were unnecessary. Exclusion of an implant infection is of the utmost importance.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is a well-recognized inflammatory joint disorder. Extensor tendon rupture associated with CPPD deposition has rarely been described. We report herein the case of a 58-year-old woman who underwent reconstruction for subcutaneous extensor tendon ruptures of the extensor tendons for the ring and little fingers on both wrists associated with CPPD deposition. The significance of this case is the occurrence at an earlier age compared to previous papers and the appearance on bilateral wrists.

Purpose of review Calcium pyrophosphate dihydrate and basic calcium phosphate crystals are common components of osteoarthritic synovial fluids and define subsets of patients with inflammatory or rapidly destructive arthritis. Recent literature concerning clinical and etiologic aspects of calcium pyrophosphate dihydrate and basic calcium phosphate crystal arthritis are reviewed. Recent findings Recent literature reminds us of the propensity of calcium pyrophosphate dihydrate deposition disease to mimic other syndromes affecting the elderly. Several new studies reinforce the prevalence and significance of extra-articular calcium pyrophosphate dihydrate deposits, and demonstrate the presence of basic calcium phosphate-like whitlockite crystals in intervertebral discs. Current work serves to increase our appreciation for the complex role of the putative pyrophosphate transporter, ANKH, in healthy and diseased cartilage. The application of newer radiographic techniques to the diagnosis of calcium pyrophosphate dihydrate deposition disease holds promise for easier and more accurate identification of these crystal deposits in vivo. Work demonstrating the efficacy of a crystal poison in an animal model of osteoarthritis provides good evidence for a pathogenic role of calcium crystals in osteoarthritis, and hope for new therapies for these diseases. Summary Continued work will further our understanding of these common crystals and their associated clinical syndromes.

We examine the major genes in mice and humans involved in the pathogenesis of monosodium urate, calcium pyrophosphate dihydrate and hydroxyapatite crystal-induced arthritis.Several genetic causes of renal disease associated with hyperuricemia and gout provide insight into genes involved in renal urate handling. Mutations or polymorphisms in exons 4 and 5 and intron 4 of urate transporter 1 may be independent genetic markers of hyperuricemia and gout. Genetic analysis supports the role of ANKH mutations in calcium pyrophosphate dihydrate-induced arthritis. ANKH gain-of-function mutations were confirmed by functional studies; however, the crystals formed in ATD5 cells were basic calcium phosphate, not calcium pyrophosphate dihydrate, underlying the significance of chondrocyte differentiation state and the factors regulating normal and pathological mineralization. Animal models have implicated a general model of crystal-induced inflammation involving innate immunity through the NALP3 (Natch domain, leucine-rich repeat, and PYD-containing protein 3) inflammasome signaling through the interleukin-1 receptor and its signaling protein myeloid differentiation primary response protein 88.Genetic analysis has elucidated genes responsible for crystal formation and animal models have unveiled mechanisms in the development of crystal-induced arthritis. Future studies will hasten understanding of the pathology of crystal-induced arthritis and provide new therapies.

Summary Objective To compare characteristics of patients with severe osteoarthritis with and without calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. Study methods Patients undergoing total knee replacement surgery participated in this study and completed questionnaires. Radiographs of the index knee (extended anteroposterior, lateral and skyline) were reviewed for the presence of chondrocalcinosis. Synovial fluids were obtained during surgery and analyzed under compensated polarized light microscopy. Results The presence of CPPD crystals was identified in 52.9% of 102 patients. The use of both radiographs and synovial fluid analysis increased the identification of crystals. There was no difference in the following characteristics of the patients with and without CPPD crystals: age of pain onset, gender, difficulty in performing daily functions (including cooking, standing up from chairs, using restroom, going upstairs, and going shopping), history of previous joint inflammation, use of walking aids, and number and types of medications ever used. CPPD patients underwent knee arthroplasty at older age compared to non-CPPD patients (70.3±6.37 and 67.5±7.15 years old, respectively) ( P =0.037). All but one CPPD patients were unaware of the presence of crystals. Conclusion High prevalence of CPPD crystals was found in patients undergoing total knee replacement surgery. All but one CPPD patients were unaware of calcium deposition in the index joints. Patients with these crystals experienced similar difficulties in performing daily activities and received similar treatment to patients without CPPD crystals. CPPD patients did not undergo knee arthroplasty at earlier age than non-CPPD patients.

Tumoral pseudogout is a rare clinical form of calcium pyrophosphate dihydrate crystal deposition disease. Tumoral pseudogout can mimic other diseases such as chondroid tumor, tophaceous gout, or tumoral calcinosis. Its radiological features have been presented in some case reports, but no specific radiographic features have been identified. Here, we report an unusual case of recurrent tumoral pseudogout involving the proximal interphalangeal joint of the right long finger. This case presents with progressive radiological findings of the disease with an enlarging and recurrent calcified mass and secondary bony erosion and remodeling, along with a radiological–pathological correlation. We also review previously reported imaging findings of this disease entity, differential points in comparison to other diseases, and some key points for making the correct diagnosis.

A 66-year-old woman developed firm, painless, slowly growing nodular masses over her elbows, fingers, toes, and left hip over four years. Aspiration of the elbow mass revealed a white chalky material that was shown to be carbonate apatite on infrared spectroscopy and energy dispersive X-ray spectroscopy. We discuss the classification of tumoral calcinosis and the nature of the calcium deposits. Tumoral calcinosis should be differentiated from tophaceous gout and calcium pyrophosphate dihydrate crystal deposition disease. Polarizing light microscopy and crystal analysis by X-ray and infrared spectroscopy, electron or X-ray diffraction will confirm the diagnosis. Secondary causes of tumoral calcinosis should also be excluded.

The cervical spine may be specifically involved in crystal-associated arthropathies. In this article, we focus on the three common crystals and diseases: hydroxyapatite crystal deposition disease, calcium pyrophosphate dihydrate (CPPD) deposition disease, and monosodium urate crystals (gout). The cervical involvement in crystal-associated diseases may provoke a misleading clinical presentation with acute neck pain, fever, or neurological symptoms. Imaging allows an accurate diagnosis in typical cases with calcific deposits and destructive lesions of the discs and joints. Most of the cases are related to CPPD or hydroxyapatite crystal deposition; gout is much less common.

Basic calcium phosphate, calcium pyrophosphate dihydrate, and monosodium urate crystals are the most common types of crystals associated with human disease. Although there is a well-established association between these crystals and various forms of joint disease, recent evidence points to an association of basic calcium phosphate crystals with breast cancer and atherosclerosis. Crystal-induced tissue damage is affected by degradative proteases, cytokines, chemokines, and prostanoids produced by cells stimulated by crystals. In the case of basic calcium phosphate and calcium pyrophosphate dihydrate crystals, these responses are augmented by the cellular proliferation that results from their induction of mitogenesis. The understanding of the molecular mechanisms involved in generating these pathologic effects has been significantly advanced in recent years. Such advances are essential to the ongoing search for more effective therapies for crystal-associated diseases.

Extracellular inorganic pyrophosphate (ePPi) both inhibits and promotes different forms of pathologic mineralization. Basic calcium phosphate (BCP) deposition results from depressed levels of ePPi while excess levels of ePPi leads to calcium pyrophosphate dihydrate crystal deposition (CPPD) disease. These crystals are also often identified in patients with osteoarthritis, the most prevalent form of arthritis causing significant morbidity.The two primary hypotheses for generation of ePPi, export of inorganic pyrophosphate through the multipass transmembrane protein ANK and generation of ePPi by ectoenzyme activity, continue to be supported and better understood through animal models and study of families with CPPD deposition disease.As the pathophysiology of crystal formation in both articular cartilage and synovial fluid is better understood, the opportunity for prevention and treatment of pathologic mineralization increases. In particular, a more complex understanding of the ank gene, ectoenzyme PC-1, and the transglutaminase enzyme family may eventually translate into therapeutic application for both BCP deposition and CPPD deposition disease.

We report a case of a 76-year-old man with cervical spondylotic myelopathy acconpanied by calcification of the ligamentum flavum. The patient complained of numbness with bilateral fingers and precise motion disturbance a year and a half ago, and expressed conspicuous spastic gaits three months ago. MRI scanning showed spinal canal stenosis and CTM revealed calcification of the ligamentum flavum especially at C3/4. We performed spinous process-splitting laminoplasty, which decreased their symptoms.Under a scanning electron microscope, we examined the surgical specimen extracted from the ligamentum flavum. It included shaped crystalline structures extensively. Results of chemical composition analysis suggested crystal as calcium pyrophosphate dihydrate (CPPD), but did not confirm the existence of hydroxyapatites (HAP).

Eine Beteiligung des Kiefergelenks im Rahmen von Kristallarthropathien ist selten. Klinisch und radiologisch ist die Abgrenzung dieser Erkrankung insbesondere gegen maligne Tumoren der Glandula parotis und des Kiefergelenks ebenso schwierig wie bedeutsam. Der Kalziumpyrophosphat-Arthropathie liegt eine Uberproduktion von anorganischem Pyrophosphat mit Ablagerung von Kristallen im Gelenk zugrunde. Insbesondere bei Erkrankung des Kiefergelenks kommt es durch Ablagerung der Kristalle im umgebenden Weichteilgewebe zur Ausbildung von Pseudotumoren. Anhand der Darstellung eines ungewohnlich ausgedehnten Falles einer Kalziumpyrophosphat-Arthropathie des Kiefergelenks mit Ausbildung eines Pseudotumors wird daher im Rahmen einer Literaturubersicht auf die wesentlichen klinischen, atiologischen, diagnostischen und therapeutischen Aspekte der Erkrankung eingegangen. Aktuelle Forschungsergebnisse zu Atiologie und Pathogenese der Erkrankung werden referiert.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease has multiple clinical features with variable courses creating several pitfalls in clinical diagnosis. There are number of reported cases mimicking malignant skeletal tumors such as chondrosarcoma. However, no case of CPPD disease with radiographic noncalcified soft tissue mass has been reported in the literature. Here we report a case of CPPD disease clinically mimicking soft tissue tumor with its magnetic resonance imaging appearance and histopathology.

Objectives : Thyroid hormones induce features of the hypertrophic phenotype in mature articular chondrocytes as well as in growth plate chondrocytes. Hypertrophic chondrocytes are responsible for extracellular matrix mineralization, with formation of bone mineral in growth plate cartilage and pathologic calcium crystals in aging articular cartilage. Elevated activity levels of the two transglutaminase (Tgase) enzymes (type II Tgase and Factor XIIIA (FXIIIA)) have recently been described as additional features of hypertrophic growth plate chondrocytes. Because Tgases may participate in pathologic mineralization in aging cartilage, we explored the effects of thyroid hormones on Tgase activity in articular chondrocytes. Methods : Adult porcine articular chondrocytes were incubated with or without 250–750nM l-thyroxine (T4) or 10–100nM 3,3′,5-tri-iodothyronine (T3). Tgase activity was measured with a standard radiometric assay. The effects of thyroid hormones on protein and mRNA levels of type II Tgase and FXIIIA were determined. As Tgase activity can be stimulated by proteases, endoproteinase levels were also measured. The mechanisms of these effects were explored. Results : T4 (750nM) or T3 (100nM) stimulated Tgase activity by twofold in articular chondrocytes at 4h and increased the percentage of Tgase activity in the extracellular matrix. Chondrocytes rapidly converted T4 to T3, but the time course suggests similar mechanisms for T4 and T3. T4-induced Tgase activity was suppressed with cycloheximide and protein kinase C inhibitors. The effects of T4 on type II Tgase and FXIIIA levels were modest, but T4 strongly induced endoproteinase activity in chondrocytes. Conclusions : We report in this study that thyroid hormones increase Tgase activity in articular chondrocytes via a non-genomic mechanism, which may involve increased endoproteinase secretion.

Development and deposition of amorphous or crystalline inorganic phases, a process referred to as mineralization, occur in a large numbers of biological systems. In the human body, physiological mineralization is vital for the development and maintenance of the skeleton. However, crystals are often formed and accumulated in various other sites of the body as a result of metabolic disorders. Calcium pyrophosphate dihydrate, is among the most common types of pathological deposits and the condition associated with the presence of such crystals is referred to as calcium pyrophosphate (dihydrate) deposition disease. This chapter discusses the current knowledge regarding calcium pyrophosphate deposition disease and further focuses on the characterization methods and the in vitro model systems for studying the conditions under which these crystals develop

Ultrasonography has been increasingly used the last years for the identification of calcium pyrophosphate dihydrate crystal deposition (CPPD) in joints and has demonstrated to be a reliable and feasible tool in most of the studies published. However, it is common experience between sonographers that in daily clinical practice CPP identification by US is rather challenging as crystal deposits are not always numerous and diffuse. Furthermore, other conditions can mimic CPP deposition leading to a wrong diagnosis. During this section will be exposed the main US features of CPP deposition as well as the principal pitfals that could mislead diagnosis. Some tips and tricks that could help sonographers to identify correctly CPP deposition will also be explained. Disclosure of Interest None declared

Articular cartilage calcification caused by deposition of calcium pyrophosphate dihydrate (CPPD) is more common in women than in men. The prevalence increases with age; the condition is uncommon under 50 years, but is seen in the knee in up to 60% of individuals aged over 85 years. It may be asymptomatic, may occur in association with osteoarthritis (in which the possible pathogenic role of the crystal is uncertain) or may present as acute pseudogout or associated with chronic arthritis.

Resume Objectifs. Evaluer l’interet de la microponction articulaire des doigts et des orteils pour etablir un diagnostic chez un patient avec une atteinte de l’une ou l’autre des petites articulations. Methodes. L’etude a porte sur l’ensemble des patients ayant subi une ponction d’une petite articulation, dans le cadre de la consultation de rhumatologie entre 1994 et 1998. La ponction s’est effectuee avec des aiguilles de petit calibre et le materiel aspire a ete immediatement soumis a analyse microscopique pour la numeration des globules blancs et la recherche de cristaux en lumiere polarisee. Resultats. Soixante et onze cas ont ete ponctionnes. Pour 20 patients (28 % du collectif), un diagnostic specifique d’arthropathie microcristalline a pu etre pose : goutte 14 fois, arthropathie pyrophosphatique six fois. Parmi les 51 patients restants, le materiel etait en quantite insuffisante pour realiser une analyse chez 28 d’entre eux. Dans 23 cas, l’analyse a mis en evidence un liquide d’aspect inflammatoire chez huit patients et de formule mecanique chez 15. Conclusion. La microponction des petites articulations des doigts et des orteils qui est une technique aisement realisable a permis de preciser l’etiologie d’une atteinte rhumatismale, notamment si elle etait de nature microcristalline, dans deux tiers des cas environ.

Rates of growth of triclinic calcium pyrophosphate dihydrate microcrystals of columnar shape are reported for pH 4.5, 5.0, 5.5, and 6.5. These rates can be explained by the polynuclear growth mechanism in which nuclei of critical size form, grow laterally, and intergrow while spreading over the surface. The surface energy is found to be 75 ± 5 mJ/m2. The frequency for attachment of calcium ions to the crystal surface is found to be (2 ± 1) × 105 s-1, close to the theoretical value for a calcium ion to partially dehydrate and simultaneously make a diffusion jump into a kink site, 1.6 × 105 s-1.