Calcium Pyrophosphate Dihydrate Research Articles

The Incidence and Significance of Calcium Pyrophosphate Dihydrate Deposits in Histologic Examinations of Total Hip, Knee, and Shoulder Joint Arthroplasties.

The incidence, distribution, and significance of calcium pyrophosphate dihydrate deposition (CPPD) disease have not been extensively compared among various total joint resections. To investigate and define the clinical and pathologic features of CPPD in hip, shoulder, and knee arthroplasties. We retrospectively reviewed consecutive total hip, knee, and shoulder arthroplasty cases (N = 3195) confirmed pathologically between January 1, 2017, and October 10, 2018, comparing clinical and pathologic data. Among 2004 hip arthroplasties, 61 (3%) had CPPD on pathologic examination; the majority had a histologic diagnosis of osteoarthritis, followed by fracture and avascular necrosis. Of 1113 knee arthroplasties, 98 (9%) had CPPD; all had a histologic diagnosis of osteoarthritis. Among 78 shoulder arthroplasties, 10 (13%) had CPPD; all but one had a histologic diagnosis of osteoarthritis. Patients with hip and knee CPPD were significantly older than those without CPPD. Of the 169 pathologically detected CPPD cases, only 35 (21%) were documented on preoperative radiologic images or by other clinical means; radiology reports were significantly more likely to document chondrocalcinosis in the knees than in the hips. Histologically, CPPD was noted almost exclusively in the separately submitted soft tissues/joint capsule, concomitantly involving the articular cartilage surface in only 3.0% (5 of 169) of cases. Calcium pyrophosphate dihydrate deposition is more than twice as likely to occur in the knees and shoulders compared with the hips. Patients with CPPD in the knees or hips are usually not recognized preoperatively/radiologically and constitute a significantly older population. Reliably establishing the diagnosis of CPPD requires pathologic examination of the submitted soft tissue/joint capsule.

Hemochromatosis Arthropathy in Heterozygous HFE H63D Mutation Without Iron Overload- An Entity Less Commonly Touched

Human homeostatic iron regulator protein gene (HFE gene) H63D mutations even when homozygous are rarely associated with iron overload. These mutations, independent of iron status, are associated with calcium pyrophosphate dihydrate crystal deposition disease (CPPD) leading to arthropathy even for heterozygotes. The arthropathy does not respond to iron depletion. We report a case of a 62-year-old male with chronic generalized arthralgias with no evidence of iron overload or elevated inflammatory markers with characteristic radiographic hook-like osteophytes suggestive of hemochromatosis arthropathy. Further, he was found to be a carrier of HFE H63D mutation. Recognition of the association can help guide goal directed management.

Effect of Apium graveolens extract on the surface morphology and characteristics of calcium pyrophosphate crystals

This aim of the present study was to investigate the crystallization and physical characteristics of the triclinic calcium pyrophosphate dihydrate (t-CPPD) and monoclinic calcium pyrophosphate tetrahydrate β (m-CPPT β) crystals created in pure media and in the presence of Apium graveolens extract. The structure, functional groups, crystal morphology, and size of the crystals were investigated experimentally using X-ray diffraction, Fourier transform infrared (FTIR) spectroscopy, scanning electron microscopy, atomic force microscopy, and a particle size analyzer. The smaller crystals were created in the presence of the extract media and displayed changes in the t-CPPD crystal shapes from rod like to rounded in addition to rod-like crystals. Zeta potential analyses showed that adding A. graveolens extract resulted in a more negative crystal surface energy (−36.7 ± 1.1 mV) than that in pure media, which was −28.6 ± 1.3 mV. In addition, the thermal decomposition characteristics of the t-CPPD and m-CPPT β crystals were simultaneously investigated using thermogravimetric analysis combined with FTIR and the main evolved product was determined as H2O. The present study analyzed the structural, morphological, and thermal properties of t-CPPD and m-CPPT β to provide more comprehensive information on how A. graveolens extract helps prevent the formation of t-CPPD and m-CPPT β crystals. This information can be an important step in long-term development of an effective therapeutic treatment.

Xanthine Oxidoreductase Is Involved in Chondrocyte Mineralization and Expressed in Osteoarthritic Damaged Cartilage.

Pathologic calcification of cartilage consists of the formation of basic calcium phosphate (BCP) and/or calcium pyrophosphate dihydrate (CPPD) containing calcium crystals in mature hyaline or articular cartilage and is associated with aging, cartilage injury and likely plays a role in accelerating the pathology of osteoarthritis (OA). The pathways regulating joint calcification, in particular cartilage calcification, are not completely understood, but inflammation and the formation of reactive oxygen species (ROS) are contributory factors. The xanthine oxidase (XO) form of xanthine oxidoreductase (XOR), the key enzyme in xanthine and uric acid metabolism, is a major cellular source of superoxide. We hypothesized that XOR could be implicated in chondrocyte mineralization and cartilage calcification and degradation in OA. We showed both in murine primary chondrocyte and chondrogenic ATDC5 cells, that mineralization was inhibited by two different XOR inhibitors, febuxostat and allopurinol. In addition, XOR inhibition reduced the expression of the pro-mineralizing cytokine interleukin-6 (IL-6). We next generated XOR knock-out chondrocyte cell lines with undetectable XOR expression and XO activity. XOR knock-out chondrocyte cells showed decreased mineralization and reduced alkaline phosphatase (Alp) activity. To assess the precise form of XOR involved, primary chondrocytes of XOR mutant mice expressing either the XDH form (XDH ki) or the XO form (XO ki) were studied. We found that XO ki chondrocytes exhibited increased mineralization compared to XDH ki chondrocytes, and this was associated with enhanced Alp activity, ROS generation and IL-6 secretion. Finally, we found increased XOR expression in damaged vs. undamaged cartilage obtained from OA patients and XOR expression partially co-localized with areas showing pathologic calcification. Altogether, our results suggest that XOR, via its XO form, contribute to chondrocyte mineralization and pathological calcification in OA cartilage.

Articular and periarticular spinal calcifications in relation to synovial fluid findings in patients with calcium pyrophosphate dihydrate deposition disease (CPPD)

BackgroundCalcium pyrophosphate dihydrate deposition disease (CPPD) is the second most common form of the crystal-associated arthritis. Diagnosis is achieved by detection of crystals by polarized light microscopy and/or detection of hyaline cartilage or fibrocartilage calcifications characteristic of CPPD deposition by musculoskeletal ultrasound (MSUS). Axial involvement with intervertebral disc calcification, sacroiliac erosions, and sub-chondral cysts of the facet joints occurs with CPPD deposition.AimTo assess the presence and relation between calcification of intervertebral discs, other articular and periarticular spinal structures, and synovial fluid analysis (SFA) and MSUS calcifications in patients with CPPD deposition disease.MethodsOne hundred patients with CPPD disease diagnosed according to the modified proposed diagnostic criteria by McCarty 1994 were included. Plain radiography on the spines, pelvis, and affected joints, MSUS on affected joints, and synovial fluid analysis (SFA) were done.ResultsSpinal calcification was present in 55% of patients. The commonest site was anterior longitudinal ligament (43%). Characteristic CPPD calcifications by plain radiography on the knee and wrist joints were present in 38% and 16% respectively. Characteristic CPPD calcifications by MSUS on the knee and wrist joints presented in 93% and 27% respectively. CPPD crystal detection by SFA was 97%. The accuracy of MSUS to diagnose CPPD deposition disease is more than double that of plain radiography, and it is comparable to that of synovial fluid analysis. The result of intra-rater analysis between SFA by polarized light microscopy and MSUS was kappa 0.767 (p < 0.001); this indicates substantial level of agreement between SFA and MSUS; between plain radiography and MSUS, it was kappa 0.188 (p = 0.32) which indicates slight agreement, and between plain radiography and SFA, it was kappa 0.037 (p = 0.1) which fails to reach a significant level of agreement. There was a significant positive relation between spinal calcification and wrist joint calcification by plain radiography.ConclusionConsiderable spinal affection by CPPD deposition disease can be detected. Although the most definitive, reliable direct approach for CPPD deposition disease diagnosis is SFA using polarized light microscopy, MSUS is considered a useful non-invasive diagnostic tool in this situation. In CPPD deposition disease, MSUS has proven to be an excellent technique for detecting calcification in the articular tissue disease compared to conventional radiography.

Calcium Pyrophosphate Dihydrate (CPPD) Crystal Deposition Disease, Crowned Dens Syndrome (CDS) and Its Mimicries: Case Report

Calcium Pyrophosphate Dihydrate (CPPD) Crystal Deposition Disease, Crowned Dens Syndrome (CDS) and Its Mimicries: Case Report

Pathophysiology and MRI Findings of Infectious Spondylitis and the Differential Diagnosis

MRI에서 추간판의 이상 신호와 위, 아래 척추체 종판의 파괴, 종판 주변의 골수부종 등은 감염성 척추염의 전형적인 소견으로 여겨지나 퇴행성 척추질환, acute Schmorl's node, 척추관절병증, synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO)/chronic recurrent multifocal osteomyelitis, 척추신경관절병증, calcium pyrophosphate dehydrate 결절침착질환 등 다양한 비감염성 척추질환에서도 나타날 수 있다. MRI에서 이러한 비감염성 척추질환과 감별되는 감염성 척추염의 영상 소견은 추간판의 고신호와 농양, 척추 연부조직의 농양, 그리고 T1 강조영상에서 저신호로 보이는 종판의 경계가 불명확해지는 점 등이다. 그러나 이러한 감별점이 항상 적용되는 것은 아니며 감염성, 비감염성 질환의 영상 소견에 유사점이 많기 때문에 정확한 진단을 위해서는 감염성 척추염뿐만 아니라 감염과 감별해야 하는 다양한 질환의 병태생리와 연관된 영상학적 특징을 아는 것이 중요하다.

Imaging of Calcifying and Ossifying Disorders of the Spine

Substantial advances in the availability of spinal imaging have led to the increasing use of spinal imaging in the evaluation of patients with neck and back pain. This has resulted in the recognition of a diverse collection of spinal disorders, characterized by heterotopic calcification and ossification. Despite the increasing frequency at which these conditions are being diagnosed, there still exists a lack of awareness of the imaging characteristics of some of these calcifying and ossifying spinal disorders. Here, we review the imaging characteristics of ankylosing spondylitis, arachnoiditis ossificans, calcific discitis, calcific tendonitis of the longus colli, calcium pyrophosphate dihydrate deposition, crowned dens syndrome, diffuse idiopathic skeletal hyperostosis, ossification of the ligamentum flavum, and ossification of the posterior longitudinal ligament. Radiologists and clinicians alike should be familiar with these calcifying and ossifying spinal disorders to aid in an accurate diagnosis and to guide clinical management.Learning Objectives: Recognize the clinical features and imaging findings of various calcifying and ossifying disorders of the spine.

Calcium Pyrophosphate Dihydrate Crystals Increase the Granulocyte/Monocyte Progenitor (GMP) and Enhance Granulocyte and Monocyte Differentiation In Vivo.

Calcium pyrophosphate dihydrate (CPPD) crystals are formed locally within the joints, leading to pseudogout. Although the mobilization of local granulocytes can be observed in joints where pseudogout has manifested, the mechanism of this activity remains poorly understood. In this study, CPPD crystals were administered to mice, and the dynamics of splenic and peripheral blood myeloid cells were analyzed. As a result, levels of both granulocytes and monocytes were found to increase following CPPD crystal administration in a concentration-dependent manner, with a concomitant decrease in lymphocytes in the peripheral blood. In contrast, the levels of other cells, such as dendritic cell subsets, T-cells, and B-cells, remained unchanged in the spleen, following CPPD crystal administration. Furthermore, an increase in granulocytes/monocyte progenitors (GMPs) and a decrease in megakaryocyte/erythrocyte progenitors (MEPs) were also observed in the bone marrow. In addition, CPPD administration induced production of IL-1β, which acts on hematopoietic stem cells and hematopoietic progenitors and promotes myeloid cell differentiation and expansion. These results suggest that CPPD crystals act as a “danger signal” to induce IL-1β production, resulting in changes in course of hematopoietic progenitor cell differentiation and in increased granulocyte/monocyte levels, and contributing to the development of gout.

Calcium Pyrophosphate Dihydrate Crystal Deposition in Gouty Tophi.

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. 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. 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. 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.

Cervical myelopathy due to subaxial calcium pyrophosphate dihydrate (CPPD) deposition with simultaneous asymptomatic crowned dens syndrome: two case reports

BackgroundThere are few reports of cervical myelopathy caused by an attack of subaxial calcium pyrophosphate dihydrate (CPPD) deposition. Moreover, there has been no report on cervical myelopathy by subaxial CPPD deposition with simultaneous asymptomatic crowned dens syndrome (CDS) at the same time.Case presentationThe first case was a 68-year-old male complaining of cervical myelopathic symptoms. Plain radiographs, computed tomography (CT) and magnetic resonance imaging (MRI) findings revealed spinal cord compression by calcified round lesions at C4 as well as a calcified lesion behind the dens. The second case was a 77-year-old female complaining of cervical myelopathic symptoms. Plain radiographs, CT and MRI findings revealed spinal cord compression by calcified round lesions at C3 and C4 as well as a calcified lesion behind the dens. In both cases, we believed that the calcified lesion behind the dens was an asymptomatic lesion. Therefore, the first patient received decompressive laminectomy of C3 and C4, removal of calcified round lesions, and posterior fixation from C3 to C5 due to associated kyphosis. The second patient underwent decompressive laminectomy of C3 and C4 and removal of calcified round lesions. Microscopic examination under polarized light showed dark blue calcifications with rhomboid crystals that were positively birefringent. The findings were consistent with those of CPPD.ConclusionsThis is the first study to report cervical myelopathy caused by subaxial CPPD deposition with simultaneous asymptomatic CDS. Surgical removal of the subaxial CPPD deposition alone achieved a satisfactory surgical outcome without recurrence.

Lumbar Facet Joint Cyst Caused by Calcium Pyrophosphate Arthropathy of the Spine: Case Report and Review of Literature

Background Data: Calcium pyrophosphate dihydrate (CPPD) deposition disease is a metabolic disorder caused by the deposition of CPPD crystals in the articular or periarticular structures that leads to inflammation of the joints. Spine affection is rare. Purpose: To present a rare case of lumbar facet joint cyst caused by calcium pyrophosphate arthropathy. Study Design: A case report with a brief review of the literature. Patient and Methods: Seventy-three-year-old man, who underwent PLIF L5/S1 ten years ago, presented with right L4 nerve root compression symptoms that have started two months ago. Clinical examination revealed no motor function disturbance but hypoesthesia in the L4 dermatome. He has no history of crystal deposition disorder. The patient underwent decompression and fusion at this level. Results: The symptoms were completely resolved postoperatively and after one-year follow-up. Histopathological examination of the cyst revealed fibrous granulation tissue. Examination of the tissue under polarized light showed positively birefringent, short blunt crystals of calcium pyrophosphate dihydrate. Conclusion: Calcium pyrophosphate arthropathy, although rare, should be incorporated into the differential diagnosis of cystic lesions of the facet joints. (2020ESJ221)

Imaging of crystalline arthropathy in 2020.

Crystal-related arthropathies are the result of crystal deposition in joint and periarticular soft tissues. Identification of urate crystals is mandatory to distinguish gout from other crystalline arthropathies, including calcium pyrophosphate dihydrate and basic calcium phosphate crystal deposition diseases. ACR/EULAR classification criteria for gout included dual-energy computed tomography and ultrasound with equal impact to the final score. Different diagnostic strengths of these imaging modalities depend on disease duration and scanned anatomic site. While ultrasound has been indicated as the first-choice imaging technique, especially in the early stages of the disease, dual-energy computed tomography has shown to be highly specific, allowing the detection of crystal deposits in anatomic sites not accessible by ultrasound, such as the spine. At the spinal level, MRI findings are usually nonspecific. Finally, there is preliminary evidence that at the knee, dual-energy computed tomography may discriminate calcium pyrophosphate dihydrate from basic calcium phosphate crystal deposits.

Spinal pseudogout is a joker. Commentary on “Calcium pyrophosphate deposition disease of the cervical and thoracolumbar spine: A report of two cases”

In this issue, Moon et al. provide a detailed report on two cases of Calcium pyrophosphate deposition disease (CPDD), causing compression of the spinal cord and conus medullaris requiring surgical decompression and reconstruction [[1]Moon A.S. Mabry S. Pittman J.L. Calcium pyrophosphate deposition disease of the cervical and thoracolumbar spine: a report of two cases.North American Spine Society J (NASSJ). 2020; 3: 100026https://doi.org/10.1016/j.xnsj.2020.100026Abstract Full Text Full Text PDF Scopus (1) Google Scholar]. Both cases presented on elderly patients, with known advanced degenerative disease of the spine. In both cases the mass was likely forming from the facet joint and both cases presented with a combination of severe pain and symptoms of neural compression (in different degrees, causing alteration of the spinal cord motor tracts in one case and unilateral lower limb pain mimicking radiculopathy in the second one). Both patients gained full resolution of symptoms and neurological function after surgery. A number of cases of CPDD affecting the spine have been described in the literature, but most reports include one or few cases, which suggests that CPDD requiring surgery is relatively unfrequent. This is in contrast with the finding of high prevalence (as high as 25%) of deposits of calcium pyrophosphate in the cervical spine of patients with pseudogout affecting peripheral joints [[2]Moshrif A. Laredo J.D. Bassiouni H. et al.Spinal involvement with calcium pyrophosphate deposition disease in an academic rheumatology center: a series of 37 patients.Semin Arthritis Rheum. 2019; 48: 1113-1126https://doi.org/10.1016/j.semarthrit.2018.10.009Crossref PubMed Scopus (31) Google Scholar]. While the association of pseudogout with lumbar and cervical stenosis has been well described, some aspects of this condition deserve some attention. The prognosis of spinal canal decompression in patients with CPDD does not seem to be worse than that on patients with degenerative lumbar stenosis [[3]Ariyawatkul T. Pichaisak W. Chavasiri C. Vamvanij V. Wilartratsami S. Luksanapruksa P. The role of calcium pyrophosphate dihydrate deposition in the postoperative outcome of lumbar spinal stenosis patients.Asian Spine J. 2019; 13: 1001-1009https://doi.org/10.31616/asj.2018.0280Crossref PubMed Scopus (2) Google Scholar]. CPDD can also need to be distinguished from other spinal conditions, such as tumors [[4]Turaga S. Thomas M. Savy L. Schreiber B.E. Pseudogout or pseudolymphoma? Calcium pyrophosphate deposition disease of the cervical spine: a rare presentation and literature review.BMJ Case Rep. 2019; 12 (Published 2019 Dec 2)e231508https://doi.org/10.1136/bcr-2019-231508Crossref PubMed Scopus (6) Google Scholar], spinal infection [[5]Bridges K.J. Bullis C.L. Wanchu A. Than K.D. Pseudogout of the cervical and thoracic spine mimicking infection after lumbar fusion: case report.J Neurosurg Spine. 2017; 27: 145-149Crossref PubMed Scopus (12) Google Scholar], hematoma of the yellow ligament [[6]Cruz-Conde R. Berjano P. Buitron Z. Ligamentum flavum hematoma presenting as progressive root compression in the lumbar spine.Spine. 1995; 20: 1506-1509https://doi.org/10.1097/00007632-199507000-00012Crossref PubMed Scopus (42) Google Scholar]. One of the two cases in this report presented with severe spinal sagittal misalignment that might be related to either the spinal cord compression or inflammation of the facet joints, and resolved after surgery, which suggests that CPDD can also be misinterpreted as spinal deformity of functional nature [[7]Redaelli A. Berjano P. Aebi M. Focal disorders of the spine with compensatory deformities: how to define them.Eur Spine J. 2018; 27: 59-69https://doi.org/10.1007/s00586-018-5501-8Crossref PubMed Scopus (9) Google Scholar]. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Download .pdf (.12 MB) Help with pdf files Calcium pyrophosphate deposition disease of the cervical and thoracolumbar spine: A report of two casesNorth American Spine Society Journal (NASSJ)Vol. 3PreviewSpinal calcium pyrophosphate deposition disease (CPPD) is uncommon, and often resembles more common spine pathologies causing pain and neural compression. Here, we present two unusual cases of CPPD of the cervical and thoracolumbar spines. Full-Text PDF Open Access

Dual-energy CT collagen density mapping of wrist ligaments reveals tissue remodeling in CPPD patients: first results from a clinical cohort

ObjectivesTo evaluate differences in collagen density as detected by dual-energy computed tomography (DECT) of wrist ligaments between patients with calcium pyrophosphate-dihydrate deposition disease (CPPD) and a control group in order to gain insight into changes of the extracellular matrix in response to crystal deposition.Materials and methodsThis retrospective study included 28 patients (18 with CPPD, 10 controls) who underwent DECT of the wrist. Collagen density maps were reconstructed from the DECT datasets and used to measure densities in regions of interest (ROIs) placed in the scapholunate (SL) ligament (dorsal, palmar, proximal), lunotriquetral (LT) ligament, and extensor carpi radialis (ECR) tendon, (n = 260 measurements). The presence of calcifications on standard CT images in these regions was assessed by a blinded reader. Densities were compared with nonparametric tests, and linear regression analysis was performed to investigate the impact of age, sex, and CT- detected calcium deposition on collagen density.ResultsCollagen density in the SL ligament was significantly higher in CPPD patients than in controls (overall mean: 265.4 ± 32.1 HU vs. 196.3 ± 33.8 HU; p < 0.001). In the ECR tendon, collagen densities did not differ significantly (p = 0.672): 161.3 ± 20.1 HU in CPPD vs. 163.6 ± 12.0 HU in controls. Regression analysis showed that diagnosis, but not age or calcification, had a significant impact on collagen density.ConclusionCollagen density of the SL ligament is significantly higher in CPPD patients than in control patients. Further research is needed to understand these changes in the extracellular matrix of ligaments in CPPD.

White blood cell count and total protein concentration to predict the absence of microcrystals in synovial fluid

BackgroundSynovial fluid analysis is essential for diagnosing crystal-induced arthritis. Monosodium urate monohydrate (MSU) crystals in gout and calcium pyrophosphate dihydrate (CPP) crystals in pseudogout trigger inflammatory reactions that result in white blood cell (WBC) activation. This study aimed to evaluate the predictive value of synovial fluid WBC count and total protein concentration for the absence of microcrystals. Materials and methodsThis prospective study analyzed all synovial fluid samples collected at a single center in a 6–month period. The absolute WBC count and total protein concentration were recorded for each sample. A single expert used polarized light microscopy to detect microcrystals. Mann-Whitney U-tests was used to compare mean counts and concentrations in samples with and without crystals. Diagnostic performance was assessed through the area under the receiver-operating characteristic curve (AUC). ResultsA total of 205 samples were included. The absolute WBC count was significantly higher in samples with crystals than in those without. No differences were found between MSU and CPP. The ROC curve showed an AUC 0.773, and an absolute WBC count <1650/mm3 yielded 95.7% sensitivity, 53.1% specificity, and 97.7% negative predictive value for predicting the absence of microcrystals. Total protein concentration was not significantly different between samples with and without crystals. ConclusionThe WBC count is useful for screening for the absence of microcrystals in synovial fluid; the cutoff <1650 WBC/mm3 accurately predicts the absence of crystals, obviating the need for polarized light microscopy and thus simplifying and shortening laboratory analysis of synovial fluid, leading to a reduction in laboratory turnaround time.

Multidimensional Population Balance Modeling for Pathological Calcium Pyrophosphate Dihydrate Crystals in the Presence of Amino Acids

AbstractA multidimensional population balance model was applied to elaborate the effects of amino acids on the crystallization mechanisms of calcium pyrophosphate dihydrate crystals. Breakage and growth terms defined in the model were expressed in two dimensions depending on the sizes. The exponential hyperbolic function based on the particle sizes was selected for expressing the growth. The model was resolved by using the finite differences method. It was detected that in the non‐additive media, the growth along the length‐1 is extremely dominant against both the growth along the length‐2 and the breakage. However, it was discovered that the amino acids made the crystals more fragile, and the breakage at certain size ranges and certain concentrations of amino acids was the dominant mechanism. In any case, it was proven that both growth and breakage are suppressed considerably in the amino acid‐containing media.

Tophaceous pseudogout of the temporomandibular joint with erosion into the middle cranial fossa

This report presents a case of extensive tophaceous pseudogout involving the temporomandibular joint (TMJ), causing erosion into the middle cranial fossa. Pseudogout is a benign metabolic arthropathy caused by calcium pyrophosphate dihydrate crystal deposition within joints and peri-articular tissue. Pseudogout more frequently occurs in large joints such as the knee, wrist, symphysis pubis, and shoulder. Tophaceous pseudogout involving the TMJ is rare, with only seven cases involving erosion into the middle cranial fossa reported previously. Despite skull base erosion being a rare consequence of this erosive disease, this case highlights the importance of appropriate investigation and multidisciplinary team management.

Correlation between synovial fluid calcium containing crystal estimation and varying grades of osteoarthritis created using a rabbit model: Potential diagnostic tool

ObjectivesAccurate diagnosis of osteoarthritis (OA) is the first important step in ensuring appropriate management of the disease. A multitude of tests involving assessment of biomarkers help in assessment of severity and grading of osteoarthritic damage. However, most tests are time consuming and are limited by the paucity in synovial fluid volume. In majority of OA effusions, calcium containing crystals are found. The aim of our study was to evaluate whether a correlation existed between the amount of calcium containing crystals present in synovial fluid and severity scoring of OA to propose a quick and inexpensive technique for disease assessment. Materials and methodsMonosodium-iodoacetate was used to induce high- and low-grade knee OA in adult New Zealand white rabbits (n = 6 joint each group). At 16 weeks, synovial fluid and joints were harvested for histopathological analysis. OA grading was established based on OARSI scoring. Synovial fluid calcium crystal count was assessed by light microscopy (Alizarin red) and confirmed by Fluo-4, AM imaging and polarized microscopy. Statistical analysis was performed using unpaired Student t-test and Pearson correlation. Results and conclusionThe clumps counted in low-grade OA were significantly lower than high-grade OA, in addition to showing a positive correlation (coefficient: 0.65; P=0.021) between calcium crystal count and the grade of OA created. Fluo-4, AM staining, and polarized microscopy were indicative of calcium pyrophosphate dihydrate crystals. This is the first study to suggest that Alizarin red could serve as an effective and rapid, bed-side method for screening and assessing disease progression.

Clinical manifestations of the patients with glenohumeral osteoarthritis who underwent shoulder arthroplasty ーa comparison with cuff tear arthropathy

Purpose: Mechanisms underlying development and progression of primary glenohumeral osteoarthritis (GHOA) have not been proven conclusively yet. As an anatomical factor, Critical Shoulder Angle (CSA) has been received attention and Bjarnison AO et al. recently reported that CSA < 30 degree was a significant risk factor for developing GHOA. Meanwhile, GHOA is possibly a part of generalized OA affected in multiple joints. The aim of this study was to investigate clinical manifestations of the patients with GHOA who underwent shoulder arthroplasty compared with cuff tear arthropathy (CTA) patients. Methods: In 40 consecutive cases who underwent shoulder arthroplasty (TSA/RSA/Hemiarthroplasty) in our hospital, patients with RA, humeral head necrosis, fracture, hemodialysis, and who underwent contralateral shoulder arthroplasty before were excluded, and remaining 27 cases (20 female), with a mean age of 78 years (64−86) were retrospectively analyzed. Patients were allocated to GHOA group (n=16) and CTA group (n=11) according to preoperative imaging studies. 1) Age, sex, 2) Bilateral CSA, 3) Serum CRP, 4) Detection of calcium pyrophosphate dihydrate (CPPD) crystals in ipsilateral synovial fluid, 5) Motion pain and radiological change in contralateral shoulder, and 6) History of TKA/THA, were assessed and compared between the groups. Mann-Whitney U test and Fisher’s exact test were used for statistical analyses and P<0.05 was considered significant. Results: 1) Age and sex were similar between the groups. 2) CSA was bilaterally smaller in GHOA (Figure 1) and patients with CSA < 30 degree was more frequent in GHOA (13/16) compared with CTA (3/11). 3) Serum CRP was similar between the groups. 4) Positive CPPD shoulder was more frequent in GHOA (10/16) compared with CTA (2/11). 5) Motion pain and radiological change in contralateral shoulder were more frequent in GHOA compared with CTA (Figure 2). 6) History of TKA/THA was more frequent in GHOA (11/16) compared with CTA (3/11). All patients in GHOA group had at least 1 factor in 2), 4), 5), 6). Mean number of these factors was significantly higher in GHOA (2.9) than in CTA (1.0). Conclusions: Both anatomical and systemic factors possibly associate with pathogenesis for developing end stage GHOA, which are completely different from CTA. CSA is an important anatomical factor as reported, however, severe GHOA possibly underlies generalized OA, and CPPD deposition disease would associate with the pathology. Although multicenter study including larger number of patients is warranted, our results would provide better understanding for GHOA development and progression. When clinicians undertake arthroplasty for severe GHOA, it should be careful for contralateral shoulder and other joints to achieve better clinical outcome after the surgery.View Large Image Figure ViewerDownload Hi-res image Download (PPT)