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BACKGROUND: To summarize clinical presentations, baseline characteristics, diagnosis, treatment, and treatment outcomes through a systematic review of cases of crystal-induced arthritis in prosthetic joints in the literature. METHODS: A systematic review of case reports and case series was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A literature search was performed through PubMed/MEDLINE, Google Scholar, Embase, Cumulative Index to Nursing & Allied Health, and Web of Science. We identified case reports/case series in English of adult patients presenting with crystal-induced arthritis (gout, calcium pyrophosphate deposition disease) in prosthetic joints. Articles that met the inclusion criteria were utilized for qualitative data synthesis. RESULTS: We found 44 cases of crystal-induced arthritis in prosthetic joints from 1984 to 2021. Crystal-induced arthritis in periprosthetic joints most frequently affects patients who had knee arthroplasty and most often presents as monoarticular arthritis that is usually acute in onset. However, several cases in the literature involved patients who had bilateral knee replacements and presented with a concurrent flare of gout or calcium pyrophosphate deposition disease in bilateral knees. Patients with crystal-induced arthritis in prosthetic joints show elevated white blood cell counts with neutrophil predominance and respond favorably to anti-inflammatory treatments, usually within one week. In many cases, crystal-induced arthritis was challenging to differentiate from prosthetic joint infection, with approximately one-third of patients undergoing surgical intervention and 35% receiving antibiotic treatment. CONCLUSION: Crystal-induced arthritis in prosthetic joints can mimic prosthetic joint infections and should always be considered in the differential diagnoses of joint pain in prosthetic joints. We present the first systematic review of crystal-induced arthritis in prosthetic joints to increase awareness of the diagnosis and proper management.

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OBJECTIVE: To investigate the occurrence of meniscal calcifications in individuals with and without knee osteoarthritis (OA). Additionally, we aim to identify the specific types of calcifications: basic calcium phosphate (BCP) and calcium pyrophosphate dihydrate (CPP). METHOD: We analyzed 82 meniscal posterior horn samples (medial and lateral) collected from 41 human subjects. Among them, 20 individuals underwent total knee replacement due to medial compartment OA, while 21 deceased donors had no known knee OA. The assessment of meniscal calcifications and Pauli's histopathological scoring was conducted using histological sections. Furthermore, adjacent sections underwent measurement using Raman spectroscopy to characterize BCP and CPP calcifications based on their distinct spectral fingerprints. RESULTS: All OA individuals exhibited calcifications in at least one meniscus, compared to 9.5% (95%CI 1%, 30%) of donors. Among 35 OA menisci with calcifications, 28(80%) had BCP, 5(14%) had CPP and 2(6%) had both types. In 4 donor menisci, 3(75%) had CPP while 1(25%) had both types. We estimated the association between Pauli score and presence of BCP in OA individuals, yielding an odds ratio of 2.1 (95%CI 0.8, 5.3) per 1 Pauli score. The association between Pauli score and presence of CPP (in whole study sample) seemed weaker, with odds ratio of 1.3 (95%CI 1.1, 1.7). CONCLUSION: The presence of BCP was predominant in menisci of OA individuals, whereas CPP exhibited similar prevalence in individuals with and without OA. The formation of BCP crystals in menisci may represent an important and specific characteristic of OA disease process that warrants further attention.

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PURPOSE OF THE REVIEW: This review provides an overview of medical conditions and risk factors associated with CPPD. RECENT FINDINGS: Recent studies have indicated that CPPD patients may have a higher risk for systemic conditions such as cardiovascular diseases. Calcium pyrophosphate deposition disease (CPPD) is a common crystal arthropathy that primarily affects older adults, and, in most cases, the aetiology is idiopathic. Age is the most remarkable risk factor and due to the aging population, the prevalence of this condition is expected to increase. Strong evidence supports an association between CPPD and several metabolic and endocrine conditions, including hemochromatosis, hyperparathyroidism, hypomagnesemia, and hypophosphatasia. Additionally, there is growing evidence of an increased risk for cardiovascular diseases among CPPD patients, alongside potential links to rheumatic disorders, gender, medications, and joint trauma. Further research is needed to explore the underlying mechanisms linking CPPD to associated conditions and to develop targeted therapies with the aim of improving patient outcomes.

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Dual-energy computed tomography (DECT) has emerged as a transformative tool in the past decade. Initially employed in gout within the field of rheumatology to distinguish and quantify monosodium urate crystals through its dual-material discrimination capability, DECT has since broadened its clinical applications. It now encompasses various rheumatic diseases, employing advanced techniques such as bone marrow edema assessment, iodine mapping, and collagen-specific imaging. This review article aims to examine the unique characteristics of DECT, discuss its strengths and limitations, illustrate its applications for accurately evaluating various rheumatic diseases in clinical practice, and propose future directions for DECT in rheumatology.

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The frequency and risk factors for the development of diastolic dysfunction (DD) in patients with CPPD and OA have not been studied. The objective of this study was to determine the frequency and identify risk factors (RF) for the development of DD of the left and right ventricles (LV and RV) in patients with calcium pyrophosphate crystal deposition disease (CPPD) and osteoarthritis (OA). The study included 26 patients with CPPD and with knee OA 18-65 years old, matched in age and gender, without cardiovascular disease (CVD), type 2 diabetes mellitus (DM2), and rheumatic diseases. Conventional risk factors (TRF) of CVD were assessed, and echocardiography was performed. The frequency of DD in patients with CPPD and OA was quite high and almost did not differ in both groups: it was detected in 19 patients, of which 11 (42%) had CPPD and 8 (31%) had OA (p = 0.39). Type 1 LV DD was detected in 10 (39%) patients with CPPD and in 8 (31%) with OA (p = 0.11); type 1RV DD was detected in 8 (31%) patients with CPPD and in 7 (27%) patients with OA (p = 0.17); and type 1 LV DD and RV DD was detected in 7 (27%) patients with both CPPD and with OA. DD types 2 and 3 were not detected in both groups. There were no differences in both groups in CV risk factors, except for the level of CRP (it was higher in CPPD) (p = 0.03). In the CPPD group, mean values of LV E/E' (p = 0.02), LVDT (p = 0.03), LVMI (p = 0.04) were significantly higher than in patients with OA. On the contrary, in patients with OA, indices EDV (p = 0.004) and TVC (p = 0.02) were higher. There were direct correlations between diastolic function indices and the following factors in CPPD: LVL, PWLV and PTH level (r = 0.7, p <0.005), LV E' and PTH level (r = 0.7, p < 0.005). Inverse correlations were found between the level of PTH and IS (r = -0.5, p < 0.005), LVMI (r = -0.5, p < 0.005), and the level of vitamin D and VDDT (r = -0.6, p < 0.005). Direct correlations in OA were found between the level of CRP and PVAdiast (r = 0.6, p < 0.005), and the level of sUA (r = 0.7, p < 0.005), and the level of vitamin D and E/E'LV (r = 0.6, p < 0.005). A high prevalence of LV and RV DD was found in patients with CPPD and OA. The presence of DD in CPPD was associated with lower vitamin D levels, and in OA with a higher level of sUA and a lower level of PTH.

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Calcium pyrophosphate deposition disease is categorized into radiographic chondrocalcinosis, acute calcium pyrophosphate arthritis, chronic calcium pyrophosphate arthritis, and osteoarthritis with calcium pyrophosphate deposition. These entities collectively are characterized by the deposition of calcium into joints, which then may cause localized and systemic inflammation, resulting in pain and swelling in the affected joints. Patients with the ANKH gene are more susceptible to the development of CPP arthritis as are those with primary hyperparathyroidism, hypomagnesemia, and hemochromatosis. Radiographic chondrocalcinosis is asymptomatic. Acute calcium pyrophosphate arthritis results in self-limited periods of joint pain and swelling in the affected joint. Along with localized inflammation, there may also be systemic inflammation characterized by fever and elevated inflammatory markers. Chronic calcium pyrophosphate arthritis results in periods of quiescence interrupted by flares that are identical to acute periods of disease. Osteoarthritis associated calcium pyrophosphate arthritis presents with chronic pain well described in osteoarthritis with periods of acute flares. In 2023, a joint effort by the American College of Rheumatology and the European League Against Rheumatism developed guidelines meant to aid in the recognition of calcium pyrophosphate deposition diseases. The diagnosis is made if there is proof of either crowned dens syndrome or synovial fluid analysis demonstrating calcium pyrophosphate crystals or when more than 56 points are summed utilizing the criteria described in the guidelines. Radiographic chondrocalcinosis requires no therapy. Acute calcium pyrophosphate arthritis is treated with the goal of aborting the flare. Treatment options include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, oral corticosteroids, parenteral corticosteroids, intraarticular corticosteroids, IL-1 inhibitors, or parenteral adrenocorticotropic hormone (ACTH). The goal in treatment for chronic calcium pyrophosphate arthritis is the suppression of acute flares. The drugs used for acute flare treatment may be given as maintenance therapy with the additional options of methotrexate and hydroxychloroquine.

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The deposition of calcium pyrophosphate (CPP) crystals in joint tissues causes acute and chronic arthritis that commonly affect the adult and elderly population. Experimental calcium pyrophosphate deposition disease (CPPD) models are divided into genetically modified models and crystal-induced inflammation models. The former do not reproduce phenotypes overlapping with the human disease, while in the latter, the direct injection of crystals into the ankles, dorsal air pouch or peritoneum constitutes a useful and reliable methodology that resembles the CPP induced-inflammatory condition in humans. The translational importance of the induced model is also strengthened by the fact that the key molecular and cellular mediators involved in inflammation are shared between humans and laboratory rodents. Although, in vivo models are indispensable tools for studying the pathogenesis of the CPPD and testing new therapies, their development is still at an early stage and major efforts are needed to address this issue. Here, we analyze the strenghts and limitations of each currently available CPPD in vivo model, and critically discuss their translational value.

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OBJECTIVE: Recent studies have shown that CPPD might be associated with a higher risk of cardiovascular events related to inflammation. Thus, we aim to examine the outcomes of patients admitted for acute coronary syndrome (ACS) with and without CPPD. METHODS: We used data from the US National Inpatient Sample (NIS) Database to identify patients who were admitted for ACS between 2006 and 2019. The ICD-9 and -10 codes were used to determine the patients with ACS related hospitalizations and of those, we classified two groups of patients: those with and those without any CPPD code. Data collection included demographics and comorbidities. Outcomes were in-hospital mortality, length of stay, hospital charges, and in-hospital complications. Associations between CPPD and specific morbidity were evaluated with chi-square tests. T-tests were used for continuous variables. We have also presented odds ratio (OR) along with 95 % confidence intervals (CI) for the outcomes of interest. RESULTS: A total of 17,322,362 patients were admitted for ACS. Among them, 7,458 had CPPD, with a mean age of 75 years and 48 % were females. CPPD patients were more likely to be older (75 vs 68 years; p < 0.001) compared to non-CPPD patients. Among the comorbidities, chronic kidney disease was more frequently observed in CPPD patients. Regarding the inpatient complications, acute ischemic stroke and post-procedural hemorrhage were more frequently seen in CPPD patients. Interestingly, the in-hospital mortality was lower in the CPPD patients than the non-CPPD patients (OR: 0.77; CI 95 % 0.70-0.85). ACS in CPPD patients was associated with a longer mean length of stay than those without CPPD (OR: 3.35; 95 % CI 3.17-3.53). In addition, mean total charges were higher in the CPPD group (OR: 1.04; 95 % CI 1.01-1.10). CONCLUSION: ACS in CPPD patients is associated with higher healthcare utilization, including cost and length of hospital stay, and lower in-hospital mortality than non-CPPD patients.

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Immune checkpoint inhibitors (ICIs) sometimes induce immune-related adverse events (irAEs), and arthritis is one of the irAE symptoms. Recently, crystal-induced arthritis, such as calcium pyrophosphate (CPP) crystal deposition disease and gout, has been reported to occur after ICI administration. However, the distinction between ICI-associated crystal arthritis and ICI-induced non-crystal arthritis is difficult because their symptoms are similar. Besides, optimal treatment for ICI-associated crystal arthritis has not been established. Here, we report a patient who developed CPP crystal arthritis twice after pembrolizumab (ICI) administration and was successfully treated with intra-articular glucocorticoid injection. He suffered arthritis and acute interstitial nephritis simultaneously after ICI administration. Musculoskeletal ultrasound of his affected joint suggests that his arthritis was crystal-induced arthritis, and arthrocentesis detected CPP crystal in synovial fluid. Thus, we diagnosed his arthritis as ICI-associated cystal arthritis. Therefore, our case encourages the use of musculoskeletal ultrasound in patients with arthritis after treatment with ICI because it may distinguish between ICI-associated crystal arthritis and ICI-induced non-crystal arthritis. Besides, ICI-associated crystal arthritis could be treatable by intra-articular glucocorticoid injection.

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Calcium pyrophosphate deposition (CPPD) arthritis is the second most common type of crystal-induced arthritis after gout. Acute flares are commonly treated with non-steroidal anti-inflammatory drugs, intra-articular or short-term systemic glucocorticoids or colchicine. However, since there is no pharmacological treatment to reduce CPPD crystal burden, relapsing or chronic CPPD arthritis may be challenging to treat, particularly in patients with end-stage renal disease who are at risk for toxicity of the above medications. Since IL-1ß appears to be driving CPPD arthritis, we treated two patients with chronic CPPD arthritis and end-stage renal disease on haemodialysis with the IL-1ß receptor antagonist anakinra. In both patients, arthritis resolved quickly, while continuation of anakinra maintained remission and allowed complete glucocorticoid withdrawal. Therefore, anakinra may be a safe and effective option both for short and long-term treatment of CPPD arthritis in patients on chronic renal replacement therapy.

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OBJECTIVE: Ectopic articular calcification is a common phenomenon of osteoarthritic joints, and closely related to disease progression. Identification of the involved calcium crystal types represents an important topic in research and clinical practice. Difficulties in accurate detection and crystal type identification have led to inconsistent data on the prevalence and spatial distribution of Basic calcium phosphate (BCP) and calcium pyrophosphate (CPP) deposition. METHOD: Combining multiple imaging methods including conventional radiography, histology and Raman spectroscopy, this study provides a comprehensive analysis of BCP and CPP-based calcification, its frequency and distribution in cartilage and synovial membrane samples of 92 osteoarthritis patients undergoing knee replacement surgery. RESULTS: Conventional radiography showed calcifications in 35% of patients. Von Kossa staining detected calcified deposits in 88% and 57% of cartilage and synovial samples, respectively. BCP crystals presented as brittle deposits on top of the cartilage surface or embedded in synovial tissue. CPP deposits appeared as larger granular needle-shaped clusters or dense circular pockets below the cartilage surface or within synovial tissue. Spectroscopic analysis detected BCP crystals in 75% of cartilage and 43% of synovial samples. CPP deposition was only detected in 18% of cartilage and 15% of synovial samples, often coinciding with BCP deposits. CONCLUSION: BCP is the predominant crystal type in calcified cartilage and synovium while CPP deposition is rare, often coinciding with BCP. Distinct and qualitative information on BCP and CPP deposits in joint tissues gives rise to the speculation that different disease entities are involved that might need different treatment strategies.

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Background: Spinal epidural abscess (SEA) is a rare condition that may result in catastrophic outcomes. On the other hand, calcium pyrophosphate (CPP) deposition disease (CPPD) causes inflammatory arthritis. Spinal involvement of a crystal-induced inflammation caused by CPPD is also common. Surgery is a common risk factor for both SEA and CPPD; however, the postoperative acute onset of SEA complicated with CPPD is extremely rare. Case Description: A man in his 70s presented to our hospital, complaining of right upper limb weakness, loss of dexterity, and gait disturbance. The diagnosis of cervical spondylotic myelopathy was made, and he performed laminectomy at C3, C4, and C5 levels. Four days after the laminectomy, he suffered from acute neck pain, weakness, and hypoesthesia in his arms and legs. Magnetic resonance imaging revealed a mass occupying the dorsal epidural space of C6 and C7, compressing the cervical spinal cord. Considering the acute symptomatology, an acute spinal epidural hematoma after surgery was suspected; therefore, emergency C6 and C7 laminectomy was performed. Surgical findings indicated that the pressure inside the spinal canal was elevated, and the mass was purulent exudate. Pathological examination showed suppurative inflammation with concomitant deposition of CPP. SEA complicated with CPPD was considered; therefore, antibiotics and non-steroidal anti-inflammatory drugs were administered. The motor weakness and hypoesthesia were improved despite a slight residual deficit in his dexterity. Conclusion: An acute onset of SEA complicated with CPPD after cervical surgery has rarely been reported. The suppurative inflammation fostered by the crystal-induced inflammation may account for the acute symptomatology.

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CPPD disease can affect patients' quality of life through its various clinical presentations. This mini-review discusses the evolution of CPPD from its discovery to current knowledge of its pathogenesis, genetic associations, diagnostics, and treatment options. Despite extensive research, the exact mechanisms of CPPD are not well understood, and there is a notable lack of knowledge about psychosocial impacts and patient experiences. This study aims to present a CPPD Disease Timeline identifying gaps in current knowledge and potential directions for future research. These findings contribute to a broader understanding of CPPD disease and emphasize the importance of continued research and innovation in this field.

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Hypophosphatasia is a rare genetic disease characterized by abnormal alkaline phosphatase activity and deficiency of bone and teeth mineralization. Hypophosphatasia is well known in pediatrics with typical presentations in children, but mild forms can also be present in adults and are difficult to detect. We present the case of a 50-year-old woman referred for pain management, with a previous diagnosis of fibromyalgia. The association of clinical features (diffuse pain syndrome, early dental loosening, personal history of two fractures with osteoporosis, and family history of osteoporosis) with radiographic (heterotopic calcifications of the yellow and interspinous lumbar ligaments) and biological (low levels of total alkaline phosphatase) indices was suggestive of hypophosphatasia, which was confirmed by genetic analysis. We review and discuss the association between hypophosphatasia, musculoskeletal pain, and calcium pyrophosphate deposition and the importance of raising the diagnosis of adult-onset hypophosphatasia when facing these two rheumatologic entities.

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Calcium pyrophosphate deposition disease (CPPD), known as pseudogout, is characterized by the accumulation of calcium pyrophosphate crystals in musculoskeletal structures, primarily joints. While CPPD commonly affects various joints, involvement in the cervical spine leading to myelopathy is rare. Surgical intervention becomes necessary when conservative measures fail, but reports on full endoscopic surgeries are extremely rare. We present two successful cases where full endoscopic systems were used for CPPD removal in the cervical spine. The surgical technique involved a full endoscopic approach, adapting the previously reported technique for unilateral laminotomy bilateral decompression. Full-endoscopic removal of cervical CPPD inducing myelopathy were successfully removed with good clinical and radiologic outcomes. The scarcity of endoscopic cases for cervical ligamentum flavum CPPD is attributed to the condition's rarity. However, our successful cases advocate for endoscopic surgery as a potential primary treatment option for CPPD-induced cervical myelopathy, especially in elderly patients or those with previous cervical operation histories. This experience encourages the consideration of endoscopic surgery for managing cervical ligamentum flavum CPPD as a viable alternative.

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Calcium pyrophosphate deposition (CPPD) disease is a form of crystal-induced arthropathy that arises from the accumulation of calcium pyrophosphate crystals within joints and soft tissues. This process leads to inflammation and damage to the affected joints. It can present asymptomatically or as acute or chronic inflammatory arthritis. Risk factors and comorbidities, including prior joint injury, osteoarthritis, hereditary or familial predisposition, and metabolic diseases, should be evaluated in CPPD cases. The management of CPPD remains a challenge in the sparsity of randomized controlled trials. The lack of such trials makes it difficult to establish evidence-based treatment protocols for CPPD. This review provides an overview of the current pharmacological management of CPPD, focusing on reducing inflammation, alleviating symptoms, and preventing acute flares. Non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and colchicine are effective in managing acute CPP arthritis. Colchicine may also be used prophylactically to prevent recurrent flares. In cases where other treatments have failed, anakinra, an interleukin-1 receptor antagonist, can be administered to alleviate acute flares. The management of chronic CPP inflammatory arthritis includes NSAIDs and/or colchicine, followed by hydroxychloroquine, low-dose glucocorticoids, and methotrexate, with limited data on efficacy. Tocilizumab can be used in refractory cases. In small studies, synovial destruction using intra-articular injection of yttrium 90 can decrease pain. To date, no disease-modifying therapies exist that reduce articular calcification in CPPD.

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Odontoid osteomyelitis is a rare infectious disease that manifests as fever and posterior neck pain, while crowned dens syndrome is a relatively common inflammatory disorder with similar signs and symptoms. We describe the case of a 90-year-old woman presenting with fever, posterior neck pain, throat pain, and headache. Crowned dens syndrome was initially diagnosed based on the clinical picture and calcification around the odontoid process on cervical spine CT. However, the diagnosis was revised to odontoid osteomyelitis following the detection of Staphylococcus aureus in blood cultures that were performed due to the presence of headache. Infectious complications included spinal epidural abscess extending to the hypoglossal canal and osteomyelitis spreading to the clivus. Nonetheless, the patient achieved complete recovery after 13 weeks of antimicrobial therapy. No reports of odontoid osteomyelitis with calcification around the odontoid process have been reported. This case underscores the importance of avoiding a hasty diagnosis of crowned dens syndrome when calcification around the odontoid process is observed in patients presenting with fever and posterior neck pain. It is crucial to perform a thorough medical history review and physical examination to exclude other conditions. In cases where infection is suspected, blood cultures and cervical spine MRI are essential to investigate odontoid osteomyelitis and other complications.

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Calcified chondroid mesenchymal neoplasms (CCMN) represent a morphologic spectrum of related tumors. Historically, chondroid matrix or chondroblastoma-like features have been described in soft tissue chondroma, tenosynovial giant cell tumors (especially of the temporomandibular joint (TMJ) region), and in a subset of tophaceous pseudogout. Recently, these tumors have been found to share FN1-receptor tyrosine kinase (RTK) fusions. This review discusses the clinical, morphologic, immunohistochemical, and molecular genetic features of CCMN. The distinction from morphologic mimics is also discussed.

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Calcium pyrophosphate dihydrate (CPPD) deposition disease is an inflammatory arthritis induced by calcium pyrophosphate (CPP) crystals and clinically it is called pseudogout. It usually deposits in articular cartilage and in periarticular soft tissues. But no cases of pseudogout in the rotator cuff without cartilage deposition or destruction have been reported so far. We present a case of a 57-year-old woman who was diagnosed as pseudogout with rotator cuff tear.

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