Calcium pyrophosphate crystal deposition (CPPD) is common and mainly associates with increasing age and osteoarthritis (OA). Recent studies suggest that CPPD occurs as the result of a generalized articular predisposition and may also associate with low cortical bone mineral density. The epidemiology of basic calcium phosphate (BCP) crystal deposition is poorly understood. Although periarticular BCP crystal deposits occurs at all ages and in both sexes, intra-articular BCP crystal deposition tends to associate with increasing age and OA. Calcium pyrophosphate and BCP crystals frequently coexist in joints with OA.
Key points
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Calcium pyrophosphate (CPP) and basic calcium phosphate (BCP) crystal deposition may be asymptomatic, or cause arthritis, commonly in the elderly.
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CPP deposition (CPPD) is common, and strongly associates with age and osteoarthritis (OA), although it does not seem to associate with OA progression.
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Hyperparathyroidism, hemochromatosis, hypomagnesemia, and hypophosphatasia are other recognized risk factors for CPPD.
Introduction
Calcium pyrophosphate (CPP) and basic calcium phosphate (BCP) crystal deposition may be asymptomatic, or cause arthritis, commonly in the elderly. Although CPP crystals predominantly deposit intra-articularly, abnormal BCP crystal deposition occurs in both intra-articular and periarticular locations. However, it is difficult to study their epidemiology because their presence is frequently asymptomatic. Any estimate of incidence and prevalence is further impaired by the fact that synovial fluid aspiration is required to definitively establish their presence. Moreover, BCP crystals are identified with confidence only by sophisticated techniques such as electron microscopy and x-ray diffraction, which are not available routinely. Thus, the epidemiologic studies of CPP and BCP crystal deposition use radiographic calcification as a surrogate. Within these limitations, the epidemiology of CPP deposition (CPPD) and BCP deposition are described in this review.
Epidemiology of CPPD
The first description of articular cartilage calcification is attributed to Robert Adams, a Dublin surgeon (c. 1854). Radiographic articular cartilage calcification (chondrocalcinosis [CC]) was first described in the late 1920s, and was identified as the cardinal manifestation of a distinct disease entity (chondrocalcinosis articularis) by Zitnan and Sitaj. In 1962, McCarty and colleagues identified CPP crystals in joints of patients with apparently acute gouty arthritis with or without coexistent CC. Subsequently, other calcium phosphate crystals (such as hydroxyapatite, brushite, and octacalcium phosphate) were shown in joints with CC, suggesting that CC is not exclusively caused by CPPD.
Over the last 50 years, the clinical classification of CPPD has evolved from a complex system based on phenotypic similarity with several other conditions (eg, pseudogout, pseudo-rheumatoid arthritis, pseudo-osteoarthritis), to a simple system that recognizes the key manifestations of CPPD ( Box 1 ). Of these manifestations, the epidemiology of CC, and osteoarthritis (OA) with CC have been relatively well studied. The epidemiology of acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis, and other pseudosyndromes associated with CPPD have not been examined formally.
Asymptomatic CPPD: CPPD with no apparent clinical consequence (ie, isolated CC)
OA with CPPD: CPPD in a joint that also shows changes of OA, on imaging or histologic examination
Acute CPP crystal arthritis: acute-onset, self-limiting synovitis with CPPD (previously pseudogout)
Chronic CPP crystal inflammatory arthritis: chronic inflammatory arthritis associated with CPPD
Joints affected by CPPD
CPPD occurs in the knees, wrists/symphysis pubis, and hips, in descending order of frequency. Studies are conflicting as to whether the wrist or the symphysis pubis is the second most commonly affected joint. Although previous studies reported that it is rare to have CC at other joints in the absence of knee involvement, a recent cross-sectional plain radiographic study suggested that up to 40% of participants with CC do not have knee involvement.
Incidence
The incidence of CPPD has not been studied in the general population. However, in middle-aged and older adults with knee OA without knee CC at baseline and followed up for 8 to 12 years, the estimated annual incidence of radiographic knee CC was 0.8% to 2.1%, and that of CPPD (CPP crystals or CC) at the knee was 2.7% to 5.5%.
Prevalence
The prevalence of CPPD has been studied in several community-based radiographic studies, using CC as a surrogate ( Table 1 ). The prevalence of CC depends on the joint radiographed and the age of the population. In the 3 studies of middle-aged and older people from Europe and the United States, the prevalence of CC was 7.0% to 8.1% if just knees were examined, 10.0% if knees, wrists, and hands were radiographed, and 10.4% if knees and hips were radiographed. In an Italian study involving community-dwelling adults older than 18 years, CPPD was the fourth most prevalent condition after OA, rheumatoid arthritis (RA), and gout, with a prevalence (95% confidence interval [CI]) of 0.42 (0.33–0.58)%. Studies restricted to older people, or hospital-based studies, report a higher prevalence of CPPD (≤34.0%).
| Study | Age Range (y) | Joints | CC Prevalence (%) |
|---|---|---|---|
| Salaffi et al, 2005 | 18–91 | Symptomatic joints | 0.42 |
| Neame et al, 2003 | 40–86 | Knee | 7.0 |
| Felson et al, 1989 | 63–93 | Knee | 8.1 |
| Ramonda et al, 2009 | >65 | Knee, pelvis | 10.4 |
| Sanmarti et al, 1993 | 60–88 | Wrist, hand, knee | 10.0 |
| Bergstrom et al, 1986 | 70–79 | Wrist, hand, knee | 11.5 |
| Bergstrom et al, 1986 | 79 | Wrist, hand, knee | 16.0 |
| Zhang et al, 2006 | >60 | Wrist | 0.7 |
| Zhang et al, 2006 | >60 | Knee | 1.79 a , 2.67 b |
| Al-Arfaj & Al-Boukai, 2002 | 50–93 | Wrist, hand, knee | 3.9 c |
CPPD has been reported in people from all ethnic backgrounds. However, CPPD seems to be more common in whites than in Asians. For example, the prevalence of CC is lower in Beijing, China than in Framingham, MA. A suggested environmental cause for this difference is the 15-fold higher concentration of calcium in the tap water in Beijing, which can suppress parathyroid hormone secretion.
As expected, the incidence and prevalence of CPPD depends on the method used for its identification. Standard plain radiographs underestimate the prevalence of CPPD. For example, 17% patients without radiographic knee CC had CPP crystals at the time of total knee replacement for OA. Other studies also suggest that between one-quarter and half of OA knees with CPP crystals do not have radiographic CC. However, because it is not feasible to perform arthrocentesis in population studies, it is likely that epidemiologic studies using ultrasonography (which is more sensitive for detection of CC) would better define the epidemiology of CPPD.
CPPD: a systemic predisposition or a local abnormality?
A recent study suggests that common sporadic CPPD also results from a generalized predisposition. In a cross-sectional radiographic study, joints with CC clustered together more often than would be expected by chance alone. This clustering was present in patients with and without OA. In addition, CC at 1 joint associated with CC at distant joints, and bilateral CC at 1 joint area associated with CC at distant joints compared with unilateral CC. These associations were independent of age, sex, body mass index (BMI), and OA at the distant joint. This finding further supports the view that CC at least in part results from a systemic predisposition. Although polyarticular CC is well recognized, this was the first systematic study confirming systemic predisposition to CC. A smaller ultrasonographic study also suggested that most patients with CPPD have oligoarticular or polyarticular rather than monoarticular CC.
Risk factors
There are several established risk factors for CPPD ( Box 2 ).
Increasing age
OA
Meniscectomy and joint injury
Metabolic diseases: hyperparathyroidism, hemochromatosis a , hypomagnesemia, hypophosphatasia, chronic kidney disease stage 5 b
Hereditary: mutations in ANKH , part of severe dysplastic OA phenotype
a Associates with structural arthropathy.
b Risk factor for acute CPP crystal arthritis.
Age
The prevalence of CPPD increases with age. In a community-based study in Nottinghamshire, United Kingdom, the prevalence of knee CC increased from 3.7% at age 55 to 59 years to 17.5% at age 80 to 84 years ( Fig. 1 ). Similarly, in the Framingham study, there was more than a doubling in the prevalence of knee CC with each 10-year increase in age after the age of 60 years (relative risk [RR] [95% CI] 2.40 [1.97–2.91]). Similarly, in Swedish studies, the prevalence of knee CC at age 70, 75, and 79 years was 6.8%, 8.0%, and 12.3%, respectively; whereas that of CC at knee, wrist, or hand was 7.5%, 10.1%, and 16.0%, respectively.
Sex
Large community-based studies suggest that sex does not predispose to CPPD. However, some smaller community-based studies and 1 large study from China have reported a higher prevalence of CC in women. A recent meta-analysis suggested that sex does not predispose to CPPD (odds ratio [OR] [95% CI] 0.89 [0.58–1.38]).
Heredity
Rarely, CPPD is inherited as a monogenic autosomal-dominant characteristic, and most instances of such hereditary CPPD have been attributed to mutations in the ANKH gene. Familial CPPD can also occur as part of a severe dysplastic OA phenotype associated with mutations in procollagen type 2 and CCAL1 genes. Although small hospital-based cross-sectional studies suggest that up to a quarter of CPPD cases are inherited, there seems to be either no or only a small contribution of genetic predisposition to prevalent sporadic CPPD. For example, the prevalence of CC in 122 siblings of index cases with knee CC and OA awaiting total joint replacement was similar to that of 1727 community-dwelling adults after adjusting for age, sex, BMI, and OA (adjusted OR [aOR] [95% CI] 1.16 [0.58–2.29]). Similarly, only 1 case of familial CPPD and premature OA was identified (E490del mutation in ANKH ) in a study of 95 UK whites with apparently sporadic CC. However, the genetic contribution to sporadic CPPD is supported by a UK-based case-control study, which reported that the -4 bp G to A single nucleotide polymorphism (SNP) in the 5′-UTR of ANKH associates with CPPD (OR [95% CI] for CPPD in homozygous state = 6.00 [2.2–16.5]). SNPs in plasma cell glycoprotein 1 and tissue nonspecific alkaline phosphatase do not seem to associate with sporadic CPPD.
OA
OA associates with CPPD. This finding is independent of age. Although OA associates with CPPD at knees, wrists, scaphotrapezoid joint, and metacarpophalangeal joints (MCPJs), recent studies suggest that hip OA does not associate with CPPD. In a large case-control study, knee OA associated with CC at wrists, hips, and knees, whereas hip OA did not associate with CC at any joint.
The prevalence of CPPD at an index joint depends on the severity of OA. For example, the prevalence of knee CC + OA in community-dwelling adults is 3.4%, whereas in clinic-based studies of knee OA, the prevalence of knee CPPD varies between 8% and 33%, increasing to 30% to 53% in end-stage knee OA.
Although small hospital-based case series and case-control studies have suggested that CPPD associates with a rapidly progressive destructive form of OA, larger prospective community-based studies have shown that at least at the knee, CC either protects against or does not associate with knee OA progression. The adjusted RR (aRR) (95% CI) for progression of knee OA was 0.4 (0.2–0.7) in the Boston OA Knee Study and 0.9 (0.6–1.5) in the Health ABC Study. Another study did not find any evidence for an association between CC and progression of knee OA. In addition, knee CC does not associate with incident knee OA (aRR [95% CI] 1.20 [0.50–2.70]), suggesting that CC is at least in part a consequence, and not a cause, of OA. The key facts concerning the association between OA and CPPD are summarized in Box 3 .
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Association between OA and CC is independent of age
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OA associates with CC except at the hip
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Prevalence of CC increases with severity of OA
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Presence of CC does not seem to associate with OA progression
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CC does not associate with incident OA
Other musculoskeletal conditions
Hospital-based case-control studies have suggested that CC associates with gout but not with hyperuricemia. This finding suggests that the association between CC and gout may be mediated by a generalized predisposition to crystal formation, or by epitaxy (the formation of 1 crystal type on another). Current evidence suggests that there is either a negative or no association between CPPD and RA. However, defleshed skeletal studies have suggested a possible association between CPPD and both RA and spondyloarthropathy. A retrospective hospital-based case series also reported a high (25.8%) prevalence of CPP crystals in RA synovial fluid aspirates. However, this study lacked a control group, and the high prevalence of CPP crystal may be caused by older age (mean age: 64.5 years), and long disease duration (mean: 12 years), which may result in secondary OA. A recent meta-analysis of published studies supported a strong negative association between RA and CPPD (pooled OR [95% CI] 0.18 [0.08–0.41]). There is no association between Paget disease and CC.
Meniscectomy/Joint injury
Meniscectomy is a risk factor for knee CC. In an early study of people who had undergone unilateral meniscectomy more than 25 years before, knee CC was 5-fold more likely in the operated knee than in the contralateral unoperated knee. Similarly, some case reports have suggested that recurrent joint injury caused by joint hypermobility can also result in CPPD.
Knee alignment
In a cross-sectional study of UK adults, self-reported constitutional varus knee alignment in the third decade (20s) associated with subsequent knee CC (aOR [95% CI] 1.77 [1.05, 2.98]). This finding was independent of age, sex, BMI in the 20s, and knee OA. However, current knee malalignment did not associate with knee CC, supporting a causal association between early life knee malalignment and CC.
Metabolic diseases
Several metabolic diseases are reported to associate with CC. Although the association between diabetes and CC may be confounded by age, other reported associations between rare diseases such as Wilson disease and ochronosis are based on case reports of florid CC in young patients. One case-control study reported no association between hypothyroidism and CC. Hemochromatosis, hyperparathyroidism, hypomagnesemia, and hypophosphatasia are recognised risk factors for CC, and these should be screened for specifically in young (<55 years) patients, especially those with polyarticular CPPD.
Hemochromatosis
The association between hemochromatosis and CPPD was first reported by Schumacher. Subsequent hospital-based case series reported that structural arthropathy with CC was present at the knees, wrists, hips, pubic symphysis, or MCPJs in 12 of 32 cases with hemochromatosis. CC was present in 1 in 3 patients with hemochromatosis in a recent large hospital-based study. As with sporadic CPPD, knees and wrists were the commonest sites of CC in those with hemochromatosis. Large population-based studies have not identified any association between C282Y homozygosity and CPPD. However, homozygosity for H63D, which carries a smaller risk of iron overload, has been associated with knee and hip CC in those younger than 65 years (OR [95% CI] 4.7 [1.2–18.5]). This situation may be caused by variable penetrance of HFE mutations, channeling bias, or the possibility that factors unrelated to iron overload predispose to CPPD in hemochromatosis.
Hyperparathyroidism
The association between CC and hyperparathyroidism is supported by several studies. One age-matched and sex-matched case-control study found CC to be 9 times more likely in those with hyperparathyroidism than in those without (30.7% vs 3.4%). Furthermore, hyperparathyroid patients with CC tend to be younger than those with CC in the absence of hyperparathyroidism; however, as expected, the association between CC and hyperparathyroidism is not independent of age, because hyperparathyroid patients with CC are older than hyperparathyroid patients without CC. A meta-analysis of published literature carried out by a European League Against Rheumatism (EULAR) task force in 2011 confirmed a strong association between hyperparathyroidism and CPPD (pooled OR [95% CI] 3.03 [1.15–8.02]).
A recent case-control study found an association between low metacarpal index (a measure of cortical bone mineral density) and CC (aOR [95% CI] 1.41 [1.06–1.89]), and this was independent of age, sex, BMI, OA, and vascular and soft tissue calcification. There was no association between calcaneal bone mineral density measured using dual-energy X-ray absorptiometry and CC (aOR [95% CI] 1.15 [0.76–1.73]). The differential association between metacarpal index, calcaneal bone mineral density, and CC raises the possibility that this may be mediated by subclinical hyperparathyroidism.
Hypomagnesemia
A case of postparathyroidectomy acute CPP crystal synovitis with acute hypomagnesemia was first described in 1966. Subsequently, several cases of CC were described in patients with idiopathic hypomagnesemia and hypomagnesemia caused by renal loss. CPPD was identified as a manifestation of the Gitelman variant of Bartter syndrome. Hypomagnesemia caused by gastrointestinal loss also leads to CPPD. In a cross-sectional study, prevalence of CC was investigated in patients with intestinal failure, and age-matched and sex-matched controls. The prevalence of CC was higher in patients with intestinal failure (OR [95% CI] 7.0 [1.45–66.1]) and was significantly higher in patients with lower serum magnesium levels (OR [95% CI] 13.5 [2.76–127.3]).
The reported association between diuretic use and knee CC has been hypothesized to be mediated by diuretic-induced hypomagnesemia. Although severe hypomagnesemia associates with CC, it is unclear if there is a role of mild hypomagnesemia in the pathogenesis of CPPD, because serum magnesium levels are similar in people with apparently sporadic CPPD and matched controls.
Hypophosphatasia
The association between hypophosphatasia and CC is based on several case reports of florid polyarticular CC at a young age. However, low alkaline phosphatase levels do not seem to play a role in the occurrence of sporadic CPPD, because there is no difference in serum alkaline phosphatase levels in those with and without CPPD in the absence of a history of hypophosphatasia. Although some laboratory-based studies have reported low synovial fluid alkaline phosphatase levels in joints with CPP crystals, others have reported no difference in synovial fluid alkaline phosphatase levels in those with and without CPPD. Although gross hypophosphatasia associates with CPPD, these studies do not support a role of low alkaline phosphatase activity in the cause of CPPD at a population level.
Risk factors for acute CPP crystal arthritis
A recent population-based age-matched and sex-matched case-control study using data from the THIN (The Health Improvement Network) database reported that hyperparathyroidism (aOR [95% CI] 4.87 [2.10, 11.3]), OA (aOR [95% CI] 2.91 [2.48, 3.43]), and loop diuretic use (aOR [95% CI] 1.35 [1.09, 1.67]) were independent associations for acute CPP crystal arthritis. Patients with stage 5 chronic kidney disease were also more likely to have acute CPP crystal arthritis (aOR [95% CI] 2.29 [1.30–4.01]). As with gout, it is possible that risk factors for crystal deposition may differ from those that predispose to acute crystal-induced synovitis, which is generally considered to be caused by crystal shedding from preformed deposits within cartilage.
Epidemiology of BCP Crystal Deposition
BCP crystals are the umbrella term for several BCP crystals including carbonate-substituted hydroxyapatite, octacalcium and tricalcium phosphates, and whitlockite. Of these crystals, hydroxyapatite is the most abundant in man. The current understanding of calcium crystal deposition suggests that Robert Adams’ first pathologic description of joint calcification could have been at least in part caused by BCP crystal deposition. Subsequently, calcific periarthritis of the shoulder and radiographic periarticular shoulder calcification were identified in 1870 and 1907, respectively. In 1966, McCarty and Gatter identified hydroxyapatite crystals in such calcific material, and in 1976, Dieppe and colleagues identified BCP crystals in synovial fluid from OA knees. Soon after this, McCarty and colleagues and Halverson and colleagues identified apatite-associated destructive arthropathy (AADA) or Milwaukee shoulder as a distinct clinical entity. A formal classification of articular and periarticular syndromes associated with BCP crystal deposition has never been devised. A simple clinical classification system similar to that proposed by the EULAR task force for CPPD is presented in Box 4 .
Asymptomatic BCP crystal deposition: BCP crystal deposits with no apparent clinical consequences
OA with BCP crystal deposition: BCP deposition in a joint that also shows changes of OA on imaging or histologic examination
Acute BCP crystal periarthritis: acute-onset, self-limiting synovitis with CPPD
Apatite-associated destructive arthropathy: destructive arthropathy associated with BCP crystals
The epidemiology of BCP crystal deposition is less well understood, and there are scant data, particularly on BCP crystal-associated arthropathy. Calcific periarthritis occurs in all age groups and in both sexes. Hospital-based case series have suggested that it is more common in women, and occurs at all ages, including childhood. Pseudopodagra caused by calcific periarthritis seems to be especially common in women. The best epidemiologic data on calcific periarthritis comes from a US study of more than 12,000 shoulder radiographs undertaken as part of an insurance medical assessment. This study showed a crude adult prevalence of calcific periarticular deposits at the shoulder of 3%. Most calcifications were asymptomatic, with just more than one-third of these having shoulder symptoms. Calcifications were more common in women, and unlike other crystal deposition (urate, CPPD), the prevalence was highest in those younger than 40 years. Calcific shoulder periarthritis is 3-fold more common in people with type II diabetes mellitus than in age-matched and sex-matched controls. Calcific shoulder periarthritis associates with long-standing and poorly controlled diabetes, hyperlipidemia, minor trauma, and hypomagnesemia. A hospital-based case-control study suggested that diabetics with shoulder calcification were more likely to have renal and retinal complications of diabetes. Periarticular calcification is also common in connective tissue diseases and may result in acute calcific periarthritis.
In contrast to calcific periarthritis, AADA seems to be more common in elderly women. AADA seems to target the shoulders, knees, hips, elbows, and ankles. In a comprehensive review using data from more than 72 patients with Milwaukee shoulder syndrome, the mean (range) age of patients was 72 (50–90) years, and there was a 4:1 female preponderance. The dominant shoulder was more commonly affected and usually had more severe disease. Trauma/overuse, neurologic involvement, dialysis, and CPPD were the identifiable risk factors, whereas no risk factors were apparent in a large proportion of patients. Patients with knee arthropathy along with Milwaukee shoulder syndrome were more likely to have valgus than varus knees. Further studies are required to better identify and define the subset of patients with AADA at other joints, and then to study its epidemiology.
The prevalence of intra-articular BCP crystal deposition in OA joints has been relatively well studied. In 2 recent studies, BCP crystals were present in all end-stage OA joints, suggesting that BCP crystal deposition is integral to the process of end-stage OA. BCP crystals frequently coexist with CPP crystals in OA joints. In hospital-based studies of symptomatic knee OA, BCP crystals (or alizarin red positivity) coexists with CPP crystals in 16% to 40% of cases. Just as for CPPD, BCP crystals become more prevalent with increasing severity of OA. In a prospective study involving sequential analysis of knee OA synovial fluids, BCP crystals developed as the disease progressed. For example, BCP crystals were identified in less than a quarter of patients at first aspiration but were present in more than half of patients at final aspiration (mean interval 3.6 years). However, large prospective studies are required to identify the epidemiology of BCP crystal deposition diseases, and to confirm if BCP crystals result in progression of OA.
CPP and BCP crystal deposition diseases are common. Research over the last 50 years has helped understand the prevalence and disease associations of CPPD. This research has translated into routine clinical practice. For example, polyarticular CPPD, especially in those younger than 50 years, triggers screening to identify metabolic diseases and familial predisposition. On the contrary, CPPD in the context of severe OA at the index joint, or in commonly affected joints in the elderly, should not result in detailed metabolic screening. However, the epidemiology of clinical manifestations of CPPD like chronic CPP crystal inflammatory arthritis, acute CPP crystal arthritis, and that of clinical syndromes associated with BCP crystal deposition is poorly understood. Further research using noninvasive imaging modalities like ultrasonography, which is able to identify both intra-articular and periarticular calcium deposits with greater sensitivity than plain radiographs, may be able to better define the epidemiology of chronic CPP crystal inflammatory arthritis or clinical features associated with BCP crystal deposition.
Introduction
Calcium pyrophosphate (CPP) and basic calcium phosphate (BCP) crystal deposition may be asymptomatic, or cause arthritis, commonly in the elderly. Although CPP crystals predominantly deposit intra-articularly, abnormal BCP crystal deposition occurs in both intra-articular and periarticular locations. However, it is difficult to study their epidemiology because their presence is frequently asymptomatic. Any estimate of incidence and prevalence is further impaired by the fact that synovial fluid aspiration is required to definitively establish their presence. Moreover, BCP crystals are identified with confidence only by sophisticated techniques such as electron microscopy and x-ray diffraction, which are not available routinely. Thus, the epidemiologic studies of CPP and BCP crystal deposition use radiographic calcification as a surrogate. Within these limitations, the epidemiology of CPP deposition (CPPD) and BCP deposition are described in this review.
Epidemiology of CPPD
The first description of articular cartilage calcification is attributed to Robert Adams, a Dublin surgeon (c. 1854). Radiographic articular cartilage calcification (chondrocalcinosis [CC]) was first described in the late 1920s, and was identified as the cardinal manifestation of a distinct disease entity (chondrocalcinosis articularis) by Zitnan and Sitaj. In 1962, McCarty and colleagues identified CPP crystals in joints of patients with apparently acute gouty arthritis with or without coexistent CC. Subsequently, other calcium phosphate crystals (such as hydroxyapatite, brushite, and octacalcium phosphate) were shown in joints with CC, suggesting that CC is not exclusively caused by CPPD.
Over the last 50 years, the clinical classification of CPPD has evolved from a complex system based on phenotypic similarity with several other conditions (eg, pseudogout, pseudo-rheumatoid arthritis, pseudo-osteoarthritis), to a simple system that recognizes the key manifestations of CPPD ( Box 1 ). Of these manifestations, the epidemiology of CC, and osteoarthritis (OA) with CC have been relatively well studied. The epidemiology of acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis, and other pseudosyndromes associated with CPPD have not been examined formally.
Related posts:
Gout and Crystal Arthropathies
Diagnosis and Clinical Manifestations of Calcium Pyrophosphate and Basic Calcium Phosphate Crystal Deposition Diseases
Comorbidities in Patients with Crystal Diseases and Hyperuricemia
Nonpharmacologic and Pharmacologic Management of CPP Crystal Arthritis and BCP Arthropathy and Periarticular Syndromes
Long-Term Management of Gout
Emerging Therapies for Gout
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