Impacts of ‘understudied’ calcium pyrophosphate deposition remain unknown
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Among the many unanswered questions about calcium pyrophosphate deposition — formerly called “pseudogout” — perhaps the most important is whether it causes osteoarthritis, a speaker said at the Congress of Clinical Rheumatology East.
“I am hoping I can drum up some enthusiasm for what really has been an understudied disease, yet very common,” Sara K. Tedeschi, MD, MPH, co-director of the Fast Track Clinic for Giant Cell Arteritis at Brigham and Women’s Hospital, and assistant professor of medicine at Harvard Medical School, told attendees.
According to Tedeschi, CPPD is a “very common crystalline arthritis” that is caused by calcium crystals commonly found in the knee and wrist.
Risk factors include older age, previous joint trauma, family history of mutations in osteoprotegerin or the ANKH protein, hemochromatosis, hyperparathyroidism, hypophosphatasia, hypomagnesemia or Gitelman syndrome.
Approximately 8 million to 10 million U.S. adults experience this complication, with greater incidence among older adults, according to Tedeschi. Despite these figures, Tedeschi noted that CPPD is currently understudied compared with gout, which impacts about the same number of adults in the United States.
“In the past decade, there have been about 7,000 publications on gout and about 500 publications on CPPD,” Tedeschi said.
Regarding the nomenclature, the condition can be known as both calcium pyrophosphate deposition, or calcium pyrophosphate deposition disease, or calcium pyrophosphate dihydrate deposition, both of which are abbreviated as CPDD.
“This is really relevant to how we study this disease,” she said, suggesting that the inability to arrive at a consensus on a name or abbreviation contributes to the inability to study the condition.
With so few publications and unclear nomenclature, it follows that there remain so many unanswered questions. One such question pertains to the natural history of asymptomatic radiographic chondrocalcinosis, while others deal with risk factors. It is unknown why some patients have several CPPD manifestations in a lifetime, while others only have one. The long-term extra-articular consequences of CPPD are also unclear.
“A literal billion-dollar question is whether CPPD causes osteoarthritis,” Tedeschi said.
She noted that the two conditions are “so linked,” and that if researchers found a causative effect, it would be of great interest to the rheumatology in general.
That said, it is known that the calcium pyrophosphate crystals found in CPPD can induce cartilage damage, she added. In addition, there is speculation that subchondral bone remodeling in OA may lead to increased CPP crystal formation.
“The consensus is that, currently, it remains unclear whether these CPP crystals are the cause, or, potentially, the effect of osteoarthritis,” Tedeschi said.
The American College of Rheumatology and EULAR are currently working on a document for the condition, which Tedeschi believes could aid in everything from diagnosis to treatments.
“Classification criteria and core outcome domain sets will establish a framework for future CPPD clinical research,” she said.
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Tedeschi SK. CPPD: What have we learned and where are we going? Presented at: The Congress of Clinical Rheumatology East; May 12-15, 2022; Destin, Fla.
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