Chondrocalcinosis means “calcium in the cartilage.” In this condition, very tiny crystals made from a salt called calcium pyrophosphate build up inside the smooth cartilage that covers the ends of the bones in a joint. These crystals can make the cartilage and the lining of the joint become irritated and inflamed. When the joint is inflamed, it can become painful, swollen, warm, and stiff, in a way that looks very similar to gout or other types of arthritis. Doctors often use the name calcium pyrophosphate deposition (CPPD) disease for the whole illness, and use chondrocalcinosis for the visible calcium lines seen on X-ray pictures of the joint.
Over time, these calcium pyrophosphate crystals can damage the joint structure. They may speed up “wear-and-tear” arthritis, and in some people they can cause repeated attacks that come suddenly, with a very painful, hot, swollen joint that lasts for days or weeks. In other people, the crystals sit in the cartilage quietly with no pain and are only found by chance on an X-ray taken for another reason. Because the signs can copy other diseases, doctors must look carefully at symptoms, joint fluid, blood tests, and imaging to make sure the problem is really chondrocalcinosis / CPPD and not gout, osteoarthritis, or rheumatoid arthritis.
Other names
Doctors and books may use several names for the same basic problem, which can be confusing. Chondrocalcinosis is often used when talking about the X-ray picture of calcium lines in cartilage. Calcium pyrophosphate deposition (CPPD) disease is the broader medical name for the illness caused by these crystals. Pseudogout is a common name when the disease causes sudden, very painful attacks that look like gout but are caused by calcium pyrophosphate crystals instead of uric acid crystals. Other terms that may be used include pyrophosphate arthropathy and articular chondrocalcinosis. All of these names point to the same basic idea: calcium pyrophosphate crystals in and around joints that can cause arthritis.
Types of chondrocalcinosis
Doctors describe several main types or patterns of CPPD disease. One person can sometimes move from one pattern to another over time.
Asymptomatic chondrocalcinosis – In this type, X-rays or ultrasound show calcium lines or spots in the cartilage, but the person has no pain, swelling, or stiffness in that joint. The crystals are present but are not actively inflaming the joint. Many older adults have this “silent” form, discovered only when images are taken for another reason, such as after an injury.
Acute CPP crystal arthritis (pseudogout attacks) – This type causes sudden attacks of severe joint pain, swelling, warmth, and redness, often in the knee or wrist. The joint may become very tender, and the person can feel unwell, sometimes with a mild fever. These attacks develop over hours or a day, then improve over several days or weeks, like gout flares, but the crystals are calcium pyrophosphate, not uric acid.
Chronic CPP crystal inflammatory arthritis – In some people, instead of sharp attacks, the disease causes long-lasting joint pain and stiffness that can look like rheumatoid arthritis. More than one joint can be involved, often wrists, knuckles, or knees, and the symptoms may be present most days rather than only in short flares. This form can slowly damage joints if not treated.
Osteoarthritis with CPPD (“OA with chondrocalcinosis”) – Here, the person has typical wear-and-tear joint changes, but images also show calcium pyrophosphate crystals. The joint pain may be like usual osteoarthritis, but it can sometimes flare more suddenly or be more severe because of the extra irritation from crystals. Knees, hips, wrists, and shoulders are common sites.
Severe destructive or “pseudo-neuropathic” CPPD arthritis – Rarely, CPPD causes very aggressive joint damage, almost as if the person had a loss of normal joint feeling, like in some nerve diseases. The joint may become unstable, deformed, and difficult to use. This form is not common but is important to recognize because large joint replacement surgery may eventually be needed.
These patterns help doctors predict how the disease may behave and which tests and treatments may be most useful in each person.
Causes and risk factors
Chondrocalcinosis / CPPD does not have one single cause. Many different body and joint problems can raise the chance that calcium pyrophosphate crystals will form.
Older age – Age is the strongest risk factor. CPPD is much more common in people over about 60 years old. As cartilage ages, its structure and the way it handles minerals change, making it easier for crystals to form and stay trapped.
Inherited (familial) CPPD disease – Some families carry changes in certain genes, such as the ANKH gene, that affect how cartilage controls pyrophosphate levels. These changes can cause earlier and more severe crystal deposits, sometimes starting in middle age instead of late life.
Previous joint injury – A bad sprain, fracture that goes into the joint, or meniscus tear can damage cartilage. Damaged cartilage is less smooth and more likely to trap crystals. Joints that have been injured often show more chondrocalcinosis later in life.
Previous joint surgery – Operations such as meniscectomy (removal of part of the knee cartilage) or other joint procedures may change the joint’s structure and mechanics. This can speed up wear and encourage crystal deposits in the remaining cartilage.
Osteoarthritis (OA) – CPPD often lives in the same joints as osteoarthritis. It is not fully clear which comes first, but worn cartilage in OA seems more likely to calcify. OA and CPPD together can cause more pain and faster joint damage than either alone.
Rheumatoid arthritis (RA) – Some people with RA also develop CPPD. Long-lasting inflammation and joint damage in RA may change cartilage and bone, making the joint more friendly for CPP crystals. The two diseases together can be hard to tell apart and may make symptoms worse.
Co-existing gout – Gout and CPPD are different crystal diseases, but they can occur in the same person. High uric acid and urate crystals can damage cartilage and may share risk factors with CPP crystals, so a person with gout may also form calcium pyrophosphate deposits.
Primary hyperparathyroidism – In this hormone disorder, the parathyroid glands make too much parathyroid hormone (PTH), which changes calcium and phosphate balance in the blood and cartilage. This disturbed mineral control strongly increases the risk of early and widespread CPPD and chondrocalcinosis.
Hemochromatosis (iron overload) – In this condition, too much iron is stored in the body and organs. It can damage cartilage and change enzymes that handle pyrophosphate, leading to early crystal deposits and sometimes severe arthritis in middle age.
Hypomagnesemia (low magnesium) – Magnesium helps control crystal formation by affecting enzymes that break down pyrophosphate. Low magnesium in the blood, due to gut disease, kidney loss, certain medicines, or poor intake, makes CPP crystals more likely to form in cartilage.
Hypophosphatasia – This rare genetic disease involves low levels of an enzyme called alkaline phosphatase. Without enough of this enzyme, pyrophosphate builds up around bones and cartilage, encouraging calcium pyrophosphate crystal deposits.
Hypothyroidism (low thyroid hormone) – Underactive thyroid can change metabolism and body water balance. It has been linked to a higher chance of CPPD, although the exact reason is not fully understood. Treating thyroid disease may help reduce future risk.
Chronic kidney disease – Long-term kidney problems disturb the balance of calcium, phosphate, and other minerals. This can favor many types of abnormal calcification in the body, including chondrocalcinosis.
Acromegaly (excess growth hormone) – In this rare hormonal condition, abnormal growth hormone levels affect cartilage, bone, and mineral handling. People with acromegaly have an increased risk of CPPD and unusual joint changes.
Wilson disease (copper overload) – Wilson disease causes abnormal copper storage in several organs. It has been reported together with CPPD, probably because of metabolic stress and damage to cartilage and bone.
Amyloidosis – In amyloidosis, abnormal protein deposits build up in tissues, including joints. These deposits can change the cartilage environment and may promote calcium pyrophosphate crystals in affected joints.
X-linked hypophosphatemic rickets and other phosphate disorders – Some inherited diseases change phosphate balance in bone and cartilage. These conditions can make pyrophosphate levels in joint cartilage rise, which supports crystal formation.
Diabetes mellitus and metabolic syndrome – Diabetes and related metabolic problems are linked to many joint diseases. They may increase CPPD risk through low-grade inflammation, cartilage damage, and changes in mineral handling in the joint.
Previous joint infection (septic arthritis) – A serious infection inside a joint can permanently damage cartilage and bone. After healing, the joint surface may be irregular and more prone to trapping and growing crystals such as CPP.
Idiopathic or “no clear cause” – In many older adults with chondrocalcinosis, no single cause or disease is found. In these people, natural aging of cartilage plus genetic and lifestyle factors probably work together to allow CPP crystals to form.
Symptoms and signs
Not everyone with chondrocalcinosis has symptoms, but when the crystals inflame the joint, they can cause many different problems.
Sudden severe joint pain – A very common symptom is a sudden, strong pain in a joint, often the knee or wrist. The pain may start over a few hours, sometimes even overnight, and can make it hard to move or put weight on the joint.
Joint swelling – The affected joint often becomes visibly swollen because extra fluid builds up inside. The swelling can make clothes or watches feel tight and can make the joint look bigger than usual.
Warmth of the joint – The skin over the sick joint can feel warm or hot to the touch. This warmth shows that there is active inflammation inside, with more blood flow going to that area.
Redness or color change – The joint skin can become pink or red, especially during sharp attacks. Sometimes the color change is mild and easier to see by comparing with the same joint on the other side of the body.
Joint stiffness – When the joint is inflamed, it often feels stiff, especially after resting or in the morning. People may say the joint “won’t bend” or “feels stuck” for a while before it loosens with gentle movement.
Limited range of motion – Because of pain, swelling, and stiffness, the joint may not move through its normal full arc. This can make it hard to fully straighten or fully bend the knee or to twist and bend the wrist or shoulder.
Tenderness to touch – The joint is often very sensitive when pressed or when moved by someone else. Even light touch or small movements can cause a strong pain sensation during a flare.
Recurrent attacks in the same or different joints – Many people have repeated episodes over months or years. One attack might affect the knee, and the next one might affect the wrist, ankle, or shoulder. This pattern can lead to a long history of “mysterious” joint flares.
Chronic joint pain between flares – Some people move from sharp attacks to continuous, dull pain that is present most days. This chronic pain may be achy and worse after activity, similar to osteoarthritis.
Knee pain and swelling – The knee is the most often involved joint in CPPD. People may notice that stairs, walking, or standing become painful. The knee can look enlarged or slightly bowed from long-term damage.
Wrist and hand symptoms – The wrists are another common site. Pain, stiffness, and swelling here can make it difficult to grip objects, open jars, or do fine hand work. Sometimes it can look like carpal tunnel or rheumatoid arthritis.
Ankle and shoulder involvement – Ankles and shoulders can also be affected. Ankle pain may make walking or standing hard, while shoulder involvement can limit lifting the arm, combing hair, or reaching overhead.
Mild fever and feeling unwell – During an acute attack, some people develop a low-grade fever and feel tired or sick in general. Because these signs are similar to infection, doctors must often test joint fluid to be sure infection is not present.
Long-term joint deformity – If CPPD and other joint problems continue for many years without good control, the joint may become misshapen or unstable. This can lead to bowing of legs, loss of normal alignment, or “collapse” of parts of the joint surface.
Loss of function and disability – Ongoing pain, stiffness, and deformity can make walking, climbing stairs, working, or self-care tasks difficult. Some people may need walking aids or, in severe cases, joint replacement surgery.
Diagnostic tests
Physical examination
Because CPPD can look like many other joint diseases, careful examination is the first step. The doctor will compare several joints and look for patterns.
Overall joint inspection – The doctor looks at both sides of the body, checking for swelling, redness, and differences in joint shape or size. Asymmetry, sudden swelling in a single large joint such as the knee, and sparing of the big toe joint can suggest CPPD more than gout or RA.
Palpation for warmth and tenderness – By gently pressing on the joint and feeling its temperature, the doctor can confirm active inflammation. Local warmth, soft fluid around the joint, and strong tenderness support an inflammatory arthritis like CPPD rather than only simple osteoarthritis.
Range-of-motion testing – The doctor will ask the patient to bend and straighten the joint and may also move it passively. Pain at the end of movement, a firm “stop,” or creaking sensations (crepitus) can show cartilage damage and fluid in the joint, which are common in CPPD.
Gait and function assessment – Watching how the person walks, stands from a chair, and uses their hands helps the doctor judge which joints are most affected and how much disability is present. Limping, favoring one leg, or avoiding certain movements can all reflect painful joints with CPPD.
Manual and bedside tests
Manual tests are simple hands-on maneuvers done in the clinic without machines.
Passive movement and crepitus check – The doctor slowly moves the joint while the patient relaxes. In CPPD, movement may produce a crackling or grinding feeling from the rough crystal-damaged cartilage, and the patient often reports pain at certain angles.
Joint line compression or “grind” test (knee) – For the knee, the doctor may gently press the kneecap or joint line while bending and straightening the leg. Pain, grinding, or popping sounds can suggest cartilage damage from osteoarthritis plus CPPD crystals in the meniscus or cartilage.
Ligament and stability tests – The doctor may check the stability of the knee, ankle, or wrist by gentle side-to-side or forward-backward stress. Normal ligaments with painful but stable joints suggest arthritis such as CPPD rather than ligament tears or major instability problems.
Comparison with the opposite joint – Manually comparing the painful joint with the same joint on the other side helps show differences in swelling, warmth, or movement. In CPPD, one side may be noticeably more swollen, tender, and stiff despite similar use.
Lab and pathological tests
Lab tests, especially tests on joint (synovial) fluid, are central for confirming CPPD.
Synovial fluid aspiration and crystal analysis – The most important test is arthrocentesis, where the doctor uses a needle to draw fluid from the swollen joint. In the lab, this fluid is examined under a special polarized light microscope. CPPD shows weakly positively birefringent, rhomboid or rod-shaped crystals, which confirms the diagnosis and helps separate CPPD from gout and infection.
Synovial fluid cell count and culture – The same fluid is checked for white blood cell numbers and sent for bacterial culture. A high white cell count with bacteria suggests septic arthritis, which is an emergency, while sterile fluid with CPP crystals supports CPPD. This testing makes sure the pain is not from a dangerous joint infection.
Serum calcium and parathyroid hormone (PTH) – Blood tests for calcium and PTH help detect hyperparathyroidism, a strong and treatable risk factor for CPPD. Finding high calcium and PTH levels may lead to further tests of the parathyroid glands and treatment to correct the hormone problem.
Serum magnesium level – Measuring blood magnesium is important because low magnesium is a reversible risk factor. Correcting low magnesium can help reduce new crystal formation and may improve joint symptoms over time.
Iron studies and ferritin – Tests such as serum iron, transferrin saturation, and ferritin help diagnose hemochromatosis. When iron overload is found in a person with early or severe CPPD, treating the iron problem (for example with regular blood removal) may slow joint damage.
Alkaline phosphatase, phosphate, and related bone markers – These tests can point to hypophosphatasia or other bone/mineral disorders. Abnormal results may explain premature chondrocalcinosis and guide more specific genetic or endocrine testing.
Electrodiagnostic studies
Electrodiagnostic tests are not used to prove CPPD, but sometimes they help exclude other conditions when joint damage is severe or unusual.
Nerve conduction studies (NCS) – If joint destruction looks like it might be due to a nerve problem (for example, in a “pseudo-neuropathic” pattern of CPPD), nerve conduction tests can check how well signals travel along the nerves. Normal nerve conduction with severe joint changes points more toward crystal arthritis than true neuropathic arthropathy.
Electromyography (EMG) – EMG uses a small needle in muscles to record their electrical activity. It can show whether muscle weakness or wasting is due to nerve damage or muscle disease. In people with very damaged joints and odd movement patterns, normal EMG findings can support the idea that the main problem is destructive CPPD arthritis rather than a nerve disease.
Imaging tests
Imaging tests show the physical structure of joints and are very important for recognizing chondrocalcinosis.
Plain X-rays (conventional radiography) – Standard X-rays often show chondrocalcinosis as thin, bright white lines or small spots of calcium in the cartilage or menisci of the knees, wrists, and other joints. X-rays can also show joint space narrowing, bone spurs, and other arthritis changes. While useful, X-rays can miss early disease and are not perfectly specific, so they are combined with other tests.
Ultrasound of the joint – Ultrasound uses sound waves to show soft tissues and cartilage. In CPPD, ultrasound can display crystal deposits as bright bands or spots inside cartilage and can also show extra fluid and inflammation. It is very helpful at the bedside and has good accuracy when done by trained staff. Recent guidelines highlight ultrasound, along with X-rays, as a first-line imaging test for suspected CPPD.
Computed tomography (CT) and dual-energy CT (DECT) – CT scans give very detailed pictures of bone and can reveal crystal deposits in deep or complex joints, such as the spine or hips, where ultrasound and X-rays are less clear. Dual-energy CT can sometimes help distinguish different crystal types. These scans are especially useful when there is suspected spine or axial joint involvement.
Magnetic resonance imaging (MRI) – MRI shows cartilage, ligaments, bone marrow, and fluid in great detail. CPPD itself is harder to see on MRI than on X-rays or ultrasound, but MRI can reveal bone marrow edema, soft tissue swelling, and other joint damage. In complex cases, MRI helps rule out other causes of pain and supports the overall picture of CPPD-related arthritis.
Non-pharmacological treatments
1. Rest and temporary joint protection
During a painful flare, short-term rest helps lower stress on the inflamed joint and reduces pain. Doctors often suggest avoiding heavy use of the joint for a few days and sometimes using a soft splint or brace to limit movement until the worst pain settles.
2. Cold packs (ice therapy) in acute attacks
Cool packs or wrapped ice placed on the painful joint for 10–15 minutes at a time can numb the area, shrink blood vessels and reduce swelling. This is especially helpful in the first 48 hours of an acute CPPD flare, similar to how it is used in gout and other crystal arthritis.
3. Elevation and gentle compression
Keeping the affected limb raised above heart level and using light elastic bandages (if safe) can help fluid drain away from the joint and reduce swelling. This is more useful in leg joints such as the knee or ankle, and must not be tight enough to block blood flow.
4. Early guided joint movement
Once the sharp pain improves, careful movement helps prevent stiffness. A physiotherapist can teach gentle bending and straightening exercises that keep the joint fluid moving and stop the tissues from becoming tight and weak.
5. Muscle-strengthening exercises
Strong muscles around a joint act like natural shock absorbers. Quadriceps strengthening for knees, hip and core strengthening for hips and spine, and shoulder girdle exercises for shoulder CPPD can improve function and may reduce future pain episodes.
6. Low-impact aerobic activity
Regular activities such as walking on flat ground, cycling, and water aerobics improve blood flow, lubricate joints and support weight control without over-loading the cartilage. The aim is most days of the week, but intensity must be adjusted to pain level.
7. Hydrotherapy and pool exercises
Exercising in warm water reduces joint loading because water supports body weight. Many people with chronic CPPD-related arthritis find it easier to move, stretch, and strengthen in a pool than on land, which can improve pain and function over time.
8. Weight management
Extra body weight puts more mechanical stress on weight-bearing joints like knees and hips. In people with osteoarthritis-type CPPD, even modest weight loss can reduce pain and improve mobility by lowering the pressure on damaged cartilage.
9. Assistive devices (sticks, walkers, braces)
Using a cane in the opposite hand to a painful knee or hip, or using a walker for balance, can take significant load off the joint. Braces and orthoses can improve alignment, reducing stress on specific parts of the joint that are badly damaged by CPPD crystals and osteoarthritis.
10. Occupational therapy and joint-protection techniques
An occupational therapist can suggest new ways of doing daily tasks, such as using jar openers, long-handled tools, or raised chairs. These changes spread the load across larger joints and help avoid repeated strain on the most affected joints.
11. Footwear and orthotic inserts
Supportive shoes and custom or off-the-shelf insoles can improve alignment from the feet up. Better alignment reduces abnormal forces at knees, hips and spine that may already be affected by CPPD-related cartilage damage.
12. Heat therapy in chronic stiffness (not acute flare)
Warm packs, heated pads, or warm showers may relax tight muscles and improve joint flexibility in chronic, non-inflamed phases. Heat should not be used during red, hot, very swollen acute attacks, where cold is usually safer.
13. Transcutaneous electrical nerve stimulation (TENS)
TENS uses small electrical pulses on the skin to interfere with pain signals going to the brain. Some patients with chronic CPPD-related knee or wrist pain report helpful short-term relief when TENS is used along with exercise and medicines.
14. Acupuncture as an adjunct
Acupuncture may help some people with chronic arthritis pain when used together with standard care. Evidence in CPPD is limited, but studies in osteoarthritis and other arthritis types show modest pain relief for some patients.
15. Pain-education and cognitive-behavioural strategies
Understanding how chronic pain works and learning coping skills (relaxation, pacing, goal setting, cognitive-behavioural therapy) can reduce pain distress, improve sleep and support long-term self-management in people with persistent CPPD symptoms.
16. Sleep hygiene and fatigue management
Good sleep habits (regular sleep times, dark and quiet bedroom, limiting caffeine and screens) help reduce fatigue and make joint pain easier to tolerate. Treating sleep apnoea or depression, if present, can also lower the overall pain experience.
17. Fall-prevention and home safety modifications
Joint pain and stiffness can increase fall risk. Simple changes such as removing loose rugs, adding grab bars, using non-slip mats and keeping good lighting can prevent serious injuries, especially in older adults with CPPD.
18. Managing associated metabolic conditions (non-drug parts)
Some people with CPPD have low magnesium, high iron (hemochromatosis) or over-active parathyroid glands. Lifestyle steps like balanced diet, limiting alcohol and following medical nutrition advice are part of the overall plan alongside any specific medical treatment.
19. Smoking cessation
Smoking is linked to worse outcomes in many inflammatory and degenerative joint diseases. Stopping smoking improves general health, circulation, healing and response to treatment, even though it does not directly remove CPP crystals.
20. Regular follow-up and self-monitoring
Keeping a simple symptom diary (pain scores, triggers, activities) and attending regular reviews helps your doctor adjust therapy, spot side effects early and decide when to change from simple to more intensive treatment.
Drug treatments
Important: None of these drugs is specifically approved to “cure” CPPD or dissolve CPP crystals. Most are approved for gout, osteoarthritis or rheumatoid arthritis and are used off-label for CPPD based on expert opinion and small studies. Only a doctor can decide which medicine and dose is safe for you.
1. Naproxen (oral NSAID)
Naproxen is a non-steroidal anti-inflammatory drug (NSAID) that blocks cyclo-oxygenase (COX) enzymes, lowering prostaglandins that drive pain and swelling. It is often used in short courses for acute CPPD flares, typically twice daily with food, at the lowest effective dose. Main risks are stomach ulcer or bleeding, kidney problems and heart risk, especially with long-term use.
2. Ibuprofen (oral NSAID)
Ibuprofen works in a similar way and can be used for milder flares or in people who have used it safely before. Over-the-counter labels usually suggest 200–400 mg every 4–6 hours up to a daily limit for pain and fever, but for CPPD the exact dose and time must be set by a doctor because of GI, kidney and heart side-effects.
3. Indomethacin (stronger NSAID)
Indomethacin is a potent NSAID often used in gout and sometimes in CPPD for severe acute pain. Because it has higher risk of stomach and nervous-system side effects than some other NSAIDs, it is usually reserved for short, carefully supervised courses in people without major heart, kidney or ulcer disease.
4. COX-2 inhibitor celecoxib
Celecoxib is a COX-2 selective NSAID that aims to reduce pain and inflammation with somewhat less stomach ulcer risk, though heart and clot risks remain. It is taken once or twice daily as capsules; dose and duration are chosen based on age, kidney function and cardiovascular risk.
5. Topical NSAIDs (diclofenac gel and similar)
In people with milder, more superficial joint pain, gels or creams containing diclofenac or other NSAIDs can be rubbed onto the skin over the joint, giving local pain relief with lower blood levels than tablets. They are often used in knees and hands when skin is intact.
6. Low-dose colchicine for flare prevention
Colchicine interferes with microtubules in white blood cells and reduces their ability to respond to CPP crystals, which can lower frequency of attacks. Low daily doses (for example 0.5–1 mg/day in adults) are used for months in people with recurrent CPPD, but dose must be adjusted in kidney or liver disease and with interacting drugs. Diarrhoea and stomach upset are common side effects.
7. Short-course colchicine in acute flares
For some patients, short bursts of colchicine at the start of an attack can shorten the flare if started early. Modern gout regimens use lower, safer total doses than older high-dose schedules, to reduce the risk of serious toxicity such as bone-marrow suppression and multi-organ failure with overdose.
8. Oral prednisone or prednisolone (systemic glucocorticoids)
When NSAIDs and colchicine are not suitable, oral steroids like prednisone or prednisolone can quickly reduce joint inflammation by broadly suppressing immune responses. A typical approach is a short tapering course over 5–14 days at the lowest dose that relieves symptoms. Long-term or repeated courses increase the risk of diabetes, bone thinning, infection and many other complications, so careful monitoring is needed.
9. Intramuscular or intravenous methylprednisolone
In people with many joints flaring at once or who cannot take tablets, injected methylprednisolone (Solu-Medrol) can give fast relief. It acts like a strong systemic steroid and carries similar risks, so it is usually given as a single or very short course in hospital or clinic settings.
10. Intra-articular steroid injections (e.g., methylprednisolone acetate)
A doctor can inject steroid directly into a swollen joint after aspirating fluid. This delivers a high local dose with lower total body exposure. It is effective for mono- or oligo-articular CPPD flares, but should not be done if infection is suspected. Repeated injections must be spaced out to reduce cartilage or tendon damage.
11. Adrenocorticotropic hormone (ACTH) injections
ACTH stimulates the adrenal glands to release the body’s own steroids. Small studies in crystal arthritis, including CPPD, show that intramuscular ACTH can rapidly reduce pain and swelling in patients with multiple medical problems who cannot safely take NSAIDs or colchicine. It is still relatively uncommon and used mainly in specialised centres.
12. Methotrexate (low-dose, weekly)
Methotrexate is a disease-modifying drug widely used in rheumatoid arthritis. In CPPD, trials show mixed results; some patients with chronic, recurrent inflammation improve, while others do not. It works by dampening many immune pathways. Because it can affect liver, bone marrow and lungs, it must be given in low weekly doses with folic acid and regular blood tests.
13. Hydroxychloroquine
Hydroxychloroquine modulates immune activity and is used in lupus and RA. An older controlled trial and case series suggest it may reduce pain and swelling in chronic CPPD in some patients. Eye exams and blood monitoring are needed because of rare retinal and other toxicities.
14. Anakinra (IL-1 receptor antagonist)
Anakinra is a biologic drug that blocks interleukin-1, a key inflammatory signal activated by CPP crystals. Daily subcutaneous injections for a few days have been reported to help severe, refractory CPPD flares and some chronic forms, especially when standard drugs fail or are unsafe. Main concerns are injection-site reactions and increased infection risk.
15. Tocilizumab (IL-6 receptor inhibitor)
Tocilizumab blocks IL-6, another inflammatory cytokine. Case series suggest benefit in difficult, chronic CPPD with persistent inflammation. It is given as intravenous infusion or subcutaneous injection. Because it suppresses the immune system and can affect liver tests, blood counts and cholesterol, it is reserved for highly selected patients.
16. TNF inhibitor adalimumab and biosimilars
Adalimumab and its biosimilars block tumour necrosis factor-α and are approved for many autoimmune diseases. Some doctors have tried them in severe CPPD overlapping with other inflammatory arthritis, but evidence is limited, and they carry notable infection and malignancy warnings in their labels.
17. Baricitinib (JAK inhibitor – under study)
Baricitinib blocks JAK1/2 signalling pathways used by many cytokines. A phase-2 study is exploring its use in chronic CPPD disease compared with standard drugs like colchicine and steroids. At present it is an experimental option, with known risks such as infection, blood clots and cholesterol changes from its use in RA.
18. Experimental NLRP3 inflammasome inhibitor dapansutrile
Dapansutrile targets the NLRP3 inflammasome, a critical sensor in crystal-induced inflammation. It is being studied in gout and may later be tested in CPPD, but it is not yet an approved standard treatment. Safety and real-world benefits are still being investigated.
19. Simple analgesics such as paracetamol (acetaminophen)
Paracetamol does not reduce inflammation but can help background pain in people who cannot take NSAIDs or need extra pain control. Doses must stay within recommended daily limits to avoid liver damage, especially when combined with alcohol or other hepatotoxic drugs.
20. Short-term weak opioids (for example, tramadol)
In very severe pain when other options cannot be used, doctors may briefly prescribe weak opioid painkillers. They act on the nervous system to change pain perception. Because of dependence, dizziness, constipation and other risks, doses and duration should be as low and short as possible and monitored closely.
Dietary molecular supplements
Note: Current research shows no specific “CPPD diet” and no supplement that dissolves CPP crystals. Diet mainly supports general joint health, bone strength and control of other diseases (like obesity, diabetes or heart disease) that can worsen overall outcomes.
1. Vitamin C
Vitamin C is essential for collagen production in cartilage, ligaments and bone and acts as an antioxidant. Adequate intake from food or low-dose supplements may support joint structure, but very high doses can cause kidney stones and stomach upset. Typical supplement doses for adults are in the range of 75–500 mg/day, but the exact amount should be chosen with a doctor or dietitian.
2. Vitamin D
Vitamin D helps the gut absorb calcium and supports bone and muscle health. Low vitamin D is common in older adults and can worsen bone problems and falls. Usual replacement doses depend on blood levels and local guidelines; taking too much can cause high calcium and kidney damage, so blood monitoring is important.
3. Omega-3 fatty acids (fish oil, EPA/DHA)
Omega-3 fats from fish oil reduce production of some inflammatory molecules and may improve joint pain and function in several arthritis types. Studies in osteoarthritis and inflammatory conditions show modest pain reduction, but doses, purity and bleeding risk (especially with blood thinners) must be reviewed with a doctor.
4. Vitamin E and other antioxidants
Vitamin E and plant antioxidants help neutralise free radicals that can damage cartilage cells. Some studies suggest small benefits in osteoarthritis, but high-dose vitamin E may increase bleeding risk and stroke in certain people, so supplements should stay within safe limits and be discussed with a clinician.
5. Magnesium
Magnesium participates in many enzyme reactions, including those related to bone and cartilage mineralisation. Low magnesium is linked to chondrocalcinosis in some studies. Food-based magnesium (dark greens, nuts, whole grains) is preferred; supplements must be used carefully in kidney disease due to risk of high magnesium levels.
6. Calcium (within normal needs)
Although CPPD crystals contain calcium, CPPD is not caused by eating too much calcium. Adequate calcium is still needed to prevent osteoporosis. Many patient guidelines recommend getting calcium mainly from food and using supplements only when diet is insufficient, to avoid kidney and vascular problems from excessive intake.
7. Glucosamine
Glucosamine is a building block of cartilage matrix. Some osteoarthritis trials show small symptom benefits, while others do not. If used, it is usually taken daily for several months before judging effect. It should be avoided in people with shellfish allergy to some formulations and used cautiously in diabetes because of possible sugar effects.
8. Chondroitin sulfate
Chondroitin is another cartilage component. Like glucosamine, evidence is mixed, but some people report less pain and better function in knee OA. Typical doses are split across the day. Because it can affect blood clotting slightly, people on anticoagulants should discuss it with their doctor first.
9. Curcumin (from turmeric)
Curcumin has anti-inflammatory and antioxidant actions in laboratory and some clinical studies. It may modestly reduce joint pain and stiffness, especially when combined with piperine to improve absorption. High doses can upset the stomach and may interact with blood thinners, so medical advice is needed.
10. Boswellia and mixed joint-support formulas
Extracts from Boswellia serrata and mixed “joint support” capsules often combine plant anti-inflammatories with vitamins and minerals. Some small studies in OA show pain reduction, but quality and content vary widely between brands. Any supplement plan should be checked against your current medicines to avoid harmful interactions.
Immunity-booster, regenerative and stem-cell-related drugs
There are no approved “stem cell drugs” that specifically fix CPPD in routine practice. The options below are advanced immune-modifying treatments or therapies being studied for crystal arthritis; they are mentioned for completeness, not as routine advice.
1. Anakinra (IL-1 receptor antagonist)
By blocking IL-1 signalling, anakinra directly interferes with one of the main inflammatory pathways activated by CPP crystals. This can be seen as “immune resetting” during severe flares, helping the body calm down excessive inflammation that damages cartilage. It is not a classic stem-cell drug but is an important biologic option in very resistant CPPD.
2. Tocilizumab (IL-6 inhibitor)
Tocilizumab blocks IL-6 receptors and may help patients with chronic CPPD whose inflammation stays high despite steroids, colchicine and NSAIDs. By dampening IL-6-driven immune activity, it can improve pain and inflammation but also lowers immune defences, so infection risk and lab tests must be closely monitored.
3. Baricitinib (JAK inhibitor)
Baricitinib acts on JAK1/2, “downstream” of many cytokines. In CPPD trials it aims to reduce joint inflammation by interrupting several inflammatory messages at once. Because it affects wide immune pathways, it can increase infection and clot risk, so it is reserved for research settings or highly specialist care.
4. Anti-IL-1β monoclonal antibodies (e.g., canakinumab – pipeline)
Monoclonal antibodies targeting IL-1β are approved for some rare autoinflammatory diseases and gout and are now being studied in crystal arthritis more broadly. They provide longer-lasting IL-1 blockade than anakinra but are expensive and carry similar infection risks. Their place in CPPD care is still under investigation.
5. NLRP3 inflammasome inhibitors (e.g., dapansutrile – pipeline)
NLRP3 is a key “danger sensor” activated by CPP crystals. Blocking it with small-molecule inhibitors like dapansutrile may prevent the cascade of inflammation that leads to flares. Clinical trials are ongoing in gout and could later include CPPD, but these drugs are not yet available for routine clinical use.
6. Mesenchymal stem-cell and regenerative injections for osteoarthritis-type damage (experimental)
For patients with severe cartilage loss and CPPD-related osteoarthritis, some research centres are testing injections of mesenchymal stem cells or platelet-rich plasma to support cartilage repair. Evidence is still mixed, these treatments are not specific to CPPD, and some advertised “stem-cell clinics” offer unproven and risky therapies. They should only be considered within well-regulated studies.
Surgeries (Procedures and why they are done)
1. Arthroscopic joint lavage and debridement
Through small keyhole cuts, a surgeon can wash out inflamed joint fluid and remove loose cartilage fragments. This may temporarily reduce symptoms in severely affected joints but does not fully remove or prevent CPP crystals, so long-term benefit can be limited.
2. Arthroscopic synovectomy and crystal removal
In joints with repeated flares, surgeons may remove thickened synovial tissue that is heavily loaded with CPP crystals. This can reduce the amount of inflamed tissue and sometimes lowers the frequency of flares, especially in single-joint disease such as a repeatedly inflamed knee.
3. Corrective osteotomy (bone realignment)
If CPPD and osteoarthritis have led to crooked joints (for example, bow-legged knees), cutting and realigning the bone can redistribute weight more evenly and slow further damage. This is more common in younger or more active patients where joint replacement would be too early.
4. Joint replacement (arthroplasty)
In end-stage joint damage with constant pain and major disability, total knee, hip, or sometimes shoulder replacement may be recommended. The surgeon replaces the damaged surfaces with artificial components. CPP crystals do not usually damage the metal or plastic implants, but surgery still carries risks and needs careful planning.
5. Joint fusion (arthrodesis)
For small joints (such as some wrist or ankle joints) that are severely damaged, fusing the bones together can remove pain by stopping movement in that joint. Mobility is reduced in that segment, but overall function may improve if pain had been very severe. This is usually a last-line option.
Prevention tips
1. Control metabolic risk factors
Treating low magnesium, high iron levels, over-active parathyroid, thyroid disease or kidney problems can reduce triggers that may worsen CPPD or its symptoms. Regular blood tests guided by your doctor are key.
2. Avoid unnecessary joint trauma and surgery
CPPD flares often appear after joint injury or operations such as joint replacement or parathyroid surgery. Careful surgical planning, joint protection and good rehabilitation may lower this risk.
3. Maintain healthy body weight
Keeping weight in a healthy range reduces mechanical stress on knees, hips and spine, which may already be vulnerable due to CPP crystals and osteoarthritis.
4. Keep joints moving with safe exercise
Regular low-impact movement maintains cartilage nutrition, muscle strength and balance, which all help protect joints from further damage and falls.
5. Use medicines exactly as prescribed
Using NSAIDs, colchicine, steroids or biologics at the right dose and duration lowers the risk of both undertreatment (continued inflammation) and overtreatment (side effects such as ulcers, infections or organ damage).
6. Vaccinations before strong immunosuppressive therapy
For people starting biologics or long-term steroids, being up to date on vaccines (influenza, pneumococcal, shingles, etc., according to local guidelines) can reduce infection risk during treatment.
7. Avoid dehydration and acute illnesses when possible
CPPD flares may follow serious illness or surgery. Good hydration, early treatment of infections and careful management of hospital stays can sometimes reduce inflammatory triggers.
8. Protect bones (calcium, vitamin D, weight-bearing exercise)
Because many CPPD patients are older and may use steroids, protecting bone density is important to prevent fractures. Adequate calcium and vitamin D intake plus weight-bearing activities help maintain bone strength.
9. Do not smoke and limit alcohol
Smoking harms blood vessels, bone and immune function. Excess alcohol can worsen bone and liver health and interact with many medicines. Avoiding both helps overall outcomes.
10. Regular rheumatology follow-up
CPPD can change over time. Regular visits allow adjustment of medicines, checking for side effects and screening for associated diseases such as osteoarthritis, hemochromatosis or hyperparathyroidism.
When to see a doctor
You should see a doctor urgently (or go to emergency care) if:
A joint suddenly becomes very painful, hot, red and swollen, especially if you also have fever or feel very unwell (to rule out joint infection, which is an emergency).
You have severe pain not relieved by usual pain medicines, or you cannot put any weight on the leg or move the joint at all.
You are on steroids, biologics, or chemotherapy-type drugs (like methotrexate) and develop signs of infection such as high fever, chills, cough, burning urine, or unexplained shortness of breath.
You should book a routine appointment with your doctor or rheumatologist if:
You are getting more frequent flares or chronic daily pain from CPPD.
Your current medicines cause side effects such as stomach pain, black stools, swelling of legs, mood changes or high blood sugars.
You are thinking about starting supplements or alternative treatments and want to check for safety and interactions.
What to eat and what to avoid
1. Eat a balanced, anti-inflammatory style diet
Plenty of colourful vegetables, fruits, whole grains, healthy fats (olive oil, nuts, seeds) and lean proteins supports overall health and may modestly reduce inflammation, similar to Mediterranean-style eating patterns.
2. Include calcium-rich foods in normal amounts
Milk, yoghurt, cheese and calcium-fortified foods are safe in normal portions and help protect bones. CPPD is not caused by normal dietary calcium intake.
3. Ensure enough vitamin D and vitamin C from food
Fatty fish, eggs and fortified foods provide vitamin D, while citrus fruits, berries and peppers provide vitamin C, both important for bone and cartilage health.
4. Focus on omega-3-rich foods
Eating oily fish (salmon, sardines, mackerel) 1–2 times per week or using plant sources like flaxseed and walnuts may support joint health and heart health at the same time.
5. Avoid very high doses of unproven supplements
More is not always better. High doses of vitamins A, E, C, D or fish-oil supplements can cause harm, including kidney stones, bleeding or heart rhythm problems. Use only doses your doctor or dietitian recommends.
6. Limit ultra-processed and sugary foods
Processed snacks, sweet drinks and fast foods can promote weight gain and systemic inflammation, which may worsen overall joint and heart health.
7. Moderate alcohol intake
While diet is not a direct cause of CPPD, heavy alcohol use can damage liver, bone and overall health, and may complicate medication safety. Low or moderate intake (or avoiding alcohol completely) is usually safest, especially with many arthritis drugs.
8. Stay well hydrated
Good fluid intake supports kidney function, especially important if you are using NSAIDs or other drugs that can affect the kidneys. Dehydration can also make you feel more fatigued and headachy.
9. Manage salt intake
Limiting added salt can help control blood pressure and reduce swelling in people on steroids or NSAIDs, which can cause fluid retention.
10. Tailor diet to other conditions (diabetes, kidney disease, heart disease)
Because many CPPD patients are older and have other illnesses, diet should be personalised. For example, people with kidney disease may need to control potassium and phosphate; people with diabetes must manage carbohydrate intake carefully.
Frequently asked questions (FAQs)
1. Can chondrocalcinosis be completely cured?
At present, there is no cure that removes existing CPP crystals or guarantees they will not form again. Treatment aims to control pain and swelling, protect joint function and reduce how often attacks happen. Research into crystal-targeted drugs is ongoing.
2. Is chondrocalcinosis the same as gout?
No. Both are crystal arthritides and can look similar, but gout is caused by uric acid crystals, while CPPD is caused by calcium pyrophosphate crystals. They may sometimes occur together in the same person.
3. Does diet cause CPPD like it can trigger gout?
Current evidence says no. Diet is not a main cause of CPPD, and foods that trigger gout attacks (like purine-rich meats or alcohol) do not clearly trigger CPPD flares. However, diet still matters for weight, heart health and bone strength.
4. Will drinking milk or taking calcium tablets make my CPPD worse?
Normal dietary calcium and appropriate calcium supplements to protect bones do not appear to worsen CPPD. The disease is related to local crystal formation inside the joint, not simply to how much calcium you eat.
5. Should everyone with CPPD take colchicine every day?
No. Daily low-dose colchicine is one option for people with frequent flares, but it is not suitable for everyone. Kidney function, liver function, other medicines and side-effects must be checked, and the dose must be tailored by a doctor.
6. Are NSAIDs safe to use long-term?
Long-term NSAID use can increase the risk of stomach ulcers, bleeding, kidney disease and cardiovascular events, especially in older adults. Many people can use them safely for short periods, but long-term daily use needs close medical supervision and sometimes gastro-protective drugs.
7. When is a biologic drug like anakinra or tocilizumab considered?
Biologics are usually considered only in severe CPPD with frequent flares or chronic inflammation that does not respond to NSAIDs, colchicine and steroids, or when these standard drugs are unsafe. They are specialist treatments with high cost and infection risks.
8. Can exercise make CPPD worse?
During an acute flare, high-impact or heavy use of the affected joint can worsen pain. But in the long term, carefully chosen low-impact exercise is protective, not harmful, and helps reduce stiffness, muscle weakness and falls.
9. Is CPPD always a disease of older people?
CPPD is much more common after age 60, but it can appear earlier, especially in people with certain genetic forms or with underlying metabolic conditions like hemochromatosis or hyperparathyroidism. Younger patients often need thorough investigation for these causes.
10. Does CPPD always progress and destroy the joint?
No. Some people have only mild, occasional flares with little long-term damage, while others develop chronic arthritis with joint space narrowing and deformity similar to osteoarthritis. Early diagnosis, good flare control and lifestyle measures can slow progression.
11. Can CPPD crystals move to other organs?
CPPD crystals mainly stay inside joints and the tissues around them. Unlike some metabolic diseases, they do not usually deposit in organs like kidneys or heart, although associated conditions such as hemochromatosis can affect many organs.
12. Is there a role for joint aspiration even when I am not in a flare?
Joint aspiration is mainly used to diagnose CPPD and to treat acute flares by removing inflammatory fluid. It is less often used when symptoms are quiet, unless there is suspicion of infection or another problem needing fluid analysis.
13. Can CPPD be inherited?
Yes, some families have genetic forms where CPPD appears at a younger age and may be more severe. Genetic testing is sometimes considered in early-onset or multi-joint chondrocalcinosis.
14. Are stem-cell injections recommended outside clinical trials?
At present, most professional societies advise that stem-cell injections for joint disease should only be given in regulated clinical trials. Many commercial clinics offer expensive treatments with uncertain benefit and potential risks.
15. What is the outlook for new CPPD treatments?
The research field is growing fast. New trials are testing targeted inflammasome inhibitors, IL-1 and IL-6 blockers, JAK inhibitors and other experimental drugs. While we still lack a true crystal-dissolving therapy, understanding of CPPD biology is improving, and future disease-modifying options are becoming more realistic.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: January 12, 2026.
