Chondrocalcinosis

Definition. Chondrocalcinosis is radiographically visible calcification within cartilage: hyaline articular cartilage, or a fibrocartilaginous structure such as the meniscus, triangular fibrocartilage complex, symphysis pubis, acetabular labrum, glenoid labrum or annulus fibrosus. It is a radiographic sign; calcium pyrophosphate dihydrate (CPPD) crystal deposition is its commonest cause, not its synonym.

Hyaline cartilage. A thin, dense, linear band running parallel to the subchondral bone and separated from it by the uncalcified cartilage layer. It is best seen at the femoral condyles, humeral head and radial head.

Fibrocartilage. Thicker, shaggier, more amorphous or punctate calcification within the substance of the structure. The classic examples are the triangular density in the meniscus on an anteroposterior knee film, and the dense wedge between the ulnar head and triquetrum at the TFCC.

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Confirming it is genuinely present. Three checks:

1. The density is intra-articular and conforms to the shape of a cartilage structure, rather than following a tendon, capsule or vessel.
2. It is present at more than one site. Screening films of the knees (anteroposterior), wrists (posteroanterior) and pelvis (symphysis pubis) form the standard "chondrocalcinosis series", and establish whether deposition is monoarticular or systemic.
3. Ultrasound agrees, if the radiograph leaves doubt. What it shows is in Next Investigation.

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Saying it out loud. "There is linear calcification paralleling the subchondral bone of both femoral condyles and amorphous calcification within the body of the medial meniscus. This is chondrocalcinosis involving both hyaline and fibrocartilage. There is patellofemoral joint space narrowing with subchondral sclerosis. The pattern favours calcium pyrophosphate deposition disease. I would examine the wrists and symphysis pubis for further deposition, and given the patient's age I would screen for haemochromatosis and hyperparathyroidism."

Mimics. Calcification within the capsule, synovium, ligaments or tendons is not chondrocalcinosis, and shifts the differential toward hydroxyapatite deposition or gout. The false positives, and what gives each away:

• Calcific tendinopathy (hydroxyapatite deposition) - globular, homogeneous, and located in the supraspinatus tendon, gluteus medius insertion or longus colli, outside the joint line
• Synovial osteochondromatosis - multiple discrete rounded bodies of equal size with ring-and-arc chondroid mineralisation, distending the capsule rather than confined to a cartilage layer
• Vascular calcification - tram-track parallel lines following a known vessel course, popliteal or femoral
• Meniscal ossification - a true ossicle with cortex and trabeculae, not amorphous density
• Gouty tophus - soft tissue density with eccentric erosions and overhanging edges; usually only mineralised in chronic renal disease
• Pellegrini–Stieda - post-traumatic calcification at the medial femoral condyle along the medial collateral ligament, extra-articular

The screening radiograph series is first-line in every case and is described above.

The metabolic screen. Serum calcium, phosphate, PTH, ferritin with transferrin saturation, magnesium, alkaline phosphatase, and thyroid function. It is mandatory under age 55, in polyarticular disease, or if any systemic feature is present. A low alkaline phosphatase is the specific clue to hypophosphatasia and is easily overlooked as a normal-range result.

Joint aspiration with polarised light microscopy. The only test that positively confirms CPPD, and it simultaneously excludes sepsis and urate. It is mandatory in any acutely inflamed joint and useful electively when the diagnosis is uncertain. A cell count above 50,000 per cubic millimetre with neutrophil predominance is treated as infection until cultures return.

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Ultrasound. Hyperechoic deposits within the substance of the hyaline cartilage layer, which do not produce the posterior acoustic shadow typical of hydroxyapatite and do not disappear at differing insonation angles the way the surface double contour sign of urate does. It is more sensitive than radiography at the knee and wrist and useful for guiding aspiration, so its place is the equivocal radiograph or the technically difficult aspiration.

Dual-energy CT. Colour-codes monosodium urate, separating gout from CPPD in the selected cases where clinical and radiographic features overlap. It does not replace aspiration where infection is a consideration.

CT of the cervical spine. For acute neck pain with pyrexia and raised inflammatory markers in a patient with known chondrocalcinosis. It demonstrates the calcification around the odontoid peg and prevents an unnecessary infection or malignancy workup.

When to stop. An asymptomatic incidental meniscal calcification in a patient over 70 with normal bloods and no systemic features needs no follow-up imaging and no treatment. Say this explicitly; recognising when to stop is a mark-scoring answer.

The crystal differential. CPPD, urate and basic calcium phosphate part on tissue, appearance, microscopy and site. Gout travels with CPPD as an associated crystal disease, and mixed deposition occurs.

Related pages. The disease behind the sign: Pseudogout and CPPD Disease covers acute CPP crystal arthritis and its management, and Arthritis on Radiographs places chondrocalcinosis in the deposition family alongside gout. The metabolic causes: Haemochromatosis Arthropathy is the must-not-miss and carries the metacarpophalangeal pattern that actually discriminates, with Hyperparathyroidism and Renal Osteodystrophy for the calcium-PTH axis and Ochronosis for the dense multilevel disc calcification that mimics it in the spine. The crystal differential: Gout and Crystal Arthropathy for negatively birefringent needles against positively birefringent rhomboids, and Milwaukee Shoulder for basic calcium phosphate, which is periarticular rather than cartilage-based. What it does to joints: SLAC Wrist is the scapholunate collapse pattern CPPD drives at the wrist, and Osteoarthritis Pathophysiology is the co-traveller that rises with age independently rather than because of the crystals. Septic Arthritis Pathophysiology is the pathway an acutely hot joint enters regardless of what the radiograph shows.

The shape of the list. Idiopathic, age-related CPPD is overwhelmingly the commonest cause, commoner than all the metabolic causes combined, and its prevalence rises with each decade. It is a finding of ageing cartilage, usually asymptomatic, and does not by itself explain a painful knee. The rest of the table exists to stop you missing the treatable minority.

The must-not-miss. Haemochromatosis, because chondrocalcinosis may precede cirrhosis and diabetes by years and the arthropathy can be the presenting feature. What discriminates it is the metacarpophalangeal arthropathy in the table, not the chondrocalcinosis: isolated cartilage calcification is non-specific.

The counterintuitive one. Hypophosphatasia is the reason alkaline phosphatase is on the panel. A persistently low value dismissed as a laboratory artefact is the classic miss, and bisphosphonates are contraindicated because they worsen the disease.

The reversible one. Hypomagnesaemia is the most easily reversible cause on the list and the one most often left off the request form. Think of long-term proton pump inhibitors, thiazides, short bowel, alcohol excess, or Gitelman syndrome in a young patient.

The questions, in the order the viva asks them.

Is it truly cartilage calcification? Decide which structure the density lies in before anything else: parallel to subchondral bone, or within a meniscus, TFCC, labrum or symphyseal disc. Globular and in a tendon means hydroxyapatite deposition; a rounded ossicle with a cortex is a loose body or meniscal ossification. This step alone eliminates half the mimics, and it is the step most often skipped.

How old is the patient? Take the age before ordering anything; it is the single most important branch point. Over 65 with knee-limited deposition and no systemic features, idiopathic age-related CPPD is overwhelmingly likely and a blood screen may be all that is needed. Under 55, chondrocalcinosis is a metabolic disease until proven otherwise, and reciting "degenerative" without the screen is the single commonest viva failure.

One joint or many? Screen the knees, wrists and pelvis rather than imaging only the symptomatic joint, and ask specifically about previous injury or surgery to that joint. Monoarticular deposition in a previously injured or operated joint is post-traumatic or degenerative and needs no systemic workup. Polyarticular deposition, particularly including the symphysis pubis and both wrists, substantially raises the probability of a metabolic driver or familial disease and triggers blood testing.

What are the joints themselves doing? Look past the calcification, especially at the second and third metacarpophalangeal joints and the radiocarpal joint. Degenerative change at joints osteoarthritis spares (radiocarpal, elbow, glenohumeral, ankle, second and third metacarpophalangeal) is the flag for CPPD or haemochromatosis, not primary osteoarthritis. The metacarpal-head and joint-space patterns of haemochromatosis and acromegaly are in the table; the CPPD patterns are these:

• Isolated radiocarpal and scapholunate disease with proximal capitate migration is CPPD-driven scapholunate advanced collapse
• Patellofemoral-predominant wear with large subchondral cysts is CPPD
• Normal joint spaces with pure deposition is early or asymptomatic disease

Is the spine involved? Review any available spinal imaging for disc calcification, ligamentum flavum calcification and the region of the odontoid peg. Fused sacroiliac joints alongside multilevel disc calcification suggests ochronosis. Calcification of the transverse ligament of the atlas is crowned dens syndrome, which can present as acute neck pain with pyrexia mimicking meningitis, and which the 2023 ACR/EULAR criteria treat as sufficient on its own to classify CPPD disease.

Are there systemic clues? Examine the skin and liver, ask about renal stones, childhood dental loss and tremor, and take a drug history for proton pump inhibitors and thiazides. Each answer maps onto the setting column of the table.

Is the joint acutely inflamed? If the joint is hot, swollen and painful, stop and aspirate before starting antibiotics, sending fluid for cell count, Gram stain, culture and polarised microscopy. The pathway is now a suspected septic arthritis pathway, and chondrocalcinosis on the radiograph does not change that: crystals in the fluid do not exclude coexisting infection. Never attribute an acutely hot joint to pseudogout on the basis of the radiograph alone.