Chondrocalcinosis is a chronic disease characterized by an inflammatory lesion of the joints due to the deposition of calcium pyrophosphate in them. Clinically, it can occur both asymptomatically and with manifestations of acute monoarthritis or minor joint pain. The diagnosis is made on the basis of symptoms, anamnesis, detection of calcium pyrophosphate crystals in the synovial fluid by polarization microscopy, radiography and ultrasound examination of the joints. Treatment consists in the use of nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, intra-articular administration of glucocorticosteroids. If necessary, endoprosthesis is performed.
Chondrocalcinosis (pyrophosphate arthropathy, pseudopodagra) is a chronic rheumatological disease that belongs to the group of microcrystalline arthritis. This pathology is characterized by the deposition of calcium pyrophosphate deposits in articular cartilage and periarticular tissues (ligaments, tendons, joint bags), which leads to their inflammation and degeneration.
Chondrocalcinosis is considered a “disease of the elderly” and occurs in 30-40% of people over 70 years old. There are no exact data on the prevalence among young people. Pseudopodagra is characterized by imitation of symptoms of other rheumatological pathologies. The acute form in the form of monoarthritis is more often observed in men. Osteoarthritis-type arthropathy is specific to the female sex.
There are several reasons for the development of chondrocalcinosis, but most often it is not possible to accurately determine the etiological factor. Risk factors are old age and a history of joint injuries. Conditions that can cause shifts in the metabolism of calcium pyrophosphate are as follows:
- Hereditary predisposition. In the course of genetic studies, a mutation of the ANKH gene (locus 5p15.2) encoding a protein that transports intracellular inorganic pyrophosphate is detected in some patients. As a result of a genetic defect, a compound accumulates in the articular tissue. The inheritance of the gene is carried out according to the autosomal dominant type.
- Diseases. Metabolic and endocrine pathologies that disrupt the exchange of calcium pyrophosphate include hemochromatosis, hyperparathyroidism, hepatolenticular degeneration (Wilson-Konovalov disease). There is also an association of chondrocalcinosis with alkaptonuria, hypomagnesemia, and alkaline phosphatase deficiency.
- Medicines. Some medications cause calcium dysmetabolism, which can lead to chondrocalcinosis. Such medications include thyroid hormones and diuretics. Deposition of inorganic pyrophosphate also occurs with prolonged parenteral administration of iron and calcium preparations.
The main pathogenetic mechanism in chondrocalcinosis is the formation and accumulation of crystals of inorganic calcium pyrophosphate in the cartilage of joints. Under the influence of various factors (genetic defect, diseases, medication intake), the activity of enzymes of the nucleoside triphosphate-pyrophosphohydrolase group increases, which catalyze the reactions of pyrophosphate formation by hydrolysis of adenosine triphosphate. The transition of crystals into synovial fluid provokes the development of synovitis.
Further deposition of pyrophosphate crystals leads to degradation of articular cartilage, fibrosis of the synovial membrane and calcification of periarticular tissues (tendons, ligaments, aponeurosis). Pathoanatomically revealed swelling of the synovial membrane, its infiltration by macrophages, lymphocytes and giant multinucleated cells, hypertrophy and apoptosis of chondrocytes. Synoviocyte proliferation, erosion of cartilage tissue and fragmentation of the surface layer of cartilage are also characteristic.
According to the clinical course, pseudopodagra, pseudosteoarthrosis, pseudorheumatoid arthritis are distinguished, simulating the symptoms of other joint diseases. Isolated cases of pseudoneuropathic chondrocalcinosis resembling Charcot’s joint in diabetes mellitus are also described. According to the etiological factor , the following forms are distinguished:
- Family (hereditary). The disease is caused by a genetic mutation. It develops more often in young patients (30-40 years old). The most severe form of pathology leading to disability.
- Primary (idiopathic). The most common type of chondrocalcinosis with an unclear cause. The main contingent of patients are elderly people.
- Secondary. It occurs in various diseases, as well as when taking medications that disrupt the metabolism of calcium and inorganic pyrophosphate.
The clinical picture of pyrophosphate arthropathy is diverse. In some cases, the disease is completely asymptomatic. Any joints can be affected, but the favorite localization is the knee and wrist joints. The most rare localizations of calcium pyrophosphate deposits are the cervical spine, pubic symphysis, temporomandibular joint.
Acute monoarthritis (pseudopodagra) develops in 25% of patients. Seizures occur more often in the spring. There is a strong acute pain in the joint, swelling, redness of the skin over the joint, difficulty and soreness of movements. The skin feels hot to the touch. The intensity of the pain increases within 24-36 hours, then slowly weakens within a week. The first metatarsophalangeal joint may be involved, which significantly complicates differential diagnosis with gout. The distinguishing signs of chondrocalcinosis from gout are the absence of fever and specific tofuses (nodes) on the skin. Nothing bothers the patient outside of the attack.
Approximately half of the patients have symptoms resembling osteoarthritis – moderate symmetrical aching pains in large joints, increasing with movement and weakening at rest, osteophytes (Bouchard and Geberden nodules) on distal interphalangeal joints, ranging in size from a rice grain to a pea. When the menisci of the knee joints are affected, an O-shaped curvature of the lower extremities occurs. 5% of patients suffer from pseudorheumatoid arthritis, characterized by pain and swelling in the metacarpophalangeal joints with morning stiffness.
Chondrocalcinosis is a benign disease with minimal complications. The formation of pronounced deformities or rough contractures of the joints that violate their functions occurs only with a hereditary form. The main problem is the pathological conditions that served as a background for the development of arthropathy. These include damage to the liver and central nervous system in Wilson-Konovalov disease, calcification of blood vessels and renal tubules in hyperparathyroidism, cardiovascular catastrophes in hemochromatosis.
Rheumatologists are involved in the curation of patients with chondrocalcinosis. When making a diagnosis, the clinical picture, family history, prescription of the disease, the presence of concomitant diseases, taking medications are taken into account. To confirm the diagnosis , the following research methods are carried out:
- Blood test. There are no specific changes. In the pseudorheumatoid form, markers of inflammation are sometimes detected – leukocytosis, an increase in the rate of erythrocyte sedimentation, C-reactive protein and rheumatoid factor. To exclude diseases associated with chondrocalcinosis, the level of iron, ionized calcium, copper, and parathyroid hormone is determined.
- Instrumental methods. During joint radiography, an X–ray sign specific to chondrocalcinosis is noted – calcification of hyaline articular cartilage, which is presented in the form of a narrow shadow repeating the contour of the articular surface. There is also a narrowing of the articular gap, the presence of sclerosis of the subchondral bone, subchondral cysts, calcification of tendons and ligaments. Ultrasound of the joints is more sensitive, which makes it possible to identify smaller calcium deposits that look like hyperechoic spots in the hyaline cartilage area.
- Synovial fluid analysis. A crucial test that allows you to reliably establish a diagnosis. The liquid is transparent, viscous, and contains a small number of white blood cells. Using polarization microscopy using a compensator, monoclinic or triclinic crystals of calcium pyrophosphate are detected, having a diamond-shaped shape and a blue glow.
Acute attacks of chondrocalcinosis should first of all be differentiated with gouty arthritis. It also needs to be distinguished from other rheumatological diseases that occur with similar symptoms – rheumatoid arthritis, infectious arthritis. Orthopedists and surgeons take part in the differential diagnosis.
There are no strict indications for hospitalization for this disease. Treatment can be carried out both on an outpatient basis and in a hospital. There is no etiotropic therapy. Non-drug methods of exposure are reduced to cold applications, balneotherapy, unloading of the affected joint and performing special physical exercises to strengthen the muscles that stabilize the joint. In the secondary form of the disease, it is necessary to cancel causal medications and treat the underlying disease (hyperparathyroidism, hemochromatosis, hepatolenticular degeneration).
Non-narcotic analgesics (diclofenac, naproxen, lornoxicam) are used to relieve pain. Taking into account the need for patients to take NSAIDs for a long time, additional administration of proton pump inhibitors (omeprazole, pantoprazole) is necessary to prevent the development of NSAID-induced gastropathies. In acute pseudopodagric attacks, the combination of NSAIDs with colchicine is effective. Intra-articular injections of glucocorticosteroids (triamcinolone, betamethasone) are used for anti-inflammatory purposes. With pronounced degenerative changes in the joints, surgical intervention (endoprosthetics) is performed.
Prognosis and prevention
Chondrocalcinosis in the vast majority of cases has a favorable prognosis. Pronounced deformities and rough contractures of the joints, leading to violations of their functions, occur rarely and mainly in the genetic form of pathology. With the cancellation of medications that cause the development of pyrophosphate arthropathy, a regression of symptoms quickly occurs without any residual effects. No specific prevention methods have been developed. To prevent the progression of the disease, treatment of pathologies that are associated with chondrocalcinosis should be carried out.