Periarticular Calcifications Research Articles

Association between low cortical bone mineral density, soft-tissue calcification, vascular calcification and chondrocalcinosis: a case-control study

ObjectivesTo examine the association between bone mineral density (BMD), soft-tissue calcification, vascular calcification and chondrocalcinosis (CC).MethodsA case-control study within the Genetics of Osteoarthritis and Lifestyle (GOAL) database (n=3170). All GOAL...

FRI0378 Chondrocalcinosis – a fresh look at established and novel risk factors

BackgroundChondrocalcinosis (CC), predominantly a result of calcium pyrophosphate crystal deposition (CPPD) occurs due to a combination of excess synovial fluid extracellular pyrophosphate (PPi) and favourable cartilage matrix changes. The association...

THU0438 Predictive value of ultrasound on the response to steroid infiltrations in the painful shoulder: A prospective controlled single-blind study of 70 patients

BackgroundAcute shoulder pain is a common rheumatologic symptom. Although there are multiple causes, it usually responds well to local steroid infiltration. Ultrasound (US), a simple non-invasive and accessible imaging modality...

Multiple bilateral symmetrical recurrent hyperphosphatemic tumoral calcinosis in a young adolescent girl: A rare entity

Tumoral calcinosis is an uncommon disease characterized by periarticular soft-tissue hyperplasia and calcification. Large joint such as hip, shoulder and elbow are most commonly involved. This entity usually manifest in adolescent females as slowly growing, painless, mobile soft-tissue tumor like mass around the large joint that may interfere with joint function when large. A familial predisposition has been reported. Exact cause is not known, but there is deposition of calcium phosphate with normal calcium and elevated phosphorus levels. Here, we report a case of 15-year-old female presented with symmetrical, recurrent swellings on various joints with milk like fluid extrusion and scar mark of previous excision.

Tumoral calcinosis: a dental literature review and case report

Tumoral calcinosis (TC) is a rare familial disease characterized by abnormal peri-articular calcification in affected joints, without any associated renal, metabolic or collagen vascular disease. It is characterized by usual hyperphosphataemia with normal serum calcium and alkaline phosphatase values. There are only a few reported cases ofTC patients with dental findings. This article reviews the dental literature and describes progressive gingival, alveolar and mandibular tori enlargement in a 41-year-old female from Zimbabwe with tumoral calcinosis. Tumoral calcinosis is a rare disorder of mineral metabolism with oral manifestations.

Kidney and bone update : the 5-year history and future of CKD-MBD. Disorders of musculoskeletal system in CKD ; bone fracture and periarticular calcification

Chronic kidney disease-mineral and bone disorder (CKD-MBD) affects life expectancy through vascular calcification, and impairs patient's activity of daily living (ADL) and quality of life (QOL) through bone fracture and periarticular calcification. In CKD patients, vitamin D deficiency and secondary hyperparathyroidism impairs bone strength, and muscle dysfunction related to vitamin D deficiency also causes easy fall, leading to the high risk of bone fracture. Bone fracture not only aggravates ADL and QOL but increases the risk of mortality. Periarticular calcification such as tumoral calcinosis in relation to CKD-MBD causes restricted range of articular motion, leading to the deterioration of patient's ADL and QOL. Because bone fragility and tumoral calcinosis occurs in relation to CKD-MBD, the appropriate management of CKD-MBD is madatory.

Adult hypophosphatasia with painful periarticular calcification treated with surgical resection

Hypophosphatasia is a rare inherited disorder characterized by a low serum alkaline phosphatase (ALP) activity and defective bone mineralization. Adult hypophosphatasia typically manifests in middle-age as a result of osteomalacia with recurrent stress fractures of the lower limb. However, considerable variation occurs in the clinical expression of hypophosphatasia, and no curative treatment has yet been established. We herein report a case of adult hypophosphatasia with painful calcific periarthritis, which showed improvement after surgical resection. A 32-year-old male was referred to our clinic complaining of pain in his elbows and knees. A painful subcutaneous mass was palpable on his right lateral epicondyle, where periarticular calcification was detected by plain radiography. The laboratory data showed a slight decrease in serum ALP activity and bone mineral density, and an elevation in the urinary phosphoethanolamine. Genomic DNA sequencing revealed an F310L mutation and a Y246H polymorphism in the tissue-nonspecific alkaline phosphatase gene, confirming the diagnosis of hypophosphatasia. The pain in the patient's right elbow was not responsive to nonsteroidal anti-inflammatory drugs, and triamcinolone diacetate was locally injected for treatment. His symptoms were ameliorated after the injection; however, they recurred in 3months, and he became refractory to additional steroid injection. Surgical debridement of the calcified lesion was performed, and his symptoms were successfully ameliorated after the surgery.

Short-Term and Long-Term Outcome of Anti-Jo1-Positive Patients with Anti-Ro52 Antibody

The aims of the present study were to (1) assess clinical features and long-term outcome in anti-Jo1-positive patients with anti-Ro52 antibody; (2) compare characteristics of anti-Jo1-positive patients with and without anti-Ro52 antibody; and (3) compare features of anti-Ro52-positive patients with and without anti-Jo1 antibody. The medical records of 89 consecutive anti-Jo1-positive patients with antisynthetase syndrome (ASS) were reviewed; 36 of these patients had coexistent anti-Ro52 antibody. Furthermore, the medical records of 13 consecutive anti-Ro52-positive patients without anti-Jo1 antibody were also reviewed. Nine anti-Jo1-positive patients (25%) with anti-Ro-52 antibody achieved remission of ASS, whereas 19 other patients (52.8%) improved and 8 patients (22.2%) worsened their clinical status. Anti-Jo1-positive patients with anti-Ro52 antibody experienced ASS-related complications: interstitial lung disease (n = 28), esophageal dysfunction (n = 9), and joint manifestations (n = 25), including periarticular hydroxyapatite calcifications and erosions of metacarpophalangeal and interphalangeal joints and wrists (n = 3); 7 anti-Ro52-positive patients (19.4%) had cancer. Anti-Jo1-positive patients with anti-Ro52 antibody, compared with those without, more commonly experienced deterioration of myositis and joint involvement, symptomatic form of ILD, and cancer; they also had decreased survival rate (P = 0.05). We further found that anti-Ro52-positive patients with anti-Jo1 antibody, compared with those without, were younger and more frequently exhibited ILD with poorer prognosis. Our series underlines that the presence of anti-Ro52 antibody is associated with a particular phenotype of ASS, leading to more severe myositis and joint impairment. Moreover, the coexistence of anti-Ro52 antibody seems to be associated with an increased risk of cancer. We therefore suggest that anti-Jo1-positive patients should routinely undergo the search for anti-Ro52 antibody, as this autoantibody appears to impact patients' prognosis.

Tophaceuos Calcium Pyrophosphate Dihydrate Deposition Disease of the Temporomandibular Joint: The Preferential Site?

Calcium pyrophosphate dihydrate deposition disease (CPPD) is a metabolic disorder characterized by noninfectious joint inflammation with intra- or periarticular calcification.1 In 1962, Kohn et al2 were the first to describe the association of CPPD crystals in the synovial fluid of the knees of patients with cartilage calcifications visible on standard radiographs, termed “chondrocalcinosis,”3 and acute symptoms commonly associated with gout. Most population-based research uses chondrocalcinosis as the basis for the presence of CPPD, and this is strongly associated with an increase in age.

Massive, painful tumoral calcinosis in a long‐term hemodialysis patient

In chronic dialysis patients, ectopic, extraosseous calcifications can cause significant morbidity. Uremic tumoral calcinosis is an uncommon and severe complication of dialysis therapy. It is defined as deposition of dense nodular calcium-containing masses surrounding the large joints of the body, generally associated with the presence of high serum calcium-and-phosphorus product. We describe a 69-year-old woman submitted to long-term chronic hemodialysis that developed painful, bilateral hip tumors. Radiographic investigation showed extensive periarticular calcifications, and a bone biopsy was suggestive of adynamic bone disease and contained substantial amounts of aluminum. The lesions were surgically excised, and the histological analysis demonstrated amorphous, calcified material associated with densely collagenized connective tissue.

Rhumatismes apatitiques

Hydroxyapatite crystals are a common cause of periarticular disease. Virtually, any joint can be involved, but the shoulder is by far most commonly involved. These calcifications, often asymptomatic, can lead to an acute microcrystalline tendinitis or bursitis, which may simulate infection. The diagnosis of periarticular calcifications relies on imaging techniques using X-rays or ultrasounds. Treatment of acute tendinitis or bursitis includes icing, rest, analgesics or non steroidal anti-inflammatory drug and oral steroids or local steroids injection. Removal of the deposit can be considered in patients with chronic pain, particularly at the shoulder.

AJR Teaching File: Periarticular Calcifications in Two Patients With Acute Hand Pain

AJR Teaching File: Periarticular Calcifications in Two Patients With Acute Hand PainEmily N. Vinson1, Shivang V. Desai1, Suraj Reddy1 and Richard D. Goldner1Audio Available | Share

Hand Radiological Damage in Systemic Sclerosis: Comparison with a Control Group and Clinical and Functional Correlations

To define the burden of hand radiological damage in systemic sclerosis (SSc) patients, compared with a control group. Both hands of 167 SSc patients and 168 hands (82 right and 86 left) of age- and gender-matched controls were imaged by conventional radiograph. Two musculoskeletal radiologists semiquantitatively scored the following lesions: tuft acro-osteolysis, tuft calcinosis, joint space narrowings, marginal erosions, surface erosions, collapse arthropathies, periarticular calcifications, and juxta-articular osteoporosis, at the following areas: tufts, distal interphalangeal, proximal interphalangeal, metacarpophalangeal, carpal, and first carpometacarpal joints. Clinical and functional characteristics of the 167 SSc patients were obtained from the Belgian Systemic Sclerosis Cohort database. Tuft acro-osteolysis and calcinosis were the most common findings observed in SSc patients and were almost absent in controls. SSc patients displaying tuft acro-osteolysis/calcinosis suffered from more severe disease. Arthropathies were infrequently detected and mainly consisted of a mixture of osteoarthritis-related changes (joint space narrowing and surface erosions)-also observed in controls-and of 2 types of rare SSc-associated arthropathies: a rheumatoid arthritis-like pattern, characterized by marginal erosions (n = 7 patients), and a collapse arthropathy (n = 6 patients), characterized by pressure erosions and joint subluxation. Although a rheumatoid arthritis-like or a collapse arthropathy can be observed in SSc patients, arthropathies are less common than previously reported.

La calcinose tumorale : à propos d’un cas

Tumoral calcinosis is a rare benign disease, defined by the presence of calcified deposits in periarticular tissues. The pathogenesis is unclear. We report a new case of tumoral calcinosis in a young girl, involving the left hip and both elbows. The clinical exam found a voluminous mass of soft tissues and the radiological exam showed the presence of voluminous periarticular calcifications with no bone involvement. The diagnosis was confirmed by the anatomopathological exam. The treatment remains essentially surgical and the prognosis is very good.

Chondrosarcoma in Metachondromatosis

Mavrogenis, Andreas F. MD1; Skarpidi, Evangelia MD2; Papakonstantinou, Olympia MD3; Papagelopoulos, Panayiotis J. MD, DSc4 Author Information

Loss-of-Function ENPP1 Mutations Cause Both Generalized Arterial Calcification of Infancy and Autosomal-Recessive Hypophosphatemic Rickets

The analysis of rare genetic disorders affecting phosphate homeostasis led to the identification of several proteins that are essential for the renal regulation of phosphate homeostasis; for example, fibroblast growth factor 23 (FGF23), which inhibits renal phosphate reabsorption and 1,25-dihydroxyvitamin D synthesis. Here, we report presumable loss-of-function mutations in the ENPP1 gene (ectonucleotide pyrophosphatase/phosphodiesterase) in members of four families affected with hypophosphatemic rickets. We provide evidence for the conclusion that ENPP1 is the fourth gene-in addition to PHEX, FGF23, and DMP1-that, if mutated, causes hypophosphatemic rickets resulting from elevated FGF23 levels. Surprisingly, ENPP1 loss-of-function mutations have previously been described in generalized arterial calcification of infancy, suggesting an as yet elusive mechanism that balances arterial calcification with bone mineralization.

Local effects of intra-articular corticosteroids

Intra-articular corticosteroid injection (IACI) is a very popular procedure. In this review, we wanted to review all that had been published about local effects of IACIs. English literature search was made through PubMed using the terms intra-articular and local effect. Effects on subjective, functional, structural, cellular, humoral, molecular, and imaging aspects were included. Also, all local adverse effects were documented. The main beneficial effect of IACI is pain relief. The duration of this effect is variable and depends on underlying disease, type of disease, amount of structural damage, type of IACI, dose of IACI, presence of joint effusion, level of inflammatory mediators, emptiness of joint effusion, availability of imaging, and others. At large, inflammatory problems had higher rate of favorable response in terms of pain and function. IACI at the knee joint in juvenile idiopathic arthritis patients resulted in remission for >6 months in >80% of the patients with a mean duration of approximately 1.2 years, while in the osteoarthritic knee there was a pain relief for 3 weeks only and in rheumatoid arthritis (RA) knee for 8 weeks. There was no joint space loss at the knee joint following multiple IACI in osteoarthritis and also no increase in cartilage or bone erosions in RA following a single IACI. IACI guide imaging is important in achieving better results in particular joints. Joint infection rate is very low. Other adverse effects included intra-articular and periarticular calcifications, cutaneous atrophy, cutaneous depigmentation, avascular necrosis, rapid destruction of the femoral head, acute synovitis, Charcot's arthropathy, tendinopathy, Nicolau's syndrome, and joint dislocation. IACI is associated with a wide range of local effects. Subjective and functional favorable response is prominent mainly in juvenile idiopathic arthritis patients. Adverse effects are either rare or insignificant.

Displaced medial epicondyle fractures of the humerus: surgical treatment and results. A report of 139 cases

Elbow instability is a common feature after medial epicondyle fractures, displaced or not, even in the absence of dislocation. Undisplaced or minimally displaced fractures often have an underestimated degree of instability secondary to unrecognised capsuloligamentous and muscular injuries. The purpose of this retrospective study was to analyze and to assess objectively the results of the surgical treatment of these acute injuries. One hundred and thirty-nine displaced medial epicondyle fractures were surgically treated and reviewed. A valgus stress test was performed on each child under general anesthesia or sedation. Functional outcome was assessed using a scoring system based on a series of clinical and radiographic criteria. The mean age of patients at the time of accident was 11.9 years. Mean follow-up was 3.9 years. All fractures had associated with instability of the elbow. A posterolateral elbow dislocation was associated in 80 fractures. The medial epicondylar fragment was anatomically reduced and fixed in all cases. The final result was excellent in 130 cases and good in 9 cases. Elbow were stable and pain free in all patients. Normal elbow range of motion was reported in 133 cases. Union was achieved in all cases. Among these cases, nine had presented a <<fibrous>> union with no change on valgus stress views. No cases of cubitus valgus >/=10 degrees were observed. Anatomical abnormalities of the elbow were present in 28 cases: periarticular calcification in 18 cases, medial condyle groove formation in 4 cases, moderate hypertrophy and fragmentation of the medial epicondyle, respectively, in 3 cases. The positive valgus stress test performed at the time of surgery for all epicondyle fractures without associated dislocation regardless of there degree of displacement justified our operative approach. Operative intervention is a good management of these fractures and results in an anatomic reduction, a solid bone union and prevents valgus instability. Even with postoperative immobilization of the elbow (mean of 4 weeks), stiffness is rare. Damage to the medial stabilizing structure of the elbow rather than the extent of medial epicondyle displacement has a far greater influence on joint stability and outcome.

Periarticular Calcification Causing Acute Carpal Tunnel Syndrome: A Case Report

We report a case of acute carpal tunnel syndrome caused by periarticular calcification (hydroxyapatite deposition disease) around the wrist joint in a 64-year-old woman. She had acute severe pain, exacerbated by wrist movements and extension of the fingers. Her full blood count, urea, electrolytes, uric acid, calcium, phosphate, alkaline phosphatase, and thyroid function levels were all within normal ranges, and her serum was negative for rheumatoid factor. Computed tomography revealed lobulated calcification close to the volar capsule. She underwent an emergency surgical decompression of the carpal tunnel under general anaesthesia within 3 hours of presentation. The flexor tendon sheaths were excised, and 'toothpaste-like' chalky material (hydroxyapatite crystals) in the capsule was removed. The pain was relieved dramatically and her median nerve function recovered. She was symptom-free at the one-year follow-up.

Familial Tumoral Calcinosis: A Forty-Year Follow-up on One Family

Familial tumoral calcinosis is a rare autosomal recessive disorder that was first described well in a report on four patients from one family in 1969. The disease leads to periarticular ectopic calcifications. The original report described patients from black, healthy, unrelated parents with sixteen children, seven of whom had the disease. On the basis of retrospective chart reviews and interviews with surviving family members, we describe the long-term follow-up of this one family, encompassing as long as forty years. Of the sixteen siblings, seven had tumoral calcinosis. All seven affected children had hyperphosphatemia. There were two subsequent generations comprising thirteen children and seven grandchildren with no instances of tumoral calcinosis. The seven affected patients were followed for as many as forty years and underwent an average of twenty-one operations (range, four to thirty-six operations) for the treatment of calcified lesions. The genetic defect has been identified as the GALNT3 gene, thus leading to the hyperphosphatemic form of the disease. Although two of the patients had died by the time of the present study, the remaining five provided accounts of the disease course, the response to surgery and to medical therapy, and the effect of therapy on their lives. Some members had relatively few lesions and surgical procedures (as few as four), whereas others had an unrelenting course of lesions, recurrences, and surgical procedures (as many as thirty-six, with numerous other procedures). Three patients had multiyear periods with few symptoms--one for seven years, one for twelve years, and one for fifteen years. No effective medical therapy was found to control the lesions, and operations were associated with a high recurrence rate. Familial tumoral calcinosis has a varied natural history; some patients have an unrelenting course, while others may experience quiescent periods. The GALNT3 gene is responsible for the hyperphosphatemic form as seen in this family. Molecular testing may be of benefit to members of affected families, and future studies may help to explain the phenotypic variability among affected individuals. No medical or surgical treatment plan seemed to be effective for controlling the lesions in this family.