Musculoskeletal Radiology

Juvenile idiopathic arthritis (JIA), formerly known as juvenile rheumatoid arthritis, is a heterogeneous group of inflammatory diseases characterized by inflammation of 1 or more joints and is the most common pediatric rheumatic disease. Juvenile idiopathic arthritis is classified according to its clinical presentation, and diagnosis is made with examination findings as well as confirmatory lab testing showing evidence of inflammation and characteristic X-ray findings. Treatment is directed at preventing loss of function and controlling or limiting joint damage, with a variable prognosis depending on the type.

Gout medications include antiinflammatory and urate-lowering medications. Colchicine is an antiinflammatory medication that can be used for acute gout flares. The urate-lowering drug classes include the xanthine oxidase inhibitors, uricosuric agents, and uricases. These medications are beneficial for the prevention of gout exacerbations and work through a variety of mechanisms. Xanthine oxidase inhibitors are the most commonly used urate-lowering therapy; these work by inhibiting the enzyme necessary for the conversion of purines to uric acid. Uricosuric agents reduce reabsorption of uric acid by the proximal tubule, thereby increasing renal excretion. Lastly, the urases are recombinant enzymes that metabolize uric acid to allantoin. In addition to gout, urate-lowering treatment can also be used for other indications, such as the prevention of tumor lysis syndrome and uric acid nephrolithiasis.

Bone, while seemingly inert, is an active, growing, and changing part of the human body, in addition to being the body's primary calcium reservoir. In the correct homeostatic conditions, bone can remodel in response to damage, stress, or hormonal signaling (parathyroid hormone and calcitonin). Osteocytes located deep in the bone sense damage and signal bone-lining cells that will begin the process of remodeling. This process is vital not only for damage repair but also to adapt to a new environment and conditions.

Reactive arthritis is a seronegative autoimmune spondyloarthropathy that occurs in response to a previous gastrointestinal (GI) or genitourinary (GU) infection. The pathophysiology of this disease is unclear, but a significant proportion of affected patients are positive for HLA-B27. The disease manifests as asymmetric oligoarthritis (particularly of large joints in the lower extremities), enthesopathy, dactylitis, and/or sacroiliitis. Ocular, mucocutaneous, GI, GU, and cardiac manifestations may also occur. The diagnosis is clinical, and efforts should be made to rule out alternative diagnoses. Management focuses on controlling symptoms, typically with nonsteroidal anti-inflammatory drugs. An active infection should also be treated, particularly Chlamydia trachomatis.

A fracture is a disruption of the cortex of any bone and periosteum and is commonly due to mechanical stress after an injury or accident. Open fractures due to trauma can be a medical emergency. Fractures are frequently associated with automobile accidents, workplace injuries, and trauma. Clinical presentation varies depending on the cause and location of the injury, but generally includes deformity, pain, edema, and inflammation. Diagnosis is made clinically and confirmed with imaging, and management may be with splinting or may require surgery.

Disease-modifying antirheumatic drugs are antiinflammatory medications used to manage rheumatoid arthritis. The medications slow, but do not cure, the progression of the disease. The medications are classified as either synthetic or biologic agents and each has unique mechanisms of action and side effects. Common side effects among the disease-modifying antirheumatic drugs include bone marrow suppression and hepatotoxicity. Leflunomide, methotrexate, and tumor necrosis factor (TNF)-ɑ inhibitors are avoided in pregnancy due to their potential teratogenicity. Hydroxychloroquine and sulfasalazine are safe for use during pregnancy.

Bone marrow, the primary site of hematopoiesis, is found in the cavities of cancellous bones and the medullary canals of long bones. There are 2 types: red marrow (hematopoietic with abundant blood cells) and yellow marrow (predominantly filled with adipocytes). Human marrow composition changes with age. In the young, the entire bone marrow is red, as there is increased blood cell production. As age increases, there is gradual change to the yellow marrow variety. The yellow marrow can revert to red marrow when hematopoiesis is needed (e.g., anemia). The red marrow, by hematopoiesis, produces about 6 billion cells per kilogram per day. The process relies on hematopoietic cells (stem cells and progenitors) producing mature effector cells (lymphocytes, platelets, granulocytes, erythrocytes) with the aid of nonhematopoietic elements. Production is regulated by cytokines released in the bone marrow environment and feedback from target tissues. The marrow structure allows hematopoiesis to take place in the extravascular area, and after staged differentiation, blood cells are released into circulation.

Bone is a compact type of hardened connective tissue composed of bone cells, membranes, an extracellular mineralized matrix, and central bone marrow. The 2 primary types of bone are compact and spongy. Because the matrix is mineralized (rather than aqueous), nutrients and waste cannot diffuse through the matrix. Bone has developed a unique structure to allow the functions to occur. The structure of bone allows the bone to be hard, but not too brittle, and gives bone the strength to resist compressive and bending forces. As a result, bone is ideally suited for the functions of support, protection of vital organs, and movement. In addition, bone produces blood cells in the marrow and is the body's primary storage site for calcium.

The process of bone formation is called ossification. The 2 types of ossification are intramembranous ossification, in which bone is developed directly from mesenchyme cells, and endochondral ossification, in which a hyaline cartilage model is created 1st and then later replaced with bone. Bone continues to grow into early adulthood at the epiphyseal plates, where chondrocytes continue to divide, die, and be replaced with mineralized bone. Bone mineralization occurs because the osteoblasts allow high levels of calcium and phosphate to accumulate above critical threshold levels within bone.

Septic arthritis is an infection of the joint due to direct inoculation, contiguous extension, or hematogenous spread of infectious organisms into the joint space. This process causes an acute, inflammatory, monoarticular arthritis. A variety of organisms have been implicated, most commonly Staphylococcus aureus. Previously damaged joints (e.g., rheumatoid arthritis) are at the highest risk of infection. Patients present with a swollen, warm, and tender joint, most commonly involving the knee. Positive cultures from arthrocentesis are diagnostic, with antibiotic therapy tailored to the specific organism. Repeated joint aspiration, or surgical drainage, is required in some cases. If the joint space is infected with a prosthetic in place, debridement and prosthesis removal may also be required.

Rheumatoid arthritis (RA) is a symmetric, inflammatory polyarthritis and chronic, progressive, autoimmune disorder. Presentation occurs most commonly in middle-aged women with joint swelling, pain, and morning stiffness (often in the hands). Systemic inflammation can lead to extraarticular manifestations such as rheumatoid nodules, interstitial lung disease, Felty syndrome, and pericarditis. Prolonged and severe disease can lead to irreversible joint deformities. Diagnosis is based on strong clinical suspicion and confirmed by the presence of rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibodies, and characteristic imaging. Management involves long-term disease-modifying antirheumatic drugs (DMARDs), biologic agents, and physical therapy. Glucocorticoids and nonsteroidal antiinflammatory drugs (NSAIDs) are the treatment of choice for acute exacerbation.

Osteoarthritis (OA) is the most common form of arthritis, and is due to cartilage destruction and changes of the subchondral bone. The risk of developing this disorder increases with age, obesity, and repetitive joint use or trauma. Patients develop gradual joint pain, stiffness lasting < 30 minutes, and decreased range of motion. Physical exam may reveal crepitus with joint motion and osteophyte formation (Heberden's and Bouchard's nodes). The diagnosis is clinical and supported with radiographic joint findings. Management includes conservative measures, analgesic medications, glucocorticoid intra-articular injections, and surgery for advanced disease.

Gout is a heterogeneous metabolic disease associated with elevated serum uric acid levels (> 6.8 mg/dL) and abnormal deposits of monosodium urate in tissues. The condition is often familial and is initially characterized by painful, recurring, and usually monoarticular acute arthritis, or “gout flare,” followed later by chronic deforming arthritis. The kidneys can also be affected, and urate crystals can precipitate as chalkstone-like deposits (“tophi”) in the soft tissues, synovial tissues, or in bones near the joints. Hyperuricemia is due to overproduction and/or underexcretion of uric acid and is a necessary but insufficient precondition to developing urate crystal deposition disease (most hyperuricemic individuals never experience clinical gout). The most commonly involved joint is the first metatarsophalangeal joint. The identification of urate crystals in joint aspirate or tophi is diagnostic. Effective therapies to relieve the pain of a gout flare include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and glucocorticoids; the choice of therapy depends on the individual and if there are any contraindications.