The World Health Organization (WHO) lists rheumatoid arthritis and osteoarthritis as the top two chronic rheumatic conditions with the greatest impact on society. A large number of disorders are subsumed under the terms “arthritis” or “rheumatism” but present quite different manifestations and pose different diagnostic and therapeutic challenges.

Correctly diagnosing arthritis involves consideration of numerous factors, including clinical features (age and sex of the patient, duration of symptoms, clinical appearance of involved joint or joints, presence or absence of associated diseases such as skin disease, uveitis, urethritis), laboratory values (e.g., markers for inflammation, serum rheumatoid factor, serum uric acid level), and imaging features.

Radiographs represent the mainstay for diagnosis and follow up of joint damage. However, in the last two decades, magnetic resonance imaging (MRI) and sonography have emerged as powerful evaluation tools for early diagnosis and staging of rheumatic diseases. They also may give information about the prognosis of rheumatic diseases and may help in differential diagnosis. To establish a correct diagnosis of rheumatic disease, many imaging features have to be systematically addressed:

Rheumatoid arthritis (RA) is a systemic auto-immune disease which originates primarily in the synovial membrane of affected joints and may progress to joint destruction. Extra-articular manifestations involving lungs, heart, pericardium, and nerves may occur. The auto-immune reaction may possibly be related to a prior infection, and many patients are found to be carriers of certain HLA-DBRI genes. Activated T-lymphocytes stimulate B-lymphocytes to produce immunoglobulins (rheumatoid factor and anti-cyclic citrullinated peptides [anti-CCP]) and macrophages to form cytokines (interleukin-1, interleukin-6, and tumor necrosis factor α). This results in the proliferation of mesenchymal tissue elements (fibroblasts) and the influx of inflammatory cells from the blood into the synovial membrane, so that aggressive granulation tissue (pannus) develops. Synovitis develops at certain sites of predilection in joints and tendon sheaths, which probably depends on the number of synovial B-cells present and tissue perfusion. This may result in destruction of adjacent cartilage with joint space narrowing. At areas with absent or thinned hyaline cartilage covering adjacent bone (bare areas), early osseous erosion (marginal erosions) may develop, related to inflammation that stimulates osteoclasts via another cytokine, the RANK ligand. Furthermore, osteoclastic activity may result in juxta-articular osteoporosis or a more generalized arthritis-related osteoporosis of the entire skeleton. Furthermore, collagen-splitting enzymes may damage the ligaments, resulting in subluxation or dislocation, especially in the hands, feet, and atlantodental joint. Early secondary osteoarthritis may develop as a result of joint deformity and destruction. Less commonly ankylosis occurs following complete erosion of articular surfaces.

The initial radiographic manifestations of RA are soft tissue swelling and periarticular osteoporosis. These features represent indirect evidence of synovial inflammation, and their assessment is quite subjective. During the first 3 months of disease onset (referred to as early arthritis), timely initiation of treatment can favorably affect prognosis. However, standard radiographs will usually appear normal, since the disease is still predominantly confined to the synovial membrane. This can be confirmed by ultrasound or MRI.

RA typically begins in the peripheral joints, usually the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints, the wrists, and the metatarsophalangeal (MTP) joints, with a predominantly symmetrical left/right distribution. As the disease progresses, it affects more proximal joints. Early marginal erosions of bone may occur at the radial aspect of the second and third metacarpal heads, at the ulnar styloid process, and at the metatarsal heads, especially at the lateral aspect of the fifth metatarsal head. This is followed by diffuse narrowing of PIP, MCP, MTP, and wrist joints. Characteristically, the distal interphalangeal (DIP) joints are spared. There is no osseous proliferation and no involvement of entheses.

The development of new, powerful but expensive therapeutic agents for RA, such as the anti–tumor necrosis factor (TNF) agents, has created new demands on radiologists to identify patients with aggressive rheumatoid arthritis at an early stage. Sonography is often used to detect synovitis and tenosynovitis at specific joints, whereas MRI is a more global way to evaluate the small synovial joints of the appendicular skeleton and is more sensitive than radiography in detecting synovitis, bone marrow edema, and bone erosions. MRI is also an excellent means to assess spinal complications of RA, in particular subluxation at the atlantoaxial joint. Both MRI and sonography may be used to demonstrate the soft tissue changes of RA, such as tenosynovitis and rheumatoid nodules.

The spondyloarthritides are a group of rheumatic diseases, each with characteristic clinical findings and a common genetic predisposition, especially for the antigen HLA-B27. The terms seronegative spondyloarthritis or seronegative spondyloarthopathy may also be used, with seronegative referring to the serum rheumatoid factor not being elevated.

Forms of spondyloarthritis include ankylosing spondylitis (Bechterew’s disease), (infectious) reactive arthritis, psoriatic arthritis, the enteropathic arthropathies, SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, Type 2 juvenile oligoarthritis, and undifferentiated spondyloarthritis. Chronic, non-bacterial osteomyelitis (chronic recurrent multifocal osteomyelitis, or CRMO) should also be mentioned, even though it is not included in the official classifications. These diseases frequently cause symptoms in the axial skeleton, but the appendicular skeleton may also be affected, in isolation or in combination. Radiographically, these diseases differ from rheumatoid arthritis by the absence or mild nature of periarticular osteoporosis, the involvement of entheses with erosions and with new bone formation, and the asymmetrical involvement of the peripheral skeleton.

The cause of spondyloarthritis remains hypothetical, possibly taking origin from a bacterial infection. Overloading of the endoplasmic reticulum with misfolded HLA-B27 proteins is believed to result in a proinflammatory response. Whereas with rheumatoid arthritis the center of the inflammation is located in the synovial membrane and the clinical course, if left untreated, is progressive and destructive, with spondyloarthritides, the disease is predominantly located in and around the insertions of ligaments and tendons and has an intermittent course with juxtaposed bone destruction and proliferation.

Axial spondyloarthritis is characterized by inflammatory back pain along with other features such as uveitis, dactylitis, or psoriasis. In addition to characteristic radiographic features, “positive” or “highly probable” MRI findings of bone marrow edema or osteitis help make a definitive diagnosis.