1. To understand the aetiologies of bone marrow oedema syndromes.
2. To learn about the imaging characteristics of avascular necrosis of bone.
Bone marrow edema is a pattern of marrow alteration frequently observed at MRI. It is defined by the presence of an ill-delimited area of moderate and homogeneous decrease in signal intensity on SE T1 images that converts to high signal intensity on fat-saturated proton density or T2-weighted images. It is non-specific and may be associated with almost any abnormal marrow, bone or joint conditions. Epiphyseal bone marrow edema can be associated with self-limited spontaneously resolutive conditions (overuse, stress insufficiency fractures, transient osteoporosis), or with evolutive disorders including chondropathy or spontaneous osteonecrosis. The main task of the radiologist is to assess the cause for bone marrow edema and to highlight imaging features that contribute to a specific diagnosis and subsequently a prognosis (resolutive versus non-resolutive). The current lecture aims at emphasizing imaging features indicative of bone marrow edema to avoid confusion with systemic osteonecrosis. We will also highlight imaging features of prognostic significance that enable the clinician to tailor the treatment to the patient’s condition.
1. To understand the pathomechanisms of osteochondral injury and subchondral fractures.
2. To learn about the imaging techniques and prognostic values.
Bone marrow contusions are frequently identified at magnetic resonance imaging after an injury to the musculoskeletal system. These osseous injuries may result from a direct blow to the bone, from compressive forces of adjacent bones impacting one another, or from traction forces that occur during an avulsion injury. Commonly these injuries resolve without long term sequelae. However, they may also involve the cartilaginous surface with or without an associated fracture line defining these as osteochondral injuries, which may have a different prognostic relevance. Subchondral fractures have been implicated in the genesis of some well-known destructive articular conditions whose cause was previously undetermined, such as rapidly progressive osteoarthritis of the hip or spontaneous osteonecrosis of the knee. Subchondral fractures may ultimately lead to bone collapse, secondary osteonecrosis, and severe articular damage. It should be suspected in the appropriate clinical setting, as in early stages it is usually indistinct on initial plain radiographs and magnetic resonance imaging is required for a definitive diagnosis. The fracture line usually appears as a band of low signal intensity in the subchondral bone plate, adjacent to the articular surface, most often surrounded by bone marrow edema. As these injuries may be occult on radiographs, the differentiation of bone contusions from osteochondral injuries or subchondral fractures is possible only with MRI including fat-suppressed and non-fat suppressed sequences. While purely subchondral lesion may have a good prognosis if diagnosed early, disruption of the articular surface may lead to early degenerative alterations including focal cartilage loss and other features of osteoarthritis.
1. To understand the pathomechanisms that result in articular cartilage and bone damage in rheumatoid arthritis, including the clinical relevance of synovitis and BME in terms of their role as an erosion precursor.
2. To learn about the role of imaging techniques to detect early cartilage damage and bone erosions.
Rheumatoid arthritis is the most common inflammatory rheumatic disease. The pathogenesis of RA is subject to ongoing discussion. The traditional concept of inflammatory pannus, in which fibroblast-like synoviocytes provoke cartilage and bone destruction through direct invasion and indirect triggering of catabolic cascades has been termed the outside-in hypothesis. There is also evidence supporting the inside-out hypothesis, in which joint inflammation and destruction originates from the bone marrow. Next to synovium and subchondral bone, another tissue involved in cartilage and bone damage in RA is extra- or intraarticular fat tissue which produces ca. 50 adipo(cyto)kines which may be involved in degradation of all components of the connective tissue, including cartilage. Finally, the hyaline cartilage autoantigens, activated by cartilage damage, may activate and maintain synovitis and lead to joint damage. In everyday practice, the clinical relevance of synovitis and bone marrow inflammation in terms of their role as an erosions precursors is known and ultrasound and MRI are used to detect synovitis, BME, inflammatory cysts, hyaline cartilage loss, and bone erosions. Less in known about inflammatory and destructive potential of intra- and extraarticular fat tissue which may also be evaluated in US and MRI. And only research centers use quantitative MR applications to cartilage to show glucosaminoglycans loss possibly preceeding visible cartilage damage. In this presentation pathomechanisms that result in articular cartilage and bone damage in RA will be presented, including the clinical relevance of synovitis and BME in terms of their role as an erosion precursors, as well as the role of imaging techniques to detect early cartilage damage and bone erosions.