Giant cell tumor (GCT) of bone is generally a benign tumor composed of mononuclear stromal cells and characteristic multinucleated giant cells that exhibit osteoclastic activity. It usually develops in long bones but can occur in unusual locations. The typical appearance is a lytic lesion with a well-defined but nonsclerotic margin that is eccentric in location, extends near the articular surface, and occurs in patients with closed physes. However, GCT may have aggressive features, including cortical expansion or destruction with a soft-tissue component. Fluid-fluid levels, consistent with secondary formation of aneurysmal bone cysts, are seen in 14% of cases. GCT can mimic or be mimicked by other benign or malignant lesions at both radiologic evaluation and histologic analysis. Rarely, GCT is associated with histologically benign lung metastases or undergoes malignant degeneration. In the past, the mainstay of treatment was surgical, primarily consisting of curettage with cement placement, with recurrence rates of 15%-25%. Recurrence is suggested by development of progressive lucency at the cement-bone interface. Other complications include pathologic fracture and postoperative infection. Denosumab, a monoclonal antibody that targets the osteoclastic activity of GCT, has produced 90% tumor necrosis in early studies, results indicative of promise as a potential adjuvant therapy.

Morel-Lavallée lesions are posttraumatic hemolymphatic collections related to shearing injury and disruption of interfascial planes between subcutaneous soft tissue and muscle. We review the pathophysiology of Morel-Lavallée lesions, clinical presentation, and potential sites of involvement. Magnetic resonance imaging (MRI) is the modality of choice for characterization. We present the MRI classification and highlight the key imaging features that distinguish the different types, focusing on the three most common: seroma, subacute hematoma, and chronic organizing hematoma. Potential mimics of Morel-Lavallée lesions, such as soft tissue sarcoma and hemorrhagic prepatellar bursitis, are compared and contrasted. Treatment options and a management algorithm are also briefly discussed.

Stress fracture, in its most inclusive description, includes both fatigue and insufficiency fracture. Fatigue fractures, sometimes equated with the term "stress fractures," are most common in runners and other athletes and typically occur in the lower extremities. These fractures are the result of abnormal, cyclical loading on normal bone leading to local cortical resorption and fracture. Insufficiency fractures are common in elderly populations, secondary to osteoporosis, and are typically located in and around the pelvis. They are a result of normal or traumatic loading on abnormal bone. Subchondral insufficiency fractures of the hip or knee may cause acute pain that may present in the emergency setting. Medial tibial stress syndrome is a type of stress injury of the tibia related to activity and is a clinical syndrome encompassing a range of injuries from stress edema to frank-displaced fracture. Atypical subtrochanteric femoral fracture associated with long-term bisphosphonate therapy is also a recently discovered entity that needs early recognition to prevent progression to a complete fracture. Imaging recommendations for evaluation of stress fractures include initial plain radiographs followed, if necessary, by magnetic resonance imaging (MRI), which is preferred over computed tomography (CT) and bone scintigraphy. Radiographs are the first-line modality and may reveal linear sclerosis and periosteal reaction prior to the development of a frank fracture. MRI is highly sensitive with findings ranging from periosteal edema to bone marrow and intracortical signal abnormality. Additionally, a brief description of relevant clinical management of stress fractures is included.

Sclerosing bone dysplasias are skeletal abnormalities of varying severity with a wide range of radiologic, clinical, and genetic features. Hereditary sclerosing bone dysplasias result from some disturbance in the pathways involved in osteoblast or osteoclast regulation, leading to abnormal accumulation of bone. Several genes have been discovered that, when disrupted, result in specific types of hereditary sclerosing bone dysplasia (osteopetrosis, pyknodysostosis, osteopoikilosis, osteopathia striata, progressive diaphyseal dysplasia, hereditary multiple diaphyseal sclerosis, hyperostosis corticalis generalisata), many of which exhibit similar pathologic mechanisms involving endochondral or intramembranous ossification and some of which share similar underlying genetic defects. Nonhereditary dysplasias include intramedullary osteosclerosis, melorheostosis, and overlap syndromes, whereas acquired syndromes with increased bone density, which may simulate sclerosing bone dysplasias, include osteoblastic metastases, Paget disease of bone, Erdheim-Chester disease, myelofibrosis, and sickle cell disease. Knowledge of the radiologic appearances, distribution, and associated clinical findings of hereditary and nonhereditary sclerosing bone dysplasias and acquired syndromes with increased bone density is crucial for accurate diagnosis.

The knee is an intricate joint with numerous tendinous, ligamentous, and meniscal attachments, which make it particularly vulnerable to complex injuries after trauma. A variety of avulsion fractures of the knee can occur, including Segond and reverse Segond fractures; avulsions of the anterior and posterior cruciate ligaments; arcuate complex avulsion; iliotibial band avulsion; avulsions of the biceps femoris, semimembranosus, and quadriceps tendons; Sinding-Larsen-Johansson syndrome; and Osgood-Schlatter disease. These fractures often have a subtle appearance at conventional radiography, which is typically the first imaging modality performed in these cases. Advanced imaging modalities, particularly magnetic resonance imaging, are helpful and can provide valuable additional information for adequately defining the extent of damage. The onus is on the radiologist to identify the pattern of injury and to understand the substantial underlying damage that it frequently represents. Conveying this information to the referring clinician is crucial and represents the first step toward additional evaluation and probable orthopedic referral. By recognizing the significance of these injuries at initial presentation, radiologists can facilitate appropriate patient work-up and prevent the chronic morbidity associated with delayed treatment.