Over time, the reactive interface continues to develop and mature as a discrete zone at the margin of the area of ON. The next pathologic phases represent a continuum of development of a reactive interface in an attempt to wall off and repair the area of ON. The initial phase of ON is cell death, interruption of cell enzymes, and loss of cell metabolic activity. Other causes include metabolic and hematologic disorders, marrow storage disorders, pancreatitis, radiation, drug therapy, occlusive vascular disease, infection, renal disease, Caisson disease, and rheumatologic conditions. Various conditions have been associated with the development of ON, with idiopathic causes, trauma, corticosteroid use, and alcohol consumption implicated in most cases. However, this incidence markedly underestimates the true prevalence of ON, as the majority of patients are asymptomatic. It is estimated that the rate of symptomatic femoral head ON is 2–4.5 cases per patient year, resulting in 10,000–20,000 new cases annually in the United States. įemoral head osteonecrosis (ON) is a common disease and potentially disabling disorder affecting mainly middle-aged adults that can lead to early osteoarthritis due to femoral head collapse and joint incongruity.

Because of the severe consequences of undiagnosed femoral neck stress fractures, the diagnosis is based on combined imaging findings of periosteal edema, endosteal edema, and high cortical signal, regardless of visible fracture line. With any of these findings, one should carefully evaluate for a hypointense band in the marrow or focal cortical abnormality, indicating stress fracture and necessitating prolonged non-weight-bearing or rest from sporting activity. Classic MRI features include ill-defined focal or diffuse high T2 bone marrow signal due to microtrabecular fractures and intramedullary edema, with or without corresponding low T1 signal and/or periosteal edema (Fig. Radiographs are not very sensitive in the identification of stress injuries of the femoral neck. This causes temporary weakening of the marrow and cortical bone, leading to microtrabecular fractures (stress reaction) and cortical failure (stress fracture). The repetitive overloading stimulates bone remodeling, beginning with osteoclastic activity that is not matched by reparative osteoblastic activity and periosteal maturation, which lag 10–14 and 20 days, respectively. Stress fractures are classified as fatigue, resulting from normal bone being subjected to abnormal repetitive forces, and insufficiency, due to normal stress placed on abnormal bone. Stress injuries are most commonly seen in endurance athletes, such as runners and military recruits, as well as recreational athletes with sudden increase in activity. However, because stress injuries may progress to complete fracture and result in prolonged recovery or career-ending complications, it is imperative to identify these injuries early. Stress injuries are due to a mismatch between native bone strength and chronic mechanical load applied on bone over time.

Recently, high-resolution conventional MR imaging is replacing MR arthrography at many centers. If symptoms or clinical exam findings suggest intra-articular pathology, dedicated small field-of-view (FOV) MR arthrography of the hip is considered the imaging method of choice. For symptoms of generalized pain or nonspecific physical exam findings, imaging is best performed with conventional MRI of the pelvis and hip. According to the American College of Radiology Musculoskeletal Imaging Criteria, MRI is the next appropriate imaging method in those individuals with negative radiographs. Anteroposterior view of the pelvis is standard, and dedicated views of the symptomatic hip are often performed in the athletic hip which include cross-table lateral, frog-leg lateral, or Dunn lateral. The radiographic examination is a critical component in the diagnostic evaluation and treatment decision-making process and considered the first-line imaging technique in the evaluation of hip pain.

Normal hip bone xray