Ätiologie von Osteonekrosen und Knochenmarködemen

Background: The frequent use of magnetic resonance imaging (MRI) introduced “bone marrow edema” (BME) as a descriptive radiological term for hyperintense signal changes in fluid-sensitive sequences. With the optimization of MRI soft tissue contrast, BME has evolved into a valid prognostic indicator associated with pain genesis, trauma, mechanical overload, and progressive cartilage and joint destruction. Diagnostics: Both osteonecrosis and BME manifest in early MRI as intraosseous fluid accumulation, characterized by hyperintense signals in T2-weighted and STIR sequences. Conventional radiography and computed tomography (CT) are limited in BME detection due to the absence of relevant density alterations or structural osseous lesions early on. Classification: Although BME is not pathognomonic for osteonecrosis, it represents the initial phase of every primary osteonecrosis. BME can be transient (transitory osteoporosis) and regress without residuals or serve as a prodromal stage of manifest osteonecrosis. Pathophysiology: Primarily, it represents a non-specific reaction of bone marrow to various noxious stimuli such as trauma, mechanical overload, inflammatory processes, vascular insufficiency, or metabolic dysregulations. This review explores the pathophysiological mechanisms underlying BME, its clinical significance for osteonecrotic joint diseases, and its role in pain genesis.