Traumatic and non-traumatic bone marrow edema in ankle MRI: a pictorial essay

Magnetic resonance imaging (MRI) after ankle trauma often shows alteration of bone marrow signal with a low signal on T1-weighted and a high signal on T2-weighted and fluid-sensitive sequences (like short tau inversion-recovery (STIR) or fat-suppressed (FS) sequences). This is known as bone marrow edema (BME) or bone bruise (Fig. 1) [1, 2, 4, 5].

BME is associated with capillary leakage and interstitial extracellular fluid accumulation within the bone marrow, which is responsible for the “bruising” of the bone marrow [6]. Patients without injury often show changes with similar morphology on MRI, also called BME. In hyperemic BME, the extracellular fluid comes from the inflamed walls of capillaries [7]. Some authors instead use the term bone marrow lesion (BML) in those cases, which is a more universal term and use the term BME for trauma-related cases [8].

The presence of BME is an unspecific but sensitive sign of underlying pathology, so correct and systematic interpretation is crucial. Interpretation of BME is multilevel and usually starts with the patient’s history (traumatic or non-traumatic, acute, or insidious). As mentioned above, the differential diagnosis of BME is very wide (Fig. 1) [2].

The distribution of BME is like a footprint of trauma which allows for determination of the trauma mechanism by giving clues to the concomitant soft tissue injuries (Figs. 6 and 7). With an inversion injury (Figs. 2 and 6), an extensive reticular BME is visible in the medial part of the ankle joint, mainly in the medial and postero-medial part of the talus and medial malleolus, because of a contrecoup injury. Usually, small areas of BME are visible on the avulsion side in the lateral malleolus. An eversion injury usually causes an inverse BME distribution. A geographic BME in the medial part of the talar trochlea may indicate an avulsion of the deltoid ligament [8, 9].

A BME near the tendon may reveal tendinopathy (Figs. 8 and 9), impingement (Figs. 10 and 11), tendon maltracking, or enthesopathy (Fig. 12) [5, 8, 12, 13]. Tendinopathy encompasses a wide range of tendon changes involving the internal structure of the tendon (Figs. 8 and 9), most commonly associated with micro-trauma and secondary degeneration. Changes in the bone marrow in direct contact with the tendon may indicate pathology of these tendons or tendon maltracking (Fig. 8). The presence of BME is probably due to altered tendon pressure on the bone [8, 12, 13]. Several authors report BME at the tendon insertion (Figs. 10, 11, and 12) to be a sign of enthesitis in inflammatory arthropathy [8, 14‐16].

Reticular BME in the posterior half of the medial malleolus is seen with dysfunction of the tibialis posterior tendon (Fig. 8); BME in the posterior half of the lateral malleolus with pathology in the peroneal tendons (Fig. 9)—functional dysfunction, overuse, or ruptures [17, 18].

When the bony trabecular load is higher than normal, loss of mechanical integrity through injury is possible. This happens with weakened bone tissue (osteopenia) or with vigorously repeated mechanical forces (Fig. 13). In these situations, a fatigue fracture or insufficiency fracture, respectively, may occur [5, 16]. Linear low-signal disturbances oriented perpendicular to the load axis, usually surrounded by extensive BME, are consistent with stress fracture (Fig. 14). A slight periosteal edema is the first sign of stress fracture which, in the absence of treatment, is followed by BME in the medullary cavity. Intracortical changes occur while the limb is still bearing weight. MRI can detect a stress fracture in the early stages [5, 8, 12, 13].

BME can be a very sensitive sign in the different types of impingement [11, 20]. Posttraumatic changes such as local synovitis, scars, thickened articular capsule or ligaments, and osteophytes may cause different impingement syndromes based on the localization. The most common impingement is anterolateral impingement, followed by posterior and anterior impingement. BME is a bone manifestation of impingement [17, 20].

Anterolateral impingement is an uncommon complication of ATFL injury resulting in hemarthrosis and synovitis, less often in the thick inferior part of the ATFL. The anterolateral gutter becomes filled with synovitis, scar tissue, and small osseous fragments [20].

An elongated posterior process of the talus or an os trigonum causes posterior ankle impingement. BME found in the posterior process of the talus or in the os trigonum, edema in Kager’s fat pad, and effusion in the posterior ankle recess are frequent findings [20, 21].

Anterior impingement manifests by a painful limitation of dorsal ankle flexion, mostly in football players, called “footballers’ ankle.” Accumulation of micro-trauma on the talar neck and anterior distal tibia may results in synovitis, thickening of the articular capsule, or osteophytes with BME (Figs. 19 and 20) [17, 20].

An evaluation of BME allows for better identification of patients for whom surgery is indicated (Figs. 19, 20, and 21).

BME in an accessory bone shows that it is probably a symptomatic accessory bone. Accessory bones occur at various frequencies but rarely cause discomfort and are often bilateral. The most frequent problem they cause is being mistaken for a fracture. The most common accessory bones are the os peroneum, os naviculare accessorium, and os trigonum. The os trigonum and talus often articulate. The mobility produces a folding of the joint capsule, occurrence of joint fluid, and conflict with the synovial sheath of the flexor hallucis longus tendon or Kager’s fat pad. BME usually occurs both in the os trigonum and the adjacent part of the talus (Fig. 21) if it is symptomatic [21]. An accessory bone in a tendon (e.g., os peroneum) may cause tendon overload and faster tendon degeneration and rupture (Fig. 22).

A coalition is an abnormal developmental fusion between bones. It usually results from the failure of segmentation of the bones during development, which in the foot occurs in about 1% of the population [22, 23]. A coalition may be bony or fibrous. The coalition prevents proper movement in the joint, which causes deformity, pain, and soft tissue changes. The distortion in fibrous coalition results in overuse and subsequent BME. Two of the most common coalitions are between the calcaneus and the navicular bone or between the middle facet of the talus and the calcaneus [22, 24] (Figs. 23 and 24).

BME is common in patients with septic arthritis and osteomyelitis. In areas of bone with inflammation, fluid signal replaces the fat signal. Usually, the fluid shows a higher signal than usual on T1-weighted images because of an increased protein concentration [8]. In osteomyelitis, the geographic replacement of the fat signal on T1-weighted images by edematous low signal has been reported to correspond better to the distribution of infection (Figs. 26 and 27) than the more diffuse reticular BME seen on fluid-sensitive images [26]. Similar imaging findings can be seen in chronic recurrent multifocal osteomyelitis (CRMO) where, however, no pathogenic agent has been confirmed (Fig. 28) [27]. BME is suggestive rather than pathognomonic for CRMO. In CRMO, a transient BME manifests as a region of BME without trauma (Fig. 28), which usually resolves in 3–12 months. The pathogenesis is not clear, and both a vascular and a neurologic etiology have been proposed [2, 4, 7, 28].

In inflammatory arthritides like rheumatoid arthritis (RA) or spondyloarthritis, hindfoot pain is not uncommon and is especially in spondyloarthritis an important diagnostic component if caused by enthesopathy with BME. Often, synovitis and joint effusion causes the pain [29]. Retrocalcaneal bursitis may lead to BME [30, 31]. BME in RA, known as osteitis and most commonly investigated in the hand and forefoot, is associated with erosive progression and poor functional outcome [32]. In spondyloarthritis, many patients, even if asymptomatic, have BME and other arthritis-related changes [30, 33].

BME with associated soft tissue edema in patients with peripheral neuropathy can indicate neuropathic arthropathy (Fig. 29) [11, 26]. The presence of BME in the early stages shows the extent of the process, while in the later stages, it helps distinguish the vital areas from osteonecrosis [34].