Table 1.

Classification of ELMSI with known etiology, adapted from references [52, 53]

Type	Etiology	Main imaging features
Trauma	Direct or indirect damage, fracture, CRPS	- The stress injury-induced ELMSI is often subchondral and wedge-shaped with the base located at the site of greatest stress - The bone bruise/contusion appears as an area of heterogeneous ELMSI - ELMSI is larger if due to compressive rather than traction forces - If a fracture is present, ELMSI is accompanied by the hypointense line in all sequences - The CRPS-induced ELMSI typically shows a patchy pattern
Trauma/degenerative	SIF	- Ill-defined ELMSI arising from the subchondral region with a fracture line in the subarticular marrow - Ischemic low T2w-SI subchondral area subjacent to the collapsed bone plate - Fluid-filled cleft underlying the collapsed bone plate
Degenerative	Osteoarthritis	- Joint-sited ELMSI due to high metabolic activity, extracellular matrix turnover/angiogenesis, and bone formation - ELMSI is frequently associated with geodes, reactive synovitis, joint effusion and loss of joint space - More evident ELMSI when greater cartilage loss or abnormalities occur
Degenerative/inflammatory	Modic changes	- Type I (low SI in T1w and high SI in T2w) corresponds to vertebral body edema and hypervascularity - Type II (high SI in T1w and T2w) reflects fatty replacements of the red BM - Type III (low SI in T1w and T2w) consists of subchondral bone sclerosis
Inflammatory	Inflammatory arthritis, enthesitis	- ELMSI is caused by the replacement of the medullary fat with inflammatory cells with edema - Immature blood vessels containing high levels of VEGF can also contribute to ELMSI appearance - In RA patients, ELMSI is representative of bone inflammation, initially located in the bare areas - In these patients ELMSI and synovitis precede the appearance of bone erosion and joint space narrowing and - The progression of joint destruction is significantly greater in ELMSI positive rather than in negative joints
Vascular	Avascular necrosis (AVN)	- ELMSI is sited in the viable tissue and surrounds the area of necrotic marrow outlined by a low SI rim - This rim is often double-lined on T2w acquisitions: a high inner (granulation tissue) and an outer low SI band (sclerosis) - AVN-related ELMSI seems not to represent an early finding and could be secondary to a subchondral fracture
Infectious	Bone and articular infections	- ELMSI frequently surrounds a mass of infected tissue - Septic arthritis has a wide spectrum of imaging presentation and can be divided in: - Necrotic, caused by an ischemic mechanism - Exudative, induced by vascular congestion (DD with gelatinous transformation of bone marrow, due to protein loss)
Neoplastic	Benign lesions	- Benign lesions as osteoid osteoma and osteoblastoma show an important ELMSI - Usually ELMSI seems caused by trabecular destruction and local inflammation, but - Osteoid osteoma surrounding ELMSI seems due to tumor-associated inflammatory mediators (PGE2)
Neoplastic	Malignant lesions	- Generally, primary/secondary malignancy induces a minor quantity of ELM with respect to benign tumors but - Chondroblastoma and Langerhans’s cell histiocytosis are surrounded by an intense ELMSI -DwI can differentiate the neoplastic focus from the surrounding ELMSI
Iatrogenic	After surgery or RT, steroids or calcineurin inhibitors	- ELMSI RT-related is the most frequent - In this case usually presents fast onset and short duration (1-14-day time frame), however - Its presence, intensity and duration can vary significantly depending on treatment type/location
Metabolic	Hydroxyapatite deposition disease, CPPD, gout	- ELMSI is due to the inflammatory response at pathologic tendon insertion site - This reaction is due to hydroxyapatite or calcium pyrophosphate deposition - In gout can be caused by the presence of intraosseous tophi
Neurological	Charcot’s joints	- ELMSI is often associated with this disorder commonly affecting foot and ankle - ELMSI is an early sign of Charcot’s joint - MRI is sensitive to follow the course of the healing process and differentiate acute Charcot’s foot from acute osteomyelitis