Vertebral compression fracture is the collapse of the anterior column of the vertebral body due to axial or flexion forces. Approximately 1.4 million new vertebral compression fractures are diagnosed worldwide annually. The most common causes are osteoporosis (84%), trauma, and pathologic fracture (metastasis, multiple myeloma). Osteoporotic compression fractures are 2-3 times more common in women and peak at the thoracolumbar junction (T11-L2). The anterior column is the region most exposed to flexion forces and the first to fail — thus anterior height loss (wedge deformity) is the most typical finding. The posterior column and posterior wall are intact — this is the fundamental difference from burst fracture. Differentiating pathologic fracture is of critical clinical importance: convex posterior wall, pedicle signal change, epidural soft tissue mass, diffusion restriction, and diffuse T1 hypointensity favor malignancy. In benign osteoporotic fracture, band-like edema pattern, fluid cleft sign, normal pedicle signal, and absence of diffusion restriction are characteristic. MRI is the gold standard for acute-chronic and benign-malignant differentiation.
Age Range
50-90
Peak Age
70
Gender
Female predominant
Prevalence
Common
The mechanism of vertebral compression fracture is based on the mechanical strength of the vertebral body being unable to withstand applied forces. In osteoporotic fractures, low bone mineral density (BMD) weakens the trabecular bone architecture — particularly loss of horizontal trabeculae reduces vertebral load-bearing capacity. Normal vertebral body can withstand 2000-14000 N axial force, while osteoporotic vertebra may fail at 500-1500 N. Under flexion loading, the anterior column is most stressed (tension + compression) and the anterior cortex is the first structure to fracture — explaining wedge deformity. The posterior column is behind the neutral axis and experiences tension rather than compression — thus the posterior wall remains intact (difference from burst fracture). After fracture, edema and hemorrhage develop in bone marrow — seen as T1 hypointensity (long T1 of edema fluid replacing fatty marrow) and STIR hyperintensity (long T2 of free water, fat suppressed) on MRI. In the chronic phase (after 6-12 weeks), edema resolution returns T1 signal to normal fatty marrow level — the most reliable indicator of chronic benign fracture. Fluid cleft sign reflects vacuum phenomenon or fluid accumulation at the fracture line — seen as T2 hyperintense and T1 hypointense horizontal line, related to ischemic bone necrosis and specific for benign fracture.
Fluid collection seen as T2 hyperintense and T1 hypointense horizontal line at the fracture line. Related to ischemic bone necrosis and fracture instability. Has >95% specificity for benign osteoporotic compression fracture and is not seen in pathologic fracture — a very valuable finding for benign-malignant differentiation.
In acute compression fracture, STIR shows hyperintense bone marrow edema in the vertebral body. Edema pattern is generally band-like (along fracture line) or diffuse. In benign fracture, edema tends to be limited to the anterior column, while in pathologic fracture, it involves the entire vertebral body.
Report Sentence
Hyperintense bone marrow edema in the vertebral body on STIR, consistent with acute compression fracture.
In chronic compression fracture, normal fatty marrow signal is restored on T1 — T1 hyperintense signal returns in the vertebral body. This finding indicates the fracture is at least 6-12 weeks old and is the most reliable indicator of benign fracture. In pathologic fracture, T1 hypointensity persists because tumor tissue continues to replace normal fatty marrow.
Report Sentence
Restored fatty marrow signal on T1 in the vertebral body with collapse deformity, consistent with chronic benign compression fracture.
Fluid cleft sign is seen as a T2 hyperintense and T1 hypointense horizontal line at the fracture line. It is related to ischemic bone necrosis and instability at the fracture line. It has high specificity (95%+) for benign osteoporotic fracture and is not seen in pathologic fracture.
Report Sentence
T2 hyperintense fluid cleft sign in the vertebral body with compression fracture, favoring benign osteoporotic fracture.
Diffusion-weighted imaging (DWI) and ADC map play a critical role in benign-malignant compression fracture differentiation. In malignant (metastatic) fracture, high cellularity restricts water molecule movement → DWI hyperintense, ADC low. In benign osteoporotic fracture, edema fluid allows free water movement → DWI variable, ADC normal or high.
Report Sentence
ADC values within normal limits in the vertebral body with compression fracture, no diffusion restriction detected; favoring benign osteoporotic fracture.
CT sagittal reformats clearly show anterior column height loss (wedge deformity). Posterior wall is intact and concave (normal shape) — convex posterior wall suggests pathologic fracture. Cortical fracture line and fragment displacement are better evaluated on CT than MRI.
Report Sentence
Anterior column height loss and wedge deformity of the vertebral body on CT sagittal reformats with intact posterior wall; consistent with compression fracture.
Criteria
Fracture occurring with minimal or spontaneous trauma on background of low bone mineral density
Distinct Features
Most common type (84%); elderly female, T-score <-2.5; band-like edema, fluid cleft sign, normal pedicle, no diffusion restriction; treatment conservative or vertebroplasty/kyphoplasty
Criteria
Fracture developing on background of underlying malignant lesion (metastasis, myeloma)
Distinct Features
Convex posterior wall, pedicle T1 hypointensity, epidural soft tissue mass, diffusion restriction (low ADC), diffuse T1 hypointensity; no fluid cleft sign; treatment radiotherapy/surgery/medical
Criteria
Fracture occurring with significant trauma mechanism (fall, accident) in normal bone density
Distinct Features
Trauma history in young patient; acute bone marrow edema; posterior ligamentous complex injury should be assessed (STIR); TLICS score for stability assessment; treatment conservative or surgical (if unstable)
Distinguishing Feature
In vertebral metastasis, convex posterior wall, pedicle involvement (T1 hypointensity), epidural soft tissue mass, and diffusion restriction (ADC <1.0 x 10^-3) support pathologic fracture. In osteoporotic fracture, band-like edema, concave posterior wall, normal pedicle, fluid cleft sign, and absence of diffusion restriction support benignity.
Distinguishing Feature
Burst fracture involves BOTH anterior AND posterior column fracture — retropulsed fragment displaces into spinal canal, vertical fracture line (sagittal split) and increased interpedicular distance. In compression fracture, only anterior column is fractured, posterior wall intact, no retropulsion. By Denis 3-column model, burst involves at least 2 columns while compression involves only 1.
Distinguishing Feature
In Schmorl's node, focal end-plate depression is present but overall vertebral height is preserved — compression fracture shows height loss of the entire vertebral body. Sclerotic rim is typical in Schmorl's node, while cortical fracture line and diffuse edema are seen in compression fracture.
Urgency
urgentManagement
conservativeBiopsy
Not NeededFollow-up
3-monthThe most critical step in vertebral compression fracture diagnosis is differentiating benign (osteoporotic) from malignant (pathologic) fracture. MRI is the gold standard — combined T1, STIR, DWI/ADC evaluation provides >90% accuracy. In osteoporotic fractures, pain management, osteoporosis treatment (bisphosphonates, denosumab), and vertebroplasty/kyphoplasty (for refractory pain) are treatment options. In pathologic fracture, primary tumor investigation, staging, and multidisciplinary treatment planning are needed. Urgent surgery or radiotherapy is indicated for cord compression or neurological deficit. In newly diagnosed osteoporotic fracture, DEXA bone mineral density measurement and cascade fracture risk assessment should be performed — new fracture risk increases 5-fold after first compression fracture.
Osteoporotic compression fractures are very common in the elderly population and are managed with pain management. Differentiating pathologic fracture (metastasis) is critically important — convex posterior wall, pedicle signal change, epidural soft tissue mass and diffusion restriction favor metastasis. Urgent surgery may be needed if neurological deficit is present.