Osteonecrosis of the Upper Extremity: MRI-Based Zonal Patterns and Differential Diagnosis

Regarding the upper extremity, osteonecrosis can relate to the humeral head and to any carpal bone, most commonly the lunate (Kienböck's disease), scaphoid (Preiser's disease and nonunion), and capitate bone (osteonecrosis of the capitate head). In children and adolescents, osteochondrosis is an important differential diagnosis at the epiphyses. Appropriate imaging of osteonecrosis depends on knowledge about blood supply, biomechanical load, and bone repair mechanisms. Contrast-enhanced MRI (ceMRI) enables the differentiation of up to three mostly band-shaped zones: necrotic tissue (proximal), hypervascular repair tissue (intermediate), and viable bone (distal). To distinguish between necrotic and repair zones, intravenous gadolinium is recommended in MRI. Osteosclerosis and insufficiency fractures in early and intermediate stages as well as osteoarthritis in advanced stages are best depicted using high-resolution CT (HRCT). The combination of HRCT and ceMRI allows for exact classification of osteonecrosis regarding morphology and viability.

Bilateral Preiser’s disease in a patient with hypercoagulability

Reports of bilateral Preiser’s disease-avascular necrosis of the scaphoid -- are rare with only 4 cases reported in the English literature. We present the fifth reported case of bilateral Preiser’s disease in the setting of a previously undiagnosed hypercoagulability disorder.

On the history and definition of Preiser’s disease

In 1910, Georg Preiser (1876–1913) described five cases of rarifying osteitis. Based on his imaging studies, he diagnosed post-traumatic avascular necrosis (AVN) of the scaphoid without any sign of primary fracture. This was followed by an article in 1911 in which Preiser related his findings to Kienböck’s disease and Köhler’s disease of the tarsal navicular. Upon searching the literature, we found descriptions and discussions of Preiser’s imaging; however, the original images have never been published. We reproduce Preiser’s original imaging in this current review. All of these appear to show a fracture and no signs of AVN, suggesting that Georg Preiser misinterpreted his findings. There is no apparent uniformity in the literature regarding the definition, description, or aetiology of Preiser’s disease, and it is for this reason that we find the use of eponyms to be confusing.