Radiological Case: Tumoral Calcinosis

Eric M Christiansen, MD; Shane Mallon, MD; Michelle M; Alan Pitt, MD; Jeremy Hughes, MD


Appl Radiol. 2021;50(3):53-55. 

In This Article


Tumoral calcinosis (TC) is characterized by lobular, densely calcified, mass-like lesions classically confined to the soft tissues, generally at the extensor surface of a joint.[1] Reports of TC can be traced back to 1898; however, it was first described in the American literature in 1943 by Inclan et al.[2]

Tumoral calcinosis may be genetic, the result of prior traumatic injury, or the result of a metabolic derangement, most commonly chronic renal failure, which accounts for approximately 23% of cases.[3] Onset is typically in the second decade of life, with a reported increased frequency in African Americans.[4] The condition can be divided into primary and secondary varieties, and there are two primary subtypes: hyper-phosphatemic TC secondary to a gene mutation in GaINAc or FGF23, and normo-phosphatemic TC secondary to a gene mutation in the SAMD9 gene.[5] The secondary type results from chronic renal failure.

Tumoral calcinosis of the spine is rare, with only 30 cases reported in the literature, most involving the cervical (48%) and lumbar (45%) spine. Only two reported cases involve the thoracic spine.[6] In descending order of prevalence, TC most commonly involves the hip, elbow, shoulder, foot, and wrist joints.[2]

Owing to the characteristic soft-tissue calcifications of tumoral calcinosis, CT plays a primary role in diagnosis. In cases of advanced disease, the condition may be identified on radiographs. MRI is often performed after CT to evaluate for spinal cord signal abnormalities and for presurgical planning.

The characteristic CT imaging appearance of TC is multilobulated cystic or amorphous periarticular calcifications. Erosive changes of adjacent osseous structures are common. Homogeneous or layering density can also be seen on CT. These lesions typically demonstrate T1 hypointense signal on MRI. There is variable T2 signal, which may be hypo- or hyperintense despite the high amount of calcium.[1]

Imaging appearance, anatomic distribution, clinical history, and laboratory values are helpful in differentiating these processes. Treatment is individualized after the condition is subtyped into one of the above etiologies. The choice between medical and surgical therapy depends on multiple variables, including subtype, location, and severity.