Intraosseous migration of intratendinous calcification

Last revised by Arlene Campos on 22 Jan 2024

Intraosseous migration of intratendinous calcification is a process in which calcific deposits penetrate and accumulate within the adjacent bone, creating a sclerotic lesion with bone edema1,2.

This migration occurs during the resorptive stage of calcific tendinopathy natural evolution3.

In some cases, it can mimic a neoplastic or infectious lesion, and should not be overdiagnosed to avoid invasive diagnostic biopsies.

This condition is a rare complication of calcific tendinitis and there is no reported incidence rate in the literature4.

The mechanism by which calcifications erode the bone cortex and migrate into the bone is not fully understood. However, it is thought that enzymatic actions during the resorptive stage of calcific deposits may facilitate cortical osteolysis, allowing the calcifications to spread4.

Intraosseous migration can be divided into three types4:

  • cortical erosion: This is the most common type of intraosseous migration. It occurs when the calcific deposits erode the cortex and allows the deposits to spread into the bone marrow.

  • subcortical calcium migration: This type of migration occurs when the calcific deposits move from the bone cortex to the subcortical bone.

  • intramedullary diffusion: occurs when the calcific deposits spread throughout the bone marrow.

The reported locations are:

It generally presents with acute pain, with no trauma history.

  • amorphous soft tissue calcifications, usually the tendons

  • cortical erosions adjacent to the tendon insertion - the first manifestation prior to migration

  • amorphous subcortical calcification, osteolyis and sclerotic area - second phase of migration

  • vanishing of a previous calcification

  • follow up may demonstrate restitutio ad integrum, or persistence of a subcortical cyst in the previous location of the resorbed intraosseous calcification2,3

  • intratendinous T1 /T2 hypointensities corresponding to intratendinous calcifications

  • non enhancing juxtacortical lesion of bone signal (T1 and T2 hypointense) adjacent to tendon insertion

  • variable amount of bone marrow edema (T1 hypointense, T2 hyperintense)

  • surrounding soft-tissue edema

  • enhancement of adjacent tissues

  • follow up may demonstrate restitutio ad integrum, or persistence of a subcortical cyst in the previous location of the resorbed intraosseous calcification2,3

This is a self limiting condition and resolves completely with no specific treatement.

Neoplastic

The acute symptoms, the absence of soft tisse mass and joint effusion generally rules out these differentials.

Infections

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