Teaching Case

A 7-year-old female patient presented to the department of radiology complaining about spontaneous pain at the left upper extremity with movement restriction at the left elbow.  This was worsened especially at night. There is no clear history of previous trauma.

Conventional radiographs showed displacement of the posterior fat pad due to intra-articular joint effusion in the distal humerus with subtle peri-articular osteopenia (Figure 1).

Ultrasound demonstrated a significant intra-articular effusion elbow with diffuse thickening of the synovium (Figure 2).

Axial T1-weighted Magnetic Resonance Imaging (MRI) showed a hypointense round-shaped lesion involving the left olecranon fossa at the radial side (Figure 3A). Fat-suppressed (FS) T2-weighted MR images demonstrated a well-delineated hyperintense lesion with a central hypointense surrounded by bone marrow oedema at the distal left humerus diaphysis (Figures 3B, 3C).

Subsequent computed tomography (CT) confirmed a small rounded osteolytic lesion involving the distal left humerus with subtle cortical thinning and central calcified nidus (Figures 4A, 4B, 4C). There was no periosteal reaction.

Osteoid osteoma (OO) is a painful benign bone lesion that is frequently seen between 5-25 with male predominance. Patients present typically with a history of atraumatic pain worsening at night relieved by nonsteroidal anti-inflammatory drugs and salicylates [1,2,3,4,5]. The most common location for osteoid osteomas is the diaphyseal cortex of the long bones, especially the femur and tibia [1,2].

Intra-articular osteoid osteomas (IAOO) are very rare, and commonly involve the hip and elbow joint, as in our case in the distal humerus [3]. Intra-articular lesions are difficult to identify as there is a significant overlap of bony margins. Symptoms are often atypical which may result in a delayed diagnosis.

The typical radiographic appearance of a cortical OO is a well-defined lucent bone lesion with a central mineralized nidus and surrounding reactive sclerosis with periosteal thickening [1,2,3,4]. However, IAOO is usually associated with joint inflammation leading to periarticular osteopenia rather than sclerosis, which may cause a delay in the diagnosis [3].

The modality of choice for lesion characterization is computed tomography (CT) as it is better suited for demonstrating the nidus and reactive sclerosis than projection radiography due to the lack of superimposed structures.

MRI reveals bone marrow edema at the affected bone and soft tissue changes. The nidus has a low to intermediate signal on T1-weighted image and variable signal intensity on the T2-weighted image depending on the amount of mineralization [1,2,3,4,5].

Detection of the nidus is the clue to the correct diagnosis.  The presence of unexplained bone marrow oedema on MRI should alert the radiologist to the presence of a potential OO and warrants further investigation by CT to detect a nidus [1,2,4,5].

It is important to distinguish OO from the other osteolytic lesions to avoid unnecessary harmful surgical interventions.  Osteoblastoma is an important differential diagnosis. Osteoblastoma is often less painful and larger, typically measuring 2.0 cm at least. Bone marrow oedema may also be secondary to an occult fracture, stress reaction or osteomyelitis (Brodie abscess) but the clinical presentation differs.

The most effective treatment of OO is CT-guided radiofrequency ablation. However, extra caution is needed to avoid cartilage loss [1,2,3,4,5]. Accompanying synovitis requires corticosteroid infiltration therapy. Sometimes, open surgical excision is needed. The prognosis is considered excellent with recurrences being uncommon.

In conclusion, unexplained bone marrow oedema with synovitis should always alert the radiologist of the possibility of the presence of an IAOO, and supplementary CT should be performed for precise lesion characterization.