PMC6304848_01
AP and mortise radiographs of the ankle demonstrating a lytic, expansile, geographic bone lesion with no cortical disruption.
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Radiographs obtained demonstrated a lytic, expansile, geographic lesion with no cortical disruption or periosteal reaction (Figure 1).
STIR (short tau inversion recovery) weighted MRI of the ankle showing 5 x 5.2 x 3.6 cm multiloculated, expansile lesion with fluid-fluid levels.
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MRI revealed a multiloculated, minimally enhancing, expansile lesion (Figures 2 and 3).
T1 weighted MRI of the ankle showing 5 x 5.2 x 3.6 cm multiloculated, slightly hyperintense compared to surrounding muscle expansile lesion.
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MRI revealed a multiloculated, minimally enhancing, expansile lesion (Figures 2 and 3).
Photomicrographs demonstrating the wall of an ABC partially lined by proliferation of bland fibroblasts (Black arrow) with underlying osteoclast-type giant cells (star) and blood (hematoxylin and eosin, x20).
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ABC (Figure 4). A curettage, application of phenol, and allograft bone grafting were performed, and she was followed with serial radiographs.
T1 weighted MRI showing a homogeneously slightly hyperintense to muscle lobulated lesion with multiple fluid-fluid levels.
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MRI showed a homogeneously lobulated, hyperintense lesion with multiple fluid-fluid levels confirming the recurrence (Figures 5 and 6).
STIR (short tau inversion recovery) weighted MRI showing a homogeneously lobulated, hyperintense lesion with multiple fluid-fluid levels.
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MRI showed a homogeneously lobulated, hyperintense lesion with multiple fluid-fluid levels confirming the recurrence (Figures 5 and 6).
Pretreatment with denosumab: mortise radiograph showing a large lytic, expansile bone lesion with cortical disruption.
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Serial radiographs were obtained throughout her treatment which showed increased mineralization and no further expansion of her lesion throughout the course of denosumab therapy (Figures 7 and 8).
Posttreatment with denosumab after 1 year shows increased mineralization and no further expansion or cortical disruption.
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Serial radiographs were obtained throughout her treatment which showed increased mineralization and no further expansion of her lesion throughout the course of denosumab therapy (Figures 7 and 8).
Photomicrographs taken after denosumab treatment demonstrating fibrous connective tissue with bland-looking spindle cells (arrow), focal hemorrhage, and reactive bone formation (star) admixed with scattered inflammatory cells; multinucleated giant cells are absent.
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Her histopathology at the time of surgery showed numerous fragmented bones admixed with fragments of fibrous connective tissue with bland fibroblasts with no significant component of multinucleated giant cells present (Figure 9).
Mortise radiographs taken at 10 months following denosumab treatment and surgery demonstrating no local recurrence.
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She has been followed for three years with clinical and radiographic examination, has resumed all normal activity without pain, and has had no recurrence of her disease (Figures 10 and 11).
Mortise radiographs taken at 3 years following denosumab treatment and surgery demonstrating no local recurrence.
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She has been followed for three years with clinical and radiographic examination, has resumed all normal activity without pain, and has had no recurrence of her disease (Figures 10 and 11).