| |
EH of the skin and subcutaneous tissue |
EH of soft tissue |
EH of the bone |
| Neoplastic potential of the vascular component |
Reactive lesion to trauma. Angiocentric distribution around a larger vessel with evidence of mural damage often associated with trauma. |
Reactive lesion to trauma. However, a case of dermal EH was found to harbor a TEK gene mutation, which encodes the endothelial cell tyrosine kinase receptor Tie-2, indicating that certain molecular abnormalities may also contribute to pathogenesis [41]. |
Distinct cytogenetic events and lack of an eosinophilic response in some tumors suggest distinct pathogenesis compared with that in skin EH. FOS gene rearrangement and recurrent ZFP36–FOSB fusion are present in nearly one-third of bone EH cases in varied locations [32]. |
| Neoplastic potential of the inflammatory cell component |
These lesions are associated with various lymphoproliferative conditions, supporting the contention that some EH cases arise from a monoclonal T-cell process [42].Peripheral T-cell lymphoma was reported in a patient with ALHE/EH. Some cases of ALHE/EH have also been reported with T-cell receptor gene rearrangement and monoclonality [42]. |
Mostly polyclonal and reactive. No lymphoproliferative conditions documented to date. |
| Margins |
Well-marginated lesions. |
Less-marginated lesions [33]. |
Less-marginated lesions. |
| Association with an artery |
Demonstrable angiocentric distribution and symmetric association with an artery. The artery can show evidence of damage (e.g., thrombosis, fibrointimal proliferation, duplication of the internal elastic lamina, or mural disruption) [43]. |
Rarely associated with a muscular artery [33]. |
Symmetrical association with an artery is not usually demonstrable in bone lesions because the site of origin may be obliterated by the expanding tumor [2]. |
| Vasoformative tendency |
Vasoformative tendency and vessel maturation increase from the center to the periphery, resulting in central ill-defined poorly formed vessels (Fig 2) and peripheral well-formed vessels (Fig 3). The subcutaneous form has a tendency for the florid proliferation of large epithelioid endothelial cells that may become so exuberant as to form solid intraluminal nodules or clusters. These masses can obscure the vascular nature of the lesion and thus increase the diagnostic complexity [44-45]. |
Similar vasoformative tendency to EH of the skin but lesions contain more fully developed vessels, typically with patent lumina. [33]. |
Vasoformativetendency but often greater histological variability within lesions. |
| Histomorphology |
Well-defined epithelioid endothelial morphology (Figure 3). |
Less pronounced epithelioid endothelial morphology (often more cobblestone-like) [36]. |
Recognizable epithelioid endothelial morphology. Spindling and fasciculation may be observed within the lesion [37]. |
