The etiology of<unk>  is uncertain, as there is no specific characteristic abnormality or chromosomal breaking point observed, despite cytogenetic abnormalities being highly specific for some tumors. Romeo et al has noted that<unk>  arising in long bones mainly affects the epiphyses, while in other locations it is close to ossification centers. Additionally, rare prevalence of<unk>  in intra-membranous ossification suggests a close relationship with growth plate cartilage. In<unk> , growth signaling molecules may be present due to the pre-pubertal signaling network as well as cartilage growth. Sex hormones are thought to be linked to this process because of the spatial relationship of<unk>  with the growth plate and its typical occurrence before growth plate fusion. Both Indian Hedgehog/Parathyroid Hormone-related Protein (IHh/PtHrP) and fibroblast growth factor (FGF) signaling pathways, important for development of the epiphyseal growth plate, are active in<unk>  leading to greater proliferation among the cells in the proliferating/pre-hypertrophic zone (cellular-rich area) versus the hypertrophic/calcifying zone (matrix-rich area). These findings suggest that<unk>  is derived from a mesenchymal cell undergoing chondrogenesis via active growth-plate signaling pathways (see Endochondral ossification). The highly heterogeneous nature of the tumor makes classification particularly difficult especially considering the origins of<unk> . There are two opposing views on the nature of<unk> , one favoring an osseous origin and the other favoring a cartilaginous origin. The work of Aigner et al suggests that<unk>  should be reclassified as a bone-forming neoplasm versus a cartilaginous neoplasm due to the presence of osteoid matrix, type I collagen, and absence of true cartilage matrix (collagen II). However, Edel et al found that collagen II, a marker for mature chondrocytes, was expressed in<unk> , supporting the chondroid nature of the neoplasm. The results of Romeo and colleagues favor the view of Edel et al of<unk>  being cartilaginous in nature but recognize that any definitive determinations regarding the origin of this neoplasm are not possible because of the plasticity of mesenchymal cells when set into different microenvironments and static approaches used in literature. Romeo et al have observed<unk>  neoplasms to be composed of mesenchymal cells that have completed normal chondrogenesis along with the production of osteoid and collagen I that could be the result of transdifferentiation of chondrocytes towards osteoblasts.
Chondroblastoma
Mycetoma
Esthesioneuroblastoma
Ganglioneuroblastoma
Myelolipoma
Lipoblastoma
Myxoid cyst
Brown tumor