Four basic windows have provided our insights into the nature and character of osteosarcomas: Clinical, anatomic, laboratory, and radiologic. What effect does it have on the afflicted individual? What changes does it induce in “host’s” anatomy? Why does it occur (environmental and genetic factors)? How does the host respond (metabolic, hematologic, immunologic and chemical responses) and how does it alter the “host’s” appearance when viewed by the expanded radiologic study options? Additional insights derive from study of its history, not the experience of a single individual or clinical population, but as a historical phenomenon.

Artificially-prepared mummies provide one such option for such study. Mummification was a practiced procedure utilized throughout much of the ancient world, especially in some cultures (e.g., Egyptian and Chinchorro). Natural mummies additionally afford an opportunity to examine internal organs, so often removed in artificial mummification processes. Disorders affecting the musculoskeletal system still remain accessible for study. That is fortunate, as so much of neoplasia identification is now predicated upon immunologic and genetic (DNA) analysis of associated soft tissues [1]. Beyond the Holocene (past ~10,000 years), mummies are quite rare [2]. The soft tissues seem rarely preserved, so analysis is limited to what can be discerned from actual physical examination of the preserved bones. That is fortunate for study of bone tumors, as radiologic studies (of individuals in whom neoplasia is suspected) can be compared to those in modern individuals afflicted with the same diseases [3,4]. That option offers a unique opportunity, allowing observation of actual bone damage. Examining the surface of afflicted bones overcomes the limited resolution of standard radiologic techniques (e.g., 0.3 mm for high resolution x-rays; 0.6 mm for computed tomography (CT) and magnetic resonance imaging (MRI) [5]. It permits identification of previously unrecognized disease manifestations, such identification providing insights applicable to clinical disease recognition and management (e.g., myeloma character) [3,6].  

The limited amenability of fossil and sub-fossil soft tissues to histologic study is not actually disadvantageous to recognition of neoplasia. We understand that skeletal pathologists will not report an osteosarcoma diagnosis without examining the radiologic studies, because the histology often does not permit distinguishing osteosarcoma and osteomyelitis [7]. Thus, the radiologic appearance allows recognition of osteosarcomas and distinguishing among the varieties. At least, that has been the case until more recent variety subdivisions predicated on recognition of specific immunologic soft tissue (neoplastic cell) markers. As these are seemingly not preserved in the sub-fossil and fossil record, further discussion will be limited to identification of occurrence and antiquity of the originally described forms of osteosarcoma. These include parosteal, periosteal, and medullary or central and its high grade variant, telangiectatic [8].

The manifestations of medullary, parosteal and periosteal osteosarcomas, observable on bones (when soft tissues are no longer present), have been well documented [9,10]. The appearance of bones affected by the telangiectatic form of osteosarcoma responsible for 2-12% of human osteosarcomas [11] has been suggested in a dog from the 3rd-5th century CE [12], and reported as isolated cases in rhesus macaca [13], dog [14], cat [15] and horse [16], but not documented in human, until now. Also referred to as hemorrhagic osteosarcoma [17] and designated by Ewing [18] as an osteogenic sarcoma variant, it was referred by Sir James Paget [19] as “medullary cancer of bone with an excessive development of blood vessels” and by Gaylord [20], as a malignant bone aneurysm in 1903. Those descriptions reflect the septated, aneurysmally-dilated cavities recognized on histologic examination [21].

Radiologic examination reveals a purely lytic geographic, permeative process localized centrally within long bone metaphyses [17,21-26], a characterization that Matsuno et al. [27] reported as diagnostic.

A previously healthy 29 year old Swiss Caucasian male presented in the early part of the 20th century with swelling at the lateral aspect of the leg, just proximal to the ankle. There were no other physical findings. Radiologic evaluation revealed fusiform expansion of the distal third of the fibula by a centrally located, permeative process. The resected fibula was macerated to remove soft tissues. Macroscopic examination of the defleshed bone revealed an expanded distal fibula with cortical breakthrough and slight focal periosteal reaction (Figures 1A and 1B). Radiologic examination revealed cortical thinning (to egg shell thickness) and permeation with perforation. Medullary density was irregular with subtle cystic areas, focal periosteal reaction, and a Codman’s triangle (Figures 1C and 1D). Residual trabeculae were not individually identifiable. Histological studies were not permitted.

The actual bone damage caused by telangiectatic osteosarcoma is illustrated herein. The perspective provided supplements that obtainable by routine radiologic and histologic techniques. It documents the diffuse thin residual shell, highly characteristic of this disorder. This contrasts with other forms of osteosarcoma which, though less high grade than telangiectatic osteosarcomas, grow around residual cortex rather than diffusely leaving a thin rim [28]. 
The major differential consideration is aneurysmal bone cyst [8]. It was easy to dismiss in this case, given its diffuse, permeative appearance, with no evidence of internal struts or opaque rim, in contrast to the well-demarcated soap bubble appearance of aneurysmal bone cysts [11,29]. Similarly, absence of lobulation or internal struts eliminates giant cell tumor [5,30]. Internal calcifications (e.g., popcorn appearance), characteristic of chondrosarcoma and malignant fibrous dysplasia, and the lobulated nature of the latter [31-34] were not observed. Absence of a honeycomb appearance and sclerotic reaction permit hemangioendothelioma and cystic angiomatosis diagnoses to be dismissed [35]. Absence of well-defined margins and failure of survival of peri-lesional normal bone is not compatible with diagnosis of fungal disease or echinococcus (hydatid) disease [36-38]. Hyperparathyoidism and tuberculosis are associated with preservation of surrounding trabeculae and endosteal scalloping [5], at variance with what was observed in this individual. Osteomyelitis may also present as purely destructive, but associated abscesses (e.g., Brodie abscess have a sclerotic margin [5], contrasted with the subtle margins observed herein.

Telangiectatic osteosarcoma is a high grade bone tumor with characteristic amenable to its recognition in the archeologic and paleontologic record. As an expansile tumor which produces severe cortical thinning and minimal periosteal reaction, it is easily distinguished from aneurysmal bone cysts and giant cell tumors. Examination of the archeologic and paleontologic record should allow identification of the antiquity of this form of osteosarcoma and perhaps provide additional clues to its derivation.

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