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Background: Bone tumors are neoplasias with a high overall mortality; one of the main factors that reduce survival is their high capacity to develop metastases. It has been reported that finding lung metastases at diagnosis of osteosarcoma (OS), chondrosarcoma (CS) and giant cell tumor of bone (GCTb) is quite common. In this study, we inquire the relationship of metastases caused by these tumors with different clinical and pathological aspects, in order to guide medical personnel in the diagnosis and opportune treatment of metastases or micro metastases. Materials and Methods: We collected data of 384 patients with clinical, radiological and histopathological diagnosis of OS, GCTb and CS that attended the National Rehabilitation Institute (INR) during 2006 to 2014. Chi-square and Fisher's exact tests were performed for data analysis. Results: In the three tumor types, the presence of metastases at diagnosis was variable (p=0.0001). Frequency of metastases was 36.7%, 31.7% and 13.2% for OS, CS and GCTb respectively. The average age had no significant difference (p>0.05) in relation to metastases, even so, patients with OS and GCTb and metastases, were older while patients with CS and metastases were younger, in comparison to patients without metastases. Males had a higher frequency of metastases (68.2%, p = 0.09) in contrast to CS and GCTb, in which the metastases was more frequent in women with 51.9% (p = 0.44) and 57.9% (p = 0.56) respectively. Broadly, metastasis was associated with primary tumors located in the femur (44.4%), followed by the tibia (15.6%); metastases was more frequent when primary tumor of GCTb and OS were in the same bones, but were located in the hip (26.3%) for CS. Conclusions: The frequency of metastases in OS, GCTb and CS is high in our population and is determined by different clinicopathological variables related to the kind of tumor. Further studies are needed in order to evaluate metastases subsequent to diagnosis and associations with survival and clinicopathological factors , as well as to determine the sensitivity and specificity of current methods of detection.

Background: Primary and metastatic bone tumor incidence has increased in the last years. Pain is a common symptom and is one of the most important related factor to the decrease of quality of life in these patients. Different pain management strategies are not completely effective and many patients afflicted by cancer pain cannot be controlled properly. In this sense we need to elucidate the neurophysiology of cancer-induced pain contemplating other quality of life components such as inflammation, neuropathies and cognitive components regarding bone tumors, and thus pave the way for novel therapeutic approaches in this field. Aim: Identify the neurophysiology of the mechanisms related to pain management in bone tumors. Method: Advanced searches were performed in scientific databases: PubMed, ProQuest, EBSCO, and the Science Citation index to get information about the neurophysiology mechanisms related to pain management in bone tumors. Results: The central and peripheral mechanisms that promote bone cancer pain are poorly understood. Studies have shown that bone cancer could be related to neurochemicals produced by tumor and inflammatory cells, coupled with peripheral sensitization due to nerve compression and injury caused by tumor growth. Activity of mesolimbic dopaminergic neurons, substance P, cysteine/glutamate antiporter, and other neurochemical dynamic’s brings us putative strategies to suggest better and efficient treatments against pain in cancer patients. Conclusion: Cancer-induced bone pain could include neuropathic and inflammatory pain, but with different modifications to the periphery tissue, nerves and neurochemical changes in different neurological levels. In this sense, here we explore opportunity areas in pharmacological and non-pharmacological pain management, according to pain-involved mechanisms.

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Tissue engineering of bone has combined bespoke scaffolds and osteoinductive factors to maintain functional osteoprogenitor cells, and the periosteum has been confirmed as a satisfactory source of osteoblasts. Suitable matrices have been identified that support cell proliferation and differentiation, including demineralised bone matrix (both compatible and osteoinductive) and acellular human dermis. We have evaluated the osteogenic potential of an osteogenic unit, developed by combining periosteum, demineralised bone matrix, and acellular human dermis, in rodents with critical-size cranial defects. Briefly, remnants from the superior maxillary periosteum were used to harvest cells, which were characterised by flow cytometry and reverse retrotranscriptase-polymerase chain reaction (RT-PCR). Cells were cultured into the osteogenic unit and assessed for viability before being implanted into 3 rodents, These were compared with the control group (n=3) after three months. Histological analyses were made after staining with haematoxylin and eosin and Von Kossa, and immunostaining, and confirmed viable cells that stained for CD90, CD73, CD166, runt-related transcription factor, osteopontin, and collagen type I in the experimental group, while in the control group there was only connective tissue on the edges of the bone in the injury zone. We conclude that osteogenic unit constructs have the osteogenic and regenerative potential for use in engineering bone tissue.