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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Modeling Primary Bone Tumors and Bone Metastasis with Solid Tumor Graft Implantation into Bone
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Tumor-induced osteomalacia.

Pablo Florenzano1,2, Rachel I Gafni1, Michael T Collins1

  • 1Section on Skeletal Disorders and Mineral Homeostasis, National Institutes of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.

Bone Reports
|October 13, 2017
PubMed
Summary
This summary is machine-generated.

Tumor-induced osteomalacia (TIO) is a rare condition caused by tumors overproducing FGF23, leading to bone issues. Early diagnosis and tumor localization are key for curative surgical removal and patient recovery.

Keywords:
1,25-OH2-vitamin D, 1,25(OH)2DCT, computerized tomographyFDG-PET/CT, fluorodeoxyglucose positron emission tomography with computerized tomographyFGF1, fibroblast growth factor 1FGF23FGF23, fibroblast growth factor 23FGFR1, fibroblast growth factor receptor-1FISH, fluorescence in situ hybridizationFN1, fibronectin-1MAPK, mitogen-activated protein kinaseMRI, magnetic resonance imagingPMT, phosphaturic mesenchymal tumorPTH, parathyroid hormonePhosphaturic mesenchymal tumorsSPECT, single-photon emission computed tomographyTIO, tumor-induced osteomalaciaTRP, tubular reabsorption of phosphateTmP/GFR, tubular maximum reabsorption of phosphate to glomerular filtration rateTumor-induced osteomalacia

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Area of Science:

  • Endocrinology
  • Oncology
  • Nephrology

Background:

  • Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by bone pain, fractures, and muscle weakness.
  • It results from tumoral overproduction of fibroblast growth factor 23 (FGF23), causing hypophosphatemia and osteomalacia.
  • A common driver in these typically small, benign mesenchymal tumors is the FN1-FGFR1 fusion gene.

Purpose of the Study:

  • To highlight the diagnostic criteria for TIO, emphasizing FGF23 levels and phosphate wasting.
  • To outline the recommended step-wise approach for tumor localization in suspected TIO cases.
  • To discuss current and novel therapeutic strategies for TIO management.

Main Methods:

  • Diagnosis relies on identifying acquired hypophosphatemia with renal phosphate wasting, elevated FGF23, and low 1,25(OH)2D.
  • Tumor localization involves medical history, physical exam, functional and anatomical imaging, and potentially selective venous sampling for FGF23.
  • Treatment strategies include surgical resection, medical management with phosphate and vitamin D, and emerging therapies like KRN23.

Main Results:

  • Complete surgical tumor removal is curative for TIO.
  • Medical therapy with phosphate and active vitamin D can resolve osteomalacia but requires careful monitoring for complications.
  • Novel treatments targeting FGF23 or FGFR pathways show promise for TIO patients.

Conclusions:

  • Accurate and timely evaluation of hypophosphatemia and bone pain is crucial for diagnosing TIO.
  • A systematic localization strategy is essential for identifying the causative tumor.
  • Advances in medical and interventional therapies offer new hope for managing TIO.