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The locomotor system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The increased PTH levels cause an increased number of osteoclasts on the bone surface. This leads to increased bone resorption (Figure 13. 8A). This bone resorption is accompanied by increased bone formation, with increased osteoblasts lining the bone surface. Overall there is loss of bone. As the disease progresses, much bone may be resorbed and replaced by small irregular trabeculae of woven bone, with loss of the normal bony architecture. Fibrous tissue is laid down, and, in longstanding cases, the marrow spaces become filled with fibrous tissue. Cystic degeneration occasionally occurs. In ‘brown tumours’ (Figure 13.8B), the resorbed bone is replaced by numerous osteoclasts, fibrous tissue, and haemorrhage with abundant haemosiderin. This may simulate giant cell tumour of bone.
Musculoskeletal tumours
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Giant cell tumour of bone (Figure37.22) is a locally aggressive tumour with large osteoclast-like giant cells. It usually occurs between the ages of 20 and 45, after the physes have closed. Giant cell tumour of bone typically affects the epiphysis of long bones and erodes bone under the articular cartilage, especially around the knee, proximal humerus and distal radius. Metastases are rare.
Histopathologic Classification of Human Sinonasal Tumors
Published in Gerd Reznik, Sherman F. Stinson, Nasal Tumors in Animals and Man, 2017
Numerous lesions of bone can contain multinucleated giant cells and the identification of the “true” giant cell tumor of bone can thus be difficult. The true giant cell tumor is probably rare in the sinonasal tract. Possibly less rare are the giant cell lesions histologically similar to central giant cell (reparative) granulomas described in the jaws, and also the giant cell lesions (“brown tumors”) associated with hyperparathyroidism. The “true” giant cell tumor tends to have more evenly distributed and larger giant cells, with little or no fibrous areas in the stroma and with less evidence of hemosiderin deposition.
Biosimilarity of HS-20090 to Denosumab in healthy Chinese subjects: a randomized, double-blinded, pharmacokinetics/pharmacodynamics study
Published in Expert Opinion on Investigational Drugs, 2022
Yaqi Lin, Heng Yang, Xiaoyan Yang, Can Guo, Shuang Yang, Guoping Yang, Qiong Wu, Chao Pan, Changan Sun, Chuan Li, Liangliang He, Jie Huang, Qi Pei
Denosumab is a fully human monoclonal antibody that binds to nuclear factor kappa-B ligand (RANKL), a cytokine that plays an essential role in the formation, function, and survival of osteoclasts, through inhibiting osteoclast-mediated bone resorption and thereby increasing the bone mass [5]. Denosumab (Xgeva®, Amgen Inc., Thousand Oaks, CA, USA) has been approved in multiple countries including European Union, United States, Japan, and China, for the prevention of skeletal-related events (SREs) in patients with multiple myeloma and patients with bone metastases from solid tumors. It can be also prescribed to adults and skeletally mature adolescents with giant cell tumor of bone that is unresectable or where surgical resection is likely to result in severe morbidity [6]. Xgeva® is an effective therapy for oncology patients with urgent clinical needs. However, its high price makes it unaffordable for many patients in developing countries; thus, the availability of biosimilars is highly demanded to make drugs more accessible for patients at relatively low prices.
Ultrastructural changes in giant cell tumor of bone cultured cells exposed to quercetin
Published in Ultrastructural Pathology, 2021
Eréndira Estrada-Villaseñor, Andres Delgado-Cedillo, Alma Hernández-Pérez, Abelardo Meneses, Anell Olivos Meza, Alberto Hidalgo-Bravo, Mónica Santamaría, Carlos Landa Solís
Giant cell tumor of bone (GCTB) is a primary bone tumor that affects most common people between 20 and 50 years. The epiphysis of long bones is its principal location; however, GCTB can affect other bones such as sacrum that are sites of difficult surgical access. The treatment for GCTB is mainly surgical, with limitations in case of inaccessible locations and with some disadvantages.1 There are few complementary and pharmacological alternatives for the treatment of this tumor: denosumab and bisphosphonates. Both, with the possibility of secondary effects such as mandibular osteonecrosis and atypical fractures with bisphosphonates or malignant transformation with denosumab.2,3 Therefore, to find other molecules or compounds that could be potential therapeutic agents and whose administration has no secondary effects is desirable in order to offer a better outcome to the patients. Quercetin could be a potential therapeutic agent for GCTB.
Incidence and demographics of giant cell tumor of bone in The Netherlands: First nationwide Pathology Registry Study
Published in Acta Orthopaedica, 2018
Arie J Verschoor, Judith V M G Bovée, Monique J L Mastboom, P D Sander Dijkstra, Michiel A J Van De Sande, Hans Gelderblom
Giant cell tumor of bone (GCT-B) is a locally aggressive neoplasm composed of sheets of mononuclear cells admixed with uniformly distributed large osteoclast-like giant cells, primarily affecting the metaphysis of long bones (Athanasou et al. 2013). These cells express receptors of nuclear factor kappa-B ligand (RANKL) (Atkins et al. 2000, Roux et al. 2002). GCT-B are rare; however, the incidence is not exactly known and is for example not stated in the World Health Organization (WHO) classification of Tumors of Soft Tissue and Bone (Athanasou et al. 2013). The incidence was recently estimated at between 1.03 and 1.33 per million per year based on cancer registries in Australia, Japan and Sweden (Table 1) (Liede et al. 2014, Amelio et al. 2016). Median age of onset ranges between 20 and 40 years with an equal distribution between the sexes or a slight female predominance (Athanasou et al. 2013, Amelio et al. 2016).