Rare Giant Cell Tumour of the Left Parieto-Occipital Skull in an 8-Year-Old Female Patient: A Case Report

Rare Giant Cell Tumour of the Left Parieto-Occipital Skull in an 8-Year-Old Female Patient: A Case Report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Rare Giant Cell Tumour of the Left Parieto-Occipital Skull in an 8-Year-Old Female Patient: A Case Report Eyob Engidaw, Esayas Tefera, Kenean Bekele, Eyosias Belayneh, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8405513/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 14 You are reading this latest preprint version Abstract Introduction: Giant cell tumors (GCTs) are typically benign but locally aggressive lesions, typically found at the metaphyseal or epiphyseal regions of the tibia or femur, long bones. It predominantly occurs in young adults aged 20 to 40 with a high recurrence rate and the potential for aggressive behaviour. Local aggressiveness varies from focal symptoms arising from bony or cortical destruction and surrounding soft tissue expansion to the rare occurrence of metastasis.Involvement of the cranial bones, particularly in pediatric patients, is exceedingly rare. Case Presentation: We report the case of an 8-year-old female patient who presented with a progressively enlarging mass over the left parieto-occipital region of the skull for 18 months. Imaging revealed a large, lytic, expansile lesion compressing the occipital and parietal lobes. The patient underwent surgical excision via craniotomy. Histopathological examination confirmed the diagnosis of a giant cell tumor of bone. Postoperative follow-up showed no recurrence at 6 months. Discussion: This case highlights the rare presentation of GCT in the pediatric skull, underscoring the diagnostic and surgical challenges it presents. Complete surgical resection remains the mainstay of treatment, with generally favorable outcomes. Conclusion: Early identification and prompt surgical management of skull GCTs are critical to prevent neurological complications and recurrence. Long-term surveillance is essential, particularly in pediatric patients. Giant Cell Tumor Skull Pediatric Neurosurgery Parieto-Occipital Mass Case Report Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Introduction and Importance Giant cell tumors are characterized by the presence of multinucleated giant cells and are most commonly found in the metaphysis of long bones. The occurrence of GCTs in the skull is rare, especially in pediatric patients. The etiology remains unclear, but these tumors have a propensity for local aggression. Early diagnosis and appropriate surgical intervention are critical for optimal outcomes. We present a case of GCT on the skull of an 8 year old pediatric patient. Clinical presentation An 8-year-old female school-age child presented to the pediatric clinic with a 1-year and 6-month history of a progressively enlarging mass on the left posterior side of her head, associated with mild headache and localized tenderness. There was no history of trauma or significant family history of bone tumors. On examination, she was well-looking with stable vital signs. A firm to hard consistency, non-mobile, and slightly tender mass measuring 10cm × 12cm was palpated over the left parieto-occipital region. Neurological examination revealed no deficits, and there were no signs of increased intracranial pressure. There were no pertinent findings on other site examination. (Fig. 1.1 ) Upon imaging, a computed tomography (CT) scan of the skull revealed a well-defined, lytic lesion measuring approximately 8.4cm × 5.3cm × 5.8cm in size in the left parieto-occipital calvarium region expansile and soft tissue density mass with internal bony fragments. The mass had a compressive mass effect on the parietal and occipital lobes with sulci effacement and dural inward displacement. The mass infiltrated the overlying scalp and showed post-contrast avid heterogeneous enhancement. No calcifications were noted. Magnetic resonance imaging (MRI) confirmed the lesion's characteristics, showing a well-defined T1 and T2 hypointense mass with areas of hyperintensities in the left occipito-parietal calvarium. It was expansile, caused marked expansion of the outer table, and involved the scalp soft tissue. The mass also compressed adjacent brain parenchyma but showed no invasion. It had heterogeneous enhancement on post-contrast study with central non-enhancing areas. The mass showed no restriction on DWI and no blooming on SWI. (Fig. 1.2 ) Surgical Intervention The patient underwent surgical resection of the tumor. A craniotomy was performed, and the tumor was carefully excised, ensuring minimal disruption to surrounding structures. The lesion was encapsulated but adhered to the surrounding dura. The surgical margins were confirmed to be free. (Fig. 1.3 ) (Fig. 1.4 ) Histopathological Analysis The excised tumor was sent for histopathological evaluation. Microscopic examination revealed a proliferation of multinucleated giant cells, oval to spindle-shaped mononuclear cells, and a background of foamy macrophages and hemosiderin-laden cells. These findings were consistent with a giant cell tumor of bone. (Fig. 1.5 ) Postoperative Course The patient tolerated the procedure well and was monitored in the pediatric ward. Pain management was initiated, and the patient was started on physiotherapy to facilitate recovery. Margins were free upon histopathological examination. Follow-up imaging at 6 months post-surgery showed no evidence of recurrence. Discussion Giant cell tumor of bone (GCTB) is a benign but locally aggressive lesion that typically arises in the epiphysis of long bones.(Turcotte, 2006 ) It has an estimated annual incidence of 1.7 per million (Verschoor et al., 2018 ), making it a rare entity and accounting for only 4%–10% of all primary bone tumors. Primary bone tumors themselves represent approximately 0.2% of all malignancies. GCTB predominantly affects young adults between 20 and 40 years of age, with a female-to-male ratio reported between 1.3–1.5:1. The most commonly affected sites include the region around the knee (44%), distal radius (10%), proximal humerus (6%), and the bones of the hands and feet (13%). In contrast, cranial involvement is exceptionally rare. When present, it typically affects the sphenoid or temporal bones in adults. Occurrence in the occipital bone, particularly in children, is extremely uncommon and has been reported only in few literatures (Reed et al., 1994 ) . The biological nature of GCTB remains controversial. While traditionally considered benign, there is ongoing debate about whether it represents a true neoplasm or a reactive process. Supporting evidence for a neoplastic origin includes 20q11 amplification in approximately 54% of cases, p53 overexpression in about 20%, as well as centrosome amplification and increased telomerase activity with suppression of telomere shortening. However, these alterations are not universal, and similar findings may occur in rapidly proliferating non-neoplastic cells or in other reactive bone lesions. Consequently, the precise pathogenesis of GCTB remains unresolved (Haque and Moatasim, 2008 ). Despite its benign classification, GCTB can demonstrate locally aggressive behavior, with a notable tendency for recurrence. Furthermore, 1%–5% of patients develop metastases, most commonly to the lungs. The likelihood of metastasis appears to correlate strongly with local aggressiveness and repeated recurrence, it highlights the importance of surgical management and long-term follow-up . . Differential Diagnosis Lytic metastatic lesion (particularly a vascular metastasis from thyroid or renal cell carcinoma):- presents as an expansile, destructive bone lesion caused by metastatic tumor cells eroding the calvarial bone. These lesions are typically well-defined, highly vascular, and may produce a soft-tissue mass, sometimes associated with pain, swelling, or pulsatility. Primary bone tumor:- typically presents as a localized calvarial lesion arising from bone or cartilage, often manifesting as a painless, slowly enlarging mass. Common entities include eosinophilic granuloma, osteoma, osteosarcoma, and Ewing sarcoma. Depending on the tumor type, imaging may show lytic, sclerotic, or mixed patterns, sometimes with soft-tissue extension or periosteal reaction. Brown tumor of hyperparathyroidism:- a rare, benign osteolytic lesion resulting from excessive osteoclastic bone resorption due to elevated parathyroid hormone levels. It typically presents as an expansile, well-defined lytic mass with thinning of the calvarial cortex. Histologically, it contains fibrous tissue, multinucleated giant cells, and areas of hemorrhage, giving it a characteristic “brown” appearance. Nonossifying fibroma:- an extremely rare, benign fibroblastic lesion characterized by a well-defined, lytic defect with a sclerotic rim. It typically presents as an asymptomatic, slow-growing calvarial mass and shows fibrous tissue replacement of normal bone without aggressive features. Aneurysmal bone cyst:- a benign, expansile, blood-filled osteolytic lesion characterized by rapid growth and cortical thinning. It typically appears as a multiloculated, “blow-out” cystic mass that may cause swelling, pain, or deformity. Imaging often shows fluid–fluid levels and marked expansion of the calvarial bone. Fibrous metaphyseal defects:- typically seen in long bones are extremely rare in the skull. When present, they appear as well-defined, benign fibro-osseous lesions with a lytic center and sclerotic margins. In a pediatric patient, they usually present as an incidental, asymptomatic calvarial defect without aggressive features or significant expansion. Osteoblastoma:- a rare, benign but locally aggressive bone-forming tumor that presents as a painful, expansile lesion of the calvarium. Imaging typically shows a lytic or mixed lytic–sclerotic mass with internal calcifications and cortical thinning. It may cause localized swelling, tenderness, or neurologic symptoms if near critical structures. Chondroblastoma:- a rare, benign cartilaginous tumor that typically arises from the squamous or temporal bone. It presents as a well-defined, lytic lesion that may cause pain, swelling, or conductive hearing symptoms depending on location. Imaging often shows a mixed lytic–sclerotic pattern with punctate calcifications and possible cortical expansion. Malignant fibrous histiocytoma:- also called undifferentiated pleomorphic sarcoma,in a pediatric patient is a rare, aggressive soft-tissue and bone malignancy that presents as a rapidly enlarging, painful calvarial mass with destructive bone changes. Imaging typically shows an ill-defined, lytic lesion with cortical breakthrough and soft-tissue extension. It carries a high risk of local recurrence and potential metastasis. Telangiectatic osteosarcoma:- is a rare, highly aggressive variant of osteosarcoma characterized by blood-filled cystic spaces and minimal osteoid production. It presents as a rapidly enlarging, painful calvarial mass with destructive lytic bone changes, cortical breach, and prominent soft-tissue extension. Imaging often mimics an aneurysmal bone cyst but shows aggressive features and malignant cells on histology. Pathophysiology The giant cell tumor of bone (GCT) is a local osteolytic tumor with variable degrees of aggressiveness. In rare cases, pulmonary metastases can be observed. The lesion most frequently occurs in the epiphysis of long tubular bones of the knee region, predominantly affecting young adults after closure of the growth plate. The characteristic histological appearance of GCT displays a high number of osteoclast-like multinucleated giant cells, which resulted in the classification "osteoclastoma" or "giant cell tumor". Apart from the multinucleated giant cells, there are two mononuclear cell types in the GCT. The first one has a round morphology and resembles a monocyte. The second cell type is the spindle-shaped, fibroblast-like stromal cell. Cell culture experiments with GCT cells revealed the stromal cell to be the proliferating component of the GCT. The other two cell types, the monocyte and the multinucleated giant cell, were lost after a few cell culture passages. Furthermore, latest results from GCT reveal that the stromal cells secrete a variety of cytokines and differentiation factors, including MCP1, ODF and M-CSF. These molecules are monocyte chemoattractants and are essential for osteoclast differentiation, suggesting that the stromal cell stimulates blood monocyte immigration into tumor tissue and enhances their fusion into osteoclast-like, multinucleated giant cells.((Wuelling et al., 2002 )) The pathogenesis of GCT appears to be significantly influenced by the receptor activator of the nuclear factor kappa B [NF-kB] ligand (RANKL). Under normal physiologic conditions, osteoclast formation requires interaction with cells of the osteoblastic lineage, which may depend upon cell-cell contact and the interaction of RANKL with its receptor RANK. Several studies identified a high expression of RANKL by stromal cells within GCTs. These stromal cells also secrete factors that can regulate or prevent osteoclastogenesis, including osteoprotegerin, serving as a natural negative regulator of RANKLE that obstructs osteoclast and osteoblast interactions and functions as a natural negative regulator of RANKL. The expression of RANKL by the osteoblast-like mononuclear stromal cells stimulates the recruitment of the osteoclastic cells from a normal monocytic pre-osteoclast cell. The osteoclastic giant cells then actively absorb host bone via a cathepsin K and matrix metalloproteinase 13-mediated process, which would account for the osteolysis associated with these tumors.The tumor can be locally aggressive, leading to bone destruction, although they rarely metastasize ((Cowan and Singh, 2013 )). Their location in the skull can pose unique challenges in management, especially in the pediatric population, where cranial development is still ongoing ((Reed et al., 1994 )). Upon gross inspection, these lesions exhibit characteristic features such as a chocolate brown, soft, and spongy texture, and fragility. Yellow-to-orange discoloration from the hemosiderin can also be present. Commonly, cystic blood-filled cavities within the tumor may be observed. Examination typically reveals a variable degree of cortical expansion and disruption while the periosteum remains intact. Histologically, these lesions appear cellular, featuring a distinctive composition of multinucleated giant cells and a background network of mononuclear stromal cells. The mononuclear cells can exhibit a variety of shapes, including plump, oval, or spindle-shaped, and may display prominent mitotic activity, although cellular atypia is uncommon. The multinucleate giant cells have numerous centrally located nuclei, unlike the peripherally located nuclei of Langerhans-type giant cells observed in atypical infections. The nuclei of these giant cells are compact and oval, containing prominent nucleoli. Giant cells are distributed throughout the lesion, and the concentration of multinucleated giant cells can vary from tumor to tumor. While some tumors feature numerous multinucleated giant cells, others have limited giant cells settled in whirls of spindle-shaped stromal cells. In approximately 5% of cases, giant cells invade small perforating vessels((“Giant cell tumor of bone,” 2022)). Treatment Strategies The management of GCT involves a multidisciplinary approach, combining surgical, medical, and sometimes radiation therapies. The specific approach depends on factors such as the tumor's location, size, aggressiveness, and whether it is primary or recurrent. The standard care for treating GCT often involves a tailored approach considering the benign nature of most GCTs, their proximity to joints in young adults, and the goal of preserving bone anatomy. Many authors advocate for an intralesional approach rather than resection to maintain bone integrity. The primary treatment for GCTs remains surgical excision, aiming for complete resection to minimize recurrence (Tsukamoto et al., 2021 ). While wide resection has been associated with a decreased risk of local recurrence, potentially raising the recurrence-free survival rate from 84% to 100%, this approach comes with higher rates of surgical complications. It may lead to functional impairment, necessitating reconstruction. The decision between intralesional curettage and wide resection is often made based on the tumor's location, size, aggressiveness, and the patient's overall health and preferences. Resection may be the preferred option in benign tumors, particularly when bone salvageability through intralesional methods would cause a severe compromise in mechanical characteristics. This applies particularly to the "expendable bones," such as the lower ulnar and upper fibular end, where excision may be the treatment of choice. In primary and recurrent cases, especially when the tumor involves the end of a long bone and causes significant dysfunction of the joint surface, reconstruction becomes necessary. Several options are available for these cases, including mega prosthetic joint replacement, biologic reconstruction with an autograft, arthrodesis with internal/external fixation, microvascular fibula reconstruction, Ilizarov method of bone regeneration, and osteoarticular allograft. Adjunct therapies, such as curettage and bone grafting, may be employed based on the tumor's characteristics and location. The prognosis is generally favorable with complete excision, although long-term follow-up is necessary to monitor for potential recurrence. Radiotherapy is recommended for spinal, sacral, or aggressive tumors when complete excision or curettage is impractical for any functional or medical reasons. Radiation therapy may be considered when the close proximity of critical structures prevents microscopically negative surgical margins. The systemic treatment options for advanced or metastatic disease are very limited. Intralesional curettage and bone grafting are considered the limb-sparing treatment of choice, associated with acceptable functional and oncologic outcomes. However, a simple curettage with or without a bone graft presents a 27% and 55% recurrence rate. Many surgeons replace bone graft packing with PMMA packing due to its high recurrence rate. Wide en bloc resection is another option that offers the lowest recurrence rate and can be used in expendable bones. For instance, wide resection without reconstruction is often performed in the proximal fibula. In cases of GCT in the distal radius, resection and reconstruction with an allograft or an autograft are commonly undertaken. Adjuvant treatments, such as liquid nitrogen, phenol, or HO with argon beam coagulation, demonstrate excellent recurrence-free survival, especially when paired with intralesional curettage. Long-term follow-up is recommended to monitor for potential local recurrence or metastasis. Informed consent was obtained from the patient’s legal guardian for publication of this case report and accompanying images. Declarations ETHICAL APPROVAL Not applicable. INFORMED CONSENT Informed consent was obtained from the patient, and a copy of the written consent is available for review by the editor-in-chief of this journal. DECLARATIONS OF INTEREST None. FUNDING None. CLINICAL TRIAL NUMBER Clinical trial number: not applicable. CONSENT TO PUBLISH Informed consent was obtained from the patient’s legal guardian for publication of this case report and accompanying images. References Cowan, R.W., Singh, G., 2013. Giant cell tumor of bone: A basic science perspective. Bone 52, 238–246. https://doi.org/10.1016/j.bone.2012.10.002 Giant cell tumor of bone: An update, including spectrum of pathological features, pathogenesis, molecular profile and the differential diagnoses, 2022. . Histol. Histopathol. 38, 139–153. https://doi.org/10.14670/HH-18-486 Haque, A.U., Moatasim, A., 2008. Giant cell tumor of bone: a neoplasm or a reactive condition? Int. J. Clin. Exp. Pathol. 1, 489–501. Reed, L., Willison, C.D., Schochet, S.S., Voelker, J.L., 1994. Giant cell tumor of the calvaria in a child: Case report. J. Neurosurg. 80, 148–151. https://doi.org/10.3171/jns.1994.80.1.0148 Tsukamoto, S., Mavrogenis, A.F., Kido, A., Errani, C., 2021. Current Concepts in the Treatment of Giant Cell Tumors of Bone. Cancers 13, 3647. https://doi.org/10.3390/cancers13153647 Turcotte, R.E., 2006. Giant Cell Tumor of Bone. Orthop. Clin. North Am. 37, 35–51. https://doi.org/10.1016/j.ocl.2005.08.005 Verschoor, A.J., Bovée, J.V.M.G., Mastboom, M.J.L., Sander Dijkstra, P.D., Van De Sande, M.A.J., Gelderblom, H., 2018. Incidence and demographics of giant cell tumor of bone in The Netherlands: First nationwide Pathology Registry Study. Acta Orthop. 89, 570–574. https://doi.org/10.1080/17453674.2018.1490987 Wuelling, M., Engels, C., Jesse, N., Werner, M., Kaiser, E., Delling, G., 2002. Aktuelles zur Histogenese des Riesenzelltumors. Pathol. 23, 332–339. https://doi.org/10.1007/s00292-002-0552-2 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Revision requested 04 Mar, 2026 Reviews received at journal 22 Feb, 2026 Reviewers agreed at journal 12 Feb, 2026 Reviews received at journal 11 Feb, 2026 Reviewers agreed at journal 11 Feb, 2026 Reviews received at journal 11 Feb, 2026 Reviewers agreed at journal 08 Feb, 2026 Reviews received at journal 08 Feb, 2026 Reviewers agreed at journal 07 Feb, 2026 Reviewers invited by journal 06 Feb, 2026 Editor invited by journal 16 Jan, 2026 Editor assigned by journal 29 Dec, 2025 Submission checks completed at journal 29 Dec, 2025 First submitted to journal 19 Dec, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8405513","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":588040113,"identity":"69eaf51a-04dc-4fc7-afce-f6e953ed4545","order_by":0,"name":"Eyob Engidaw","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA6klEQVRIiWNgGAWjYHACNijNfABISMiQooUtAaSFhxQtPAZgkqB6fonkYw9+ttnk8UvkfH51o8aCh4H98NEN+LRIzkhLN+xtSyuWnJG7zTrnGNBhPGlpN/BpMbiRYybB23Y4ccPt3G3GOWxALRI8Zni12AO1SP5t+5+4/3bOM+Ocf0RoMZDIMZPmbTuQuEE6h/lxbhsRWiTOPEs3ljmXnDjj/jMz5tw+CR42Qn7hb08+9vBNmV1if8/hx59zvtXJ8bMfPoZXC4NAAgMDIyRq2CTAJF7lYGsOAIk/YCbzB4KqR8EoGAWjYEQCAHvDSKF8I2rtAAAAAElFTkSuQmCC","orcid":"","institution":"University of Gondar","correspondingAuthor":true,"prefix":"","firstName":"Eyob","middleName":"","lastName":"Engidaw","suffix":""},{"id":588040114,"identity":"cc1200c9-8486-4239-8fa6-fb8b28872c63","order_by":1,"name":"Esayas Tefera","email":"","orcid":"","institution":"University of Gondar","correspondingAuthor":false,"prefix":"","firstName":"Esayas","middleName":"","lastName":"Tefera","suffix":""},{"id":588040115,"identity":"a1318551-e404-4c73-95bd-0807674df27d","order_by":2,"name":"Kenean Bekele","email":"","orcid":"","institution":"University of Gondar","correspondingAuthor":false,"prefix":"","firstName":"Kenean","middleName":"","lastName":"Bekele","suffix":""},{"id":588040116,"identity":"8ca29fff-5426-423b-8b11-2618232ceab4","order_by":3,"name":"Eyosias Belayneh","email":"","orcid":"","institution":"University of Gondar","correspondingAuthor":false,"prefix":"","firstName":"Eyosias","middleName":"","lastName":"Belayneh","suffix":""},{"id":588040117,"identity":"b2bf8d16-53de-4382-8c2b-c1afd3c715d7","order_by":4,"name":"Sharon Tibebe","email":"","orcid":"","institution":"University of Gondar","correspondingAuthor":false,"prefix":"","firstName":"Sharon","middleName":"","lastName":"Tibebe","suffix":""},{"id":588040118,"identity":"1c5ed0da-4a26-47ab-8eac-d8b9f240b831","order_by":5,"name":"Habib Seid","email":"","orcid":"","institution":"University of Gondar","correspondingAuthor":false,"prefix":"","firstName":"Habib","middleName":"","lastName":"Seid","suffix":""}],"badges":[],"createdAt":"2025-12-19 13:54:06","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8405513/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8405513/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":102438979,"identity":"400c8925-6212-4040-b8fe-cf04012ebc9f","added_by":"auto","created_at":"2026-02-11 16:38:07","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":465990,"visible":true,"origin":"","legend":"\u003cp\u003eFig 1.1: Image of the tumor during physical examination\u003c/p\u003e","description":"","filename":"1.1.png","url":"https://assets-eu.researchsquare.com/files/rs-8405513/v1/b7c7d718de9f29af4adbd6d4.png"},{"id":102438977,"identity":"d3ddd93d-d95c-4425-91d7-e97f470d6102","added_by":"auto","created_at":"2026-02-11 16:38:06","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":272934,"visible":true,"origin":"","legend":"\u003cp\u003eFig 1.2 MRI images of the skull\u003c/p\u003e","description":"","filename":"1.2.png","url":"https://assets-eu.researchsquare.com/files/rs-8405513/v1/abba7737b0bb2195753639aa.png"},{"id":102438980,"identity":"c4ffb3fd-bd2e-4918-a9fd-6a1f4c89c251","added_by":"auto","created_at":"2026-02-11 16:38:07","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":1049391,"visible":true,"origin":"","legend":"\u003cp\u003eFig 1.3 Gross surface appearance of the mass upon exposure and en bloc excision, Intra-op picture.\u003c/p\u003e","description":"","filename":"1.3.png","url":"https://assets-eu.researchsquare.com/files/rs-8405513/v1/bbefd96aa9eddaaf17b03b13.png"},{"id":102438978,"identity":"aac66019-4187-4e41-bab8-dc536f3196f2","added_by":"auto","created_at":"2026-02-11 16:38:07","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":949022,"visible":true,"origin":"","legend":"\u003cp\u003eFig 1.4 Tumor comletely excised and subjected to histopathology for assesment of margins. Surface hemostasis with 3% H\u003csub\u003e2\u003c/sub\u003eO\u003csub\u003e2\u003c/sub\u003e( Background).\u003c/p\u003e","description":"","filename":"1.4.png","url":"https://assets-eu.researchsquare.com/files/rs-8405513/v1/5c84bf3c1e7bdc3a7d69b44a.png"},{"id":102438981,"identity":"729b692c-d63b-42b3-b2dc-8d4a4c23906d","added_by":"auto","created_at":"2026-02-11 16:38:07","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":803461,"visible":true,"origin":"","legend":"\u003cp\u003eFig. 1.5: Histopathological examination with H \u0026amp; E stain using a) 100x b) shows Giant cell tumor stromal cells originating from osteoblasts(Mononuclear histiocytic cells, Multinucleated giant cells belonging to an osteoclast-monocyte lineage)\u003c/p\u003e","description":"","filename":"1.5.png","url":"https://assets-eu.researchsquare.com/files/rs-8405513/v1/198e35c59178dd194c85c0bc.png"},{"id":102439016,"identity":"60c341ae-218a-4ce1-bd0c-c907d15a265f","added_by":"auto","created_at":"2026-02-11 16:38:25","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":5206215,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8405513/v1/09d8b560-cc2e-4a4d-8001-abd709f1db88.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Rare Giant Cell Tumour of the Left Parieto-Occipital Skull in an 8-Year-Old Female Patient: A Case Report","fulltext":[{"header":"Introduction and Importance","content":"\u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eGiant cell tumors are characterized by the presence of multinucleated giant cells and are most commonly found in the metaphysis of long bones. The occurrence of GCTs in the skull is rare, especially in pediatric patients. The etiology remains unclear, but these tumors have a propensity for local aggression. Early diagnosis and appropriate surgical intervention are critical for optimal outcomes. We present a case of GCT on the skull of an 8 year old pediatric patient.\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e"},{"header":"Clinical presentation","content":"\u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eAn 8-year-old female school-age child presented to the pediatric clinic with a 1-year and 6-month history of a progressively enlarging mass on the left posterior side of her head, associated with mild headache and localized tenderness. There was no history of trauma or significant family history of bone tumors. On examination, she was well-looking with stable vital signs. A firm to hard consistency, non-mobile, and slightly tender mass measuring 10cm \u0026times; 12cm was palpated over the left parieto-occipital region. Neurological examination revealed no deficits, and there were no signs of increased intracranial pressure. There were no pertinent findings on other site examination. (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1.1\u003c/span\u003e)\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eUpon imaging, a computed tomography (CT) scan of the skull revealed a well-defined, lytic lesion measuring approximately 8.4cm \u0026times; 5.3cm \u0026times; 5.8cm in size in the left parieto-occipital calvarium region expansile and soft tissue density mass with internal bony fragments. The mass had a compressive mass effect on the parietal and occipital lobes with sulci effacement and dural inward displacement. The mass infiltrated the overlying scalp and showed post-contrast avid heterogeneous enhancement. No calcifications were noted.\u003c/p\u003e \u003cp\u003eMagnetic resonance imaging (MRI) confirmed the lesion's characteristics, showing a well-defined T1 and T2 hypointense mass with areas of hyperintensities in the left occipito-parietal calvarium. It was expansile, caused marked expansion of the outer table, and involved the scalp soft tissue. The mass also compressed adjacent brain parenchyma but showed no invasion. It had heterogeneous enhancement on post-contrast study with central non-enhancing areas. The mass showed no restriction on DWI and no blooming on SWI. (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e1.2\u003c/span\u003e)\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eSurgical Intervention\u003c/h2\u003e \u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eThe patient underwent surgical resection of the tumor. A craniotomy was performed, and the tumor was carefully excised, ensuring minimal disruption to surrounding structures. The lesion was encapsulated but adhered to the surrounding dura. The surgical margins were confirmed to be free. (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e1.3\u003c/span\u003e) (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e1.4\u003c/span\u003e)\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eHistopathological Analysis\u003c/h3\u003e\n\u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eThe excised tumor was sent for histopathological evaluation. Microscopic examination revealed a proliferation of multinucleated giant cells, oval to spindle-shaped mononuclear cells, and a background of foamy macrophages and hemosiderin-laden cells. These findings were consistent with a giant cell tumor of bone. (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e1.5\u003c/span\u003e)\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e\n\u003ch3\u003ePostoperative Course\u003c/h3\u003e\n\u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eThe patient tolerated the procedure well and was monitored in the pediatric ward. Pain management was initiated, and the patient was started on physiotherapy to facilitate recovery. Margins were free upon histopathological examination. Follow-up imaging at 6 months post-surgery showed no evidence of recurrence.\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eGiant cell tumor of bone (GCTB) is a benign but locally aggressive lesion that typically arises in the epiphysis of long bones.(Turcotte, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e2006\u003c/span\u003e) It has an estimated annual incidence of 1.7 per million (Verschoor et al., \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e2018\u003c/span\u003e), making it a rare entity and accounting for only 4%\u0026ndash;10% of all primary bone tumors. Primary bone tumors themselves represent approximately 0.2% of all malignancies. GCTB predominantly affects young adults between 20 and 40 years of age, with a female-to-male ratio reported between 1.3\u0026ndash;1.5:1. The most commonly affected sites include the region around the knee (44%), distal radius (10%), proximal humerus (6%), and the bones of the hands and feet (13%).\u003c/p\u003e \u003cp\u003eIn contrast, cranial involvement is exceptionally rare. When present, it typically affects the sphenoid or temporal bones in adults. Occurrence in the occipital bone, particularly in children, is extremely uncommon and has been reported only in few literatures (Reed et al., \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e1994\u003c/span\u003e) .\u003c/p\u003e \u003cp\u003eThe biological nature of GCTB remains controversial. While traditionally considered benign, there is ongoing debate about whether it represents a true neoplasm or a reactive process. Supporting evidence for a neoplastic origin includes 20q11 amplification in approximately 54% of cases, p53 overexpression in about 20%, as well as centrosome amplification and increased telomerase activity with suppression of telomere shortening. However, these alterations are not universal, and similar findings may occur in rapidly proliferating non-neoplastic cells or in other reactive bone lesions. Consequently, the precise pathogenesis of GCTB remains unresolved (Haque and Moatasim, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e2008\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eDespite its benign classification, GCTB can demonstrate locally aggressive behavior, with a notable tendency for recurrence. Furthermore, 1%\u0026ndash;5% of patients develop metastases, most commonly to the lungs. The likelihood of metastasis appears to correlate strongly with local aggressiveness and repeated recurrence, it highlights the importance of surgical management and long-term follow-up .\u003cdiv class=\"BlockQuote\"\u003e\u003cp\u003e.\u003c/p\u003e\u003c/div\u003e\u003c/p\u003e\n\u003ch3\u003eDifferential Diagnosis\u003c/h3\u003e\n\u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003eLytic metastatic lesion (particularly a vascular metastasis from thyroid or renal cell carcinoma):- presents as an expansile, destructive bone lesion caused by metastatic tumor cells eroding the calvarial bone. These lesions are typically well-defined, highly vascular, and may produce a soft-tissue mass, sometimes associated with pain, swelling, or pulsatility.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003ePrimary bone tumor:- typically presents as a localized calvarial lesion arising from bone or cartilage, often manifesting as a painless, slowly enlarging mass. Common entities include eosinophilic granuloma, osteoma, osteosarcoma, and Ewing sarcoma. Depending on the tumor type, imaging may show lytic, sclerotic, or mixed patterns, sometimes with soft-tissue extension or periosteal reaction.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eBrown tumor of hyperparathyroidism:- a rare, benign osteolytic lesion resulting from excessive osteoclastic bone resorption due to elevated parathyroid hormone levels. It typically presents as an expansile, well-defined lytic mass with thinning of the calvarial cortex. Histologically, it contains fibrous tissue, multinucleated giant cells, and areas of hemorrhage, giving it a characteristic \u0026ldquo;brown\u0026rdquo; appearance.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eNonossifying fibroma:- an extremely rare, benign fibroblastic lesion characterized by a well-defined, lytic defect with a sclerotic rim. It typically presents as an asymptomatic, slow-growing calvarial mass and shows fibrous tissue replacement of normal bone without aggressive features.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eAneurysmal bone cyst:- a benign, expansile, blood-filled osteolytic lesion characterized by rapid growth and cortical thinning. It typically appears as a multiloculated, \u0026ldquo;blow-out\u0026rdquo; cystic mass that may cause swelling, pain, or deformity. Imaging often shows fluid\u0026ndash;fluid levels and marked expansion of the calvarial bone.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eFibrous metaphyseal defects:- typically seen in long bones are extremely rare in the skull. When present, they appear as well-defined, benign fibro-osseous lesions with a lytic center and sclerotic margins. In a pediatric patient, they usually present as an incidental, asymptomatic calvarial defect without aggressive features or significant expansion.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eOsteoblastoma:- a rare, benign but locally aggressive bone-forming tumor that presents as a painful, expansile lesion of the calvarium. Imaging typically shows a lytic or mixed lytic\u0026ndash;sclerotic mass with internal calcifications and cortical thinning. It may cause localized swelling, tenderness, or neurologic symptoms if near critical structures.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eChondroblastoma:- a rare, benign cartilaginous tumor that typically arises from the squamous or temporal bone. It presents as a well-defined, lytic lesion that may cause pain, swelling, or conductive hearing symptoms depending on location. Imaging often shows a mixed lytic\u0026ndash;sclerotic pattern with punctate calcifications and possible cortical expansion.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eMalignant fibrous histiocytoma:- also called undifferentiated pleomorphic sarcoma,in a pediatric patient is a rare, aggressive soft-tissue and bone malignancy that presents as a rapidly enlarging, painful calvarial mass with destructive bone changes. Imaging typically shows an ill-defined, lytic lesion with cortical breakthrough and soft-tissue extension. It carries a high risk of local recurrence and potential metastasis.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eTelangiectatic osteosarcoma:- is a rare, highly aggressive variant of osteosarcoma characterized by blood-filled cystic spaces and minimal osteoid production. It presents as a rapidly enlarging, painful calvarial mass with destructive lytic bone changes, cortical breach, and prominent soft-tissue extension. Imaging often mimics an aneurysmal bone cyst but shows aggressive features and malignant cells on histology.\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003ePathophysiology\u003c/h2\u003e \u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eThe giant cell tumor of bone (GCT) is a local osteolytic tumor with variable degrees of aggressiveness. In rare cases, pulmonary metastases can be observed. The lesion most frequently occurs in the epiphysis of long tubular bones of the knee region, predominantly affecting young adults after closure of the growth plate. The characteristic histological appearance of GCT displays a high number of osteoclast-like multinucleated giant cells, which resulted in the classification \"osteoclastoma\" or \"giant cell tumor\". Apart from the multinucleated giant cells, there are two mononuclear cell types in the GCT. The first one has a round morphology and resembles a monocyte. The second cell type is the spindle-shaped, fibroblast-like stromal cell. Cell culture experiments with GCT cells revealed the stromal cell to be the proliferating component of the GCT. The other two cell types, the monocyte and the multinucleated giant cell, were lost after a few cell culture passages. Furthermore, latest results from GCT reveal that the stromal cells secrete a variety of cytokines and differentiation factors, including MCP1, ODF and M-CSF. These molecules are monocyte chemoattractants and are essential for osteoclast differentiation, suggesting that the stromal cell stimulates blood monocyte immigration into tumor tissue and enhances their fusion into osteoclast-like, multinucleated giant cells.((Wuelling et al., \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e2002\u003c/span\u003e)) The pathogenesis of GCT appears to be significantly influenced by the receptor activator of the nuclear factor kappa B [NF-kB] ligand (RANKL). Under normal physiologic conditions, osteoclast formation requires interaction with cells of the osteoblastic lineage, which may depend upon cell-cell contact and the interaction of RANKL with its receptor RANK. Several studies identified a high expression of RANKL by stromal cells within GCTs. These stromal cells also secrete factors that can regulate or prevent osteoclastogenesis, including osteoprotegerin, serving as a natural negative regulator of RANKLE that obstructs osteoclast and osteoblast interactions and functions as a natural negative regulator of RANKL. The expression of RANKL by the osteoblast-like mononuclear stromal cells stimulates the recruitment of the osteoclastic cells from a normal monocytic pre-osteoclast cell. The osteoclastic giant cells then actively absorb host bone via a cathepsin K and matrix metalloproteinase 13-mediated process, which would account for the osteolysis associated with these tumors.The tumor can be locally aggressive, leading to bone destruction, although they rarely metastasize ((Cowan and Singh, \u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e2013\u003c/span\u003e)). Their location in the skull can pose unique challenges in management, especially in the pediatric population, where cranial development is still ongoing ((Reed et al., \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e1994\u003c/span\u003e)).\u003c/p\u003e \u003cp\u003eUpon gross inspection, these lesions exhibit characteristic features such as a chocolate brown, soft, and spongy texture, and fragility. Yellow-to-orange discoloration from the hemosiderin can also be present. Commonly, cystic blood-filled cavities within the tumor may be observed. Examination typically reveals a variable degree of cortical expansion and disruption while the periosteum remains intact. Histologically, these lesions appear cellular, featuring a distinctive composition of multinucleated giant cells and a background network of mononuclear stromal cells. The mononuclear cells can exhibit a variety of shapes, including plump, oval, or spindle-shaped, and may display prominent mitotic activity, although cellular atypia is uncommon. The multinucleate giant cells have numerous centrally located nuclei, unlike the peripherally located nuclei of Langerhans-type giant cells observed in atypical infections. The nuclei of these giant cells are compact and oval, containing prominent nucleoli. Giant cells are distributed throughout the lesion, and the concentration of multinucleated giant cells can vary from tumor to tumor. While some tumors feature numerous multinucleated giant cells, others have limited giant cells settled in whirls of spindle-shaped stromal cells. In approximately 5% of cases, giant cells invade small perforating vessels((\u0026ldquo;Giant cell tumor of bone,\u0026rdquo; 2022)).\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eTreatment Strategies\u003c/h3\u003e\n\u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eThe management of GCT involves a multidisciplinary approach, combining surgical, medical, and sometimes radiation therapies. The specific approach depends on factors such as the tumor's location, size, aggressiveness, and whether it is primary or recurrent.\u003c/p\u003e \u003cp\u003eThe standard care for treating GCT often involves a tailored approach considering the benign nature of most GCTs, their proximity to joints in young adults, and the goal of preserving bone anatomy. Many authors advocate for an intralesional approach rather than resection to maintain bone integrity.\u003c/p\u003e \u003cp\u003eThe primary treatment for GCTs remains surgical excision, aiming for complete resection to minimize recurrence (Tsukamoto et al., \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e2021\u003c/span\u003e). While wide resection has been associated with a decreased risk of local recurrence, potentially raising the recurrence-free survival rate from 84% to 100%, this approach comes with higher rates of surgical complications. It may lead to functional impairment, necessitating reconstruction. The decision between intralesional curettage and wide resection is often made based on the tumor's location, size, aggressiveness, and the patient's overall health and preferences.\u003c/p\u003e \u003cp\u003eResection may be the preferred option in benign tumors, particularly when bone salvageability through intralesional methods would cause a severe compromise in mechanical characteristics. This applies particularly to the \"expendable bones,\" such as the lower ulnar and upper fibular end, where excision may be the treatment of choice.\u003c/p\u003e \u003cp\u003eIn primary and recurrent cases, especially when the tumor involves the end of a long bone and causes significant dysfunction of the joint surface, reconstruction becomes necessary. Several options are available for these cases, including mega prosthetic joint replacement, biologic reconstruction with an autograft, arthrodesis with internal/external fixation, microvascular fibula reconstruction, Ilizarov method of bone regeneration, and osteoarticular allograft.\u003c/p\u003e \u003cp\u003eAdjunct therapies, such as curettage and bone grafting, may be employed based on the tumor's characteristics and location. The prognosis is generally favorable with complete excision, although long-term follow-up is necessary to monitor for potential recurrence.\u003c/p\u003e \u003cp\u003eRadiotherapy is recommended for spinal, sacral, or aggressive tumors when complete excision or curettage is impractical for any functional or medical reasons. Radiation therapy may be considered when the close proximity of critical structures prevents microscopically negative surgical margins. The systemic treatment options for advanced or metastatic disease are very limited. Intralesional curettage and bone grafting are considered the limb-sparing treatment of choice, associated with acceptable functional and oncologic outcomes. However, a simple curettage with or without a bone graft presents a 27% and 55% recurrence rate. Many surgeons replace bone graft packing with PMMA packing due to its high recurrence rate. Wide en bloc resection is another option that offers the lowest recurrence rate and can be used in expendable bones. For instance, wide resection without reconstruction is often performed in the proximal fibula. In cases of GCT in the distal radius, resection and reconstruction with an allograft or an autograft are commonly undertaken. Adjuvant treatments, such as liquid nitrogen, phenol, or HO with argon beam coagulation, demonstrate excellent recurrence-free survival, especially when paired with intralesional curettage. Long-term follow-up is recommended to monitor for potential local recurrence or metastasis.\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eInformed consent\u003c/strong\u003e \u003cp\u003e\u003cb\u003e was obtained from the patient\u0026rsquo;s legal guardian for publication of this case report and accompanying images.\u003c/b\u003e\u003c/p\u003e \u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eETHICAL APPROVAL\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eINFORMED CONSENT\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eInformed consent was obtained from the patient, and a copy of the written consent is available for review by the editor-in-chief of this journal.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDECLARATIONS OF INTEREST\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFUNDING\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e\n\u003cp\u003eCLINICAL TRIAL NUMBER\u003c/p\u003e\n\u003cp\u003eClinical trial number: not applicable.\u003c/p\u003e\n\u003cp\u003eCONSENT TO PUBLISH\u003c/p\u003e\n\u003cp\u003eInformed consent was obtained from the patient\u0026rsquo;s legal guardian for publication of\u003c/p\u003e\n\u003cp\u003ethis case report and accompanying images.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eCowan, R.W., Singh, G., 2013. Giant cell tumor of bone: A basic science perspective. Bone 52, 238\u0026ndash;246. https://doi.org/10.1016/j.bone.2012.10.002\u003c/li\u003e\n \u003cli\u003eGiant cell tumor of bone: An update, including spectrum of pathological features, pathogenesis, molecular profile and the differential diagnoses, 2022. . Histol. Histopathol. 38, 139\u0026ndash;153. https://doi.org/10.14670/HH-18-486\u003c/li\u003e\n \u003cli\u003eHaque, A.U., Moatasim, A., 2008. Giant cell tumor of bone: a neoplasm or a reactive condition? Int. J. Clin. Exp. Pathol. 1, 489\u0026ndash;501.\u003c/li\u003e\n \u003cli\u003eReed, L., Willison, C.D., Schochet, S.S., Voelker, J.L., 1994. Giant cell tumor of the calvaria in a child: Case report. J. Neurosurg. 80, 148\u0026ndash;151. https://doi.org/10.3171/jns.1994.80.1.0148\u003c/li\u003e\n \u003cli\u003eTsukamoto, S., Mavrogenis, A.F., Kido, A., Errani, C., 2021. Current Concepts in the Treatment of Giant Cell Tumors of Bone. Cancers 13, 3647. https://doi.org/10.3390/cancers13153647\u003c/li\u003e\n \u003cli\u003eTurcotte, R.E., 2006. Giant Cell Tumor of Bone. Orthop. Clin. North Am. 37, 35\u0026ndash;51. https://doi.org/10.1016/j.ocl.2005.08.005\u003c/li\u003e\n \u003cli\u003eVerschoor, A.J., Bov\u0026eacute;e, J.V.M.G., Mastboom, M.J.L., Sander Dijkstra, P.D., Van De Sande, M.A.J., Gelderblom, H., 2018. Incidence and demographics of giant cell tumor of bone in The Netherlands: First nationwide Pathology Registry Study. Acta Orthop. 89, 570\u0026ndash;574. https://doi.org/10.1080/17453674.2018.1490987\u003c/li\u003e\n \u003cli\u003eWuelling, M., Engels, C., Jesse, N., Werner, M., Kaiser, E., Delling, G., 2002. Aktuelles zur Histogenese des Riesenzelltumors. Pathol. 23, 332\u0026ndash;339. https://doi.org/10.1007/s00292-002-0552-2\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-surgery","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bsur","sideBox":"Learn more about [BMC Surgery](http://bmcsurg.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bsur/default.aspx","title":"BMC Surgery","twitterHandle":"@BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Giant Cell Tumor, Skull, Pediatric Neurosurgery, Parieto-Occipital Mass, Case Report","lastPublishedDoi":"10.21203/rs.3.rs-8405513/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8405513/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eIntroduction:\u003c/p\u003e\n\u003cp\u003eGiant cell tumors (GCTs) are typically benign but locally aggressive lesions, typically found at the metaphyseal or epiphyseal regions of the tibia or femur, long bones. It predominantly occurs in young adults aged 20 to 40 with a high recurrence rate and the potential for aggressive behaviour. Local aggressiveness varies from focal symptoms arising from bony or cortical destruction and surrounding soft tissue expansion to the rare occurrence of metastasis.Involvement of the cranial bones, particularly in pediatric patients, is exceedingly rare.\u003c/p\u003e\n\u003cp\u003eCase Presentation:\u003c/p\u003e\n\u003cp\u003eWe report the case of an 8-year-old female patient who presented with a progressively enlarging mass over the left parieto-occipital region of the skull for 18 months. Imaging revealed a large, lytic, expansile lesion compressing the occipital and parietal lobes. The patient underwent surgical excision via craniotomy. Histopathological examination confirmed the diagnosis of a giant cell tumor of bone. Postoperative follow-up showed no recurrence at 6 months.\u003c/p\u003e\n\u003cp\u003eDiscussion:\u003c/p\u003e\n\u003cp\u003eThis case highlights the rare presentation of GCT in the pediatric skull, underscoring the diagnostic and surgical challenges it presents. Complete surgical resection remains the mainstay of treatment, with generally favorable outcomes.\u003c/p\u003e\n\u003cp\u003eConclusion:\u003c/p\u003e\n\u003cp\u003eEarly identification and prompt surgical management of skull GCTs are critical to prevent neurological complications and recurrence. Long-term surveillance is essential, particularly in pediatric patients.\u003c/p\u003e","manuscriptTitle":"Rare Giant Cell Tumour of the Left Parieto-Occipital Skull in an 8-Year-Old Female Patient: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-11 16:37:59","doi":"10.21203/rs.3.rs-8405513/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-04T13:26:05+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-22T20:21:41+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"54816217850262150483104611519028761350","date":"2026-02-12T10:56:46+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-12T04:41:43+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"270769931117047901572491040508207657845","date":"2026-02-12T04:04:57+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-11T20:55:44+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"305989978860087017899962480122882717788","date":"2026-02-08T20:40:07+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-08T18:01:50+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"166069671118220009686859427508259637956","date":"2026-02-07T16:07:54+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-02-06T10:48:26+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-01-16T17:07:53+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-12-29T05:12:23+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-12-29T05:11:40+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Surgery","date":"2025-12-19T13:43:31+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-surgery","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bsur","sideBox":"Learn more about [BMC Surgery](http://bmcsurg.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bsur/default.aspx","title":"BMC Surgery","twitterHandle":"@BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"e5bc78c1-c57a-45b5-9f33-c207259d7b01","owner":[],"postedDate":"February 11th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-05-18T04:08:24+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-11 16:37:59","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8405513","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8405513","identity":"rs-8405513","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}