PVNS talus in a patient treated for chondral lesion in ipsilateral calcaneum: A case report and review of literature

Vol 3 | Issue 2 | Sep-Dec 2017 | Page 10-13 | Apurv Gabrani, Hitesh Dawar, Deepak Raina, Surbhit Rastogi

Authors: Apurv Gabrani [1], Hitesh Dawar [1], Deepak Raina [1], Surbhit Rastogi [1].

[1] Indian Spinal Injuries Centre, New Delhi.

Address of Correspondence
Dr . Apurv Gabrani
Ah-22, Shalimar Bagh, New Delhi-110088
Email: apurvgabrani@gmail.com


Introduction: PVNS is a locally aggressive synovial proliferative disorder of unknown etiology and has been described in the foot and ankle in previous literature. A case of PVNS in the talus has been described in a patient treated for ipsilateral calcaneal chondral lesion.
Case Report: A 56 year old male presented with pain in his left ankle of 4 months duration. On investigation, he was found to have a well defined lytic lesion in the left calcaneum on x-ray. MRI showed a hyper intense lesion on T2WI. A needle biopsy revealed chondrogenic tumor which was managed by extended curettage. At 12 months follow up, patient presented with recent onset pain over the anterior aspect of left ankle which showed hypo density over the supero-anterior aspect of the talus and MRI showed ill defined hypo intense lesion on T2WI and hyper intense lesion on T1WI. The lesion increased in size on repeat MRI 6 weeks later. He was managed with synovectomy and debridement with core needle biopsy of talus. Histopathological examination revealed features consistent with PVNS. Patient remains asymptomatic at 1 year follow up after surgery.
Conclusion: A double primary lesion although rare, does exist and any recurrence should be viewed at with equal degree of suspicion as the primary lesion.
Keywords: Pigmented villonodular synovitis (PVNS), Talus, Calcaneum, Double Primary lesion, Chondral lesion.


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How to Cite this article: Gabrani A, Dawar H, Raina D, Rastogi S. PVNS talus in a patient treated for chondral lesion in ipsilateral calcaneum: A case report and review of literature. Journal of Bone and Soft Tissue Tumors Sep-Dec 2017;3(2): 10-13.



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Primary Intraosseous Schwannoma

Vol 3 | Issue 2 | Sep-Dec 2017 | Page 14-15| Asawari Ambekar, Chitralekha Soman.

Authors: Asawari Ambekar [1], Chitralekha Soman [1].

[1] Department of Histopathology, Mumbai Reference Laboratory, SRL Limited, Mumbai, Maharashtra, India

Address of Correspondence
Dr. Asawari Ambekar,
Reserve Bank of India Soc number 2 B 5 Gavand Path Thane West 400602
E-mail: asawariaa61@gmail.com


Schwannomas are benign tumors arising from the peripheral nerve sheath. Neurogenic tumors of bone are extremely uncommon and they compose less than 1% of all benign tumors [1]. We present a case of intraosseous schwannoma in a 15 year old girl who presented with pain and pathological fracture of tibia. The radiology revealed an expansile and lytic lesion in the diaphysis. Histopathology confirmed the diagnosis of intraosseous schwannoma. The tumor cells were immunoreactive for S100protein. We present this case as tibial schwannoma is extremely rare and its diaphyseal location in the bone is virtually unknown.
Keywords: Schwannoma, tibia, diaphysis


1. Mark JM, Natalie C., Donald K.Schwannoma: A case report.The Foot and Ankle Online Journal 2009
2. Rosai, J., Ackerman, L. V. 1. &Rosai, J. (2004). Rosai and Ackerman’s surgical pathology (9th ed.). St. Louis, Mo. : London: Mosby
3. Fletcher, CDM. Bridge, JA. Hogendoorn, P., Mertens, F.WHO Classification of Tumours of Soft Tissue and Bone. Fourth Edition.2002
4. Ryan MI, Kevin BJ, Nathan L, Joseph AB.Intraosseous neurilemmoma involving the distal tibia and fibula: A case report.The Iowa Orthopaedic Journal.
5. K. Krishnan Unni Carrie Y. Inwards.Dahlin’s Bone Tumors, 6e.GENERAL ASPECTS AND DATA ON 10,165 CASES.
6. Chelsea P,Hamad G, Shweta B. Vikram Dogra.Schwannoma of the Tibial Nerve.Journal of Diagnostic Medical Sonography.2010
7. Manasa AM. Intraosseous Schwannoma of the Maxilla Mimicking a Periapical Lesion: A Diagnostic Challenge. Journal of Clinical and Diagnostic Research. 2015.
8. Kaihu Li et al.Giant intraosseous Schwannoma of the calcaneusInt J ClinExp Med 2016.
9. S.A. Lacerda et al.Intraosseous Schwannoma of Mandibular Symphysis: Case Report.Braz Dent J 2006.
10. Suzuki et al.Association between intraosseous schwannoma occurrence and the position of the intraosseous nutrient vessel: A case report.ONCOLOGY LETTERS.2016

How to Cite this article: Ambekar A, Soman C. Primary Intraosseous Schwannoma. Journal of Bone and Soft Tissue Tumors Sep-Dec 2017;3(2): 14-15.


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Adamantinoma; An update

Vol 3 | Issue 2 | Sep-Dec 2017 | Page 16-19 | Ashish Gulia, Pankaj Kumar Panda.

Authors: Ashish Gulia [1], Pankaj Kumar Panda [1].

[1] Surgical Oncology (Orthopedic Oncology), 93, Ground Floor, Main Building, Bone & Soft tissue Services (Disease Management Group), Tata Memorial Hospital, Mumbai – 400012, India.

Address of Correspondence
Dr. Ashish Gulia,
Surgical Oncology (Orthopedic Oncology), 93, Ground Floor, Main Building, Bone & Soft tissue Services (Disease Management Group), Tata Memorial Hospital, Mumbai – 400012, India.
Email: aashishgulia@gmail.com


Adamantinoma is a rare, malignant biphasic tumor with varied morphological patterns.Adamantinoma mostly occurs in the second to fifth decade and is slightly more common in men than women.The onset is insidious, and its course shows a slow, progressive character.Radiography is the initial and most reliable imaging modality for adamantinoma of bones because of the tumor’s classic location and appearance on a plain radiograph.Present management modalitieswhich includeen blocresection (mostly intercalary resection) with limb salvage and limb reconstruction. Chemotherapy and radiotherapy have no established role. Amputation does not improve survival but may be advisable in cases with local recurrence and in cases with few large, recurrent lesions where en bloc resection is not possible.
Keywords: Adamantinoma, malignant biphasic tumor, management.


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12. Hazelbag HM, Taminiau AHM, Fleuren GJ, Hogendoorn PC. Adamantinoma of the long bones. A clinicopathological study of thirty-two patients with emphasis on histologic subtype, precursor lesion, and biological behavior. J Bone Joint Surg Am 1994;76:1482-1499.
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14. Bridge JA, Dembinski A, DeBoer J, Travis J, Neff JR. Clonal chromosomal abnormalities in osteofibrous dysplasia. Implications for histopathogenesis and its relationship with adamantinoma. Cancer 1994;73(6):1746-1752.
15. Ueda Y, Blasius S, Edel G, Wuisman P, Böcker W, Roessner A. Osteofibrous dysplasia of long bones-A reactive process to adamantinomatous tissue. J Cancer Res ClinOncol 1992;118(2):152-156.
16. Hazelbag HM, Fleuren GJ, vdBroek LJ, Taminiau AH, Hogendoorn PC. Adamantinoma of the long bones: Keratin subclass immunoreactivity pattern with reference to its histogenesis. Am J SurgPathol 1993;17(12):1225-1233.
17. Kanamori M, Antonescu CR, Scott M, Bridge RS Jr, Neff JR, Spanier SS, et al. Extra copies of chromosomes 7, 8, 12, 19, and 21 are recurrent in adamantinoma. J MolDiagn 2001;3(1):16-21.
18. Keeney GL, Unni KK, Beabout JW, Pritchard DJ. Adamantinoma of long bones. A clinicopathologic study of 85 cases. Cancer 1989;64(3):730-7.
19. Qureshi AA, Shott S, Mallin BA, Gitelis S. Current trends in the management of adamantinoma of long bones. An international study. J Bone Joint Surg Am 2000;82-A(8):1122-1131.
20. Bovée JV, van den Broek LJ, de Boer WI, Hogendoorn PC. Expression of growth factors and their receptors in adamantinoma of long bones and the implication for its histogenesis. J Pathol 1998;184(1):24-30.

How to Cite this article: Gulia A, Panda P. Adamantinoma – an update. Journal of Bone and Soft Tissue Tumors Sep-Dec 2017;3(2): 16-19.

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Giant Cell Tumor Symposium Part 2

Vol 3 | Issue 2 | Sep-Dec 2017 | page:1 | Dr. Mandip Shah.

Author: Mandip Shah [1].

[1] Sparsh Orthopedic Oncology Clinic. Medicare Building 9th Floor, , B/H Town Hall, Ashram Road, 380006 – Ahmedabad., India.

Address of Correspondence
Dr. Mandip Shah
Sparsh Orthopedic Oncology Clinic. Medicare Building 9th Floor, , B/H Town Hall, Ashram Road, 380006 – Ahmedabad., India
Email: mandipshah@gmail.com

Giant Cell Tumor Symposium Part 2

We are back with the second part of the Giant Cell Tumor Symposium for Journal of Bone and Soft Tissue Tumors.
Two very important aspects are covered in this part. First is the histopathological concepts regarding GCT. There is lot of new knowledge that is available in recent years and that has significantly impacted the diagnosis, management and prognosis of GCT. Histopathological assessment play a major role in terms of determining the behaviour of GCT. Current understanding of molecular pathogenesis of GCTB particularly RANK on osteoclast-like GCs and RANKL on stromal cells and development of newer agents such as denosumab and INF-α has tremendously impacted management of patients with GCTB. This aspect is elaborated in the first article. The second article builds on these concepts and describes how this is used for adjuvent therapy for GCTB. Authors of both the authors have taken tremendous effort to make both these articles good and current. Also these two now conclude the GCT Symposium and cover all aspect of GCTB
Please write to us regarding your suggestions and opinions


Dr. Mandip Shah

How to Cite this article: Shah M. Giant Cell Tumor Symposium Part 2. Journal of Bone and Soft Tissue Tumors Sep-Dec 2017; 3(2):1.


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Histopathology of Giant-cell Tumor of Bone – Current Concept

Vol 3 | Issue 2 | Sep-Dec 2017 | Page 2-5| Sanjeev Shah.

Authors: Sanjeev Shah [1].

[1] Department of Pathology, Unipath Laboratory Specialty Ltd, Beside JMC House, Ahmedabad, Gujarat, India.

Address of Correspondence
Dr. Sanjeev Shah,
102, First floor, Sanoma Plaza, Opp. Parimal Garden, Beside JMC House, Ellisbridge, Ahmedabad – 380006, Gujarat, India.
E-mail: dcp72002@yahoo.com


GCTB is a primary osteolytic bone tumor which can recurrence, undergo metastasis, and malignant transformation. Current understanding of molecular pathogenesis of GCTB particularly RANK on osteoclast-like GCs and RANKL on stromal cells and development of newer agents such as denosumab and INF-α has tremendously impacted management of patients with GCTB.
Keywords: Giant-cell tumor of bone histopathology, current concept.


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15. Behjati S, Tarpey PS, Presneau N, Scheipl S, Pillay N, Van Loo P, et al. Distinct H3F3A and H3F3B driver mutations define chondroblastoma and giant cell tumor of bone. Nat Genet 2013;45:1479-82.
16. Akpalo H, Lange C, Zustin J. Discovered on gastrointestinal stromal tumour 1 (DOG1): A useful immunohistochemical marker for diagnosing chondroblastoma. Histopathology 2012;60:1099-106.
17. Cleven AG, Briaire-de Bruijn I, Szuhai K, Bovee JV. DOG1 expression in giant-cell-containing bone tumours. Histopathology 2016;68:938-45.
18. Althof PA, Ohmori K, Zhou M, Bailey JM, Bridge RS, Nelson M, et al. Cytogenetic and molecular cytogenetic findings in 43 aneurysmal bone cysts: Aberrations of 17p mapped to 17p13.2 by fluorescence in situhybridization. Mod Pathol 2004;17:518-25.
19. Oliveira AM, Perez-Atayde AR, Dal Cin P, Gebhardt MC, Chen CJ, Neff JR, et al. Aneurysmal bone cyst variant translocations upregulate USP6 transcription by promoter swapping with the ZNF9, COL1A1, TRAP150, and OMD genes. Oncogene 2005;24:3419-26.
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21. López-Pousa A, Martín Broto J, Garrido T, Vázquez J. Giant cell tumour of bone: New treatments in development. Clin Transl Oncol 2015;17:419-30.
22. Xu SF, Adams B, Yu XC, Xu M. Denosumab and giant cell tumour of bone-a review and future management considerations. Curr Oncol 2013;20:e442-7.
23. Branstetter DG, Nelson SD, Manivel JC, Blay JY, Chawla S, Thomas DM, et al. Denosumab induces tumor reduction and bone formation in patients with giant-cell tumor of bone. Clin Cancer Res 2012;18:4415-24.
24. Heymann D. Anti-RANKL therapy for bone tumours: Basic, pre-clinical and clinical evidences. J Bone Oncol 2012;1:2-11.
25. Roux S, Amazit L, Meduri G, Guiochon-Mantel A, Milgrom E, Mariette X, et al. RANK (receptor activator of nuclear factor kappa B) and RANK ligand are expressed in giant cell tumors of bone. Am J ClinPathol 2002;117:210-6.

How to Cite this article: Shah S. Histopathology of Giant-cell Tumor of Bone – Current Concept. Journal of Bone and Soft Tissue Tumors Sep-Dec 2017;3(2): 2-5.


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Systemic Adjuvant Therapies in the Management of Giant Cell Tumor of Bone: Current State of Understanding and Practice

Vol 3 | Issue 2 | Sep-Dec 2017 | Page 6-9 | Shekhar Kumta, Carol Lau, K C Wong.

Authors: Shekhar Kumta [1], Carol Lau [1], K C Wong [2].

[1] Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong,
[2] Department of Orthopaedics& Traumatology, The Prince of Wales Hospital, Hong Kong.

Address of Correspondence
Dr. Shekhar Kumta,
103-E, Learning Resource Centre, Block A, Prince of Wales Hospital, Shatin, Hong Kong.
Email: shekharkumta@gmail.com


GCT of bone is a locally aggressive bone-destroying tumor. The primary neoplastic tumor cell is a RANKL over expressing cell that drives osteoclast recruitment and activation, ultimately leading to bone resorption at the site of the lesion. Osteoclast driven destruction in GCT may be ameliorated with the use of drugs such as Bisphophonates, which target Osteoclasts as well as the primary neoplastic stromal cells. Denusomab, is a monoclonal antibody against RANKL and it has a dramatic effect on Osteoclasts. Adjuvant therapies have reduced recurrence rates in GCT of bone, but uncertainties remain as to the optimum dose-intensity of the drugs and the duration of treatment.
Keywords: Tumor, bone destruction, Giant Cell Tumor of Bone.


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4. Marcove RC, Weis LD, Vaghaiwalla MR, Pearson R. Cryosurgery in the treatment of giant cell tumors of bone: A report of 52 consecutive cases. ClinOrthopRelat Res 1978;134:275-89.
5. Gortzak Y, Kandel R, Deheshi B, Werier J, Turcotte RE, Ferguson PC, et al. The efficacy of chemical adjuvants on giant-cell tumour of bone. An in vitro study. J Bone Joint Surg Br 2010;92:1475-9.
6. Lin WH, Lan TY, Chen CY, Wu K, Yang RS. Similar local control between phenol- and ethanol-treated giant cell tumors of bone. ClinOrthopRelat Res 2011;469:3200-8.
7. Theoleyre S, Wittrant Y, Tat SK, Fortun Y, Redini F, Heymann D, et al. The molecular triad OPG/RANK/RANKL: Involvement in the orchestration of pathophysiological bone remodeling. Cytokine Growth Factor Rev 2004;15:457-75.
8. Yasuda H, Shima N, Nakagawa N, Yamaguchi K, Kinosaki M, Mochizuki S, et al. Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL. Proc Natl AcadSci U S A 1998;95:3597-602.
9. Yasuda H, Shima N, Nakagawa N, Mochizuki SI, Yano K, Fujise N, et al. Identity of osteoclastogenesis inhibitory factor (OCIF) and osteoprotegerin (OPG): A mechanism by which OPG/OCIF inhibits osteoclastogenesisin vitro. Endocrinology 1998;139:1329-37.
10. Huang L, Xu J, Wood DJ, Zheng MH. Gene expression of osteoprotegerin ligand, osteoprotegerin, and receptor activator of NF-kappaB in giant cell tumor of bone: Possible involvement in tumor cell-induced osteoclast-like cell formation. Am J Pathol2000;156:761-7.
11. Nancollas GH, Tang R, Phipps RJ, Henneman Z, Gulde S, Wu W, et al. Novel insights into actions of bisphosphonates on bone: Differences in interactions with hydroxyapatite. Bone 2006;38:617-27.
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14. Balke M, Campanacci L, Gebert C, Picci P, Gibbons M, Taylor R, et al. Bisphosphonate treatment of aggressive primary, recurrent and metastatic giant cell tumour of bone. BMC Cancer 2010;10:462.
15. Tse LF, Wong KC, Kumta SM, Huang L, Chow TC, Griffith JF, et al. Bisphosphonates reduce local recurrence in extremity giant cell tumor of bone: A case-control study. Bone 2008;42:68-73.
16. Yu X, Xu M, Xu S, Su Q. Clinical outcomes of giant cell tumor of bone treated with bone cement filling and internal fixation, and oral bisphosphonates. Oncol Lett 2013;5:447-51.
17. Cheng YY, Huang L, Lee KM, Xu JK, Zheng MH, Kumta SM, et al. Bisphosphonates induce apoptosis of stromal tumor cells in giant cell tumor of bone. Calcif Tissue Int2004;75:71-7.
18. Coleman RE, Major P, Lipton A, Brown JE, Lee KA, Smith M, et al. Predictive value of bone resorption and formation markers in cancer patients with bone metastases receiving the bisphosphonate zoledronic acid. J ClinOncol2005;23:4925-35.
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21. Kostenuik PJ, Nguyen HQ, McCabe J, Warmington KS, Kurahara C, Sun N, et al. Denosumab, a fully human monoclonal antibody to RANKL, inhibits bone resorption and increases BMD in knock-in mice that express chimeric (murine/human) RANKL. J Bone Miner Res 2009;24:182-95.
22. Thomas D, Henshaw R, Skubitz K, Chawla S, Staddon A, Blay JY, et al. Denosumab in patients with giant-cell tumour of bone: An open-label, Phase 2 study. Lancet Oncol2010;11:275-80.
23. Lewiecki EM, Miller PD, McClung MR, Cohen SB, Bolognese MA, Liu Y, et al. Two-year treatment with denosumab (AMG 162) in a randomized Phase 2 study of postmenopausal women with low BMD. J Bone Miner Res 2007;22:1832-41.

How to Cite this article: Kumta S, Lau C, Wong K C. Systemic Adjuvant Therapies in the Management of Giant Cell Tumor of Bone: Current State of Understanding and Practice. Journal of Bone and Soft Tissue Tumors Sep-Dec 2017;3(2): 6-9..


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