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Treatment and recurrence of giant cell tumors of bone - A retrospective cohort from a developing country.

ABSTRACT: Introduction:GCT is a benign primary bone tumor which is known to cause local recurrence as well as distant metastases. The standard care of treatment of GCT in our institution is the extended intralesional curettage followed by the use bone cement and either phenol or alcohol as adjunct therapy. This offers preservation of joint closest to tumor and decreased risk of recurrence compared to curettage alone. Therefore, the objective of this study was to assess the recurrence of GCT of the bone and time of recurrence-free survival after primary surgery (curettage with adjunct therapy) and determine the influence of factors like site of tumor involvement and demographic factors on the risk of recurrence. Methods:Non-funded, non-commercial single group retrospective cohort study was conducted at a tertiary care university hospital. Total of 44 patients treated for primary GCT of the bone between 1995 and 2015?at our institution were included. Medical record files were reviewed for demographic characteristics, intra-operative findings and post-operative follow-up. Risk factors for recurrence and mean recurrence free survival was calculated using appropriate statistical analysis. Results:Proximal tibia was the most commonly involved bone followed by distal femur, while intralesional curettage with either phenol or alcohol as adjunct was the most common primary treatment. Mean follow-up period for all patients was 52.1?±?43.9 months. Out of the 46 tumors operated primarily at our institution, recurrence developed in eight (17.4%) cases. Extra-compartmental spread of tumor and tumor grade were identified to have a significant association with recurrence (P?=?0.013 and 0.043 respectively). Estimated recurrence free survival at 2 and 5 - year interval was 0.85 and 0.83 respectively. Conclusion:Extra-compartmental extension of tumor and a higher-grade lesion is significantly associated with development of recurrence in cases of GCT of bone.

SUBMITTER: Hasan O

PROVIDER: S-EPMC6820075 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Treatment and recurrence of giant cell tumors of bone - A retrospective cohort from a developing country.

Hasan Obada O Ali Moiz M Mustafa Mohammad M Ali Arif A Umer Masood M

Annals of medicine and surgery (2012) 20191015

<h4>Introduction</h4>GCT is a benign primary bone tumor which is known to cause local recurrence as well as distant metastases. The standard care of treatment of GCT in our institution is the extended intralesional curettage followed by the use bone cement and either phenol or alcohol as adjunct therapy. This offers preservation of joint closest to tumor and decreased risk of recurrence compared to curettage alone. Therefore, the objective of this study was to assess the recurrence of GCT of the ...[more]

PMID: 31687136

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Project description:Giant cell tumors of bone (GCTB) are locally aggressive osteolytic bone tumors. Recently, some clinical trials have shown that denosumab is a novel and effective therapeutic option for aggressive and recurrent GCTB. This study was performed to investigate the molecular mechanism underlying the therapeutic effect of denosumab. Comparative proteomic analyses were performed using GCTB samples which were taken before and after denosumab treatment. Each expression profile was analyzed using the software program to further understand the affected biological network. One of identified proteins was further evaluated by gelatin zymography and an immunohistochemical analysis. We identified 13 consistently upregulated proteins and 19 consistently downregulated proteins in the pre- and post-denosumab samples. Using these profiles, the software program identified molecular interactions between the differentially expressed proteins that were indirectly involved in the RANK/RANKL pathway and in several non-canonical subpathways including the Matrix metalloproteinase pathway. The data analysis also suggested that the identified proteins play a critical functional role in the osteolytic process of GCTB. Among the most downregulated proteins, the activity of MMP-9 was significantly decreased in the denosumab-treated samples, although the residual stromal cells were found to express MMP-9 by an immunohistochemical analysis. The expression level of MMP-9 in the primary GCTB samples was not correlated with any clinicopathological factors, including patient outcomes. Although the replacement of tumors by fibro-osseous tissue or the diminishment of osteoclast-like giant cells have been shown as therapeutic effects of denosumab, the residual tumor after denosumab treatment, which is composed of only stromal cells, might be capable of causing bone destruction; thus the therapeutic application of denosumab would be still necessary for these lesions. We believe that the protein expression patterns and the results of the network analysis will provide a better understanding of the effects of denosumab administration in patients with GCTB.

Project description:BackgroundFollowing curettage of giant cell tumor of bone (GCTB), it is common to fill the cavity with polymethylmethacrylate (PMMA) bone cement, bone allograft, or artificial bone to maintain bone strength; however, there is a 2-14% risk of postoperative fractures. We conducted this retrospective study to clarify the risk factors for fractures after curettage for GCTB of the extremities.MethodsThis study included 284 patients with GCTBs of the extremities who underwent curettage at our institutions between 1980 and 2018 after excluding patients whose cavities were not filled with anything or who had additional plate fixation. The tumor cavity was filled with PMMA bone cement alone (n = 124), PMMA bone cement and bone allograft (n = 81), bone allograft alone (n = 63), or hydroxyapatite graft alone (n = 16).ResultsFractures after curettage occurred in 10 (3.5%) patients, and the median time from the curettage to fracture was 3.5 months (interquartile range [IQR], 1.8-8.3 months). The median postoperative follow-up period was 86.5 months (IQR, 50.3-118.8 months). On univariate analysis, patients who had GCTB of the proximal or distal femur (1-year fracture-free survival, 92.5%; 95% confidence interval [CI]: 85.8-96.2) presented a higher risk for postoperative fracture than those who had GCTB at another site (100%; p = 0.0005). Patients with a pathological fracture at presentation (1-year fracture-free survival, 88.2%; 95% CI: 63.2-97.0) presented a higher risk for postoperative fracture than those without a pathological fracture at presentation (97.8%; 95% CI: 95.1-99.0; p = 0.048). Patients who received bone grafting (1-year fracture-free survival, 99.4%; 95% CI: 95.7-99.9) had a lower risk of postoperative fracture than those who did not receive bone grafting (94.4%; 95% CI: 88.7-97.3; p = 0.003).ConclusionsFor GCTBs of the femur, especially those with pathological fracture at presentation, bone grafting after curettage is recommended to reduce the risk of postoperative fracture. Additional plate fixation should be considered when curettage and cement filling without bone grafting are performed in patients with GCTB of the femur. This should be specially performed for those patients with a pathological fracture at presentation.

Project description:Paget's disease of bone (PDB) is a late-onset chronic progressive bone disease characterized by abnormal activation of osteoclasts that results in bone pain, deformities, and fractures. PDB is very rare in Asia. A subset of PDB patients have early onset and can develop malignant giant cell tumors (GCTs) of the bone (PDB/GCTs), which arise within Paget bone lesions; the result is a significantly higher mortality rate. SQSTM1, TNFRSF11A, OPG, VCP, and HNRNPA2B1 have been identified as pathogenic genes of PDB, and ZNF687 is the only confirmed gene to date known to cause PDB/GCT. However, the molecular mechanism underlying PDB/GCT has not been fully elucidated. Here, we investigate an extended Chinese pedigree with eight individuals affected by early-onset and polyostotic PDB, two of whom developed GCTs. We identified a heterozygous 4-bp deletion in the Profilin 1 (PFN1) gene (c.318_321delTGAC) by genetic linkage analysis and exome sequencing for the family. Sanger sequencing revealed another heterozygous 1-bp deletion in PFN1 (c.324_324delG) in a sporadic early-onset PDB/GCT patient, further proving its causative role. Interestingly, a heterozygous missense mutation of PFN1 (c.335 T > C) was identified in another PDB/GCT family, revealing that not only deletion but also missense mutations in PFN1 can cause PDB/GCT. Furthermore, we established a Pfn1-mutated mouse model (C57BL/6J mice) and successfully obtained Pagetic phenotypes in heterozygous mice, verifying loss of function of PFN1 as the cause of PDB/GCT development. In conclusion, our findings reveal mutations in PFN1 as the pathological mechanism in PDB/GCT, and we successfully established Pfn1-mutated mice as a suitable animal model for studying PDB-associated pathological mechanisms. The identification of PFN1 mutations has great diagnostic value for identifying PDB individuals predisposed toward developing GCTs. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

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Treatment and recurrence of giant cell tumors of bone - A retrospective cohort from a developing country.

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Treatment and recurrence of giant cell tumors of bone - A retrospective cohort from a developing country.

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