Surgical Site Infection in Patients Managed with an Endoprosthesis for the Treatment of Cancer: Evaluation of Patient, Disease, and Index Surgical Factors.

BACKGROUND: Surgical site infection (SSI) after segmental endoprosthetic reconstruction in patients treated for oncologic conditions remains both a devastating and a common complication. The goal of the present study was to identify variables associated with the success or failure of treatment of early SSI following the treatment of a primary bone tumor with use of a segmental endoprosthesis. METHODS: The present study used the Prophylactic Antibiotic Regimens in Tumor Surgery (PARITY) data set to identify patients who had been diagnosed with an SSI after undergoing endoprosthetic reconstruction of a lower extremity primary bone tumor. The primary outcome of interest in the present study was a dichotomous variable: the success or failure of infection treatment. We defined failure as the inability to eradicate the infection, which we considered as an outcome of amputation or limb retention with chronic antibiotic suppression (>90 days or ongoing therapy at the conclusion of the study). Multivariable models were created with covariates of interest for each of the following: surgery characteristics, cancer treatment-related characteristics, and tumor characteristics. Multivariable testing included variables selected on the basis of known associations with infection or results of the univariable tests. RESULTS: Of the 96 patients who were diagnosed with an SSI, 27 (28%) had successful eradication of the infection and 69 had treatment failure. Baseline and index procedure variables showing significant association with SSI treatment outcome were moderate/large amounts of fascial excision ≥1 cm2) (OR, 10.21 [95% CI, 2.65 to 46.21]; p = 0.001), use of local muscle/skin graft (OR,11.88 [95% CI, 1.83 to 245.83]; p = 0.031), and use of a deep Hemovac (OR, 0.24 [95% CI, 0.05 to 0.85]; p = 0.041). In the final multivariable model, excision of fascia during primary tumor resection was the only variable with a significant association with treatment outcome (OR, 10.21 [95% CI, 2.65 to 46.21]; p = 0.018). CONCLUSIONS: The results of this secondary analysis of the PARITY trial data provide further insight into the patient-, disease-, and treatment-specific associations with SSI treatment outcomes, which may help to inform decision-making and management of SSI in patients who have undergone segmental bone reconstruction of the femur or tibia for oncologic indications. LEVEL OF EVIDENCE: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

MR imaging of BioCartilage augmented microfracture surgery utilizing 2D MOCART and KOOS scores.

OBJECTIVES: BioCartilage is a novel scaffold-based microfracture augmentation technique that has been shown to aid in chondrogenic differentiation of adult progenitor cells resulting in formation of more hyaline-like cartilage. As this cartilage repair technique becomes more commonplace, it is essential that the musculoskeletal radiologist and orthopedic surgeon gain familiarity with the surgical technique and its post-operative MR imaging findings. METHODS: We present several case studies regarding MRI findings (modified clinical 2D MOCART) and clinical outcome (KOOS) scores in patients who have undergone this novel surgical procedure. For data analysis KOOS scores where dichotomized to scores greater or less than 80, and MOCART scores were dichotomized to scores greater or less than 50. A fisher exact test was then performed to determine if there was any correlation between parameters of the modified 2D MOCART and KOOS scores (Tables 2 and 3). RESULTS: Marrow elements travel through the microfracture holes and interact with the scaffold created by BioCartilage, rather than creating their own fibrin scaffold, as is typically anticipated from a marrow stimulation procedure. Interestingly, the amount defect fill, presence of an intact surface, intact subchondral bone, or lack of effusion did not correlate with positive outcomes. Parameters that trended towards significance included presence of adhesions and subchondral lamina. Completeness of cartilage interface, homogeneity, and signal intensity also failed to reach statistical significance. In our experience, patients that demonstrated mild repair tissue surface irregularity, but with preservation of greater than 50% thickness compared to surrounding native cartilage, mild irregularity of subchondral plate, with vertical low signal intensity lines (sequela of prior microfracture surgery), and mild or no bone marrow edema pattern demonstrated higher KOOS scores. CONCLUSION: Biocartilage in conjunction with microfracture is an encouraging cartilage restoration technique that promotes regeneration of more robust hyaline-like cartilage compared to the fibrocartilage formed after conventional microfracture. The T2 mapping properties of the repair tissue after successful BioCartilage augmented microfracture surgery are very similar to that of the adjacent native cartilage. Although there appear to be characteristic trends in a successful repair, further research is warranted to elucidate any correlations between specific characteristics of the repair and patient clinical outcomes.

The stability of the hip after the use of a proximal femoral endoprosthesis for oncological indications: analysis of variables relating to the patient and the surgical technique.

AIMS: Instability of the hip is the most common mode of failure after reconstruction with a proximal femoral arthroplasty (PFA) using an endoprosthesis after excision of a tumour. Small studies report improved stability with capsular repair of the hip and other techniques, but these have not been investigated in a large series of patients. The aim of this study was to evaluate variables associated with the patient and the operation that affect post-operative stability. We hypothesised an association between capsular repair and stability. PATIENTS AND METHODS: In a retrospective cohort study, we identified 527 adult patients who were treated with a PFA for tumours. Our data included demographics, the pathological diagnosis, the amount of resection of the abductor muscles, the techniques of reconstruction and the characteristics of the implant. We used regression analysis to compare patients with and without post-operative instability. RESULTS: A total of 20 patients out of 527 (4%) had instability which presented at a mean of 35 days (3 to 131) post-operatively. Capsular repair was not associated with a reduced rate of instability. Bivariate analysis showed that a posterolateral surgical approach (odds ratio (OR) 0.11, 95% confidence interval (CI) 0.02 to 0.86) and the type of implant (p = 0.046) had a significant association with reduced instability; age > 60 years predicted instability (OR 3.17, 95% CI 1.00 to 9.98). Multivariate analysis showed age > 60 years (OR 5.09, 95% CI 1.23 to 21.07), female gender (OR 1.73, 95% CI 1.04 to 2.89), a malignant primary bone tumour (OR 2.04, 95% CI 1.06 to 3.95), and benign condition (OR 5.56, 95% CI 1.35 to 22.90), but not metastatic disease or soft-tissue tumours, predicted instability, while a posterolateral approach (OR 0.09, 95% CI 0.01 to 0.53) was protective against instability. No instability occurred when a synthetic graft was used in 70 patients. CONCLUSION: Stability of the hip after PFA is influenced by variables associated with the patient, the pathology, the surgical technique and the implant. We did not find an association between capsular repair and improved stability. Extension of the tumour often dictates surgical technique; however, our results indicate that PFA using a posterolateral approach with a hemiarthroplasty and synthetic augment for soft-tissue repair confers the lowest risk of instability. Patients who are elderly, female, or with a primary benign or malignant bone tumour should be counselled about an increased risk of instability. Cite this article: Bone Joint J 2017;99-B:531-7.

Effect of cytostatic proline rich polypeptide-1 on tumor suppressors of inflammation pathway signaling in chondrosarcoma.

Cytokines produced in the tumour microenvironment exert an important role in cancer pathogenesis and in the inhibition of disease progression. Cancer of the cartilage is termed metastatic chondrosarcoma; however, the signaling events resulting in mesenchymal cell transformation to sarcoma have yet to be fully elucidated. The present study aimed to characterize the cytokine expression profile in the human JJ012 chondrosarcoma cell line, as well as the effect of cytostatic proline-rich polypeptide-1 (PRP-1). Western blot experiments demonstrated that the levels of suppressor of cytokine signaling 3 (SOCS3) were upregulated in chondrocytes compared with chondrosarcoma cells. Addition of PRP-1 restored the expression of the tumor suppressors, SOCS3 and ten-eleven-translocation methylcytosine dioxygenase 1 and 2 (TET1/2), in a dose-responsive manner. It is known that methylation of histone H3K9 was eliminated from the promoters of the inflammation-associated genes. PRP-1 inhibited H3K9 demethylase activity with an IC50 (concentration required to give half-maximal inhibition) value of 3.72 µg/ml in the chondrosarcoma cell line. Data obtained from ELISA experiments indicated that the expression of interleukin-6 (IL-6) in chondrosarcoma cells was 86-fold lower compared with that in C28 chondrocytes. In the present study, a 53-fold downregulation of IL-6 expression in co-culture of chondrosarcoma cells and C28 chondrocytes was identified as well. Downregulation of IL-6 expression has been documented in numerous other tumor types, although the reasons for this have not been fully established. In chondrosarcoma, IL-6 manifests itself as an anti-inflammatory agent and, possibly, as an anti-tumorigenic factor. To explore protein-DNA interactions leading to such differences, a gel-shift chemiluminescent assay was performed. Gel shifts were observed for chondrosarcoma and chondrocytes in the lanes that contained nuclear cell extract and oligo-IL-6 DNA. Notably, the DNA-protein complexes in C28 chondrocytes were markedly larger compared with those in chondrosarcoma cells. The mechanisms that underpin such differences, and characterization of the interacting proteins, remain to be fully elucidated.

Epigenetic regulation of embryonic stem cell marker miR302C in human chondrosarcoma as determinant of antiproliferative activity of proline-rich polypeptide 1.

Metastatic chondrosarcoma of mesenchymal origin is the second most common bone malignancy and does not respond either to chemotherapy or radiation; therefore, the search for new therapies is relevant and urgent. We described recently that tumor growth inhibiting cytostatic proline-rich polypeptide 1, (PRP-1) significantly upregulated tumor suppressor miRNAs, downregulated onco-miRNAs in human chondrosarcoma JJ012 cell line, compared to chondrocytes culture. In this study we hypothesized the existence and regulation of a functional marker in cancer stem cells, correlated to peptides antiproliferative activity. Experimental results indicated that among significantly downregulated miRNA after PRP-1treatment was miRNAs 302c*. This miRNA is a part of the cluster miR302­367, which is stemness regulator in human embryonic stem cells and in certain tumors, but is not expressed in adult hMSCs and normal tissues. PRP-1 had strong inhibitory effect on viability of chondrosarcoma and multilineage induced multipotent adult cells (embryonic primitive cell type). Unlike chondrosarcoma, in glioblastoma, PRP-1 does not have any inhibitory activity on cell proliferation, because in glioblastoma miR-302-367 cluster plays an opposite role, its expression is sufficient to suppress the stemness inducing properties. The observed correlation between the antiproliferative activity of PRP-1 and its action on downregulation of miR302c explains the peptides opposite effects on the upregulation of proliferation of adult mesenchymal stem cells, and the inhibition of the proliferation of human bone giant-cell tumor stromal cells, reported earlier. PRP-1 substantially downregulated the miR302c targets, the stemness markers Nanog, c-Myc and polycomb protein Bmi-1. miR302c expression is induced by JMJD2-mediated H3K9me2 demethylase activity in its promoter region. JMJD2 was reported to be a positive regulator for Nanog. Our experimental results proved that PRP-1 strongly inhibited H3K9 activity comprised of a pool of JMJD1 and JMJD2. We conclude that inhibition of H3K9 activity by PRP-1 leads to downregulation of miR302c and its targets, defining the PRP-1 antiproliferative role.

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells.

Disruption of cell-cell junctions and the concomitant loss of polarity, downregulation of tumor-suppressive adherens junctions and desmosomes represent hallmark phenotypes for several different cancer cells. Moreover, a variety of evidence supports the argument that these two common phenotypes of cancer cells directly contribute to tumorigenesis. In this study, we aimed to determine the status of intercellular junction proteins expression in JJ012 human malignant chondrosarcoma cells and investigate the effect of the antitumorigenic cytokine, proline-rich polypeptide-1 (PRP-1) on their expression. The cell junction pathway array data indicated downregulation of desmosomal proteins, such as desmoglein (1,428-fold), desmoplakin (620-fold) and plakoglobin (442-fold). The tight junction proteins claudin 11 and E-cadherin were also downregulated (399- and 52-fold, respectively). Among the upregulated proteins were the characteristic for tumors gap junction ß-5 protein (connexin 31.1) and the pro-inflammatory pathway protein intercellular adhesion molecule (upregulated 129- and 43-fold, respectively). We demonstrated that PRP-1 restored the expression of the abovementioned downregulated in chondrosarcoma desmosomal proteins. PRP-1 inhibited H3K9-specific histone demethylase activity in chondrosarcoma cells in a dose-dependent manner (0.5 µg/ml PRP, 63%; 1 µg/ml PRP, 74%; and 10 µg/ml PRP, 91% inhibition). Members of the H3K9 family were shown to transcriptionally repress tumor suppressor genes and contribute to cancer progression. Our experimental data indicated that PRP-1 restores tumor suppressor desmosomal protein expression in JJ012 human chondrosarcoma cells and inhibits H3K9 demethylase activity, contributing to the suppression of tumorigenic potential in chondrosarcoma cells.

Classification of failure of limb salvage after reconstructive surgery for bone tumours : a modified system Including biological and expandable reconstructions.

Previous classification systems of failure of limb salvage focused primarily on endoprosthetic failures and lacked sufficient depth for the effective study of the causes of failure. In order to address these inadequacies, the International Society of Limb Salvage (ISOLS) formed a committee to recommend revisions of the previous systems. The purpose of this study was to report on their recommendations. The modifications were prepared using an earlier, evidence-based model with subclassification based on the existing medical literature. Subclassification for all five primary types of failure of limb salvage following endoprosthetic reconstruction were formulated and a complementary system was derived for the failure of biological reconstruction. An additional classification of failure in paediatric patients was also described. Limb salvage surgery presents a complex array of potential mechanisms of failure, and a complete and precise classification of types of failure is required. Earlier classification systems lacked specificity, and the evidence-based system outlined here is designed to correct these weaknesses and to provide a means of reporting failures of limb salvage in order to allow the interpretation of outcome following reconstructive surgery.

Lost miRNA surveillance of Notch, IGFR pathway--road to sarcomagenesis.

The goal of this study was to compare and analyze differentially expressed miRNA and their targets in human chondrosarcoma JJ012 and chondrocytes C 28 cell lines (control) to elucidate deregulation of major signal transduction pathways involved in sarcomagenesis. Total RNA extraction was followed by analyzing RNA quality and integrity. Exiqon human miRNA panel of 743 unique miRNA assays and Illumina microarray HT-12 platform and quantitative reverse transcriptase­PCR verification of targets were performed. The results from human miRNA Exiqon arrays with biological triplicates indicated 28 significant miRNAs (P value ≤0.01). A total 3,045 target genes were derived from the miRWalk database for these 28 miRNAs with 587 common and 2,458 unique target genes. The results of our analyses of the significantly downregulated and upregulated miRNAs in chondrosarcoma cell line indicated the predominant dysregulation of NOTCH, insulin-like growth factor receptor (IGFR), and downstream rat sarcoma, and Src pathways, compared to control. Among the upregulated targets for upregulated miRNAs were the cluster of cancer testis antigen (CTA) genes, located on X chromosome, and their expression was correlated to IGFR pathway activity. Based on our observations, lost miRNA surveillance of NOTCH and IGFR pathways is involved in and leads to sarcomagenesis. We conclude that upregulation of CTA genes is due to hypomethylation that are controlled by epi-miRNAs. We do not preclude the possibility that the upregulated miRNAs, which target CTA genes located in adjacent regions in chromosome X, are epi-miRNAs that influence target gene expression by directly regulating epigenetic processes. Future endeavors will be directed towards understanding the posttranscriptional modifications that affect miRNA expression in sarcomas.

Regulation of onco and tumor suppressor MiRNAs by mTORC1 inhibitor PRP-1 in human chondrosarcoma.

Metastatic chondrosarcoma of mesenchymal origin is the second most common bone malignancy and does not respond either to chemotherapy or radiation; therefore, the search for new therapies is relevant and urgent. This study aimed to reveal the comparative analysis of miRNAs and their targets in human JJ012 chondrosarcoma cell line between control and experimental samples, treated with mTORC1 inhibitor, cytostatic antiproliferative proline-rich polypeptide (PRP-1). Examination of tumor-specific microRNA expression profiles has revealed widespread deregulation of these molecules in diverse cancers. It was reported that microRNAs can function as novel biomarkers for disease diagnostics and therapy, as well as a novel class of oncogenes and tumor suppressor genes. mTORC 1 inhibitor PRP-1 caused significant upregulation of tumor suppressors, such as miR20a, miR125b, and miR192; and downregulation of onco miRNAs, miR509-3p, miR589, miR490-3p, miR 550 in human chondrosarcoma JJ012 cell line.

mTORC1 inhibition and ECM-cell adhesion-independent drug resistance via PI3K-AKT and PI3K-RAS-MAPK feedback loops.

Mammalian target of rapamycin (mTOR) serine threonine kinase is the enzyme that regulates cancer cell growth by altering nutrient supplies to cancer cells. The neuropeptide (proline-rich peptide 1 (PRP-1)), galarmin, produced by the brain neurosecretory cells is a mTOR kinase inhibitor with powerful 80% antiproliferative cytostatic effect in a high-grade chondosarcoma and other mesenchymal tumors. However, the negative feedback loop of phosphatidylinositol 3 kinase-Protein kinase B (PKB), PI3K-AKT and PI3K-rat sarcoma (RAS)-mitogen-activated protein kinase (MAPK) activation is well documented for mTOR inhibitors. This study explored the involvement of those loops in drug resistance after the treatment with mTOR complex 1 (mTORC1) inhibitor, PRP-1. Multidrug resistance assay (MDR) demonstrated that this cytokine did not inhibit permeability glycoprotein-mediated MDR in chondrosarcoma. Phospho-MAPK array in human chondrosarcoma cell line treated with galarmin (10 µg/ml,) showed a strong upregulation of phosphorylated glycogen synthase kinase 3ß (GSK3ß) via activation of PI3K-AKT and MAPK feedback loops. Such GSK3ß inactivation leads to ß-catenin accumulation that entails drug resistance. The ability of cells to metastasize is reflected in their capacity to adhere to extracellular matrix and endothelium. Laminin cell adhesion assay demonstrated that PRP-1 in the same concentrations that inhibit mTOR kinase inhibited JJ012 chondrosarcoma cell adhesion. The neuropeptide did not have any effect on the expression of total focal adhesion kinase and its phosphorylated form. Thus, it was not accompanied by total HAT downregulation and total HDAC upregulation. Combinatorial treatments of PRP-1 with MAPK and PI3K/AKT inhibitors most probably will lead to full cytotoxicity overcoming drug resistance.

Allograft reconstruction for bone sarcoma of the tibia in the growing child.

The outcome of tibial allograft reconstruction after resection of a tumour is inconsistent and has a high rate of failure. There are few reports on the use of tibial allografts in children with open growth plates. We performed 21 allograft reconstructions (16 osteoarticular, five intercalary) in 19 consecutive patients between seven and 17 years of age. Two had Ewing's sarcoma, one an adamantinoma and 16 osteosarcoma, one with multifocal disease. Five patients have died; the other 14 were free from disease at the time of follow-up. Six surviving patients (eight allograft reconstructions) continue to have good or excellent function at a mean of 59 months (14 to 132). One patient has poor function at 31 months. The other seven patients have a good or excellent function after additional procedures including exchange of the allograft and resurfacing or revision to an endoprosthesis at a mean of 101 months (43 to 198). The additional operations were performed at a mean of 47 months (20 to 84) after the first reconstruction. With the use of allograft reconstruction in growing children, joints and growth plates may be preserved, at least partially. Although our results remain inconsistent, tibial allograft reconstruction in selected patients may restore complete and durable function of the limb.

Incidence of clostridial contamination in donors' musculoskeletal tissue.

Reports of infection by Clostridium sordellii associated with allograft transplantation have generated considerable interest. We report our experience in recognising clostridial contamination in cadaver donors of musculoskeletal tissue. Tissues obtained from 795 consecutive donors were excised using standard surgical techniques. Samples of blood and bone marrow were also obtained. Donors with clostridia recovered from any site were matched with the preceding donor without clostridia as a procedural and environmental control. The histories of the donors were analysed to determine which variables had a relationship to contamination by running a contingency table and chi-squared test on the variables against the event of a donor being contaminated. Sixty-four donors (8.1%) had clostridia, most commonly C. sordellii. Clostridia were grown from the blood, marrow and tissue samples of 52, 37 and 30 donors, respectively. In eight cases, they were cultured from the tissue samples alone. There was no significant difference in age or gender between the contaminated donors and the control group. Open wounds were more common in control than in contaminated subjects, but only death by drowning in the contaminated group was statistically significant (p = 0.02). The time between death and the excision of tissue which was contaminated (16 hrs 10 mins) compared with control (11 hrs 10 mins) donors was also significant (p < 10(-6)). We conclude that there is clostridial contamination in a significant number of tissue donors, particularly with increasing time between death and tissue excision. Among the most commonly encountered species is C. sordellii. Multiple microbiological cultures, including blood, are necessary in order to identify clostridial contamination.

From the archives of AFIP. Imaging of giant cell tumor and giant cell reparative granuloma of bone: radiologic-pathologic correlation.

The radiologic features of giant cell tumor (GCT) and giant cell reparative granuloma (GCRG) of bone often strongly suggest the diagnosis and reflect their pathologic appearance. At radiography, GCT often demonstrates a metaepiphyseal location with extension to subchondral bone. GCRG has a similar appearance but most commonly affects the mandible, maxilla, hands, or feet. Computed tomography and magnetic resonance (MR) imaging are helpful in staging lesions, particularly in delineating soft-tissue extension. Cystic (secondary aneurysmal bone cyst) components are reported in 14% of GCTs. However, biopsy must be directed at the solid regions, which harbor diagnostic tissue. These solid components demonstrate low to intermediate signal intensity at T2-weighted MR imaging, a feature that can be helpful in diagnosis. Multiple GCTs, although rare, do occur and may be associated with Paget disease. Malignant GCT accounts for 5%-10% of all GCTs and is usually secondary to previous irradiation of benign GCT. Treatment of GCT usually consists of surgical resection. Recurrence is seen in 2%-25% of cases, and imaging is vital for early detection. Recognition of the spectrum of radiologic appearances of GCT and GCRG is important in allowing prospective diagnosis, guiding therapy, and facilitating early detection of recurrence.

Advanced imaging of melorheostosis with emphasis on MRI.

OBJECTIVE: To describe the CT and MR imaging appearance of both osseous and extraosseous manifestations of melorheostosis. DESIGN AND PATIENTS: We retrospectively reviewed the CT (n=7) and/or MR imaging findings (n=12) of 17 patients with characteristic radiographic findings of melorheostosis (undulating cortical hyperostosis with marked uptake on radionuclide bone scintigraphy). RESULTS: CT and MR imaging revealed cortical hyperostosis as high attenuation and low signal intensity on all MR pulse sequences, respectively. Encroachment on the marrow space was seen in all cases resulting from endosteal involvement. Thirteen patients demonstrated 14 soft tissue masses with infiltrative margins in 80% of cases and seven showed extensive mineralization on CT or MR imaging (low intensity on all pulse sequences). Seven soft tissue masses were predominantly nonmineralized with intermediate signal intensity on T1-weighted and intermediate to high signal on T2-weighted MR images corresponding to vascularized fibrous tissue with variable collagen content pathologically. Enhancement after intravenous gadolinium was seen in all patients imaged with soft tissue masses (n=2). Two patients demonstrated muscle atrophy resulting from nerve involvement. CONCLUSIONS: The osseous abnormalities in melorheostosis are identical on advanced imaging and radiographs. Mineralized or nonmineralized soft tissue masses should be recognized as another manifestation of this disease as opposed to a more ominous finding, making biopsy unwarrranted.

Imaging of musculoskeletal fibromatosis.

The musculoskeletal fibromatoses comprise a wide range of lesions with a common histopathologic appearance. They can be divided into two major groups: superficial and deep. The superficial fibromatoses are typically small, slow-growing lesions and include palmar fibromatosis, plantar fibromatosis, juvenile aponeurotic fibroma, and infantile digital fibroma. The deep fibromatoses are commonly large, may grow rapidly, and are more aggressive. They include infantile myofibromatosis, fibromatosis colli, extraabdominal desmoid tumor, and aggressive infantile fibromatosis. Radiographs typically reveal a nonspecific soft-tissue mass, and calcification is common only in juvenile aponeurotic fibroma. Advanced imaging (ultrasonography, computed tomography, and magnetic resonance [MR] imaging) demonstrates lesion extent. Involvement of adjacent structures is common, reflecting the infiltrative growth pattern often seen in these lesions. MR imaging may show characteristic features of prominent low to intermediate signal intensity and bands of low signal intensity representing highly collagenized tissue. However, fibromatoses with less collagen and more cellularity may have nonspecific high signal intensity on T2-weighted images. Local recurrence is frequent after surgical resection due to the aggressive lesion growth. It is important for radiologists to recognize the imaging characteristics of musculoskeletal fibromatoses to help guide the often difficult and protracted therapy and management of these lesions.

Unplanned surgical excision of tumors of the foot and ankle.

BACKGROUND: Soft-tissue tumors of the foot and ankle are relatively common and mostly benign. Thus, many malignant tumors in this region are improperly treated initially. Unplanned excisions can lead to complications that may adversely affect patient outcomes and prognosis. METHODS: A retrospective review of patients treated at our institute over a 20-year period for malignant soft-tissue tumors of the foot and ankle was performed. The effect of unplanned surgical excisions on outcomes was examined. RESULTS: When limb salvage was attempted, patients who underwent unplanned surgical excisions had more complications and more extensive surgical procedures involving free flaps, and they were more likely to require adjuvant radiotherapy. No difference in recurrence and disease-free survival was evident between the two patient populations. CONCLUSIONS: Despite the lack of statistical power to demonstrate differences in recurrence and survival, unplanned surgical excisions of soft-tissue sarcomas of the foot and ankle probably adversely affect quality of patient care. Suspicious lesions should be referred to surgeons trained in oncologic principles for evaluation and treatment.

Staging of bone neoplasms: an orthopedic oncologist's perspective.

The process of staging bone tumors is complex. The goal of staging is to define the type of tumor and its extent. Like staging for other neoplasms, it stratifies patients into groups based on prognosis and established treatment protocols. Staging is a multidisciplinary effort involving orthopedic oncologists, musculoskeletal radiologists, and orthopedic pathologists. The diagnosis is often suggested on clinical examination and review of the radiographs. The biopsy usually confirms the clinical and radiographic impression. However, biopsy is difficult and leads to errors in diagnosis in nearly 20% of cases. These errors may make limb salvage impossible and adversely affect survival. For this reason, staging and especially the biopsy should be done in the institution where definitive treatment is planned.

Management of metastatic lesions of the humerus.

The management of patients with metastatic disease in the humerus requires consideration of many factors. A careful evaluation of the patient's general condition, an understanding of the disease process, an appreciation of the degree of bone destruction, and a working knowledge of available treatment options are required. A multidisciplinary approach is essential to determine the course of treatment that best alleviates pain, preserves function, and optimizes the quality of life remaining in the patient with metastatic disease.