Is there still a role for osteoarticular allograft reconstruction in musculoskeletal tumour surgery? a long-term follow-up study of 38 patients and systematic review of the literature.

AIMS: To assess complications and failure mechanisms of osteoarticular allograft reconstructions for primary bone tumours. PATIENTS AND METHODS: We retrospectively evaluated 38 patients (28 men, 74%) who were treated at our institution with osteoarticular allograft reconstruction between 1989 and 2010. Median age was 19 years (interquartile range 14 to 32). Median follow-up was 19.5 years (95% confidence interval (CI) 13.0 to 26.1) when 26 patients (68%) were alive. In addition, we systematically searched the literature for clinical studies on osteoarticular allografts, finding 31 studies suitable for analysis. Results of papers that reported on one site exclusively were pooled for comparison. RESULTS: A total of 20 patients (53%) experienced graft failure, including 15 due to mechanical complications (39%) and three (9%) due to infection. In the systematic review, 514 reconstructions were analysed (distal femur, n = 184, 36%; proximal tibia, n = 136, 26%; distal radius, n = 99, 19%; proximal humerus, n = 95, 18%). Overall rates of failure, fracture and infection were 27%, 20%, and 10% respectively. With the distal femur as the reference, fractures were more common in the humerus (odds ratio (OR) 4.1, 95% CI 2.2 to 7.7) and tibia (OR 2.2, 95% CI 1.3 to 4.4); infections occurred more often in the tibia (OR 2.2, 95% CI 1.3 to 4.4) and less often in the radius (OR 0.1, 95% CI 0.0 to 0.8). CONCLUSION: Osteoarticular allograft reconstructions are associated with high rates of mechanical complications. Although comparative studies with alternative techniques are scarce, the risk of mechanical failure in our opinion does not justify routine employment of osteoarticular allografts for reconstruction of large joints after tumour resection. Cite this article: Bone Joint J 2017;99-B:522-30.

MRI appearances of atypical cartilaginous tumour/grade I chondrosarcoma after treatment by curettage, phenolisation and allografting: recommendations for follow-up.

AIMS: The purpose of this retrospective study was to differentiate between the MRI features of normal post-operative change and those of residual or recurrent disease after intralesional treatment of an atypical cartilage tumour (ACT)/grade I chondrosarcoma. PATIENTS AND METHODS: We reviewed the case notes, radiology and histology of 75 patients, who had been treated for an ACT/grade I chondrosarcoma by curettage, phenolisation and bone allografting between 1994 and 2005. The first post-operative Gd-enhanced MRI scan was carried out within one year of surgery. Patients had a minimum of two scans and a mean follow-up of 72 months (13 to 169). Further surgery was undertaken in cases of suspected recurrence. RESULTS: In 14 patients (18.6%) a second procedure was undertaken after a mean period of 59 months (8 to 114). Radio frequency ablation (RFA) was used in lesions of < 10 mm and curettage, phenolisation and bone grafting for those ≥ 10 mm. Only six of these (8% of total) had a histologically-proven recurrence. No increase in tumour grade was seen at time of recurrence. CONCLUSION: Based on this study, we have been able to classify the post-operative MRI appearances into four groups. These groups differ in follow-up, and have a different risk of recurrence of the lesion. Follow-up and treatment vary for the patients in each group. We present a flow diagram for the appropriate and safe follow-up for this specific group of patients. Cite this article: Bone Joint J 2016;98-B:1674-81.

Intercalary allograft reconstructions following resection of primary bone tumors: a nationwide multicenter study.

BACKGROUND: Favorable reports on the use of massive allografts to reconstruct intercalary defects underline their place in limb-salvage surgery. However, little is known about optimal indications as reports on failure and complication rates in larger populations remain scarce. We evaluated the incidence of and risk factors for failure and complications, time to full weight-bearing, and optimal fixation methods for intercalary allografts after tumor resection. METHODS: A retrospective study was performed in all four centers of orthopaedic oncology in the Netherlands. All consecutive patients reconstructed with intercalary (whole-circumference) allografts after tumor resection in the long bones during 1989 to 2009 were evaluated. The minimum follow-up was twenty-four months. Eighty-seven patients with a median age of seventeen years (range, 1.5 to 77.5 years) matched inclusion criteria. The most common diagnoses were osteosarcoma, Ewing sarcoma, adamantinoma, and chondrosarcoma. The median follow-up period was eighty-four months (range, twenty-five to 262 months). Ninety percent of tumors were localized in the femur or the tibia. RESULTS: Fifteen percent of our patients experienced a graft-related failure. The major complications were nonunion (40%), fracture (29%), and infection (14%). Complications occurred in 76% of patients and reoperations were necessary in 70% of patients. The median time to the latest complication was thirty-two months (range, zero to 200 months). The median time to full weight-bearing was nine months (range, one to eighty months). Fifteen grafts failed, twelve of which failed in the first four years. None of the thirty-four tibial reconstructions failed. Reconstruction site, patient age, allograft length, nail-only fixation, and non-bridging osteosynthesis were the most important risk factors for complications. Adjuvant chemotherapy and irradiation had no effects on complication rates. CONCLUSIONS: We report high complication rates and considerable failure rates for the use of intercalary allografts; complications primarily occurred in the first years after surgery, but some occurred much later after surgery. To reduce the number of failures, we recommend reconsidering the use of allografts for reconstructions of defects that are ≥15 cm, especially in older patients, and applying bridging osteosynthesis with use of plate fixation.

Survival from high-grade localised extremity osteosarcoma: combined results and prognostic factors from three European Osteosarcoma Intergroup randomised controlled trials.

BACKGROUND: Neoadjuvant chemotherapy improves outcome in osteosarcoma. Determination of optimum regimens for survival, toxicity and prognostic factors requires randomised controlled trials to be conducted. PATIENTS AND METHODS: Between 1983 and 2002, the European Osteosarcoma Intergroup recruited 1067 patients with localised extremity osteosarcoma to three randomised controlled trials. Standard treatment in each was doxorubicin 75 mg/m(2) and cisplatin 100 mg/m(2). Comparators were addition of methotrexate (BO02/80831), a multidrug regimen (BO03/80861) and a dose-intense schedule (BO06/80931). Standard survival analysis methods were used to identify prognostic factors, temporal and other influences on outcome. RESULTS: Five- and 10-year survival were 56% (95% confidence interval 53% to 59%) and 52%, respectively (49% to 55%), with no difference between trials or treatment arms. Median follow-up was 9.4 years. Age range was 3-40 years (median 15). Limb salvage was achieved in 69%. Five hundred and thirty-three patients received the standard arm, 79% completing treatment. Good histological response to preoperative chemotherapy, distal tumour location (all sites other than proximal humerus/femur) and female gender were associated with improved survival. CONCLUSIONS: Localised osteosarcoma will be cured in 50% of patients with cisplatin and doxorubicin. Large randomised trials can be conducted in this rare cancer. Failure to improve survival over 20 years argues for concerted collaborative international efforts to identify and rapidly test new treatments.

COX-2 expression in chondrosarcoma: a role for celecoxib treatment?

Chondrosarcomas are resistant to conventional chemo- and radiotherapy. A subset of chondrosarcomas arises secondarily in the benign tumour syndromes enchondromatosis (EC) and multiple osteochondromas (MO), and prevention of tumour development would greatly improve prognosis. We therefore investigated the effect of selective COX-2 inhibition on chondrosarcoma growth. COX-2 expression was studied in central- and peripheral cartilaginous tumours. The effect of COX-2 inhibition was assessed in four high-grade chondrosarcoma cell lines using celecoxib and NS-398 treatment. COX-2 activity (prostaglandin E(2) (PGE(2)) ELISA) and cell viability were measured. The (prophylactic) effect of celecoxib on chondrosarcoma growth in vivo was studied for 8 weeks using a xenograft model of cell line CH2879 in immunoincompetent nude mice. High COX-2 protein expression was mainly found in solitary peripheral chondrosarcoma and in enchondromatosis-related central chondrosarcoma, which was confirmed by qPCR. After 72h of celecoxib treatment, a significant decrease in cell viability was observed in three chondrosarcoma cell lines. In vivo, celecoxib initially slowed tumour growth in chondrosarcoma xenografts; however, after prolonged treatment relapsed tumour growth was observed. Tumour volume was negatively associated with celecoxib serum levels, and seemed smaller in the high-dose prophylactic treatment group. We confirmed the expression of COX-2 in 65% of chondrosarcomas, and COX-2 inhibition by celecoxib diminished cell viability in vitro. The initial response and the decrease in tumour volume with increased celecoxib serum levels in vivo supported a role for celecoxib, although relapsed tumour growth after 6 weeks was worrisome. Also the role of high-dose prophylactic celecoxib in preventing the development of benign and malignant cartilage tumours in EC and MO patients deserves further investigation.

Profiling of high-grade central osteosarcoma and its putative progenitor cells identifies tumourigenic pathways.

BACKGROUND: Osteosarcoma is the most prevalent primary malignant bone tumour in children and young adults, with poor survival in 40% of patients. To identify the signalling pathways involved in tumourigenesis, we compared gene expression in osteosarcoma with that in its presumed normal counterparts. METHODS: Genome-wide expression profiles were generated from 25 high-grade central osteosarcoma prechemotherapy biopsies, 5 osteoblastomas, 5 mesenchymal stem cell (MSC) populations and these same MSCs differentiated into osteoblasts. Genes that were differentially expressed were analysed in the context of the pathways in which they function using the GenMAPP programme. RESULTS: MSCs, osteoblasts, osteoblastomas and osteosarcomas clustered separately and thousands of differentially expressed genes were identified. The most significantly altered pathways are involved in cell cycle regulation and DNA replication. Several upstream components of the Wnt signalling pathway are downregulated in osteosarcoma. Two genes involved in degradation of beta-catenin protein, the key effectors of Wnt signalling, Axin and GSK3-beta, show decreased expression, suggesting that Wnt signalling is no longer under the control of regular signals. Comparing benign osteoblastomas with osteosarcomas identified cell cycle regulation as the most prominently changed pathway. CONCLUSION: These results show that upregulation of the cell cycle and downregulation of Wnt signalling have an important role in osteosarcoma genesis. Gene expression differences between highly malignant osteosarcoma and benign osteoblastoma involve cell cycle regulation.

Improved diagnosis and treatment of soft tissue sarcoma patients after implementation of national guidelines: a population-based study.

AIM: The majority of clinicians, radiologists and pathologists have limited experience with soft tissue sarcomas. In 2004, national guidelines were established in The Netherlands to improve the quality of diagnosis and treatment of these rare tumours. This study evaluates the compliance with the guidelines over time. PATIENTS: Population-based series of 119 operated patients with a soft tissue sarcoma (STS) diagnosed in 1998-1999 (79 before implementation of new guidelines) and in 2006 (40 after implementation). METHODS: Coded information regarding patient and tumour characteristics as well as (the results of) pathology review was collected from the medical patient file by two experienced data-managers. RESULTS: Diagnostic imaging of the tumour was performed according to the guidelines in 75-100% depending on the site of the tumour (abdominal versus non-abdominal) as well as the time of diagnosis. Adherence to the guidelines with respect to invasive diagnostic procedures in patients with non-abdominal STS improved over time. A pre-operative histological diagnosis was obtained in 42% of the patients in 1998-1999 and in 72% of the patients in 2006 (p<0.001). The guidelines for reporting on pathology were increasingly adhered to. In 2006, (nearly) all pathology reports mentioned tumour size, morphology, tumour grade, resection margins and radicality. This represents a major improvement compared to the pathology reports in 1998-1999, where these aspects were not mentioned in 14-40% of the cases. The proportion of prospective pathology reviews by (a member of) the expert panel increased from 60% in 1998-1999 to 90% in 2006 (p=0.001). DISCUSSION: The compliance with the guidelines has been optimised by the increased attention to this group of patients. Most important factors have been the reporting of the results of the first evaluation and (discussions about) the centralisation of treatment. Further improvements could be reached by the prospective web based registry monitoring logistic aspects as well as parameters useful for the evaluation of the quality of care.

The cytotoxic effect of phenol and ethanol on the chondrosarcoma-derived cell line OUMS-27: an in vitro experiment.

Surgery is considered to be the most effective treatment for cartilaginous tumours. In recent years, a trend has emerged for patients with low-grade tumours to be treated less invasively using curettage followed by various forms of adjuvant therapy. We investigated the potential for phenol to be used as an adjuvant. Using a human chondrosarcoma-derived cartilage-producing cell line OUMS-27 as an in vitro model we studied the cytotoxic effect of phenol and ethanol. Since ethanol is the standard substance used to rinse phenol out of a bone cavity, we included an assessment of ethanol to see whether this was an important secondary factor with respect to cell death. The latter was assessed by flow cytometry. A cytotoxic effect was found for concentrations of phenol of 1.5% and of ethanol of 42.5%. These results may provide a clinical rationale for the use of both phenol and ethanol as adjuvant therapy after intralesional curettage in low-grade central chondrosarcoma and justify further investigation.

Telomere biology in giant cell tumour of bone.

Giant cell tumour of bone (GCTB) is a benign bone tumour known for the unpredictable clinical behaviour of recurrences and, in rare instances, distant metastases. It consists of uniformly distributed osteoclastic giant cells in a background of mononuclear rounded and spindle-shaped cells. Cytogenetically, telomeric associations are the most common chromosomal aberrations, which, however, are normally almost exclusively found in high-grade malignancies. GCTB has often been regarded as a polyclonal tumour, but more recently a recurrent specific aberration was reported, which suggests a possible role for disturbed telomere maintenance. Here we further investigate telomere maintenance in GCTB using 19 samples from 19 patients. A combination of immunofluorescence and FISH was performed, applying antibodies directed against promyelocytic leukaemia body-related antigen and hTERT and using telomere peptide nucleic acid probes. The TRAP assay and telomere restriction fragment length analysis were performed for functional detection of telomerase activity and alternative telomere lengthening. Both osteoclastic giant cells and mononuclear cells showed positivity for hTERT and promyelocytic leukaemia body-related antigen. In most mononuclear cells, co-expression was present. The TRAP assay demonstrated heterogeneous telomerase activity, while telomere restriction fragment length analysis showed non-heterogeneous telomere lengths, indicating the absence of alternative telomere lengthening. Confocal microscopy showed stereometric co-localization of nucleolin with promyelocytic leukaemia body-related antigen in association with telomeres in the spindle-shaped cells. hTERT was more diffusely distributed throughout the nucleus. Our results show that GCTB demonstrates remarkable telomere maintenance of activated telomerase and inactivated alternative telomere lengthening in the presence of normal mean telomere restriction fragment lengths. These findings strongly suggest that these aggregates, while activating telomerase, are part of a structural telomere protective-capping mechanism rather than of a telomere-lengthening mechanism. Telomere maintenance could be considered an important key factor in the pathogenesis of GCTB.

Decreased EXT expression and intracellular accumulation of heparan sulphate proteoglycan in osteochondromas and peripheral chondrosarcomas.

Mutational inactivation of EXT1 or EXT2 is the cause of hereditary multiple osteochondromas. These genes function in heparan sulphate proteoglycan (HSPG) biosynthesis in the Golgi apparatus. Loss of heterozygosity of the EXT1 locus at 8q24 is frequently found in solitary osteochondromas, whereas somatic mutations are rarely found. We investigated the expression of EXT1 and EXT2 (quantitative RT-PCR) and of different HSPGs (immunohistochemistry) in solitary and hereditary osteochondromas and in cases with malignant progression to secondary peripheral chondrosarcoma, in relation to possible mutations and promoter methylation. The mutation status of patients with multiple osteochondromas correlated with decreased EXT1 or EXT2 expression found in their resected tumours. We could not show somatic point mutations or promoter hypermethylation in 17 solitary tumours; however, EXT1 expression was decreased in 15 cases, whereas EXT2 was not. Intracellular accumulation of syndecan-2 and heparan sulphate-bearing isoforms of CD44 (CD44v3) was found in most tumours, which concentrated in the Golgi apparatus as shown by confocal microscopy. This contrasted with the extracellular expression found in normal growth plates. In conclusion, mutational inactivation of either EXT1 or EXT2 leads to loss of mRNA expression of the corresponding gene. We hypothesize that loss of EXT expression disrupts the function of the EXT1/2 complex in HSPG biosynthesis, resulting in the intracellular accumulation of HSPG core proteins that we found in these tumours.

Peripheral chondrosarcoma progression is accompanied by decreased Indian Hedgehog signalling.

Hedgehog (HH) signalling is important for specific developmental processes, and aberrant, increased activity has been described in various tumours. Disturbed HH signalling has also been implicated in the hereditary syndrome, Multiple Osteochondromas. Indian Hedgehog (IHH), together with parathyroid hormone-like hormone (PTHLH), participates in the organization of growth plates in long bones. PTHLH signalling is absent in osteochondromas, benign tumours arising adjacent to the growth plate, but is reactivated when these tumours undergo malignant transformation towards secondary peripheral chondrosarcoma. We describe a gradual decrease in the expression of Patched (PTCH) and glioma-associated oncogene homologue 1 (GLI1) (both transcribed upon IHH activity), and GLI2 with increasing malignancy, suggesting that IHH signalling is inactive and PTHLH signalling is IHH independent in secondary peripheral chondrosarcomas. cDNA expression profiling and immunohistochemical studies suggest that transforming growth factor-beta (TGF-beta)-mediated proliferative signalling is active in high-grade chondrosarcomas since TGF-beta downstream targets were upregulated in these tumours. This is accompanied by downregulation of energy metabolism-related genes and upregulation of the proto-oncogene jun B. Thus, the tight regulation of growth plate organization by IHH signalling is still seen in osteochondroma, but gradually lost during malignant transformation to secondary peripheral chondrosarcoma and subsequent progression. TGF-beta signalling is stimulated during secondary peripheral chondrosarcoma progression and could potentially regulate the retained activity of PTHLH.

Treatment of avascular necrosis of the hip by a non-vascularised cortical graft.

This retrospective study describes the long-term results of core decompression and placement of a non-vascularised bone graft in the management of avascular necrosis of the femoral head. We treated 80 hips in 65 patients, 18 by a cortical tibial autograft and 62 by a fibular allograft. The mean age of the patients was 36 years (SD 13.2). A total of 78 hips were available for evaluation of which pre-operatively six were Ficat-Arlet stage 0, three stage I, 31 stage IIA, 16 stage IIB, 13 stage III and nine stage IV. A total of 34 hips (44%) were revised at a mean of four years (SD 3.8). Survivorship analysis using a clinical end-point showed a survival rate of 59% five years after surgery. We found a significant difference (p = 0.002) in survivorship, when using a clinical and radiological end-point, between the two grafts, in favour of the tibial autograft. We considered this difference to be the result of the better quality and increased volume of tibial bone compared with that from the trochanteric region used with the fibular allograft. This is a relatively simple, extra-articular and reproducible procedure. In our view core decompression, removal of the necrotic tissue and packing of the cancellous grafts into the core track are vital parts of the procedure.

Clinico-histologic parameters of osteosarcoma patients with late relapse.

Primary high-grade intramedullary osteosarcoma of the extremities is a clinically aggressive bone tumour. There is an ongoing effort to further improve efficacy of neo-adjuvant chemotherapy and reduce chemotoxicity by trying to identify osteosarcoma patients who are at risk of treatment failure as well as to identify those who can do with less chemotherapy. In only 5% of patients, first distant metastasis or local relapse occurs 5 years or more after initial treatment for osteosarcoma. Patients and physicians can therefore easily erroneously consider a patient with osteosarcoma cured if he or she is disease-free for more than 5 years following diagnosis and treatment. To investigate if these rare late relapsing patients are characterised by specific clinico-pathological features, we examined clinical and histological variables of late relapse (first local recurrence or metastasis 5 years or more after initial diagnosis) out of a total of 2,243 patients, with a special interest in the histological osteosarcoma subtype. In total, 33 patients had a documented relapse 5 years or more after diagnosis. Half of the patients had good response (>or=90% necrosis) to pre-operative chemotherapy and the other half a poor response (<90% necrosis) and late relapses seemed to be more frequently proportionately in those who had a good initial response to chemotherapy. The occurrence of late relapse did not appear to be associated with age or gender. Although not statistically significant, there was a trend for patients with a chondroblastic subtype of osteosarcoma, or a location in the tibia or fibula, to have a higher risk for late relapse.

Epidiaphyseal versus other intercalary allografts for tumors of the lower limb.

Epidiaphyseal intercalary reconstruction has become possible for bone tumors that extend into the epiphysis because advances in magnetic resonance imaging and chemotherapy allow close resection while sparing the juxtaarticular bone and joint. In a retrospective study, we questioned whether epidiaphyseal reconstructions around the knee had a clinical outcome (measured as long-term survival, complication rate, and functional score) comparable with metadiaphyseal and diaphyseal reconstructions. Between 1988 and 1999, 14 epidiaphyseal, nine metaphyseal, and 12 diaphyseal reconstructions were done, and the median followup was 7.2 years. Kaplan-Meier analysis showed a 10-year survival rate of 79% for epidiaphyseal reconstructions, which did not differ from an 89% rate for metadiaphyseal and a 75% rate for diaphyseal reconstructions. Epidiaphyseal complications included two infections, five fractures, and three nonunion treatments. Complications for all 35 grafts included three infections, 12 fractures, and nine nonunion treatments. Ultimately, six grafts failed, with infection and length of resection as predisposing factors. All epiphyseal osteotomies had tumor-free margins and no local recurrences. The mean Musculoskeletal Tumor Society score for each type of intercalary reconstruction was between 23 and 24. Because the epidiaphyseal reconstruction avoids complications associated with joint reconstruction and the results are comparable with those of other types of intercalary grafts, these reconstructions should be considered if at least 1 cm of tumor-free juxtaarticular bone can be maintained.

Overexpression of the HER-2 oncogene does not play a role in high-grade osteosarcomas.

The aim of our study was to determine whether or not the tyrosine kinase receptor, HER2 (also known as ErbB2/Her2/neu), is overexpressed in human osteosarcomas (OS). We studied 15 biopsy and 18 resection specimens at the mRNA and protein levels. HER2 status in the OS specimens was assessed by immunohistochemistry (IHC) and quantitative Real-Time Polymerase chain reaction (PCR). In moderately immunopositive cases fluorescent in situ hybridisation (FISH) analysis was used in order to identify any possible gene amplification. 27 samples were evaluable for IHC and only 1 case showed a moderately positive membrane staining. The remaining samples showed no staining or focal cytoplasmic staining (2 samples). In the moderately positive case, FISH analysis showed no HER-2 gene amplification. There was also no overexpression of HER2 mRNA suggesting this sample was a false-positive immunostain. HER2 mRNA expression was present in all samples at a similar level to that in the breast cancer cell line, MCF7, which does not overexpress HER2 and was used as a negative control. In conclusion, this study shows that HER2 mRNA or membranous HER2 protein overexpression is absent in human OS. We noted various inconsistencies in previous published studies, with regard to methodology and the interpretation of the results based on poor methodology. We therefore conclude that the positive data with regard to HER2 overexpression reported in these previous studies is not reliable. Our results suggest that the monoclonal antibody trastuzumab (Herceptin(R)), directed against the HER2-receptor, is not likely to be an effective therapeutic agent in OS.

Expression of cartilage growth plate signalling molecules in chondroblastoma.

Chondroblastoma (CB) is a rare benign tumour (<1% of all bone tumours) involving epiphyseal long bones (male:female 1.5:1). During development, and in the postnatal period, IHh/PTHrP and FGF signalling molecules control the space and timing of chondrocyte differentiation. Considering the close relationship of CB with the growth plate (age and location), the expression of proteins involved in epiphyseal growth regulation was studied. Twelve cases of CB were retrieved. Immunohistochemistry was performed using antibodies against fibroblast growth factor-2 (FGF-2), fibroblast growth factor receptor-1 (FGFR-1), FGFR-3, bcl-2, p21, parathyroid hormone-related peptide (PTHrP), and parathyroid hormone-related peptide receptor (PTHR1). Three observers evaluated haematoxylin and eosin (H&E)-stained and immunostained slides independently. Semi-quantitative estimation of the matrix, the type of matrix, and immunostaining was performed. Cellular and matrix-rich areas were evaluated separately. Diverse amounts and types of matrix were present in different tumours, as well as within individual tumours. Signalling molecules were expressed in 50-100% of the cases. Higher levels of expression were found in cellular areas than in matrix-rich areas, especially for PTHR1, bcl-2, and FGFR-3. CB is an unusual entity affecting specific sites, showing that both IHh/PTHrP and FGF signalling are active. Higher expression was found in cellular than in matrix-rich areas, as in the proliferating/pre-hypertrophic growth plate zone in comparison with the hypertrophic/calcifying zone. Previous studies have shown the same molecules to be expressed with a similar pattern in chondrosarcomas. The sum of the evaluated features indicates that CB is a neoplasm originating from a mesenchymal cell committed towards chondrogenesis via active growth plate signalling pathways.

Hemicortical allograft reconstruction after resection of low-grade malignant bone tumours.

Low-grade surface tumours of bone may theoretically be treated by hemicortical resection, retaining part of the circumference of the cortex. An inlay allograft may be used to reconstruct the defect. Since 1988 we have performed 22 hemicortical procedures in selected patients with low-grade parosteal osteosarcoma (6), peripheral chondrosarcoma (6) and adamantinoma (10). Restricted medullary involvement was not a contraindication for this procedure. There was no evidence of local recurrence or distant metastasis at a mean follow-up of 64 months (27 to 135). Wide resection margins were obtained in 19 patients. All allografts incorporated completely and there were no fractures or infections. Fractures of the remaining hemicortex occurred in six patients and were managed successfully by casts or by osteosynthesis. The functional results were excellent or good in all except one patient. Hemicortical procedures for selected cases of low-grade surface tumours give excellent oncological and functional outcomes. There was complete remodelling and fewer complications when compared with larger intercalary procedures. The surgery is technically demanding but gives good clinical results.