Total shoulder arthroplasty for glenohumeral arthritis associated with posterior glenoid bone loss: results of an all-polyethylene, posteriorly augmented glenoid component.

BACKGROUND: Posterior glenoid bone loss is commonly encountered in total shoulder arthroplasty (TSA). The purpose of our study is to report the clinical and radiographic findings of patients with a minimum of 2 years' follow-up treated with an all-polyethylene, augmented glenoid component. METHODS: Twenty-two shoulders with posterior glenoid bone loss were treated by a single surgeon. All underwent primary TSA using a posteriorly augmented, all-polyethylene, stepped glenoid component. Outcome data included visual analog scale, Western Ontario Osteoarthritis of the Shoulder index, and Short Form 36 scores. Radiographic analysis was performed to evaluate bone-cement interface lucency, implant seating, and osseous integration of the central peg. RESULTS: The mean follow-up period was 36 months. Average preoperative retroversion measured with computed tomography scan was 23.5°. In addition to statistically significant increases in forward flexion and external rotation, the visual analog scale score, Western Ontario Osteoarthritis of the Shoulder score, and Short Form 36 physical component summary score all improved significantly (P < .001). Twelve shoulders had osseous integration between the central-peg flanges, 6 had bone adjacent to the central-peg flanges but without identifiable osseous integration, and 1 showed osteolysis. The mean Lazarus score was 0.5. All glenoids had perfect seating scores. Two patients sustained a total of 3 episodes of prosthetic instability. CONCLUSIONS: Early results of a posteriorly augmented, all-polyethylene, stepped prosthetic glenoid component to address posterior glenoid loss in TSA are encouraging. Continued evaluation will determine prosthetic longevity and maintained clinical improvement.

Osteosarcoma in a Marfan patient with a novel premature termination codon in the FBN1 gene.

Osteosarcoma is a malignant neoplasm of mesenchymal origin that is presumed to arise from osteoblasts. Considered a rare tumor, approximately 1000 cases of osteosarcoma are diagnosed in the United States each year, and osteosarcoma of the foot is rarer still. Marfan syndrome (MFS) is a rare genetic disorder that affects 1 in 5000 individuals and is caused by mutations in the fibrillin 1 (FBN1) gene. MFS phenotype affects several body systems, including soft connective tissue and bone. Here we report, for the first time, an individual with MFS that was treated for osteosarcoma. Surgically resected tissue was used to initiate an osteosarcoma cell line (PSU-OS-M) that exhibits attachment-independent growth and loss of contact inhibition in vitro. Genomic DNA was isolated from the tumor cells, and primers that anneal to intronic regions were used to amplify and sequence all 65 coding exons of the FBN1 gene. A two base pair insertion that results in a novel premature termination codon (PTC) was found in exon 52. Protein from the normal allele is detectable in PSU-OS-M cell-conditioned medium, but protein from the mutant allele was not detectable. Immunofluorescent microscopy demonstrates that PSU-OS-M cells can assemble fibrillin 1 microfibrils in culture, and fibronectin assembly is normal. As such, the PSU-OS-M cell line is to our knowledge the first oncogenically transformed cell line with a mutant fibrillin gene and may serve as a useful tool for studying molecular mechanisms of MFS and nonsense-mediated decay.