ABSTRACT
INTRODUCTION: Osteonecrosis of the femoral head (ONFH) is a disabling condition that often results in secondary arthritis necessitating total hip arthroplasty (THA). Short-stem THA has constantly gained popularity. It remains controversial, whether ONFH represents a risk factor for failure after the implantation of short stems with pronounced metaphyseal anchorage. The potential spread of the osteonecrotic area and bone marrow edema into the metaphyseal bone might result in compromised stability. Early implant migration is considered predictive of subsequent aseptic loosening. The purpose of this study was a migration analysis of a modern, calcar-guided short-stem implant in patients with ONFH in a mid-term follow-up. MATERIALS AND METHODS: This retrospective analysis investigated the migration pattern of 45 calcar-guided short stems in patients with ONFH, using Einzel-Bild-Roentgen-Analyse Femoral-Component-Analysis (EBRA-FCA). Influencing factors such as ARCO categories, age, gender, body weight and BMI were analyzed. Complications and adverse events were documented. RESULTS: At mid-term [48.1 months (SD 20.7 months)], mean axial migration was 1.56 mm (SD 1.77 mm). Mean migration rate stabilized after 2 years. No influence of ARCO categories, age and BMI was found. A tendency of increased axial migration was observed in male patients and in overweight patients. No revision surgeries had to be performed during follow-up. CONCLUSION: The results indicate a migration pattern comparable to that of primary osteoarthritis patients with slight initial migration under full load followed by subsequent stabilization in the metaphyseal femur. The 100% survival rate at mid-term supports the usage of this short-stem design in patients with ONFH.
Subject(s)
Arthroplasty, Replacement, Hip/methods , Femur Head Necrosis/surgery , Hip Prosthesis , Osteoarthritis, Hip/surgery , Prosthesis Design , Prosthesis Failure , Adult , Aged , Aged, 80 and over , Body Weight , Female , Femur/surgery , Femur Head/surgery , Femur Head Necrosis/complications , Follow-Up Studies , Humans , Male , Middle Aged , Osteoarthritis, Hip/etiology , Retrospective Studies , Risk Factors , Time Factors , Young AdultABSTRACT
Vestibular schwannomas (VS) are benign tumors of the nervous system that are usually sporadic but also occur in the inherited disorder neurofibromatosis type 2 (NF2). The NF2 gene is a tumor suppressor gene located on chromosome 22. Loss of the NF2 protein product, Merlin, is universal in both sporadic and NF2-related schwannomas and the loss or mutation of the gene is the only established causative event underlying schwannoma formation. Comparative genomic hybridization (CGH) was used to screen 20 sporadic VS to identify additional chromosomal regions that may harbor genes involved in VS-tumorigenesis. The most common change were losses on chromosome 22q. Additionally, losses were observed on chromosome 9p indicating a possible participation of the CDKN2A tumor suppressor gene in the genesis of VS. Gains were observed on 17q, 19p and 19q, which have been reported before in malignant peripheral nerve sheath tumors that are associated with neurofibromatosis type 1. Importantly, high level amplifications have been observed on 16p and 16q as well as on 9q, suggesting the possible involvement of several oncogenes in the tumorigenesis of VS. Our data suggest the involvement of various oncogenes and tumor suppressor genes might play a role in the genesis of the vestibular schwannomas apart from the inactivation of the NF2 gene.
