ABSTRACT
OBJECTIVE: To investigate the application of impaction bone grafting (IBG) combined with Ti-alloy mesh for acetabular bone defect reconstruction in total hip arthroplasty (THA) revision and follow up the clinical outcomes and imaging findings. METHODS: The clinical and imaging data of patients who were admitted to our hospital from January 2000 to December 2020 and underwent acetabular bone defects reconstruction using IBG combined with titanium mesh were retrospectively analyzed. Preoperative and post-revision Oxford and Harris scores, and post-revision complications were evaluated. Radiographs were used to determine center of rotation (COR) of the hip joint, transparency line, bone graft fusion, and bone mineral density (BMD) around the hip joint. RESULTS: Significant improvement was observed in both Oxford and Harris scores (P < 0.05). The radiographs taken at the last follow-up examination showed no significant differences in the acetabulum COR, offsets, inclination angle, mean ratio of vertical value, and BMD analysis between the post-revision side and contralateral side (P > 0.05). The follow-up data showed restoration of the mesh implant and graft bone fusion. CONCLUSIONS: The application of IBG combined with titanium-alloy mesh in revision THA patients with acetabular defects was found to provide satisfactory outcomes. However, large-scale studies are still needed to further elucidate the long-term outcomes.
Subject(s)
Arthroplasty, Replacement, Hip , Hip Prosthesis , Acetabulum/surgery , Alloys , Arthroplasty, Replacement, Hip/methods , Bone Transplantation/methods , Follow-Up Studies , Humans , Prosthesis Failure , Reoperation/methods , Retrospective Studies , Surgical Mesh , TitaniumABSTRACT
The prognosis for osteosarcoma (OS) is dismal due to the aggressive tumor growth and high incidence of metastasis. The long noncoding RNA human homeobox A transcript at the distal tip (HOTTIP) and the transcription factor forkhead box C1 (FOXC1) present oncogenic activities in OS. Here, we aimed at gaining insights into the underlying mechanisms and their crosstalk. The expression of FOXC1 and HOTTIP in OS tissues or cell lines was examined by real-time PCR (RT-PCR) and western blot. The in vitro effects of FOXC1 or HOTTIP on cell viability, proliferation, migration, invasion, and expression of target genes were examined using MTT, colony-forming assay, wound-healing, Transwell invasion, and western blot, respectively; the in vivo effects were examined using xenograft and experimental metastasis models. Molecular control of HOTTIP on large tumor suppressor 2 (LATS2) or transactivation of FOXC1 or Sp1 on HOTTIP was assessed by combining RNA immunoprecipitation, qRT-PCR, western blot, ChIP, and luciferase assay. Both FOXC1 and HOTTIP were potently up-regulated in OS tissues and cell lines. FOXC1 and HOTTIP essentially maintained viability, proliferation, migration, and invasion of OS cells in vitro and contributed to xenograft growth or lung metastasis in vivo. Mechanistically, HOTTIP recruited enhancer of zeste homolog 2 (EZH2) and lysine-specific demethylase 1 (LSD1) to silence LATS2 and thus activated YAP/ß-catenin signaling. Upstream, Sp1 activated FOXC1 and they both directly transactivated HOTTIP. In summary, we showed that the Sp1/FOXC1/HOTTIP/LATS2/YAP/ß-catenin cascade presented oncogenic activities in OS cells. Targeting FOXC1 or HOTTIP may therefore prove beneficial for OS treatment.
Subject(s)
Adaptor Proteins, Signal Transducing/metabolism , Disease Progression , Forkhead Transcription Factors/metabolism , Osteosarcoma/pathology , Protein Serine-Threonine Kinases/metabolism , RNA, Long Noncoding/metabolism , Sp1 Transcription Factor/metabolism , Transcription Factors/metabolism , Tumor Suppressor Proteins/metabolism , beta Catenin/metabolism , Animals , Base Sequence , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Cell Survival/genetics , Enhancer of Zeste Homolog 2 Protein/metabolism , Gene Expression Regulation, Neoplastic , Humans , Mice, Inbred BALB C , Mice, Nude , Models, Biological , Neoplasm Invasiveness , Neoplasm Metastasis , Osteosarcoma/genetics , Osteosarcoma/metabolism , Phenotype , Promoter Regions, Genetic/genetics , Signal Transduction , Transcription, Genetic , Up-Regulation/genetics , Xenograft Model Antitumor Assays , YAP-Signaling ProteinsABSTRACT
BACKGROUND: Joint stiffness after elbow surgery is not a rare complication, and is always accompanied by deformity. The causes of joint stiffness are multiple in different patients, and divided into intrinsic and extrinsic causes. Herein, we report an unusual case of posttraumatic elbow stiffness due to multiple and rare causes. CASE SUMMARY: A 19-year-old male was hospitalized with the loss of motion of the left elbow for over ten years. Left limb computed tomography revealed left elbow stiffness with bony block and connection. The patient underwent surgery, and the etiology of joint stiffness was found to be a rare combination of common and uncommon causes. During an 18-mo follow-up period, the patient's left elbow had normal motion and he was symptom-free. CONCLUSION: However, this case combined with multiple and rare causes highlights that the patient with scar physique is likely to be accompanied with more severe soft tissue, nerve contracture, and heterotypic ossification, even during recurrence.
