The role of implant alignment on stability and particles on periprosthetic osteolysis?A rabbit model of implant failure

2004 ◽  
Vol 70B (2) ◽  
pp. 179-186 ◽  
Author(s):  
V. L. Fornasier ◽  
S. B. Goodman ◽  
K. Protzner ◽  
M. Kamel ◽  
Y. Song ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Implant Failure ◽  
Periprosthetic Osteolysis ◽  
Implant Alignment

scholarly journals Orthopaedic implant failure: aseptic implant loosening–the contribution and future challenges of mouse models in translational research

2014 ◽  
Vol 127 (5) ◽  
pp. 277-293 ◽  
Author(s):  
Luis Alberto Cordova ◽  
Verena Stresing ◽  
Bérengère Gobin ◽  
Philippe Rosset ◽  
Norbert Passuti ◽  
...  
Keyword(s):  
Aseptic Loosening ◽  
Mouse Models ◽  
Implant Failure ◽  
Orthopaedic Implant ◽  
Implant Loosening ◽  
Periprosthetic Osteolysis ◽  
New Era ◽  
Future Challenges

Aseptic loosening as a result of wear debris is considered to be the main cause of long-term implant failure in orthopaedic surgery and improved biomaterials for bearing surfaces decreases significantly the release of micrometric wear particles. Increasingly, in-depth knowledge of osteoimmunology highlights the role of nanoparticles and ions released from some of these new bearing couples, opening up a new era in the comprehension of aseptic loosening. Mouse models have been essential in the progress made in the early comprehension of pathophysiology and in testing new therapeutic agents for particle-induced osteolysis. However, despite this encouraging progress, there is still no valid clinical alternative to revision surgery. The present review provides an update of the most commonly used bearing couples, the current concepts regarding particle–cell interactions and the approaches used to study the biology of periprosthetic osteolysis. It also discusses the contribution and future challenges of mouse models for successful translation of the preclinical progress into clinical applications.

Immune complex binding Streptococcus pyogenes type M12/emm12 in experimental glomerulonephritis

2013 ◽  
Vol 62 (9) ◽  
pp. 1272-1280 ◽  
Author(s):  
Larissa Burova ◽  
Peter Pigarevsky ◽  
Nadezhda Duplik ◽  
Vlada Snegova ◽  
Alexander Suvorov ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Complement C3 ◽  
Poststreptococcal Glomerulonephritis ◽  
Tnf Α ◽  
Rabbit Igg ◽  
Renal Changes ◽  
Group A ◽  
Study Type ◽  
Binding Component

In a rabbit model, we have previously reported evidence for a pathogenic role of streptococcal IgG Fc-binding proteins (IgGFcBP) in poststreptococcal glomerulonephritis (PSGN). These proteins, of the M protein family, were shown to trigger anti-IgG production and enhance renal deposition of IgG and/or immune complexes (ICs), with resulting activation of complement and cytokine cascades. In the present study, type M12/emm12, group A streptococci (GAS) were found often to bind artificial ICs, viz. peroxidase–anti-peroxidase rabbit IgG (PAP) or tetanus toxoid–anti-tetanus human IgG (TAT), rather than monomeric IgG. Animals injected with each of four IC binding clinical isolates (from patients with scarlet fever or PSGN) showed pronounced inflammatory and degenerative glomerular changes, morphologically similar to human PSGN, with membrane thickening and IgG and complement C3 deposition, as well as secretion of IL-6 and TNF-α by mesangial and endothelial cells. In contrast, non-binding strains (two from asymptomatic carriers and one from a PSGN case) failed to trigger any renal changes. Only the IC binding strains induced elevated titres of anti-IgG. Though the streptococcal binding component(s) has not been demonstrated, the selective binding of ICs by type M12/emm12 strains appears important for the well-known, marked nephritogenic potential of this GAS type.

Abstract 15655: Safety and Efficacy of Subclavian Fibroplasty in Patients With Prior Left Ventricular Lead Implant Failure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
MALIK SHEHADEH ◽  
Nebu Alexander ◽  
Cyrus Hadadi ◽  
John Costello ◽  
Vijaywant Brar ◽  
...  
Keyword(s):  
Fibrous Tissue ◽  
Balloon Dilation ◽  
Vascular Complications ◽  
High Volume ◽  
Left Ventricular ◽  
Implant Failure ◽  
Distal Embolization ◽  
Interventional Techniques ◽  
Ventricular Lead

Introduction: Fibrous subclavian vein obstruction (SVO) is a common primary cause of left ventricular (LV) lead implant failure. Such obstruction might be apparent or unrecognized. Balloon dilation of the aggressive fibrosis that develops in response to chronic leads (fibroplasty) can be employed safely to achieve a successful implant. Hypothesis: To describe the experience of high-volume referral center with balloon dilation of fibrous tissue in patients with prior LV lead implant failure. Methods: We evaluated the role of balloon dilation in 187 patients referred to our institute because of prior LV lead implant failure between June 2017 and November 2019. Results: Of the 187 patients, 35 (19%) had apparent SVO as the primary explanation for implant failure. In 152 (81%), SVO was not recognized as contributing to implant failure. In 32 of 35 with apparent SVO (91.4%), it was possible to cross the obstruction and perform fibroplasty successfully. Three cases (8.6%) failed due to inability to advance a wire through the obstruction, none had existing leads to follow. In 33 of 152 (22%) cases without recognized SVO, fibroplasty of the subclavian was required, in addition to another interventional techniques, for successful implantation. There were no major or minor vascular complications related to fibroplasty. There was no distal embolization and no damage to the existing leads. Conclusions: In the setting of chronic leads, apparent SVO is commonly recognized as a cause of LV lead implant failure. However, 22% of prior LV lead implant failures without obvious obstruction also required fibroplasty (in addition to another interventional techniques) for success. In conclusion, subclavian fibroplasty is essential for successful implantation in patients with prior LV lead implant failure with and without obvious obstruction and can be safely performed by the implanting physician.

scholarly journals Role of Erythromycin-Regulated Histone Deacetylase-2 in Benign Tracheal Stenosis

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Zhenjie Huang ◽  
Peng Wei ◽  
Luoman Gan ◽  
Tonghua Zeng ◽  
Caicheng Qin ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Tracheal Stenosis ◽  
Type I Collagen ◽  
Rabbit Model ◽  
Immunohistochemical Method ◽  
Type Iii Collagen ◽  
Type I ◽  
Histone Deacetylase 2 ◽  
Budesonide Group

Objective. This study aims to explore the role of erythromycin-regulated histone deacetylase-2 in benign tracheal stenosis. Methods. The rabbit model of tracheal stenosis was established. The rabbits were randomly divided into 8 groups. Histone deacetylase-2 (HDAC2) expression was detected by immunofluorescence. The expression of type I collagen and type III collagen was detected by immunohistochemical method. The expression of TGF-β1, VEGF and IL-8 in serum and alveolar lavage fluid was detected by ELISA. The expression of HDAC2, TGF-β1, VEGF and IL-8 in bronchi of each group was detected by Western blotting method. Results. In Erythromycin (ERY) group, ERY + Budesonide group, ERY + Vorinostat group and ERY + Budesonide + Vorinostat group, the degree of bronchial stenosis was alleviated, and the mucosal epithelium was still slightly proliferated. The effect of ERY combined with other drugs was more obvious. The HDAC2 protein expression increased significantly in ERY group, ERY + Budesonide group and ERY + Budesonide + Vorinostat group and decreased significantly in Vorinostat group, the expression of collagen I and III decreased significantly in ERY group, ERY + Budesonide group and ERY + Budesonide + Vorinostat group (P<0.05). The TGF-β1, IL-8 and VEGF levels decreased significantly in ERY group, ERY + Budesonide group, ERY + Vorinostat group and ERY + Budesonide + Vorinostat group (P<0.05). Conclusions. Erythromycin inhibited inflammation and excessive proliferation of granulation tissue after tracheobronchial mucosal injury by up-regulating the expression of HDAC2, it promoted wound healing and alleviated tracheobronchial stenosis. When combined with budesonide, penicillin and other glucocorticoids and antibiotics, it had a good synergistic effect. However, vorinostat could attenuate erythromycin’s effect by down-regulating the expression of HDAC2. It may have good clinical application prospects in the treatment of tracheal stenosis.

scholarly journals The Fate of Bone Graft for Periprosthetic Osteolysis in Total Ankle Arthroplasty

2017 ◽  
Vol 2 (3) ◽  
pp. 2473011417S0000 ◽  
Author(s):  
Yoo Jung Park ◽  
Dong-Woo Shim ◽  
Yeokgu Hwang ◽  
Jin Woo Lee
Keyword(s):  
Clinical Outcome ◽  
Bone Graft ◽  
Bone Grafting ◽  
Distal Tibia ◽  
Total Ankle Arthroplasty ◽  
Implant Failure ◽  
Periprosthetic Osteolysis ◽  
Aofas Score ◽  
Ankle Arthroplasty

Category: Ankle Arthritis Introduction/Purpose: Periprosthetic osteolysis in total ankle arthroplasty (TAA) is a substantial problem. It may cause implant failure and has potential to affect long-term implant survival. To prevent major revisional arthroplasty, it is important to make an early diagnosis of osteolysis and decide an appropriate timing of surgical intervention such as bone graft. We report our experience of bone graft for osteolysis after TAA associated with clinical and radiologic outcome. Methods: Between May 2004 and Oct. 2013, 238 primary TAA were performed on 219 patients. We excluded 37 ankles with follow-up less than 24 months; thus, 201 ankles in 185 patients with mean follow-up of 61.9 (range, 24-130) months were included in the study. Nineteen patients were treated with a total of 21 bone graft procedures for periprosthetic osteolysis after TAA. Of these patients, 12 (57.1%) were males with mean follow-up length after bone graft 35.0 months. Location of osteolysis, bone grafting method and clinical outcome parameters using visual analog scale (VAS), American Orthopaedic Foot and Ankle Society (AOFAS) score were recorded. Results: Radiographs revealed total of 62 osteolysis lesions in 19 patients; 35 (56.5%) distal tibial lesions, 23 (37.0%) talar lesions. Autogenous iliac bone graft was used in 18 procedures (85.7%). The mean scores (and standard deviation) improved for the VAS from 4.8 ± 1.23 points before bone graft to 3.0 ± 0.94 points at the last follow-up (p<0.05); and for the AOFAS score from 76.8 ± 5.9 before bone graft to 84.3 ± 4.5 at the last follow-up (p<0.05). After 21 bone graft procedures, 6 demonstrated detection of newly developed osteolysis. One patient needed a repeat bone graft procedure with cementation after the primary bone grafting due to large cyst on distal tibia. There was no implant failure or major revisions after the bone graft. Conclusion: Bone graft for periprosthetic osteolysis may improve patient’s clinical outcome and give support to the structures surrounding the implant. Bone grafting in optimal timing may also improve implant survivorship. However, further study is needed for the etiology of newly developed painless osteolysis even after the bone graft.

scholarly journals The role of fibroblasts and fibroblast-derived factors in periprosthetic osteolysis

2006 ◽  
Vol 54 (10) ◽  
pp. 3221-3232 ◽  
Author(s):  
Tamas Koreny ◽  
Miklós Tunyogi-Csapó ◽  
Istvan Gál ◽  
Csaba Vermes ◽  
Joshua J. Jacobs ◽  
...  
Keyword(s):  
Periprosthetic Osteolysis

scholarly journals Insulin and Glucagon Impairments in Relation with Islet Cells Morphological Modifications Following Long Term Pancreatic Duct Ligation in the Rabbit – A Model of Non-insulin-dependent Diabete

2001 ◽  
Vol 2 (2) ◽  
pp. 101-112 ◽  
Author(s):  
J. Catala ◽  
M. Daumas ◽  
A. Pham Huu Chanh ◽  
B. Lasserre ◽  
E Hollande
Keyword(s):  
Pancreatic Duct ◽  
Islet Cells ◽  
Rabbit Model ◽  
Fold Increase ◽  
Pancreatic Duct Ligation ◽  
A Cells ◽  
Duct Ligation ◽  
Insulin Dependent

Plasma levels of glucose, insulin and glucagon were measured at various time intervals after pancreatic duct ligation (PDL) in rabbits. Two hyperglycemic periods were observed: one between 15–90 days (peak at 30 days of 15.1 ± 1.2mmol/l, p < 0.01), and the other at 450 days (11.2 ± 0.5 mmol/l, p < 0.02). The first hyperglycemic episode was significantly correlated with both hypoinsulinemia (41.8 ± 8pmol/l, r= –0.94, p < 0.01) and hyperglucagonemia (232 ± 21ng/l, r=0.95, p < 0.01). However, the late hyperglycemic phase (450 days), which was not accompanied by hypoinsulinemia, was observed after the hyperglucagonemia (390 days) produced by abundant immunostained A-cells giving rise to a 3-fold increase in pancreatic glucagon stores. The insulin and glucagon responses to glucose loading at 180, 270 and 450 days reflected the insensitivity of B- and A-cells to glucose. The PDL rabbit model with chronic and severe glycemic disorders due to the predominant role of glucagon mimicked key features of the NIDDM syndrome secondary to exocrine disease.

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