Study Design. Observational epidemiological study. Objective. To identify and comprehensively assess reasons for recalls of spinal implant devices used in patients over the past 21 years. Summary of Background Data. The number of spine implant devices on the market continues to rise. Although the Food and Drug Administration (FDA) regulates the safety of these devices, there is a paucity of literature on the reasons spine implant devices are recalled. Methods. The FDA device recall database was queried using the search term “spine” for recalls between 2003 and 2024. Data were collected regarding recall class, recall reason, FDA 510(k)/premarket approval decision date, product manufacturer, and device indication. The data was then reviewed to identify recalls for spine implant devices. Results. A total of 386 spine implant devices were identified between January 2003 and December 2024. Among all recalls classified, 3.4% (n=13) were class I, 88.1% (n=340) were class II, and 8.5% (n=33) were class III. The most common reasons for recall were “Device/Component design” (52.8%) and “Packing/Processing Control” (24.1%). The median number of devices recalled by manufacturers included in the study was two with the highest being 41 devices. Conclusions. Overall, 76.9% of spine implant recalls reviewed were primarily due to issues with device design and processing control. 88.1% of recalls were classified with a class II FDA designation. This is the first study to present a retrospective regulatory analysis of FDA spine implant recalls and highlights the importance of premarket analysis and postmarketing surveillance to improve device safety. Level of Evidence. 4.
Fibrin sealants are commonly used in cartilage repair surgeries to adhere cells or grafts into a cartilage defect. Both autologous and commercial allogeneic fibrin sealants are used in cartilage repair surgeries, yet there are no studies characterizing and comparing the mechanical properties of fibrin sealants from all-autologous sources. The objectives of this study were to investigate (i) the effect of fibrinogen and thrombin sources on failure mechanics of sealants, and (ii) how sealants affect the adhesion of particulated cartilage graft material (BioCartilage) to surrounding cartilage under physiological loading. Allogeneic thrombin and fibrinogen were purchased (Tisseel), and autologous sources were prepared from platelet-rich plasma (PRP) and platelet-poor plasma (PPP) generated from human blood. To compare failure characteristics, sealants were sandwiched between cartilage explants and pulled to failure. The effect of sealant on the adhesion of BioCartilage graft to cartilage was determined by quantifying microscale strains at the graft-cartilage interface using an in vitro cartilage defect model subjected to shear loading at physiological strains well below failure thresholds. Fibrinogen sources were not equivalent; PRP fibrinogen created sealants that were more brittle, failed at lower strains, and resulted in sustained higher strains through the graft-cartilage interface depth compared to PPP and allogeneic sources. PPP clotted slower compared to PRP, suggesting PPP may percolate deeper into the repair to provide more stability through the tissue depth. There was no difference in bulk failure properties or microscale strains at the graft-cartilage interface between the purely autologous sealant (autologous thrombin + PPP fibrinogen) and the commercial allogeneic sealant. Clinical Significance: All-autologous fibrin sealants fabricated with PPP have comparable adhesion strength as commercial allogeneic sealants in vitro, whereas PRP creates an inferior all-autologous sealant that sustains higher strains through the graft-cartilage interface depth.
The incidence of coexisting osteochondral lesions (OCLs) of the tibia and talus has been negatively correlated with successful clinical outcomes, yet these lesions have not been extensively characterized.To determine the incidence of coexisting tibial and talar OCLs, assess the morphologic characteristics of these lesions, and evaluate whether these characteristics are predictive of outcome.Case series; Level of evidence, 4.A total of 83 patients who underwent surgery for a talar OCL were evaluated for coexisting OCLs of the distal tibia with preoperative magnetic resonance images. Size, location, containment, International Cartilage Repair Society (ICRS) grade, patient age, and patient sex were analyzed for predictors of coexisting lesions or patient outcome. The talar and tibial surfaces were each divided into 9 zones, with 1 corresponding to the most anteromedial region and proceeding laterally and then posteriorly. The Foot and Ankle Outcome Score (FAOS) was evaluated pre- and postoperatively.Twenty-six patients (31%) had coexisting tibial and talar OCLs, with 9 (35%) identified as kissing lesions. Age correlated with coexisting lesion incidence, as older patients were more likely to have a coexisting tibial OCL (P = .038). More than half of talar OCLs were found in zone 4 (61%), whereas the majority of tibial OCLs were located in zones 2, 4, and 5 (19% each). Patients with coexisting lesions were more likely to have a lateral talar OCL (P = .028), while those without a coexisting tibial lesion were more likely to have a talar OCL in zone 4 (P = .016). There was no difference in FAOS result or lesion size between patients with and without coexisting OCLs, but patients with coexisting lesions were more likely to have an ICRS grade 4 talar OCL (P = .034). For patients with coexisting lesions, kissing lesions were more likely to be located in zone 6 (P = .043). There was no difference in OCL size or containment between kissing and nonkissing coexisting OCLs.The incidence of coexisting talar and tibial OCLs may be more prevalent than what previous reports have suggested, with older patients being more likely to present with this pathology. The location of a talar OCL correlates with the incidence of a coexisting tibial OCL.
The phenomenon of intercellular mitochondrial transfer from mesenchymal stromal cells (MSCs) has shown promise for improving tissue healing after injury and has potential for treating degenerative diseases like osteoarthritis (OA). Recently MSC to chondrocyte mitochondrial transfer has been documented, but the mechanism of transfer is unknown. Full-length connexin 43 (Cx43, encoded by GJA1) and the truncated, internally translated isoform GJA1-20k have been implicated in mitochondrial transfer between highly oxidative cells, but have not been explored in orthopaedic tissues. Here, our goal was to investigate the role of Cx43 in MSC to chondrocyte mitochondrial transfer. In this study, we tested the hypotheses that (a) mitochondrial transfer from MSCs to chondrocytes is increased when chondrocytes are under oxidative stress and (b) MSC Cx43 expression mediates mitochondrial transfer to chondrocytes. Oxidative stress was induced in immortalized human chondrocytes using tert-Butyl hydroperoxide (t-BHP) and cells were evaluated for mitochondrial membrane depolarization and reactive oxygen species (ROS) production. Human bone-marrow derived MSCs were transduced for mitochondrial fluorescence using lentiviral vectors. MSC Cx43 expression was knocked down using siRNA or overexpressed (GJA1 + and GJA1-20k+) using lentiviral transduction. Chondrocytes and MSCs were co-cultured for 24 h in direct contact or separated using transwells. Mitochondrial transfer was quantified using flow cytometry. Co-cultures were fixed and stained for actin and Cx43 to visualize cell-cell interactions during transfer. Mitochondrial transfer was significantly higher in t-BHP-stressed chondrocytes. Contact co-cultures had significantly higher mitochondrial transfer compared to transwell co-cultures. Confocal images showed direct cell contacts between MSCs and chondrocytes where Cx43 staining was enriched at the terminal ends of actin cellular extensions containing mitochondria in MSCs. MSC Cx43 expression was associated with the magnitude of mitochondrial transfer to chondrocytes; knocking down Cx43 significantly decreased transfer while Cx43 overexpression significantly increased transfer. Interestingly, GJA1-20k expression was highly correlated with incidence of mitochondrial transfer from MSCs to chondrocytes. Overexpression of GJA1-20k in MSCs increases mitochondrial transfer to chondrocytes, highlighting GJA1-20k as a potential target for promoting mitochondrial transfer from MSCs as a regenerative therapy for cartilage tissue repair in OA.
