Aims. Unicompartmental and total knee arthroplasty (UKA and TKA) are successful treatments for osteoarthritis, but the solid metal implants disrupt the natural distribution of stress and strain which can lead to bone loss over time. This generates problems if the implant needs to be revised. This study investigates whether titanium lattice UKA and TKA implants can maintain natural load transfer in the proximal tibia. Methods. In a cadaveric model, UKA and TKA procedures were performed on eight fresh-frozen knee specimens, using conventional (solid) and titanium lattice tibial implants. Stress at the bone-implant interfaces were measured and compared to the native knee. Results. Titanium lattice implants were able to restore the mechanical environment of the native tibia for both UKA and TKA designs. Maximum stress at the bone-implant interface ranged from 1.2 MPa to 3.3 MPa compared with 1.3 MPa to 2.7 MPa for the native tibia. The conventional solid UKA and TKA implants reduced the maximum stress in the bone by a factor of 10 and caused > 70% of bone surface area to be underloaded compared to the native tibia. Conclusion. Titanium lattice implants maintained the natural mechanical loading in the proximal tibia after UKA and TKA, but conventional solid implants did not. This is an exciting first step towards implants that maintain bone health, but such implants also have to meet fatigue and micromotion criteria to be clinically viable. Cite this article: Bone Joint Res 2022;11(2):91–101

Introduction. Initial post-operative implant instability leads to impaired osseointegration, one of the most common reasons for aseptic loosening and revision surgery. In this study, we developed a novel murine model of implant instability and demonstrated the anabolic effect of immediate and delayed intermittent Parathyroid Hormone (iPTH) treatment in the setting of instability-induced osseointegration failure. Methods. 3D-printed titanium implants were inserted in an oversized drill-hole in the tibia of C57Bl/6 mice (n=54). After implantation, the mice were randomly divided in 3 treatment groups (control: PBS-vehicle; iPTH; delayed iPTH). Radiographic analysis was performed to confirm signs of implant loosening. Peri-implant tissue formation was assessed through histology. Osseointegration was assessed through µCT and biomechanical pullout testing. Results. Immediate iPTH treatment reduced radiolucencies and induced a distinct pedestal sign distal to the implant stem (white arrow Fig 1A). The PBS treated mice had fibrous tissue implant encapsulation, whereas new mineralized tissue and no fibrous tissue was observed with immediate iPTH treatment (Fig 1E). Delayed iPTH treatment was also able to exhibit significant peri-implant bone mineralization, osteoblasts, angiogenesis, and a reduction of fibrous tissue (Fig 2A-B). iPTH treatment increased the force required to pull out the implant significantly from 8.41 ± 8.15N in the PBS group to 21.49 ± 10.45N and 23.68 ± 8.99N, in the immediate and delayed iPTH treatment groups, respectively (Fig 2D). PBS vehicle resulted in a bone volume/trabecular volume (BV/TV) of 0.23 ± 0.03, while immediate and delayed iPTH treatment increased BV/TV significantly to 0.46 ± 0.07 and 0.34 ± 0.10, respectively (Fig 2E). Conclusion. Immediate iPTH treatment prevents peri-implant fibrous tissue formation and enhances peri-implant bone formation in our murine model of mechanical instability. Delayed iPTH treatment was able to resolve the peri-implant fibrous tissue and stimulate bone formation. This study potentially addresses a leading cause of aseptic loosening by demonstrating that initial implant instability can be rescued by iPTH even with delayed start of treatment. For any figures or tables, please contact authors directly

Introduction. Uncemented highly porous titanium implants have been shown to promote osseointegration, and may result in a durable construct for total knee arthroplasty (TKA). Given the mixed results of uncemented TKA, it is important to evaluate the early stability for this product. The objective of the following study was to use radiostereometric analysis (RSA) to assess early fixation of a highly porous tibial baseplate and metal backed patella. Methods. Twenty-seven patients (mean age 64 years, 30% female) undergoing primary TKA consented to participate in this prospective cohort study. All patients received a highly porous tibial baseplate, a metal backed patella and tantalum RSA bone markers. Implant migration was assessed using model-based RSA at 1.5, 3, 6, 12 and 24 months post-operative. Patient reported outcome measures were captured using the same follow-up schedule, and compared to pre-operative measures. Results. There were no adverse events affecting implant fixation, and no revisions. Patient function significantly improved by 3 months post-operation (p < 0.001). The highest rate of tibia and patellar component migration occurred over the first six post-operative weeks, with minimal migration thereafter. Mean maximum total point motion (MTPM) at 24 months was 0.72 (SD 0.34) mm for the tibia, and 0.44 (SD 0.25) mm for the patella. Three tibia baseplates migrated more than 1 standard deviation greater than the mean at 24 months, and also had continuous migration (> 0.2mm of MTPM) in the second post-operative year. One patellar component showed a rapid rate of migration between 6 and 24 months, whereas all other patellar components appeared to stabilize. Conclusions. Osseointegration appears to occur on the highly porous implant surface of the tibia baseplate and metal backed patella, as evidenced by implant stability. Further follow-up is required to determine if clinical loosening will manifest in the continuously migrating implants

Introduction. Poor osseointegration of cementless implants is the leading clinical cause of implant loosening, subsidence, and replacement failure, which require costly and technically challenging revision surgery. The mechanism of osseointegration requires further elucidation. We have recently developed a novel titanium implant for the mouse tibia that maintains in vivo knee joint function and allows us to study osseointegration in an intra-articular, load-bearing environment. Vascular endothelial growth factor (VEGF) is one of the most important growth factors for regulation of vascular development and angiogenesis. It also plays critical roles in skeletal development and bone repair and regeneration. A specialized subset of vascular endothelium, CD31. hi. EMCN. hi. cells displaying high cell surface expression of CD31 and Endomucin, has been reported to promote osteoblast maturation and may be responsible for bone formation during development and fracture healing. Because of their potential role in osseointegration, the aim of this study was to use our mouse implant model to investigate the role of VEGF and CD31. hi. EMCN. hi. endothelium in osseointegration. Methods. Under an IACUC-approved protocol, the implant was inserted into the right tibia of 16-week-old female C57BL/6 mice (N = 38). The mice were then randomized into 2 groups: Control group (N=19) and Anti-VEGFR group (N=19). A cocktail of VEGFR-1 antibody (25mg/kg) and VEGFR-2 antibody (25mg/kg) was given to the mice in the Anti-VEGFR group by intraperitoneal injection every third day starting immediately after surgery until euthanasia. An equivalent amount of an isotype control antibody was given to the control group. Flow cytometric (N = 4/group) and immunofluorescencent (N = 3/group) analyses were performed at 2 weeks post-implantation to detect the distribution and density of CD31. hi. EMCN. hi. endothelium in the peri-implant bone. Pull-out testing was used at 4 weeks post-implantation to determine the strength of the bone-implant interface. Results. Flow cytometry revealed that Anti-VEGFR treatment decreased CD31. hi. EMCN. hi. vascular endothelium percentage in the peri-implant bone vs. control (p = 0.039) at 2 weeks post-implantation (Fig. 1). This was confirmed by the decrease of CD31 and EMCN double positive cells detected with immunofluorescence at the same time point (Fig. 2). More importantly, anti-VEGFR treatment decreased the maximum load of pullout testing compared with control (p = 0.042) (Fig. 3). Conclusion. VEGF is a key mediator of osseointegration and the development of CD31. hi. EMCN. hi. endothelium. This may provide a new drug target for the enhancement of osseointegration. We have also developed a system to run flow cytometric analysis and perform fluorescent staining on the limited tissue around the implant in this mouse model. This will be a powerful platform for future mechanistic studies on osseointegration. For any figures or tables, please contact authors directly

Aims

It is increasingly appreciated that coordinated regulation of angiogenesis and osteogenesis is needed for bone formation. How this regulation is achieved during peri-implant bone healing, such as osseointegration, is largely unclear. This study examined the relationship between angiogenesis and osteogenesis in a unique model of osseointegration of a mouse tibial implant by pharmacologically blocking the vascular endothelial growth factor (VEGF) pathway.

Aims

The aim of this study was to compare the ability of tantalum, 3D porous titanium, antibiotic-loaded bone cement, and smooth titanium alloy to inhibit staphylococci in an in vitro environment, based on the evaluation of the zone of inhibition (ZOI). The hypothesis was that there would be no significant difference in the inhibition of methicillin-sensitive or methicillin-resistant Staphylococcus aureus (MSSA/MRSA) between the two groups.