Truss implant technology™ for interbody fusion in spinal degenerative disorders: profile of advanced structural design, mechanobiologic and performance characteristics.

Introduction: Interbody fusion devices are customarily used in fusion of the anterior spinal column for treatment of degenerative disc disease. Their traditional role is to reestablish and maintain intervertebral disc height, contain bone graft and provide mechanical support for the spine while osseointegration takes place. Utilizing the principles of mechanobiology, a unique biokinetic interbody fusion device has been developed that employs an advanced structural design to facilitate and actively participate in the fusion consolidation process.Areas covered: This article profiles and characterizes 4WEB Medical's Truss Implant Technology™ which includes a range of 3D-printed titanium spinal interbody implants and non-spinal implants whose design is based on truss structures enabled by advances in additive manufacturing. Four main areas of the implant design and functionality are detailed: bio-architecture, mechanobiologic underpinnings, bioactive surface features, and subsidence resistance. Pre-clinical and clinical examples are provided to describe and specify the bioactive roles and contributions of each design feature.Expert opinion: The distinct and unique combination of features incorporated within the truss cage design results in a biokinetic implant that actively participates in the bone healing cascade and fusion process.

Strains in trussed spine interbody fusion implants are modulated by load and design.

Titanium cages with 3-D printed trussed open-space architectures may provide an opportunity to deliver targeted mechanical behavior in spine interbody fusion devices. The ability to control mechanical strain, at levels known to stimulate an osteogenic response, to the fusion site could lead to development of optimized therapeutic implants that improve clinical outcomes. In this study, cages of varying design (1.00 mm or 0.75 mm diameter struts) were mechanically characterized and compared for multiple compressive load magnitudes in order to determine what impact certain design variables had on localized strain. Each cage was instrumented with small fiducial sphere markers (88 total) at each strut vertex of the truss structure, which comprised of 260 individual struts. Cages were subjected to a 50 N control, 1000 N, or 2000 N compressive load between contoured loading platens in a simulated vertebral fusion condition, during which the cages were imaged using high-resolution micro-CT. The cage was analyzed as a mechanical truss structure, with each strut defined as the connection of two vertex fiducials. The deformation and strain of each strut was determined from 50 N control to 1000 N or 2000 N load by tracking the change in distance between each fiducial marker. As in a truss system, the number of struts in tension (positive strain) and compression (negative strain) were roughly equal, with increased loads resulting in a widened distribution (SD) compared with that at 50 N tare load indicating increased strain magnitudes. Strain distribution increased from 1000 N (+156 ± 415 µÎµ) to 2000 N (+180 ± 605 µÎµ) in 1.00 mm cages, which was similar to 0.75 mm cages (+132 ± 622 µÎµ) at 1000 N load. Strain amplitudes increased 42%, from 346µÎµ at 1000 N to 492µÎµ at 2000 N, for 1.00 mm cages. At 1000 N, strain amplitude in 0.75 mm cages (481µÎµ) was higher by 39% than that in 1.00 mm cages. These amplitudes corresponded to the mechanobiological range of bone homeostasis+formation, with 63 ± 2% (p < .05 vs other groups), 72 ± 3%, and 73 ± 1% of struts within that range for 1.00 mm at 1000 N, 1.00 mm at 2000 N, and 0.75 mm at 1000 N, respectively. The effective compressive modulus for both cage designs was also dependent on strut diameter, with modulus decreasing from 12.1 ± 2.3 GPa (1.25 mm) to 9.2 ± 7.5 GPa (1.00 mm) and 3.8 ± 0.6 GPa (0.75 mm). This study extended past micro-scale mechanical characterization of trussed cages to compare the effects of design on cage mechanical behavior at moderate (1000 N) and strenuous (2000 N) load levels. The findings suggest that future cage designs may be modulated to target desired mechanical strain regimes at physiological loads.

Ex vivo loading of trussed implants for spine fusion induces heterogeneous strains consistent with homeostatic bone mechanobiology.

A truss structure was recently introduced as an interbody fusion cage. As a truss system, some of the connected elements may be in a state of compression and others in tension. This study aimed to quantify both the mean and variance of strut strains in such an implant when loaded in a simulated fusion condition with vertebral body or contoured plastic loading platens ex vivo. Cages were each instrumented with 78 fiducial spheres, loaded between platens (vertebral body or contoured plastic), imaged using high resolution micro-CT, and analyzed for deformation and strain of each of the 221 struts. With repeated loading of a cage by vertebral platens, the distribution (variance, indicated by SD) of strut strains widened from 50N control (4±114µÎµ, mean±SD) to 1000N (-23±273µÎµ) and 2000N (-48±414µÎµ), and between 1000N and 2000N. With similar loading of multiple cages, the strain distribution at 2000N (23±389µÎµ) increased from 50N control. With repeated loading by contoured plastic platens, induced strains at 2000N had a distribution similar to that induced by vertebral platens (84±426µÎµ). In all studies, cages exhibited increases in strut strain amplitude when loaded from 50N to 1000N or 2000N. Correspondingly, at 2000N, 59-64% of struts exhibited strain amplitudes consistent with mechanobiologically-regulated bone homeostasis. At 2000N, vertically-oriented struts exhibited deformation of -2.87±2.04µm and strain of -199±133µÎµ, indicating overall cage compression. Thus, using an ex vivo 3-D experimental biomechanical analysis method, a truss implant can have strains induced by physiological loading that are heterogeneous and of amplitudes consistent with mechanobiological bone homeostasis.