Journal of Biomechanical Engineering-Transactions of the Asme最新文献

Collagen XI is ubiquitous in tissues such as joint cartilage, cancellous bone, muscles, and tendons and is an important contributor during a crucial part in fibrillogenesis. The COL11A1 gene encodes one of three alpha chains of collagen XI. The present study elucidates the role of collagen XI in the establishment of mechanical properties of tendons and ligaments. We investigated the mechanical response of three tendons and one ligament tissues from wild type and a targeted mouse model null for collagen XI: Achilles tendon (ACH), the flexor digitorum longus tendon (FDL), the supraspinatus tendon (SST), and the anterior cruciate ligament (ACL). Area was substantially lower in Col11a1ΔTen/ΔTen ACH, FDL, and SST. Maximum load and maximum stress were significantly lower in Col11a1ΔTen/ΔTen ACH and FDL. Stiffness was lower in Col11a1ΔTen/ΔTen ACH, FDL, and SST. Modulus was reduced in Col11a1ΔTen/ΔTen FDL and SST (both insertion site and midsubstance). Collagen fiber distributions were more aligned under load in both wild type group and Col11a1ΔTen/ΔTen groups. Results also revealed that the effect of collagen XI knockout on collagen fiber realignment is tendon-dependent and location-dependent (insertion versus midsubstance). In summary, this study clearly shows that the regulatory role of collagen XI on tendon and ligament is tissue specific and that joint hypermobility in type II Stickler's Syndrome may in part be due to suboptimal mechanical response of the soft tissues surrounding joints.

Background: Cigarette smoking adversely affects fracture repair, causing delayed healing or nonunion rates twice those seen in nonsmokers.

Purpose: We sought to investigate if cigarette smoke differentially affects intramembranous and endochondral healing of fractures. We hypothesize that healing via endochondral ossification will be preferentially impaired compared to intramembranous ossification.

Methods: We utilized a bilateral femur fracture model in Sprague Dawley rats to examine effects of cigarette smoke exposure on healing of femur fractures, treated with either locked intramedullary nail or compression plating to induce endochondral and membranous ossification, respectively. Animals were exposed to tobacco smoke 30 days before and after surgery; evaluations included radiographs, histomorphometry, and micro-CT at 10 days, 1, 3, and 6 months postoperation, and biomechanical testing at 3 and 6 months.

Results: Sixty-eight animals were randomized to control or exposure (two died perioperatively); 89% of femora achieved union when harvested at 3 or 6 months. Smoke exposure delayed cartilaginous callus formation and bone maturation in nailed fractures compared to plated fractures and controls in the same animals. Plated fractures in exposed animals exhibited little cartilage callus and healed like control animals. At 3 months, plated fractures were stiffer and stronger than nailed fractures in both groups. These differences vanished by 6 months.

Conclusions: Plated fractures healed more rapidly and completely than nailed fractures under both control and smoke-exposed conditions.

Clinical relevance: Using compression plating instead of IM nailing for closed long bone fractures may lead to better outcomes in patients who smoke compared to current results with nailing.

Design and analysis are presented for a new device to test the response of endothelial cells to the simultaneous action of cyclic shear stresses and pressure fluctuations. The design consists of four pulsatile-flow chambers connected in series, where shear stress is identical in all four chambers and pressure amplitude decreases in successive chambers. Each flow chamber is bounded above and below by two parallel plates separated by a small gap. The design of the chamber planform must ensure that cells within the testing region experience spatially uniform time-periodic shear stress. For conditions typically encountered in applications, the viscous unsteady flow exhibits order-unity values of the associated Womersley number. The corresponding solution to the unsteady lubrication problem, with general nonsinusoidal flowrate, is formulated in terms of a stream function satisfying Laplace's equation, which can be integrated numerically to determine the spatial distribution of shear stresses for chambers of general planform. The results are used to optimize the design of a device with a hexagonal planform. Accompanying experiments using particle tracking velocimetry (PTV) in a fabricated chamber were conducted to validate theoretical predictions. Pressure readings indicate that intrachamber pressure variations associated with viscous pressure losses and acoustic fluctuations are relatively small, so that all cells in a given testing region experience nearly equal pressure forces.

Functional electrical stimulation (FES) is often used in poststroke gait rehabilitation to address decreased walking speed, foot drop, and decreased forward propulsion. However, not all individuals experience clinically meaningful improvements in gait function with stimulation. Previous research has developed adaptive functional electrical stimulation (AFES) systems that adjust stimulation timing and amplitude at every stride to deliver optimal stimulation. The purpose of this work was to determine the effects of a novel AFES system on functional gait outcomes and compare them to the effects of the existing FES system. Twenty-four individuals with chronic poststroke hemiparesis completed 64-min walking trials on an adaptive and fixed-speed treadmill with no stimulation, stimulation from the existing FES system, and stimulation from the AFES system. There was no significant effect of stimulation condition on walking speed, peak dorsiflexion angle, or peak propulsive force. Walking speed was significantly faster and peak propulsive force was significantly larger on the adaptive treadmill (ATM) than the fixed-speed treadmill (both p < 0.0001). Dorsiflexor stimulation timing was similar between stimulation conditions, but plantarflexor stimulation timing was significantly improved with the AFES system compared to the FES system (p = 0.0059). Variability between and within subjects was substantial, and some subjects experienced clinically meaningful improvements in walking speed, peak dorsiflexion angle, and peak propulsive force. However, not all subjects experienced benefits, suggesting that further research to characterize which subjects exhibit the best instantaneous response to FES is needed to optimize poststroke gait rehabilitation using FES.

Dentin is a biological composite exhibiting multilevel hierarchical structure, which confers excellent damage tolerance to this tissue. Despite the progress in characterization of fracture behavior of dentin, the contribution of composite structure consisting of peritubular dentin (PTD), intertubular dentin (ITD) and tubules to fracture resistance remains elusive. In this study, calculations are carried out for energy release rate associated with crack propagation in the microstructure of dentin. Crack penetration and deflection at the PTD-ITD interface are accounted for in the numerical analyses. It is found that high stiffness of the PTD plays a role in increasing crack driving force, promoting crack growth in the microstructure of dentin. For crack penetration across the PTD-ITD interface, the crack driving force increases with increasing tubule radius; and thick PTD generates amplified crack driving force, thereby leading to weak fracture resistance. The driving force for crack deflection increases with the increase in tubule radius in the case of short cracks, while for long cracks, there is a decrease in driving force with increasing tubule radius. Furthermore, we show that the competition between crack penetration and deflection at the PTD-ITD interface is controlled by the ratio of PTD to ITD elastic modulus, tubule radius and thickness of PTD. High PTD stiffness can increase the propensity of crack deflection. The microstructure of dentin with large tubule radius favors crack deflection and thick PTD is beneficial for crack penetration.

To the best of the author's knowledge, this paper presents the first attempt to develop a mathematical model of the formation and growth of inclusions containing misfolded TATA-box binding protein associated factor 15 (TAF15). It has recently been shown that TAF15 inclusions are involved in approximately 10% of cases of frontotemporal lobar degeneration (FTLD). FTLD is the second most common neurodegenerative disease after Alzheimer's disease (AD). It is characterized by a progressive loss of personality, behavioral changes, and a decline in language skills due to the degeneration of the frontal and anterior temporal lobes. The model simulates TAF15 monomer production, nucleation and autocatalytic growth of free TAF15 aggregates, and their deposition into TAF15 inclusions. The accuracy of the numerical solution of the model equations is validated by comparing it with analytical solutions available for limiting cases. Physiologically relevant parameter values were used to predict TAF15 inclusion growth. It is shown that the growth of TAF15 inclusions is influenced by two opposing mechanisms: the rate at which free TAF15 aggregates are deposited into inclusions and the rate of autocatalytic production of free TAF15 aggregates from monomers. A low deposition rate slows inclusion growth, while a high deposition rate hinders the autocatalytic production of new aggregates, thus also slowing inclusion growth. Consequently, the rate of inclusion growth is maximized at an intermediate deposition rate of free TAF15 aggregates into TAF15 inclusions.

Ascending thoracic aortic aneurysms (aTAAs) can lead to life-threatening dissection and rupture. Recent studies have highlighted aTAA mechanical properties as relevant factors associated with progression. The aim of this study was to quantify in vivo aortic wall stretch in healthy participants and aTAA patients using displacement encoding with stimulated echoes (DENSE) magnetic resonance imaging. Moreover, aTAA wall stretch between surgical and nonsurgical patients was investigated. Finally, DENSE measurements were compared to reference-standard mechanical testing on aTAA specimens from surgical repairs. In total, 18 subjects were recruited, six healthy participants and 12 aTAA patients, for this prospective study. Electrocardiogram-gated DENSE imaging was performed to measure systole-diastole wall stretch, as well as the ratio of aTAA stretch to unaffected descending thoracic aorta stretch. Free-breathing and breath-hold DENSE protocols were used. Uniaxial tensile testing-measured indices were correlated to DENSE measurements in five harvested specimens. in vivo aortic wall stretch was significantly lower in aTAA compared to healthy subjects (1.75±1.44% versus 5.28±1.92%, respectively, P = 0.0004). There was no correlation between stretch and maximum aTAA diameter (P = 0.56). The ratio of aTAA to unaffected thoracic aorta wall stretch was significantly lower in surgical candidates compared to nonsurgical candidates (0.993±0.011 versus 1.017±0.016, respectively, P = 0.0442). Finally, in vivo aTAA wall stretch correlated to wall failure stress and peak modulus of the intima (P = 0.017 and P = 0.034, respectively), while the stretch ratio correlated to whole-wall thickness failure stretch and stress (P = 0.013 and P = 0.040, respectively). Aortic DENSE has the potential to assess differences in aTAA mechanical properties and progressions.

Soft biological tissues often function as highly deformable membranes in vivo and exhibit impressive mechanical behavior effectively characterized by planar biaxial testing. The Generalized Anisotropic Inverse Mechanics (GAIM) method links full-field deformations and boundary forces from mechanical testing to quantify material properties of soft, anisotropic, heterogeneous tissues. In this study, we introduced an orthotropic constraint to GAIM to improve the quality and physical significance of its mechanical characterizations. We evaluated the updated GAIM method using simulated and experimental biaxial testing datasets obtained from soft tissue analogs (PDMS and TissueMend) with well-defined mechanical properties. GAIM produced stiffnesses (first Kelvin moduli, K1) that agreed well with previously published Young's moduli of PDMS samples. It also matched the stiffness moduli determined via uniaxial testing for TissueMend, a collagen-rich patch intended for tendon repair. We then conducted the first biaxial testing of TissueMend and confirmed that the sample was mechanically anisotropic via a relative anisotropy metric produced by GAIM. Next, we demonstrated the benefits of full-field laser micrometry in distinguishing between spatial variations in thickness and stiffness. Finally, we conducted an analysis to verify that results were independent of partitioning scheme. The success of the newly implemented constraints on GAIM suggests notable potential for applying this tool to soft tissues, particularly following the onset of pathologies that induce mechanical and structural heterogeneities.

This study proposes a numerical approach for simulating bone remodeling in lumbar interbody fusion (LIF). It employs a topology optimization method to drive the remodeling process and uses a pixel function to describe the structural topology and bone density distribution. Unlike traditional approaches based on strain energy density or compliance, this study adopts von Mises stress to guide the remodeling of LIF. A novel pixel interpolation scheme associated with stress criteria is applied to the physical properties of the bone, directly addressing the stress shielding effect caused by the implanted cage, which significantly influences the bone remodeling outcome in LIF. Additionally, a boundary inverse approach is utilized to reconstruct a simplified analysis model. To reduce computational cost while maintaining high structural resolution and accuracy, the scaled boundary finite element method (SBFEM) is introduced. The proposed numerical approach successfully generates results that closely resemble human lumbar interbody fusion.

Fatigue failure in biological soft tissues plays a critical role in the etiology of chronic soft tissue injuries and diseases such as osteoarthritis (OA). Understanding failure mechanisms is hindered by the decades-long timescales over which damage takes place. Analyzing the factors contributing to fatigue failure requires the help of validated computational models developed for soft tissues. This study presents a framework for fatigue failure of fibrous biological tissues based on reaction kinetics, where the composition of intact and fatigued material regions can evolve via degradation and breakage over time, in response to energy-based fatigue and damage criteria. Using reactive constrained mixture theory, material region mass fractions are governed by the axiom of mass balance. Progression of fatigue is controlled by an energy-based reaction rate, with user-selected probability functions defining the damage propensity of intact and fatigued material regions. Verification of this reactive theory, which is implemented in the open-source FEBio finite element software, is provided in this study. Validation is also demonstrated against experimental data, showing that predicted damage can be linked to results from biochemical assays. The framework is also applied to study fatigue failure during frictional contact of cartilage. Simulating previous experiments suggests that frictional effects slightly increase fatigue progression, but the main driver is cyclic compressive contact loading. This study demonstrated the ability of theoretical models to complement and extend experimental findings, advancing our understanding of the time progression of fatigue in biological tissues.