Computation of physiological loading induced interstitial fluid motion in muscle standardized femur: Healthy vs. osteoporotic bone.

BACKGROUND AND OBJECTIVES: Physiological loading-induced mechanical environments regulate bone modeling and remodeling. Thus, loading-induced normal strain is typically considered a stimulus to osteogenesis. However, several studies noticed new bone formation near the sites of minimal normal strain, e.g., the neutral axis of bending in long bones, which raises a question on how bone mass is maintained near these sites. Secondary mechanical components such as shear strain and interstitial fluid flow also stimulate bone cells and regulate bone mass. However, the osteogenic potential of these components is not well established. Accordingly, the present study estimates the distribution of physiological muscle loading-induced mechanical environments such as normal strain, shear strain, pore pressure, and interstitial fluid flow in long bones. METHODS: A poroelastic finite element muscle standardized femur (MuscleSF) model is developed to compute the distribution of the mechanical environment as a function of bone porosities associated with osteoporotic and disuse bone loss. RESULTS: The results indicate the presence of higher shear strain and interstitial fluid motion near the minimal strain sites, i.e., the neutral axis of bending of femoral cross-sections. This suggests that secondary stimuli may maintain the bone mass at these locations. Pore pressure and interstitial fluid motion reduce with the increased porosity associated with bone disorders, possibly resulting in diminished skeletal mechano-sensitivity to exogenous loading. CONCLUSIONS: These outcomes present a better understanding of mechanical environment-mediated regulation of site-specific bone mass, which can be beneficial in developing prophylactic exercise to prevent bone loss in osteoporosis and muscle disuse.

Physiological Loading-Induced Interstitial Fluid Dynamics in Osteon of Osteogenesis Imperfecta Bone.

Osteogenesis imperfecta (OI), also known as "brittle bone disease," is a genetic bone disorder. OI bones experience frequent fractures. Surgical procedures are usually followed by clinicians in the management of OI. It has been observed physical activity is equally beneficial in reducing OI bone fractures in both children and adults as mechanical stimulation improves bone mass and strength. Loading-induced mechanical strain and interstitial fluid flow stimulate bone remodeling activities. Several studies have characterized strain environment in OI bones, whereas very few studies attempted to characterize the interstitial fluid flow. OI significantly affects bone micro-architecture. Thus, this study anticipates that canalicular fluid flow reduces in OI bone in comparison to the healthy bone in response to physiological loading due to altered poromechanical properties. This work attempts to understand the canalicular fluid distribution in single osteon models of OI and healthy bone. A poromechanical model of osteon is developed to compute pore-pressure and interstitial fluid flow as a function of gait loading pattern reported for OI and healthy subjects. Fluid distribution patterns are compared at different time-points of the stance phase of the gait cycle. It is observed that fluid flow significantly reduces in OI bone. Additionally, flow is more static than dynamic in OI osteon in comparison to healthy subjects. This work attempts to identify the plausible explanation behind the diminished mechanotransduction capability of OI bone. This work may further be extended for designing better biomechanical therapies to enhance the fluid flow in order to improve osteogenic activities in OI bone.

Kinetic and Kinematic Analysis of Gait in Type IV Osteogenesis Imperfecta Patients: A Comparative Study.

BACKGROUND: Osteogenesis imperfecta (OI) is a genetic connective tissue disorder characterized by skeletal deformity and increased risk of fracture. Independent mobility is of concern for OI patients as it is associated with the quality of life. The present study investigates the variation of kinetic and kinematic gait parameters of type IV OI subjects and compares them with age-matched healthy subjects. MATERIALS AND METHODS: Gait analysis is performed on five type IV OI patients and six age-matched normal subjects. Spatiotemporal, kinematic, and kinetic data are obtained using Helen Hayes marker placement protocol. RESULTS: The results indicate an imprecise double-humped profile for vertical ground reaction force (GRF) with reduced ankle push off power and walking speed for OI subjects. Moreover, a comparison of vertical GRFs in OI subjects with that of healthy subjects suggests lower values for the former. The results encourage and motivate for further investigation with a bigger set of subjects. CONCLUSION: This information may be useful in developing a better understanding of pathological gait in type IV OI subjects, which ultimately helps the design of subject-specific implants, surgical preplanning, and rehabilitation.

In silico modeling of bone adaptation to rest-inserted loading: Strain energy density versus fluid flow as stimulus.

In vivo studies suggest that cyclic and low-magnitude loading can be useful over pharmaceutical drugs in normalizing bone loss as it encourages osteogenesis (i.e. new bone formation) at the sites of elevated strain magnitude. In silico models assumed normal strain or strain energy density (SED) as the stimulus to predict loading-induced osteogenesis, however, these models may have limited success in fitting the in vivo new bone formation at several instances. For example, rest-inserted cyclic loading amplifies the new bone formation as compared to continuous-cyclic loading even though similar strain magnitude were induced in both the cases. It is also believed that loading-induced interstitial fluid flow can also be a potential stimulus of osteogenesis. The present study hypothesizes that fluid motion as osteogenic stimulus may explain the afore-mentioned anomalies. Accordingly, this work studies osteogenesis as functions of SED and canalicular fluid motion using an in silico model. Therefore, the new bone formation is considered roughly proportional to stimuli above their osteogenic thresholds. This model attempts to simulate in vivo new bone formation noticed in rest-inserted cantilever loading studies. The model's prediction of site-specific new bone formation improves when fluid flow is considered as the stimulus. It is also noticed that fluid motion as the stimulus closely fits the new bone formation for another in vivo study where the effects of aging on osteogenesis were examined. These attempts to establish fluid flow as a potential osteogenic stimulus can be useful in the prediction of site-specific new bone formation. The findings will ultimately be useful in designing biomechanical interventions such as prophylactic exercises to cure bone loss.