Application of Numerical Methods in Design and Analysis of Orthopedic Implant Integrity

In this paper a numerical analysis of hip implant model and hip implant model with a crack in a biomaterial is presented. Hip implants still exhibit problem of premature failure, promoting their integrity and life at the top of the list of problems to be solved in near future. Any damage due to wear or corrosion is ideal location for crack initiation and further fatigue growth. Therefore, this paper is focused on integrity of hip implants with an aim to improve their performance and reliability. Numerical models are based on the finite element method (FEM), including the extended FEM (X-FEM). FEM became a powerful and reliable numerical tool for analysis of structures subjected to different types of load in cases where solving of these problems was too complex for exclusively analytical methods. FEM is a method based on discretization of complex geometrical domains into much smaller and simpler ones, wherein field variables can be interpolated using shape functions. Numerical analysis was performed on three-dimensional models, to investigate mechanical behaviour of a hip implant at acting forces from 3.5 to 6.0 kN. Short theoretical background on the stress intensity factors computation is presented. Results presented in this paper indicate that acting forces can lead to implant failure due to stress field changes. For the simulation of crack propagation extended finite element method (XFEM) was used as one of the most advanced modelling techniques for this type of problem

Nitric oxide signaling in mechanical adaptation of bone

One of the most serious healthcare problems in the world is bone loss and fractures due to a lack of physical activity in elderly people as well as in bedridden patients or otherwise inactive youth. Crucial here are the osteocytes. Buried within our bones, these cells are believed to be the mechanosensors that stimulate bone formation in the presence of mechanical stimuli and bone resorption in the absence of such stimuli. Intercellular signaling is an important physiological phenomenon involved in maintaining homeostasis in all tissues. In bone, intercellular communication via chemical signals like NO plays a critical role in the dynamic process of bone remodeling. If bones are mechanically loaded, fluid flows through minute channels in the bone matrix, resulting in shear stress on the cell membrane that activates the osteocyte. Activated osteocytes produce signaling molecules like NO, which modulate the activity of the bone-forming osteoblasts and the bone-resorbing osteoclasts, thereby orchestrating bone adaptation to mechanical loading. In this review, we highlight current insights in the role of NO in the mechanical adaptation of bone mass and structure, with emphasis on its role in local bone gain and loss as well as in remodeling supervised by osteocytes. Since mechanical stimuli and NO production enhance bone strength and fracture resistance, these new insights may facilitate the development of novel osteoporosis treatments

Functional adaptation of bone: The mechanostat and beyond

The conceptual model of the mechanostat proposed by Harold Frost in 1983 is among the most significant contributions to musculoskeletal research today. This model states that bone and other musculoskeletal tissues including cartilage, tendon and muscle respond to habitual exercise/loading and that changes in the loading environment lead to adequate structural adaptation of (bone) tissue architecture. The analogy with a thermostat clearly indicates presence of a physiological feedback system which is able to adjust bone mass and structure according to the engendered loads. In the bioengineering community, the mechanostat has been mathematically formulated as a feedback algorithm using a set point criterion based on a particular mechanical quantity such as strain, strain energy density among others. As pointed out by Lanyon and Skerry, while it is widely thought that in a single individual, there exists a single mechanostat set point, this view is flawed by the fact that different bones throughout the skeleton require a specific strain magnitude to maintain bone mass. Consequently, different bones respond differently to increases or decreases in loading depending on the sensitivity of the mechanostat. Osteocytes, i.e., cells embedded in the bone matrix are believed to be the major bone cells involved in sensing and transduction of mechanical loads. The purpose of this chapter is to review the concept of the mechanostat and its role in bone pathophysiology. To do this we provide examples of why and how the skeleton responds to complex loading stimuli made up of numerous different parameters including strain magnitude, frequency and rest intervals among others. We describe latest in vivo and ex vivo loading models, which allow exploration of various mechanobiological relations in the mechanostat model utilising controlled mechanical environments. A review of the bone cells and signalling transduction cascades involved in mechanosensation and bone adaptation will also be provided. Furthermore, we will discuss the mechanostat in a clinical context, e.g., how factors such as sex, age, genetic constitution, concomitant disease, nutrient availability, and exposure to drugs all affect bone’s response to mechanical loading. Understanding the mechanostat and mechanobiological regulatory factors involved in mechanosensation and desensitisation is essential for our ability to control bone mass based on physiological loading, either directly through different exercise regimens, or by manipulating bone cells in a targeted manner using tailored site and individual specific stimuli including pharmaceuticals