Biomechanics of implants.

For simple constructions a mechanical analysis to determine internal stresses and deformation is possible using theoretical formulas. However, for complex constructions, like joint prostheses, this is not possible. Numerical simulation of internal stresses and deformations offers a solution for these constructions. The so-called Finite Element Analysis divides the complex structure in simple ones (elements), applies the mechanical formulas and adds the effect on each element to predict the behaviour of the complex contruction.

I.5. Biomechanics of implants.

For simple constructions a mechanical analysis to determine internal stresses and deformation is possible using theoretical formulas. However, for complex constructions, like joint prostheses, this is not possible. Numerical simulation of internal stresses and deformations offers a solution for these constructions. The so-called Finite Element Analysis divides the complex structure in simple ones (elements), applies the mechanical formulas and adds the effect on each element to predict the behaviour of the complex construction.

Microdamage detection and repair in bone: fracture mechanics, histology, cell biology.

Bone is an elementary component in the human skeleton. It protects vital organs, regulates calcium levels and allows mobility. As a result of daily activities, bones are cyclically strained causing microdamage. This damage, in the form of numerous microcracks, can cause bones to fracture and therefore poses a threat to mechanical integrity. Bone is able to repair the microcracks through a process called remodelling which is tightly regulated by bone forming and resorbing cells. However, the manner by which microcracks are detected, and repair initiated, has not been elucidated until now. Here we show that microcrack accumulation causes damage to the network of cellular processes, resulting in the release of RANKL which stimulates the differentiation of cells specialising in repair.

Living with cracks: damage and repair in human bone.

Our bones are full of cracks, which form and grow as a result of daily loading activities. Bone is the major structural material in our bodies. Although weaker than many engineering materials, it has one trick that keeps it ahead - it can repair itself. Small cracks, which grow under cyclic stresses by the mechanism of fatigue, can be detected and removed before they become long enough to be dangerous. This article reviews the work that has been done to understand how cracks form and grow in bone, and how they can be detected and repaired in a timely manner. This is truly an interdisciplinary research field, requiring the close cooperation of materials scientists, biologists and engineers.

The role of osteocytes and bone microstructure in preventing osteoporotic fractures.

The skeleton alters its geometry following trauma, the introduction of artificial defects and of fatigue-induced microcracks. The precise mechanism by which the skeleton adapts remains unclear. Microcracks might directly affect the cell by damaging the osteocyte cell network or causing apoptosis. Bone microstructure may play an important role in these processes by diverting and arresting propagating microcracks and so prevent fracture failure. This paper discusses the effects of microstructure on propagating cracks, how microdamage may act as a stimulus for bone adaptation and its potential effects on bone biochemistry.

Dynamic short crack growth in cortical bone.

It is well known for almost half a century that bones contain microcracks. Very little is known about the crack growth behaviour of very small cracks, e.g. the stage before they become macroscopically long. The aim of this work was to investigate the dynamic crack growth behaviour of sub-millimetre microcracks in cortical bone. It was found that slow stable crack growth occurs in specimens subjected to static loading conditions. Crack growth direction was dominated by the local fibre orientation of the bones. Crack angles varied between 10 and 36 degrees of the long axis of the bone. Short cracks were found to show periods of rapid growth followed by intervals of temporary crack arrest. Histological analysis showed that crack arrest occurred due to vascular canals in the bone. During these periods of crack arrest, crack opening displacements increased until the local strain was sufficient to overcome these features. These observations indicate a mechanism for growth of small cracks in bone at constant stress, involving microstructural barriers, time-dependent deformation of material near the crack tip and strain-controlled propagation.

Microdamage: a cell transducing mechanism based on ruptured osteocyte processes.

As a result of underlying pathological diseases, such as osteoporosis, osteopenia, or due to altered loading after joint replacements, bones become more susceptible to microdamage accumulation than those of normal human beings, as are those of athletes who undertake strenuous exercise [Stromsoe, 2004. Fracture fixation problems in osteoporosis. Injury 35, 107-113]. Experimental evidence has linked bone adaptation to microdamage, and to increased cell activity. In this work, we investigated whether microcrack detection is related to rupturing of the cellular material itself due to crack face displacements. Using specific cell staining techniques, it was confirmed that relative crack displacements are capable of tearing cell processes between neighbouring osteocytes. No ruptured cell processes were found near the crack tip where the displacements are less. Rupturing of cell processes due to crack opening and shear displacement is a feasible new mechanism by which bone can detect and estimate the size of a microcrack. Ruptured cell processes may directly secrete passive and active components in the extracellular matrix, triggering a repair response.

The behaviour of microcracks in compact bone.

This paper summarises four separate studies carried out by our group over the past number of years in the area of bone microdamage. The first study investigated the manner by which microcracks accumulate and interact with bone microstructure during fatigue testing of compact bone specimens. In a series of fatigue tests carried out at four different stress ranges between 50 and 80 MPA, crack density increased with loading cycles at a rate determined by the applied stress. Variations in the patterns of microdamage accumulation suggest that that at low stress levels, larger amounts of damage can build up without failure occurring. In a second study using a series of four-pont bending tests carried out on ovine bone samples, it was shown that bone microstructure influenced the ability of microcracks to propagate, with secondary osteons acting as barriers to crack growth. In a third study, the manner by which crack growth disrupts the canalicular processes connecting osteocytes was investigated. Analysis of individual cracks showed that disruption of the canalicular processes connecting osteocytes occurred due to shear displacement at the face of propagating microcracks, suggesting that this may play some role in the mechanism that signals bone remodelling. In a fourth in vivo study, it was shown that altering the mechanical load applied to the long bones of growing rats causes microcrack formation. In vivo microdamage was present in rats subjected to hindlimb suspension with a higher microcrack density found in the humeri than the femora. Microdamage was also found in control animals. This is the first study to demonstrate in vivo microcracks in normally loaded bones in a rat model.

The influence of cyclic loading on gentamicin release from acrylic bone cements.

Antibiotic-loaded acrylic bone cement is widely used in total joint replacement to reduce infections. Walking results in cyclic loading, which has been suggested to stimulate antibiotic release. The goal of this study is to compare antibiotic release from cyclically loaded bone cement with the release from unloaded bone cement. Two models of the frontal aspect of a femoral stem were cemented with CMW 1 Radiopaque G, Palacos R-G and Palamed G. Both were immersed in water, and the gentamicin concentration in the water was monitored. One model was cyclically loaded at 5 Hz during immersion achieving physiological stresses in the bone cement mantle. After 10.8 x 10(6) cycles, initial release of gentamicin from Palamed G was increased significantly for loaded over unloaded, but not from CMW 1 Radiopaque G and Palacos R-G.