A bone remodelling model coupling micro-damage growth and repair by 3D BMU-activity.

Bone as most of living tissues is able, during its entire lifetime, to adapt its internal microstructure and subsequently its associated mechanical properties to its specific mechanical and physiological environment in a process commonly known as bone remodelling. Bone is therefore continuously renewed and micro-damage, accumulated by fatigue or creep, is removed minimizing the risk of fracture. Nevertheless, bone is not always able to repair itself completely. Actually, if bone repairing function is slower than micro-damage accumulation, a type of bone fracture, usually known as "stress fracture", can finally evolve. In this paper, we propose a bone remodelling continuous model able to simulate micro-damage growth and repair in a coupled way and able therefore to predict the occurrence of "stress fractures". The biological bone remodelling process is modelled in terms of equations that describe the activity of basic multicellular units. The predicted results show a good correspondence with experimental and clinical data. For example, in disuse, bone porosity increases until an equilibrium situation is achieved. In overloading, bone porosity decreases unless the damage rate is so high that causes resorption or "stress fracture".

DISCUSSION OF MECHANISMS OF ACCELERATED AND RETARDED FATIGUE CRACK GROWTH.

The relevance of the effective stress intensity range to crack growth is considered for constant and for variable amplitude loading. The accelerated and retarded growth associated with simple programmed loadings is reported for two steels and an aluminium alloy. The load interaction effects are due to several competing mechanisms, and not due to the single, popular mechanism of crack closure.