Bone stress injury: PATHOPHYSIOLOGY

A bone stress injury (BSI) represents the inability of bone to withstand repetitive mechanical loading, which results in structural fatigue and localised bone pain and tenderness. It occurs along a pathology continuum beginning with a stress reaction, which can progress to a stress fracture and ultimately a complete bone fracture.

BSIs result from an imbalance between the formation and removal of load-induced damage. Bones deform in response to loading, with the amount of deformation (expressed in terms of strain) depending on the magnitude of load applied and the ability of the bone to resist deformation. Whilst the safety factor between exercise-induced strains and those required for complete bone fracture is large, exercise-induced strains can generate microscopic damage (termed 'microdamage'.) THe threshold for microdamage formation depends on the interaction between the number of bone loading/strain cycles, the load/strain magnitude and the speed at which the load/strain is introduced (strain rate.)

Microdamage acts as a stimulus for targeted remodelling. This involves activation of remodelling units consisting of advancing front-of-bone-resorbing osteoclasts which remove the damage, followed by rows of bone-forming osteoblasts which deposit layers of new bone. Targeted remodelling maintains homeostasis between damage formation and its removal to preserve bone mechanical properties and enable a bone to adapt over time to meet changing demands. This adaptation decreases bone strain for a given load, which means greater loads can be tolerated before the threshold for microdamage formation is surpassed.

Remodelling normally removes damage approximately as fast as it occurs and a reserve exists where additional remodelling units can be activated in response to increased microdamage formation. This means that changes in load are usually well tolerated. However, remodelling is time-dependent and, if insufficient time is given to adapt to a new mechanical stimulus, progressively more damage may form as a result of feedforward between remodelling and damage formation. Feedforward results from resorption preceding formation in remodelling so that an increase in the number of active remodelling units locally reduces bone mass and the energy absorbing capacity of the bone. This potentiates further damage formation.

Accumulating microdamage may combine to initiate the BSI pathology continuum, which includes stress reactions, stress fractures and ultimately complete fracture. Stress reactions are characterised by increased bone turnover associated with periosteal and/or marrow oedema, whereas stress fractures have the addition of a discernible fracture line.

REFERENCES

Brukner, P., 2012. Brukner & Khan's clinical sports medicine. North Ryde: McGraw-Hill.