Most people are familiar with the concept of structural failure of rigid materials due to repeated application of relatively minor stresses, individually well within the capacity of the material to resist. This phenomenon achieves worldwide notoriety when the aluminium components of aircraft fail in this way. The science of this failure now seems well understood, using concepts of crack propagation, cycles to failure and metal fatigue to describe it. Bone is also a rigid material that is routinely exposed to repeated application of stresses and may fail in an apparently similar fashion. Bone, however, is a living material, capable of growth, repair and remodelling in response to stress, but is also subject to disease and influences on its metabolism that will modulate the consequences of exposure to repeated stresses. The stresses to which bone is exposed will also vary widely, from the activities of daily living through repeated higher stresses, such as the training programme of an athlete, to the single major traumas that cause immediate fracture. Consequently, many terms are used to describe fractures that occur when a single major trauma has not occurred—march fracture, stress fracture, fatigue fracture, insufficiency fracture, incremental fracture, osteoporotic fracture and low-trauma fracture being the most common. Some of these terms are relatively site specific (march fracture in the metatarsal for example), and others imply a particular pathological predisposition (insufficiency fracture in osteoporosis and incremental fracture in Paget’s disease). Some are precipitated by a single episode of trauma not considered sufficient to break a normal bone and some of these fractures have been eponymously described—Colles’ fractures for example. In order to categorise fracture types using the terms already in widespread use, we suggest that definitions for some of these terms are developed that reflect the suspected underlying pathophysiological mechanisms.
Fatigue fracture could be used to describe fractures with an aetiology closest to that seen in aluminium metal fatigue, i.e.
cyclical repetitive injury to a rigid structure with little or no capacity for repair. Cortical bone has the lowest rate of bone turnover and this may be further reduced in some conditions (aluminium bone disease or pyknodysostosis [3
] () and bisphosphonate therapy are examples). Repetitive low-trauma fractures in cortical bone in these conditions are recognised—the mid-shaft transverse fracture of the femur in patients on bisphosphonates for example. In this fracture type, there may be no unusual frequency or magnitude to the precipitating stress. A painful pre-fracture state with characteristic imaging appearances has been described in this condition (), which may be an indication for prophylactic intramedullary nailing.
Incomplete chronic fatigue fracture (white arrow) of the anterior tibia in a male with pyknodysostosis.
Figure 2 Fatigue pre-fracture in a middle-aged female with breast cancer on bisphosphonate therapy. Plain radiograph (a) demonstrates focal cortical thickening on the lateral mid-shaft (white arrow). MRI axial short tau inversion–recovery image (b) shows (more ...)
Repetitive stresses to normal bone may also result in fracture if the magnitude of the individual stresses or the frequency of stress application exceeds the capacity of the bone to repair microfractures. This may occur from unaccustomed exercise in the non-athlete or a change in the training programme in an athlete. The bone remodelling that is needed to adapt to these altered demands requires an increase in bone turnover, the initial consequence of which is bone resorption, which paradoxically increases the risk of a fracture in the short term. In addition, the bone response is slower than that of the stressed musculature, the increased strength of which then adds to the stresses on the bones. These should be termed repetitive increased stress fractures, but this would invariably be shortened to stress fracture.
When bone is abnormally weak, owing to osteoporosis, fractures of all types will occur more easily. Fractures at sites of (normally) high trabecular bone content are particularly common in osteoporosis. When there is a single episode of identified trauma, then the term insufficiency fracture is suitable, but when fracture occurs during normal activity there may be a contribution from repetitive stress or fatigue; consequently, these terms are not exclusive and could be combined—some calcaneal fractures, for example, may be insufficiency stress fractures.
While a repetitive stress fracture in an athlete may appear to be a specific type of fracture, in practice its aetiology may also be multifactorial, particularly when the patient is a keen amateur rather than an elite athlete, or if the fracture is at a site of high trabecular bone content. Female athletes have a higher incidence of stress fractures, which may also be the result of relative insufficiency. Consideration of the mechanisms described above and a search for relevant risk factors is therefore still essential in any stress fracture.
Histological studies of stress fractures confirm that the initial response of bone to repetitive stress is increased osteoclastic activity, which is greater than the osteoblastic new bone formation, temporarily weakening the bone. With continued repetitive stress, microfractures occur and bone marrow oedema would be seen on magnetic resonance scanning. Periosteal new bone then forms and may be visible on plain radiography, but if the repetitive stress continues then full cortical fracture will ensue. This sequence can, however, be interrupted by early diagnosis and appropriate management with more rapid healing and return to pain-free training.