Overuse Bone Injuries Usually Result In Stress Fractures Biology Essay


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Overuse bone injuries usually result in stress fractures. The first written account of stress fractures was by Breithaupt in 1855 who described 'the syndrome of painful swollen feet associated with marching' among Prussian soldiers (Breithaupt 1855). The highest incidence of stress fractures occurs in track and field athletes, with rates of 10 to 31% (Bennell, Malcolm, et al. 1996). Stress fractures are also commonly seen in gymnastics, lacrosse, figure skating, ballet, basketball and football (Burr and Milgrom 2001). Most stress fractures occur in the lower limbs with over 50% occurring to the fibula and tibia (Figure 1) (McBryde 1985). Certain stress fracture sites tend to be associated with certain sports, e.g. Medial malleolus of the tibia and tarsal navicular stress fracture are common in high jumpers (Ivkovic, et al. 2007).


Fourth and Fifth


Figure 1: Distribution of the common sites of stress fractures. Adapted from McBryde, 1985.

The main characteristic of a stress fracture is localized, gradual pain which progressively increases with activity and is relieved with rest (Burr and Milgrom 2001). There is usually a recent change in training prior to the onset of pain. A radionuclide scan is used to diagnose a stress fracture. Radionuclide's collect in areas where there is increased bone activity (where bone cells are breaking down or repairing parts of the bone), appearing as 'hot spots' on the picture.


Stress fractures result from repetitive loading and tend to not be associated with a history of trauma. They are often considered to be a mechanical fatigue driven process. They typically occur after a period of 4-6 weeks of increased activity. There are two hypotheses for the cause of stress fractures. The first, described in figure 2, is described as a biological process where bone remodelling is stimulated by mechanical loading causing porosity and decreased bone mass. The second hypothesis is that a stress fracture occurs from the development and growth of microcracks within the bone.

Mechanical Loading

Osteonal Remodelling


'Focal transient osteopenia'

Local Strain

Continued Loading


Stress Fracture

Figure 2: Hypothesised mechanism for the development of stress fractures. Adapted from Burr and Milgrom (2001)

Stress fractures occur as part of a positive feedback mechanism. Increased mechanical load stimulates bone turnover. Osteoclasts resorb pre-existing bone, causing bone porosity which can last several months. Stiffness of the bone decreases rapidly in response to small changes in bone porosity. Once a threshold has been reached (either through increased porosity or loading) the bone becomes unstable and fractures occur. Injury, cytokines, altered mechanical loading and fatigue can all activate bone remodelling.

There are a number of factors that can directly or indirectly influence stress factors in athletes (shown in figure 3). There seems to be a complex interaction between these factors and some have contradictory evidence in studies conducted at present. The main factors associated with stress fracture incidence are smaller bones, leg length discrepancy, muscle fatigue and training factors.

Bone disease (Pathology)

Endocrine status and hormones

Exercise (bone loading)

Diet and Nutrition


Joint range and muscle flexibility

Foot type

Lower extremity alignment

Altered gait

Complete Fracture

Stress Fracture

Stress Injury

Stress Reaction

Accelerated Remodelling

Normal Remodelling

Continuum of clinical responses to bone loading

Body size and composition

Training surfaces


Magnitude of each strain cycle

Muscle strength

Muscle fatigue

Total number of strain cycles (training volume)

Frequency of strain cycles (training intensity)

Duration of each strain cycle

Bone disease (Pathology)

Endocrine status and hormones

Exercise (bone loading)

Joint range and muscle flexibility

Diet and Nutrition


Foot type

Lower extremity alignment

Altered gait

Bone Response

Impact attenuation


Bone Health

Gait Mechanics

Bone Loading

Figure 3: Contribution of risk factors to stress fracture pathogenesis. Adapted from Brukner, Bennell and Matheson (1999).

Repetitive mechanical loading from exercise contributes to stress fracture development. Training causes changes in levels of hormones, such as sex hormones, that may influence bone indirectly. An increase in muscle mass could be protective against stress fractures. Military studies have shown that interventions such as rest periods, elimination of running on concrete, the use of running shoes and reduction of high impact activity can decrease the incidence of stress fractures (Pester and Smith 1992). An increase in training volume has been linked to an increase in stress fracture incidence in runners (Brunet, et al. 1990) and ballet dancers, (Kadel, Teitz and Kronmal 1992) and 86% of athletes can identify a change in training prior to the onset of the fracture (Sullivan, et al. 1984). However there is little controlled research in athletes as to whether training modifications can decrease the incidence.

Foot structure determines the amount of shock absorbed and the amount of force transferred. A high arched foot is less able to absorb shock due to it being more rigid than a low arched foot. However a low arched foot tends to pronate which results in increased torsion on the tibia and muscular fatigue as they attempt to control the excessive motion (Burr and Milgrom 2001). A low arched foot is the most common foot type in athletes with stress fractures but both foot types could be at an increased risk of stress fractures (Sullivan, et al. 1984). A difference in leg length also increases stress fracture incidence (Bennell, Malcolm, et al. 1996). Stress fracture development has also been linked to an increase in hip eternal rotation and a decrease in the range of ankle dorsiflexion (Burr and Milgrom 2001).

Individuals with poor physical conditioning tend to have a lack of muscular strength and are prone to muscular fatigue which increases the risk of stress fracture (Burr and Milgrom 2001). Under normal conditions, muscles act protectively by contracting to reduce strains on bone surfaces. Once fatigued, there is increased strain at the site of muscle attachment (Yosjikawa, et al. 1994).

Alterations in calcium metabolism may predispose individuals to stress fractures by affecting bone remodelling and bone density, although there is no evidence to support this as yet (Burr and Milgrom 2001). Other factors that influence bone health and possibly stress fracture risk include glutocorticoids, growth hormone and thyroxin. Nutritional studies have generally failed to find a relationship between low calcium intake and stress fracture incidence. However one study found that calcium intake was much lower in the group with stress fractures (Myburgh, et al. 1990). The intake of salt, protein, phosphorus, caffeine and alcohol all disrupt the balance of calcium, but there are no reports of any association with these factors and stress factors as yet.

The athletes at each extremity of the training spectrum are at most risk. Novice athletes or 'weekend warriors' are more likely to sustain stress fractures. High performance athletes are also at risk. Although their physical conditioning is good, the demands on them are so high that an overuse injury may occur.


The main factor determining stress fracture risk in women is genetics. Genetic factors affect bone geometry, bone alignment, hormonal environment as well as influencing psychological traits which can affect training habits and eating and menstrual disturbances. Women also seem to be more susceptible to environmental influences such as the 'ideal' body portrayed by the media (Hausenblas and Carron 1990).

Women generally have higher incidence of stress fractures, with amenorrheic women having a higher incidence than normally-menstruating women (Feingold and Hame 2006). The reason why amenorrheic women develop more stress fractures is unclear but may not be related to low bone density (Ivkovic, et al. 2007). The tibia is the most commonly affected site in both males and females, with fractures of the tarsal navicular, femoral neck, metatarsal and pelvis predominantly associated with the female athlete (Bennell and Brukner 1997).

Women tend to consume inadequate amounts of micro and macro nutrients. Bones contain a high amount of calcium and if there is dietary insufficiencies this calcium is used by the body and could compromise bone strength. This is rare in western society and only severe dietary restriction will cause mineral depletion. However, amenhorrheic and postmenopausal women lose calcium during urinary excretion due to low oestrogen levels and therefore need an increased calcium intake. The evidence for a relationship between calcium and stress fractures is inconclusive. Studies conducted on ballet dancers and female track and field athletes found no significant difference in the calcium intake of those with stress fractures and those without (Kadel, Teitz and Kronmal 1992) (Bennell, Malcolm, et al. 1996). Childhood calcium intake could be a determining factor, but only one study has assessed this and no relationship was seen (Grimston, et al. 1991). Disordered eating patterns have been associated with increased stress fracture risk. Track and field athletes and ballet dancers with stress fractures are more likely to restrict their calorie intake and avoided high fat food (Frusztajer, et al. 1990) (Bennel, et al. 1995).

Sex hormones play an important part in influencing stress fracture risk. Athletic women tend to have a higher prevalence of menstrual disturbances than the general population (Burr and Milgrom 2001). This is usually seen in sports such as ballet, gymnastics and distance running. This relationship causes a two to four fold increased risk of stress fracture, but the mechanism of increased risk is not known. It could result in lower bone density or decreased peak bone mass.


Bone structure


Bone disease (Pathology)

Endocrine status and hormones

Exercise (bone loading)

Joint range and muscle flexibility

Diet and Nutrition


Foot type

Lower extremity alignment

Altered gaitPeak incidence of stress fractures is seen in 16-25 year olds, but may occur at any age. Kadel, Teitz and Kronmal (1992) found no relationship between age and stress fracture incidence in ballet dancers and Brunet, et al. (1990) came to the same conclusion for runners.


Tolerance limits of the physis may be exceeded by the mechanical stresses of sports such as football and hockey or by repetitive physical loading required in sports such as long distance running, gymnastics and baseball. Injury can cause a disturbance to physeal growth and can lead to length discrepancy, angular deformity or altered joint mechanisms which may cause significant long term disability.

Physeal injuries can result in irreversible damage to growing cells. The growth plate cartilage is more vulnerable to stress and forces than adult cartilage and adjacent bone. The physis may also be 2-5 times weaker than the surrounding fibrious tissue. An injury that could tear a ligament or dislocated a joint in an adult may produce a separation of the growth plate in a child due to the above reasons.

The susceptibility for fracture is far more pronounced during periods of rapid growth such as during puberty. Increased growth rates and structural changes result in a thicker and more fragile plate. Bone mineralisation also lags behind bone growth which renders the bone porous and more susceptible to injury. Micheli et al (1983) proposed a controversial concept that rapid growth may cause an increased risk of injury due to muscle-tendon tightness around the joints and a loss in flexibility. Long bones or the extremities usual grow longitudinally initially with muscle-tendon units responding to the change by elongating, which may cause an imbalance.


Transverse fractures are perpendicular to the long axis of bone. Oblique fractures occur at an angle. Spiral fractures result from a rotatory mechanism; on x-rays, they are differentiated from oblique fractures by a component parallel to the long axis of bone in at least 1 view. Comminuted fractures have > 2 bone fragments. Comminuted fractures include segmental fractures (2 separate breaks in a bone). Avulsion fractures are caused by a tendon dislodging a bone fragment. In impacted fractures, bone fragments are driven into each other, shortening the bone; these fractures may be visible as a focal abnormal density in trabeculae or irregularities in bone cortex. Childhood fractures include torus fractures (buckling of the bone cortex) and greenstick fractures (cracks in only 1 side of the cortex).


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