Stress Fractures: Their Causes and Principles of Treatment


Historical Perspective

Stress fractures were first described in 1855 by Briethaupt, a Prussian military physician who observed foot pain and swelling in young military recruits unaccustomed to the rigors of training. He considered it to be an inflammatory reaction in the tendon sheaths resulting from trauma and called the condition Fussgeschwulst . It was not until the advent of radiographs that the signs and symptoms were attributed to fractures in the metatarsals. The condition then became known as a march fracture because of the close association between marching and the onset of symptoms. Stress fractures were first noticed in civilians in 1921 by Deutschlander, who reported six cases in women. However, it was not until 1956, more than a century following their identification in military recruits, that they were recognized in athletes.

A variety of terms have been used over time to describe stress fractures. These include march fractures, Deutschlander fractures, fatigue fractures, or crack fractures. Virtually all of these terms have been intended to describe some etiologic attribute of the stress injuries of bone. In recent years the most commonly used term has been stress fracture.

Following the radiographic description of metatarsal stress fractures, many theories were set forth to explain the etiology of this injury. Most of the reports were based on series that were small, and the theories proposed were concerned with either mechanical factors, such as spasm of the interossei, or flat feet, or with inflammatory reactions, such as nonsuppurative osteomyelitis.

Etiology of Stress Fractures

It is now recognized that the development of a stress fracture represents the end product of the failure of bone to adapt adequately to the mechanical loads experienced during physical activity, typically that which is repetitive. Ground reaction forces and muscular contraction result in bone strain. It is these repetitive strains that are thought to cause a stress fracture. Bone normally responds to strain by increasing the rate of remodeling. In this process, lamellar bone is resorbed by osteoclasts, thereby creating resorption cavities that subsequently are replaced with more dense bone by osteoblasts. Because there is a lag between increased activity of the osteoclasts and osteoblasts, bone is weakened during this time. If sufficient recovery time is allowed, bone mass eventually increases. However, if loading continues, microdamage may accumulate at the weakened region. Remodeling is thought to repair normally occurring microdamage. The processes of microdamage accumulation and bone remodeling, both resulting from bone strain, play an important part in the development of a stress fracture. Running, for example, produces ground reaction forces approximately five times greater than walking. The result of excess strain is an accumulation of microdamage leading to fatigue reaction or fatigue failure.

If microdamage accumulates, repetitive loading continues, and remodeling cannot maintain the integrity of the bone; a stress fracture may result. This may occur because the microdamage is too extensive to be repaired by normal remodeling, because depressed remodeling processes cannot adequately repair normally occurring microdamage, or because of some combination of these factors. Another special consideration in the pathophysiology of stress fractures is the influence of skeletal muscle. For example, muscles may protect the tibia during activity by producing shear forces that counteract the joint reaction forces and result in reduced net shear stresses in the lower extremity. It has been hypothesized that reduced lower leg muscle strength increases the risk of stress fracture through this mechanism. There is another theory that brings in the possibility of repeated oxygen deprivation during activity. In this theory, the repeated load of an activity such as running is thought to cause decreased oxygen delivery and brief ischemia in weight-bearing bones. This ischemic environment is thought to stimulate the bone-remodeling process, specifically by increasing osteoclastogenesis. The end result is a weakened bone that is susceptible to stress fractures.


Stress fractures have been reported to occur in association with a variety of sports and physical activities. Clinical impression suggests that stress fractures are more common in weight-bearing activities, particularly those with a running or jumping component. Numerous case series have reported that stress fractures comprise between 0.7% and 15.6% of all injuries sustained by athletic populations.

It often is suggested that women sustain a disproportionately higher number of stress fractures than men. A gender difference in stress fracture rates is, however, not as evident in athletic populations. Studies either show no difference between male and female athletes or a slightly increased risk for women, up to 3.5 times that of men. Bennell et al. found no significant difference between gender incidence rates even when expressed in terms of exposure. Women sustained 0.86 stress fractures per 1000 training hours, compared with 0.54 in men. Reported increased incidence of stress fractures in women has been attributed to decreased bone density/size, hormonal aberrations, and biomechanical/anatomical differences. Korpelainen and colleagues looked into risk factors for recurrent stress fractures in athletes and found runners with a high weekly training mileage are at a high risk of recurrent stress fractures of the foot and shin. Leg-length inequality, a high longitudinal arch of the foot, forefoot varus, and menstrual irregularities may also be etiologic factors for recurrent stress fractures ( Tables 3.1 and 3.2 ).

Table 3.1
Distribution of Multiple Stress Fractures According to Anatomic Location in Both Sexes
From Korpelain R, Orava S, Karpakka J et al. Risk factors for recurrent stress fractures in athletes. J Sports Med . 2001, 29(3):304-310.
Women Men Total
Location N % N % N %
Metatarsal 15 34.1 13 18.6 28 24.6
Calcaneus 2 4.5 0 0.0 2 1.8
Tarsal 5 11.4 3 4.3 8 7.0
Distal third 7 15.9 13 18.6 20 17.5
Middle third 4 9.1 11 15.7 15 13.2
Proximal third 4 9.1 16 22.9 20 17.5
Distal third 2 4.5 5 7.1 7 6.1
Middle third 1 2.3 3 4.3 4 3.5
Proximal third 0 0.0 1 1.4 1 0.9
Distal third 1 2.3 0 0.0 1 0.9
Middle third 0 0.0 0 0.0 0 0.0
Proximal third 1 2.3 3 4.3 4 3.5
Pubic bones 2 4.5 2 2.9 4 3.5
Total 44 100.0 70 100.0 114 100.0

Table 3.2
Distribution of Multiple Stress Fractures by Sports Event According to Anatomic Location
From Korpelain R, Orava S, Karpakka J et al. Risk factors for recurrent stress fractures in athletes. J Sports Med. 2001, 29(3):304-310.
Bone Sports event Total
Long-Distance Running Sprinting Jumping Orienteering Skiing Power Events Ball Games N %
Metatarsal 20 3 2 0 0 1 2 28 24.6
Calcaneus 2 0 0 0 0 0 0 2 1.8
Tarsal 5 2 1 0 0 0 0 8 7.0
Distal third 11 1 0 0 3 2 3 20 17.5
Middle third 7 1 4 0 0 0 3 15 13.2
Proximal third 12 0 2 6 0 0 0 20 17.5
Distal third 5 1 0 1 0 0 0 7 6.1
Middle third 2 0 1 0 0 0 1 4 3.5
Proximal third 1 0 0 0 0 0 0 1 0.9
Distal third 1 0 0 0 0 0 0 1 0.9
Middle third 0 0 0 0 0 0 0 0 0.0
Proximal third 4 0 0 0 0 0 0 4 3.5
Pubic bones 3 0 0 0 0 0 1 4 3.5
Total 73 8 10 7 3 3 10 114 100.0

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