Stress Fractures

Updated: Apr 04, 2018
  • Author: Stefanos F Haddad, MD; Chief Editor: Murali Poduval, MBBS, MS, DNB  more...
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Overview

Background

The stress fracture, first described by Breithaupt in 1855, [1] is a common overuse injury seen in athletes and military recruits. [2, 3] The injury is usually seen in the lower extremities, but it has also been reported in the upper extremities and the ribs. The most common locations for stress fractures include the tibia, metatarsals, fibula, and navicular bones; less common locations include the femur, pelvis, and sacrum.

A stress fracture is caused by repetitive and submaximal loading of the bone, which eventually becomes fatigued and leads to a true fracture. The typical presentation is a complaint of increasing pain in the lower extremity during exercise or activity. The patient's history usually reveals a recent increase in either training volume or intensity.

The treatment of most stress fractures is relatively straightforward and includes decreased activity and immobilization; however, patients with some stress fractures, such as displaced femoral neck stress fractures and fifth metatarsal base stress fractures, are more likely to have complications such as nonunion. [4, 5] These complications should be monitored closely because surgical intervention may be necessary.

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Pathophysiology

Stress fractures result from recurrent and repetitive loading of bone. The stress fracture differs from other types of fractures in that in most cases, no acute traumatic event precedes the symptoms.

Normal bone remodeling occurs secondary to increased compressive or tensile loads or increased load frequency. In the normal physiologic response, minor microdamage of the bone occurs. This is repaired through remodeling. Stress fractures develop when extensive microdamage occurs before the bone can be adequately remodeled. [6, 7]

Often, the patient has a history of an increase or change in the character of activity or athletic workouts. Bones may be more prone to stress fractures if the bone is weakened, as in individuals with osteoporosis or those in whom weightbearing activities are increased.

The three factors that can predispose an individual to the development of stress fractures are as follows [8] :

  • Increase in the applied load
  • Increase in the number of applied stresses
  • Decrease in the surface area of the applied load

The applied load on the bone may be increased by decreasing the surface area that the weight is distributed across or by increasing the total weight applied to the bone. High-impact activities, such as jumping or performing plyometrics, running on a new surface, or practicing incorrect biomechanical movements or techniques, may increase the risk of stress fractures.

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Etiology

Risk factors

Although stress fractures result from repeated loading, the exact contribution of training factors (eg, volume, intensity, and surface) has not been clearly established. [9] From what we do know, menstrual disturbances, caloric restriction, decreased bone density, muscle weakness, and leg-length differences are risk factors for stress fractures. [10, 11]

Myburgh reported that stress fractures were more common in athletes who had decreased bone density, lower dietary calcium intake, current menstrual irregularity, and less oral contraceptive use, when the athletes were matched for similar training volume and intensity. [12]

Nattiv and Armsey found that genetics, female sex, white ethnicity, low body weight, lack of weightbearing exercise, intrinsic and extrinsic mechanical factors, amenorrhea, oligomenorrhea, inadequate calcium and caloric intake, and disordered eating were additional risk factors for stress fractures. [13] A decreased testosterone level in male endurance athletes has also been implicated as a risk factor for stress fractures. [14, 15, 16, 17] Individuals found to have low bone mass and hormonal disturbances may require endocrinologic management. [18]

Schnackenburg et al did a matched control study on 19 female athletes with tibial stress fractures and found that stress fracture patients had lower tibial cross-sectional areas, lower trabecular bone mineral densities, and less cortical area, as well as decreased knee extension strength. They suggested that impaired bone quality of the posterior cortex and decreased muscle strength were associated with stress fractures in female athletes. [19]

Giladi identified two anatomic risk factors in military recruits. Recruits with stress fractures had significantly narrower tibiae and increased external rotation of the hip. These two variables were independent and cumulative, and when both risk factors were present, the stress-fracture morbidity was 45%. [20]

Activity and fracture location

Particular locations of stress fractures are commonly associated with particular activities (see Table 1 below).

Table 1. Epidemiologic Features of Stress Fractures According to Location and Activity (Open Table in a new window)

Location of Fracture

Activity Involved

Metatarsals, general

Football, basketball, gymnastics, ballet, military training [21]

Metatarsal, base of the second

Ballet

Metatarsal, fifth

Tennis, [22, 23]  ballet

Sesamoids of the foot

Running, ballet, basketball, skating

Navicular

Sprinting, [24]  jumping, basketball, football

Talus

Pole vaulting

Calcaneus

Military drills, running, aerobics

Fibula

Running, jumping, ballet, repeated heavy lifting [24]

Tibia

Running sports, dancing, ballet

Patella

Running, hurdling

Femoral neck

Distance running, military training [25]

Pubic rami

Military drills, distance running

Pars articularis

Gymnastics, ballet, cricket, volleyball, diving, football

Chest, ribs

Swimming, [26]  golf, [27]  rowing [28]

Sternum

Wrestling [29]

Ulna

Racquet sports, volleyball

Olecranon

Baseball, throwing sports

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Epidemiology

Sex-related demographics

Studies of US military recruits revealed a higher percentage of stress fractures in female recruits than in male recruits. [2, 30, 31, 32] Bennell et al also found a 45% incidence of stress fractures in competitive female runners. [6] The women most at risk for stress fractures were those who restricted their food intake and those who had dysmenorrhea.

The triad of disordered eating, amenorrhea/oligomenorrhea, and osteoporosis may be extremely prevalent in female distance runners and ballet dancers, [33] as well as in other female athletes who believe that a low body weight or body-fat percentage provides a competitive advantage. This triple combination is commonly referred to as the so-called female athlete triad. [34]

The amenorrheic female athlete may experience a prolonged state of estrogen deficiency similar to that of a postmenopausal woman. The lower estrogen levels are associated with decreased bone density; even if normal menses returns, this bone loss may be irreversible in high school– and college-aged female athletes. Early identification of female athletes who are likely to develop the female athlete triad is important for the prevention of stress fractures and for maintaining overall future bone health. [34, 35]

Race-related demographics

In a study of military recruits, Markey found no difference in the incidence of stress fractures between recruits of various racial backgrounds. [36]

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