Definition

Stress fractures are complete or partial bone fractures caused by the accumulation of microtrauma [1]. Normal bone accommodates to stress through ongoing remodeling. If this remodeling system does not keep pace with the force applied, stress reaction (microfractures) and, finally, stress fracture can result. Stress fracture is the end result of a continuum of biologic responses to stress placed on bone. Adolescent, young adult, and premenopausal women athletes have a higher incidence of stress injuries to bone than men do [2,3]. Stress fractures in juveniles are rare [4]. Both extrinsic and intrinsic factors have been implicated in this imbalance between bone resorption and bone deposition [5]. Malalignment and poor flexibility of the lower extremities (intrinsic factors) and inadequate footwear, changes in training surface, and increases in training intensity and duration without an adequate ramp-up period (extrinsic factors) can lead to stress fractures [6].

Stress fractures in athletes vary by sports and are most common in the lower extremities [2,7]. The most common sites are the tibia, metatarsals, and fibula, and they affect most commonly runners and dancers. The fracture site is the area of greatest stress, such as the origin of lower leg muscles along the medial tibia [8]. A narrower mediolateral tibial width was a risk factor for femoral, tibial, and foot stress fractures in a study of military recruits [9]. Studies of female runners demonstrated greater loading rates in those with history of tibial stress fractures compared with those without injury [10,11]. In contrast, in comparison of runners with and without history of tibial stress fracture, no difference in ground reaction forces, bone density, or tibial bone geometric parameters was found between groups [12].

Military recruits have been extensively studied in regard to lower extremity stress fractures. In a study of 179 Finnish military recruits aged 18 to 20 years, tall height, poor physical conditioning, low hip bone mineral content and density, and high serum parathyroid hormone level were risk factors for stress fractures [13]. The authors postulated that given the poor vitamin D status, intervention studies of vitamin D supplementation to lower serum parathyroid hormone levels and possibly to reduce the incidence of stress fractures are warranted. Prospective studies of vitamin D and calcium in stress fracture prevention, one in female young athletes and the second in female military recruits, were the focus of a recent review paper. A longitudinal study of female athletes aged 18 to 26 years showed that greater baseline intakes of dietary calcium, dairy products, and milk were linked to significant reductions in fracture incidence; fracture risk decreased by 62% per additional cup of skim milk consumed per day, and women who consumed less than 800 mg of calcium per day had nearly six times the stress fracture rate of women who consumed more than 1500 mg of calcium and more than double the rate for women who consumed between 800 and 1500 mg [14]. The second study of female military recruits who were prescribed an 8-week trial of supplementation with 2000 mg of calcium and 800 IU of vitamin D demonstrated a statistically significant 20% reduction in fracture injuries compared with women given a placebo [14]. The study concluded that evaluation of age-appropriate dietary guidelines for calcium and vitamin D levels is needed to promote bone health, to reduce the risk of stress fracture injury in the young athlete, and to achieve peak bone density that will promote lifelong bone health [14].

A database of systematic reviews, including 13 randomized prevention trials, concluded that shock-absorbing insert use in footwear probably reduces the incidence of stress fractures in military personnel [15]. There was insufficient evidence to determine the best design of such inserts.

Stress fractures may be related to abnormalities of the bone, such as in female athletes with low bone density due to exercise-induced menstrual abnormalities [16–19]. Premature osteoporosis leads to an increased risk for stress fractures. One study looked at premenopausal women runners and collegiate athletes and concluded that those with absent or irregular menses were at increased risk for musculoskeletal injuries while engaged in active training [17]. Muscle deficits in the gastrocnemius-soleus complex in jumping athletes have also been implicated in causing tibial stress fractures. Bone injury may be a secondary event after a primary failure of muscle function [20].

Recent literature review of the influence of sports participation on bone health in the young athlete concluded that high-impact and weight-bearing activities enhance bone density, particularly in anatomic locations directly loaded by those sports [21]. It also showed that participation in sports during the age range in which growth and skeletal maturity occur may result in a higher peak bone density [21]; in particular, athletes aged 10 to 30 years who participate in impact sports (particularly high-impact or odd-impact sports) may enjoy enhanced bone density and improvements in bone geometry. Nonimpact sports such as cycling and swimming are not associated with improvements in bone health, and prolonged participation in endurance sports, including long-distance running and cycling, may be associated with decreased peak bone density [21].

During the last few years, researchers have shown a link between stress fractures and long-term bisphosphonate use. Bisphosphonate medications are indicated for patients with postmenopausal osteoporosis, and it has been shown that bisphosphonate use improves bone mineral density, prevents bone loss, and reduces the number of fractures [22,23]. Bisphosphonates inhibit osteoclastic bone resorption, and therefore bone turnover, by inducing osteoclast apoptosis. The combined and coordinated action of resorbing damaged bone and laying down new bone is fundamental to the process of bone remodeling [23]. If this coupling is impaired, the microdamage that occurs under physiologic conditions that normally is repaired may accumulate, resulting in a major reduction in the energy required to cause fracture [23]. These fractures are low-energy injuries and have characteristic findings observed on femoral radiographs: a transverse fracture line originating from the lateral tension side of the cortex and lateral cortical thickening adjacent to the fracture [23,24]. In addition, prodromal thigh pain from the insufficiency changes may be present. The subsequent minimal trauma that often is required to complete the fracture is characteristic, with patients often sustaining a spontaneous nontraumatic fracture during activities of daily living [23].