“Stress fracture” constitutes a spectrum of injury that includes bone strain, stress reaction, and stress fracture. The etiology is repetitive loading in the setting of inadequate bone remodeling. The spectrum of injury reflects to some degree the quantity of strain, although exact thresholds are not known and likely mediated by numerous individual host factors in addition to the inciting activity. In general, repetitive injury is more likely to occur in the lower extremity, which sees greater loads than the upper extremity in ambulatory athletes, and with activities that are high volume and offer repetitive loading. 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. When the area of fatigue failure is inadequately repaired, it can result in crack initiation in the bone [2] (Fig. 1.2). A simple model is illustrated in Fig. 1.3.

Stress injury may also occur with normal strain, but this is typically in the setting of depressed bone remodeling. These injuries are known as insufficiency reactions or fractures. They are more common in the setting of metabolic diseases, hormonal imbalances, and osteoporosis. In the setting of older persons with osteoporosis, both reduced remodeling and structural changes in the trabecular and cortical bone leading to reduced biomechanical strength, and contribute to the susceptibility to insufficiency fracture at physiologic loads [3]. The dichotomy of fatigue failure and insufficiency is certainly more of a continuum with respect to athletes. These individuals experience greater than physiologic strain through activity but also exhibit risk factors for insufficiency failure, putting some subpopulations of athletes at greater risk.

Another special consideration in the pathophysiology of stress fractures in athletes is the influence of skeletal muscle. Muscles may protect the tibia during running by producing shear forces that counteract the joint reaction forces and result in reduced net shear stresses in the tibia. It has been hypothesized that reduced lower leg muscle strength increases the risk of stress fracture through this mechanism [4, 5], and the concept may extend to other common areas of stress fracture. This theory has only been tested in one clinical study, where a significantly lower knee extension power was observed in a case–control study of female runners with and without stress fractures [6]. Others have hypothesized that this potential protective effect of muscle may be diminished with the fatigue associated with excessive training, or be reduced in new exercisers and military recruits [7].

Finally, there is an oxidation deprivation theory of stress fracture development, which deserves some attention. In this theory, the repeated load of an activity such as running is thought to cause decreased oxygen delivery [8] and brief ischemia [9, 10] in weight-bearing bones. This ischemic environment is thought to stimulate the bone-remodeling process, specifically by increasing osteoclastogenesis [11]. The result is weakened bone that is less able to withstand subsequent loads, thereby increasing susceptibility to further stress-related injury. This theory may explain some observations that those new to activity are more at risk [12, 13].

Bone stress injury occurs via an imbalance of repetitive stress and normal bone remodeling/recovery in response to that stress. Although the paradigms of fatigue failure (high stress overwhelming normal turnover) and insufficiency failure (normal stress overwhelming disordered turnover) are a simple means of conceptualizing this disorder. In reality components of both will contribute to stress injury in any one individual. This is further complicated when one considers that many of the host factors that influence the pathophysiology of bone stress injury are also interrelated. The findings from a study such as that performed by Cosman et al. [16] illustrate that even with the current state of knowledge, we can explain only a small proportion of the risk for stress fracture development. More research is warranted.

From a practical standpoint, the clinician who will diagnose and treat patients with bone stress injuries must understand the basics of bone biology, including stress remodeling. Once a diagnosis has been made, further probing into the potential role of etiologic factors is recommended. This may include diet and nutritional deficiencies, menstrual irregularity, family history, and training volume. Some of these factors may be modifiable and useful in both the treatment of the current stress injury, as well as the prevention of future injury.

The epidemiology of stress fractures is described as the occurrence of stress fractures in athletic populations, and is typically expressed on the basis of exposure (e.g., number of stress fractures per athlete-years or per athlete-exposures). One of the challenges in defining the incidence of stress fractures lies in accurately determining the exposure component. Stress fracture cases are comparatively easy to identify, typically through chart records or physician visits. The challenge of a retrospectively designed study is that while it may identify most or all stress fractures over a given time period, accurate information regarding athletic exposure is comparatively lacking. Consistent and accurate injury reporting data is important to identify risk factors, at-risk subpopulations, and monitor the effectiveness of interventions.

A second complicating factor in deciphering the literature defining the occurrence of stress fractures in athletes is the method of diagnosis. Older studies used modalities such as X-ray, which can have poor sensitivity in identifying changes [27]. Many newer studies utilized bone scan or MRI techniques, which offer greater sensitivity and will identify stress fractures at an earlier stage. The MRI is so sensitive that it can detect stress reaction, a precursor to stress fractures, and thus studies utilizing this method of detection will report a greater incidence/occurrence but for a broader spectrum of clinical disorder. Many of these topics are explored in further detail in the remaining chapters of this text.

This heterogeneity in diagnosis, study design, and accuracy of exposure precludes the pooling of data to formulate incidence rates by sport or activity, at the current time. Therefore, this chapter will focus on a descriptive review of the literature, the most robust of which originates from military populations. Studies from various sports will also be reviewed and interpreted. A preference towards higher level of evidence studies published in the last 10 years is given.