eMedicine Specialties > Physical Medicine and Rehabilitation > Lower Limb Musculoskeletal Conditions

Stress Fracture

Author: Jonathan C Reeser, MD, PhD, Department of Physical Medicine and Rehabilitation, Marshfield Clinic
Contributor Information and Disclosures

Updated: Feb 21, 2007

Introduction

Background

Stress fractures are overuse injuries of bone. These fractures, which may be nascent or complete, result from repetitive subthreshold loading that, over time, exceeds the bone's intrinsic ability to repair itself. Briefhaupt originally described stress fractures in military recruits in 1855. Our present understanding of the pathophysiology of stress fractures and of bone's response to loading has been advanced by numerous studies investigating the epidemiology of stress fractures in military recruits and in athletes.

Stress fractures most commonly occur in the lower limbs as a result of the ground-reaction forces (GRFs) that must be dissipated during running, walking, marching, or jumping. Stress fractures of the vertebral arch, upper limbs, ribs, and even the scapula have also been described and are not uncommon in some sports.

Pathophysiology

Bone, like muscle, is an adaptable tissue capable of repair, regeneration, and remodeling in response to environmental (particularly mechanical) signals. Bones are exposed to both stress (ie, load) and strain (ie, deformation) with weight-bearing exercise. One measure of load is GRF, which can approach 12 times body weight during jumping and landing. Factors influencing the local skeletal response to loading include bone geometry and bone density. For example, cortical (ie, long) bones are generally more resistant to compressive forces than trabecular bones, but long bones also experience more strain in response to torsion or bending forces. In addition, a bone's strength is roughly proportional to the square of its mineral density; thus, osteopenic bone is weaker than bone of normal density.

Wolff law states that bone develops the structure most suited to resist the forces acting upon it. The ability of bone to remodel has tremendous clinical consequences. For example, an individual on prolonged bed rest quickly begins to lose bone mineral density (BMD). Conversely, an athlete who engages in a sporting discipline that requires repetitive jumping and landing is likely to have a higher BMD than a sedentary person. Such adaptation is the result of a continuous process of bone resorption and subsequent repair mediated at the cellular level by osteoclasts and osteoblasts, respectively.

Advanced cross sectional imaging has demonstrated that bone responds to repetitive loading via a continuum of stress responses that precede the onset of clinical symptoms. In their study involving a cohort of military recruits, Kiuru et al reported that only 40% of the MRI findings suggestive of a low-grade bone stress injury correlated with clinical symptoms (Kiuru, 2005). The vast majority of the radiographically detected areas of bone stress reaction remained clinically silent despite uninterrupted training, and disappeared upon follow-up imaging at the conclusion of the 5-month training program. Therefore, under normal circumstances, bone appears able to keep up with necessary repairs without manifesting clinically significant injury as it remodels in accordance with Wolff law. However, when a bone's reparative and adaptive capacity is overwhelmed by chronic overload, damage can begin to accumulate. If allowed to progress, this multifactorial process may eventually result in a stress fracture.

Animal studies have demonstrated that bone subjected to repetitive cyclical loading develops what has been termed microdamage. Furthermore, a physiological threshold appears to exist, below which such microdamage is not detectable. Increased osteoclastic activity at sites of bone stress or strain may cause transient weakening of the bone locally, predisposing the area to microdamage. Unless given appropriate time for healing and osteoblastic-mediated bone deposition, adjacent sites of microdamage are thought to coalesce, giving rise to an area of stress reaction or injury. At this stage, the individual may be minimally symptomatic and conventional radiographs are likely to appear normal. With progressive overload, the bone becomes increasingly vulnerable and the individual proceeds to develop symptoms that are thought to reflect the extent of underlying bone injury.

If uninterrupted, the process may culminate in a stress fracture. Some clinicians prefer to distinguish between stress fractures of normal bone that becomes fatigued through abnormal loading (ie, fatigue fractures) and stress fractures of pathologic bone that may fail even under comparatively normal loads (ie, insufficiency fractures). However, both processes are characterized by disrupted bone homeostasis and inadequate repair in the face of repetitive overload.

Frequency

United States

Estimates of the annual incidence of stress fractures among athletes and military recruits range from 5-30%. Stress fractures are among the 5 most common injuries suffered by runners and have been reported to account for up to half of the injuries sustained by military recruits. The interaction between genetic susceptibility and other internal and external risk factors determines an individual's likelihood of sustaining a bony stress injury.

Race

Stress fractures probably occur less frequently among African Americans than among whites by virtue of the generally higher BMD found in African Americans.

Sex

Most studies suggest that females are at increased risk of developing stress fractures compared with males. The incidence of stress fractures among female military recruits and athletes has been reported to be twice that of their male counterparts. Disordered eating places females at higher risk of developing stress fractures. The clinician should be mindful that a stress fracture may herald the existence of underlying amenorrhea, disordered eating, and osteoporosis (the "female athlete's triad"). Therefore, diagnosis of a stress fracture in a female should prompt the clinician to obtain a dietary history to ensure adequate intake of both energy (calories) and calcium. Finally, in the proper clinical context, a stress fracture should alert the clinician to the possibility of osteoporosis or other underlying skeletal pathology.

Age

Stress fractures typically affect individuals who are more active, and the incidence probably increases with age due to age-related reduction in BMD. By no means, however, should the diagnosis be dismissed in children, whose bones have not reached peak density and strength.

• Interestingly, some evidence suggests that the risk of stress fracture may be lower among adult runners who have a broad athletic background that includes childhood participation in "ball sports." This finding provides additional incentive for coaches and parents to avoid promoting early sport-specialization among young athletes.

Clinical

History

The most salient historical feature in the diagnosis of stress fracture is the insidious onset of activity-related pain.

• Early on, the pain typically is mild and occurs toward the end of the inciting activity.
• Subsequently, the pain may worsen and occur earlier, limiting participation in sports activities.
  • While rest may provide transient relief of symptoms in the early stages, as the stress injury progresses, the athlete's pain may persist even after cessation of activity.
  • Night pain is a frequent complaint.
  • Pain resulting from long-bone fractures is thought to be localized, while pain associated with stress injury of trabecular bone is characteristically described as more diffuse.
• Stress fractures, like most overuse injuries, typically are multifactorial in etiology; thus, if the diagnosis has been made or is suspected, the clinician is in the position to try to determine what risk factors precipitated or contributed to the injury.
  • Details of the athlete's training history should be noted, both in terms of volume and intensity.
  • Intensive sustained muscular activity may result in bone strain and overload. This type of mechanism of injury is common in rowers, who are prone to stress fractures of the ribs.
• Muscle fatigue, perhaps because of poor conditioning or as the result of overtraining, can attenuate the shock-absorbing capacity of the muscular system, resulting in greater transmission of GRFs to the associated parts of the skeleton.
• Structural malalignments (eg, leg-length discrepancies) or biomechanical inefficiencies (eg, excessive subtalar pronation) can result in increased stress and strain on the tibiae.
• Concurrent injury may result in subclinical biomechanical adaptations along the kinetic chain, placing atypical loads on bone and precipitating a stress injury.
• Poor bone health, whether because of hormonal, dietary, or pathological causes (eg, osteoporosis, hyperparathyroidism, skeletal involvement from malignancy), can weaken bone and make it more susceptible to injury.
• These conditions and other intrinsic and extrinsic risk factors for the development of stress fractures are summarized in Causes below.

Physical

Upon physical examination, individuals with stress fractures typically report pain upon palpation or percussion of the affected area.

• Inspection of the site may reveal localized swelling and, possibly, erythema.
• Loading the affected bone using specific maneuvers (such as the "hop test" or the "fulcrum test") may reproduce the athlete's pain. Note that no single physical examination test is sufficiently sensitive and specific to permit the unequivocal diagnosis of a stress fracture. Rather, taking the individual's history and examination into consideration, the clinician must have sufficient clinical suspicion to include the diagnosis among the different possible causes of the presenting complaints.
• Some practitioners believe that application of a vibrating tuning fork over the affected bone can provoke the athlete's pain, but Brukner et al dispute the validity of this test.
• As part of a thorough physical examination, the practitioner should assess the athlete's flexibility, lower limb alignment (including leg lengths), foot structure (eg, pes cavus vs pes planus), and motor function (eg, evaluating for strength imbalances).

Causes

• Intrinsic risk factors
  • Low BMD (potentially modifiable)
  • Lower limb malalignment (potentially modifiable)
  • Foot structure (unmodifiable)
  • Height - Tall stature (unmodifiable)
  • Muscle fatigue/poor overall conditioning (modifiable)
  • Weakness/strength imbalance (modifiable)
  • Pathologic bone states (potentially unmodifiable)
  • Menstrual/hormonal irregularities (potentially modifiable)
  • Genetic predisposition (unmodifiable)
• Extrinsic risk factors
  • Excessive volume or intensity of training (modifiable)
  • Sporting discipline (modifiable): For example, runners are prone to tibial shaft stress fractures, whereas tennis players appear to be most vulnerable to navicular injuries, and volleyball players may be at a relatively increased risk of pars interarticularis injuries.
  • Change in training regimen - "New coach" phenomenon (potentially modifiable)
  • Change in training surface - Density or topography (modifiable)
  • Worn-out training shoes (modifiable)
  • Cigarette smoking (modifiable)
  • Inadequate nutrition - Energy (calories), calcium, vitamin D (modifiable)
  • Medication usage - For example, chronic steroid use (potentially modifiable)

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