Stress Fractures in Athletes : Topics in Magnetic Resonance Imaging

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Stress Fractures in Athletes

Fredericson, Michael MD*; Jennings, Fabio MD*; Beaulieu, Christopher MD, PhD; Matheson, Gordon O. MD, PhD*

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Topics in Magnetic Resonance Imaging 17(5):p 309-325, October 2006. | DOI: 10.1097/RMR.0b013e3180421c8c
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A stress fracture may best be described as accelerated bony remodeling in response to repetitive submaximal stresses. Studies1,2 that have investigated the histology of stress fractures show that repetitive response to stress leads to osteoclastic activity that surpasses the rate of osteoblastic new bone formation, resulting in temporary weakening of bone. If the physical activity is continued, trabecular microfractures result, which are believed to explain the early bone marrow edema seen on magnetic resonance imaging (MRI) scanning. The bone responds by forming periosteal new bone for extra reinforcement. However, if the osteoclastic activity continues to exceed the rate of osteoblastic new bone formation, eventually a full cortical break occurs. Whether stress fractures occur owing to the increased load after fatigue of supporting structures or to contractile muscular forces acting across and on the bone has been debated;1,3,4 in principle, both factors contribute. It is important to realize that this process is on a continuum both physiologically and clinically and that early intervention is associated with more rapid healing.5 Given this spectrum of injury, we find it useful to distinguish earlier injuries, called stress reactions, from responses from more advanced injuries, called stress fractures, in which a distinct fracture line is visible on imaging.


Most studies of stress injuries cite some alteration in the training program as the most significant factor in producing the injury.6-8 It has been well documented that there is an increased injury rate with increasing distance beyond approximately 32 km/wk.9 Also important is any rapid change in the training program, whether a sudden increase in mileage, pace, volume, or cross-training activity that has been inserted into the program without adequate time for physiologic adaptation to accommodate the new forces. Hard or cambered training surfaces also are important precursors to lower extremity overuse injuries.8 Failure to follow intensive training days with easy ones also can contribute to injury.

It is difficult to correlate specific anatomical abnormalities and abnormal biomechanics of the lower extremity with specific injuries on a predictable basis.10,11 Giladi et al12 studying 300 military recruits, found only 2 independent anatomical variables they considered major risk factors for stress fracture: a narrow width of the tibia and increased external rotation of the hip. These factors were independent of each other. Bennell et al13 found that female runners with stress fractures had a smaller calf girth and less lean mass in the lower limb. This correlates with the work by Garrett etal14 who have shown that one of the major roles of muscles is energy absorption. When muscles become fatigued, they transmit greater energy to the surrounding bone. Thus, it is hypothesized, the relatively lesser muscle and bone mass of the lower leg, particularly around the tibia, may explain the greater frequency of tibial stress fractures.

Recently, Crossley et al15 published a cross-sectional study comparing 23 running athletes with a history of tibial stress fracture and 23 who have never sustained a stress fracture. The stress fracture group had a significantly smaller tibial cross-sectional area (measured by computed tomography [CT] scan and dual-energy x-ray absortiometry) than the non-stress fracture group. These findings support the contention that bone geometry plays a role in stress fracture development and that athletes with smaller bones in relation to body size are at greater risk for bony injury. Newer work by Cleek and Whalen16 also suggests that the repetitive loading history of runners in a single plane leads to asymmetric cross-sectional geometry of the tibia. This is in contrast to soccer players who load in multiple directions and were found to have a much more robust and symmetric bone geometry.

Statistics suggest that females are at greater risk for sustaining stress fractures than males.17 This has been seen in the military where female recruits undergoing identical training programs have an increased incidence of stress fractures, ranging from 1.2 to 10 times that of male recruits.7,18-20 Brukner17 believes this is because of lower initial fitness in the female recruits. In athletes, the results are less clear. The female athlete triad (menstrual irregularity, disordered eating, and osteoporosis) emphasizes the susceptibility of young female athletes to stress fractures and contributes to the clinical impression that females are at an increased risk for such injuries compared with young men.21,22 Some studies23-25 have reported an increased incidence in female athletes ranging from 1.5 to 3.5 times that of males, although methodological details were inadequate in some of these.17 Other studies26,27 have failed to show a sex effect for the incidence of stress fractures.


The typical history of a stress fracture is that of localized pain that is not present at the start but occurs after or toward the end of physical activity. This pattern is opposite to that of many soft tissue injuries that have pain first thing in the morning and with day-to-day activities but reduced during physical activity. Untreated stress reactions display pain that occurs earlier during the physical activity and lingers longer; with continued training, pain will be present throughout the training and persist into daily ambulation.

A careful history often reveals some change in the training regimen during the preceding 2 to 6 weeks, and it is critical the physician ask detailed questions to identify training changes as a cause. Subtle changes in training, footwear, running surfaces, and so forth provide an opportunity for intervention; in many cases, small adjustments in these precipitating factors can reduce the total load to the affected area and ameliorate symptoms.


The physical examination typically reveals local tenderness over the involved bone.5 It is important to be aware of surface and deep bone anatomy to comprehensively examine the affected area and compare the injured with the uninjured side. For example, palpation of the distal tibia in cases of stress fracture reveals focal tenderness and swelling. Certain bones, such as the tibia, fibula, and metatarsals, lend themselves well to palpation because of their well-defined anatomical boundaries and the absence of overlying muscle. Others, such as the pars interarticularis of the spine and the femur, make direct palpation impossible. Other tests for the clinical detection of stress fracture such as the hop test (tibia), fulcrum test (femur), and spinal extension test (pars interarticularis) are helpful but not as reliable as direct palpation.

In the foot and ankle, as well as for lesions in the femoral neck, it is helpful to perform successive articular manipulation. This maneuver can cause pain in a joint in proximity to a stress fracture or in a joint that may have direct subchondral involvement of the bone or joint affected.28

As with the history, risk factors that can be detected on physical examination should be looked for. Varus alignment of the lower extremity, true leg length discrepancies, femoral neck anteversion, muscle weakness, excessive Q angles, and excessive subtalar pronation or a pes cavus style foot should be noted.6,29,30 For example, it has been suggested that excessively pronated feet may be more common in tibial and tarsal bone stress fractures, whereas cavus feet may be a feature of metatarsal and femoral fractures.29 Another example is Morton foot with a short hypermobile first ray and long second ray, which is associated with second metatarsal fractures.31 Adjustments, such as muscular strengthening or the prescription of corrective foot orthotics, can lessen the overall magnitude of the load imparted to the affected site. Treadmill gait analysis may be useful to bring out more subtle aspects of malalignment.


Radiographic findings are usually seen after 2 to 8 weeks of symptoms, and in the early stages of these injuries, the sensitivity of radiography may be as low as 10%; at follow-up, 30% to 70%. The sensitivity of this method also depends on the bone involved. Radiography findings correlate with the MRI signs of the fracture line or callus, but the early phases of bone stress injuries verified with MRI cannot reliably be seen with radiographs.21

The most common sign in early stress fractures is a region of focal periosteal bone formation, often subtle in nature. The "gray cortex" sign (a cortical area of decreased density) also may be seen and is an early sign of stress fracture.32 It is postulated that focal hyperemia and edema with early resorption of calcium deposits are responsible for this initial "graying" of the cortex. Other radiological abnormalities may include osteopenia, endosteal reaction, ill-defined cortical margin, and, in severe cases, a discrete partial or complete fracture.

Radionuclide scanning is a more sensitive but less specific method for imaging bony stress injuries.33-36 Radionuclide technetium Tc 99 diphosphonate triple-phase scanning can provide the diagnosis as early as 2 to 8 days after the onset of symptoms.37 In acute stress fractures, all 3 phases of the bone scan are positive. The first and second phases, taken immediately and 1 minute after intravenous injection of the tracer, can gauge the age and severity of bony injuries and help to differentiate soft tissue inflammation from bony injury. On the 3- to 6-hour delayed image, the uptake of tracer is proportional to the rate of osteoblastic activity, extraction efficiency, and the amount of tracer delivered per unit time or blood flow.38 One must be aware of the possibility of increased uptake in nonpainful sites, indicating subclinical accelerated remodeling.39 Reproducible classification schemes have been devised that correlate the degree and extent of radionuclide uptake with the severity and acuteness of injury.36 As the bony lesion heals, the perfusion returns to normal first, followed by the normalization of the blood pool image a few weeks later. Focal increased uptake on the delayed scan resolves last because of ongoing bony remodeling and generally lags behind the disappearance of pain.38 False-negative bone scans involving injuries to the proximal femur and tibia have been reported.40-42 Occasionally, this has led to an undetected early stress injury that has progressed to complete fracture.

Pathological conditions such as infections and inflammatory disorders, tumors, arthropathies, or bone infarctions can also result in a positive bone scan.21

Ultrasound has limited diagnostic value in bone stress injuries. Occasionally, ultrasound can detect, mainly in metatarsals and in the lower leg, changes such as periosteal and muscle edema, cortical fracture line, and callus. Power Doppler imaging shows increased perfusion at the injury. However, the diagnosis must be confirmed with some other imaging modality.21

Computed tomography scan is useful in differentiating conditions that mimic stress fractures on bone scan, such as osteoid osteoma, osteomyelitis with Brodie abscess, and various malignancies. It is also helpful in detecting fracture lines as evidence of stress fractures and often can differentiate between stress fracture and stress reaction.43

Magnetic resonance imaging with fat suppression technique has shown promise in grading the progressive stages of stress fracture severity.44-46 A 4-stage grading system has been developed for tibial stress injuries at our institution, and in our experience, a modified version of this protocol also can be used with other types of stress fractures. A grade 1 injury simply shows periosteal edema on the fat-suppressed images. With grade 2, abnormal increased signal intensity is also seen within the marrow cavity or along the endosteal surface on fat-suppressed T2-weighted images. In grade 3 injuries, signal abnormalities are also present on T1-weighted images. This abnormal signal is secondary to edema or hemorrhage related to accumulating microdamage and the associated reparative response.44,45,47,48 In grade 4 injuries, an actual fracture line is present often seen on both T1- and T2-weighted images. Magnetic resonance imaging offers the advantages of multiplanar capability, high sensitivity for pathology, ability to precisely define the location and extent of bony injury, lack of exposure to ionizing radiation, and significantly less imaging time than a 3-phase bone scan.

Several fat-suppression techniques such as short tau inversion recovery are used to maximize the sensitivity of MRI in bone stress injuries and consequently to improve its diagnostic accuracy. Short tau inversion recovery and fat-suppressed T2-weighted images have shown higher sensitivity and accuracy rates than T1-weighted images.

Reported false-negative MR findings have been because of reader errors, suboptimal choice of imaging planes and sequences, inhomogeneities in fat suppression, and partial volume effects.21 As with any MR examination, it is important to use dedicated radiofrequency coils for high-quality imaging and to have the patient mark the area of pain with MRI-visible marker capsules.

It has not, however, been well established whether stress reactions detected on MRI are always related to clinical symptoms. Twenty-one asymptomatic runners were followed by Bergman et al39 with MRI of the tibia. Nine (43%) of them showed abnormalities indicating stress injuries. After at least 12 months, none of the asymptomatic runners developed a bone stress injury. These findings underscore the importance of correlating MRI findings with clinical findings for both type and location before making therapeutic decisions.


It is important to distinguish those stress fractures at risk for delayed union, nonunion, fracture with displacement, or any stress fracture with an intra-articular component (Table 1). In general, treatment of these higher risk stress fractures mandates immediate diagnosis, aggressive treatment, and occasionally internal fixation.30

Critical and Less Critical Stress Fractures

Less critical or not-at-risk fractures can be treated witha 2-phase protocol.30 Phase 1 includes pain control through local physiotherapy, nonsteroidal anti-inflammatory medication, ice massage, and physical therapy modalities. Weight bearing is allowed for normal activities within the tolerance of pain. The offending activity, such as running, is discontinued. If the athlete is unable to ambulate pain-free, they should be temporarily immobilized using, for example, a walking boot. A modified activity program is designed, one that maintains strength and fitness but reduces impact loading to the skeleton. Activities such as pool running, elliptical exercise machines, cycling, or StairMaster can maintain strength and fitness before the reintroduction of impact loading activities.49 Underwater and antigravity treadmills are also used in our clinics as an excellent way to gradually reintroduce the body to running activity.

Phase 2, graduated return to sport, begins when the athlete has been pain-free for 10 to 14 days. The specific length of time will depend on a host of factors, including the severity and chronicity of the condition and premorbid functional level of the athlete. As a rule, 1 week after the resolution of focal bony tenderness, the athlete can return to running, starting at half their usual pace and distance, running only every other day for the first 2 weeks. Then, during a 3- to 6-week period, a gradual increase in distance and frequency is permitted. Once they can run the distance required for training, the pace may be increased.30

In the athlete who has an abnormally pronated or supinated foot, the likelihood of additional stress fractures developing may be diminished using an orthosis. Functional foot orthoses are capable of either reducing abnormal pronation in those patients with a markedly everted hindfoot or introducing normal pronation in athletes with a rigid inverted hindfoot. If inadequate shock absorption has precipitated the stress fracture (typically, a fifth metatarsal or fibular stress fracture) and the athlete does not have adequate subtalar motion at the heel contact to reach a vertical heel position (uncompensated or partially compensated hindfoot varus), attempts should be made to increase shock absorption through the use of a softer type of orthotic material.50

Emphasis needs to be placed on careful evaluation of the athlete's shoes.51 Footwear should be regularly inspected and replaced to prevent loss of shock-absorption function. This typically occurs in running athletes after 300 to 350 miles of use, depending on the type of shoe, type of surface, and body weight. There are now shoe designs available for all types of foot structures. Shoe characteristics such as proper heel width, proper heel counter support, a firm midsole, and a straight last are all important factors in trying to maintain neutral alignment of the subtalar joint in the athlete who excessively pronates. The rigid cavus foot does best with an air sole, softer midsole, narrow flair, and curved slip lasting.

Many female runners who sustain stress fractures have menarche at a later age, fewer menses per year, and lower bone mineral density at the spine. Those who sustain stress fractures in the tibia often have lower tibia bone density.13,52-55 It is thus recommended that any female distance runner with a stress fracture should be questioned for a history of late onset menarche or history of irregular menses or amenorrhea. If there is a positive history, then consideration should be given to obtaining a bone mineral density test and endocrine workup.56,57 Calcium supplementation as well as hormonal replacement therapy in the form of a birth control pill should be prescribed when indicated. Barrow and Saha56 found that estrogen replacement in the form of birth control pills had a protective effect on bone breakdown if taken for 1 year; however, the optimal treatment is always resumption of normal menses and eating habits.58 Additionally, female distance runners are known to have a higher incidence of eating disorders, which itself may lead to amenorrhea or nutritional deficiencies.55 This should be thoroughly evaluated and psychological and nutritional counseling recommended as appropriate.

One promising treatment in stress fractures is pamidronate, which is a biphosphonate currently used in the management of osteoporosis, hypercalcemia, and metastatic bone disease. Stewart et al59 reported on the use of intravenous pamidronate on 5 symptomatic collegiate athletes who had tibial stress fractures. Four of 5 subjects improved and were able to continue training without symptoms within 72 hours. These investigators believe that the treatment is promising and plan to do a prospective study.



One of the most common location of stress fractures in the pelvis is the ischiopubic ramus, often in the inferior pubic ramus adjacent to the symphysis.60,61 These can be mistaken for an adductor strain or even osteitis pubis. Stress fractures also can occur in the sacrum62-66 and typically present with unilateral pelvic pain localized to the sacroiliac joint area, mimicking sacroiliitis (Fig. 1). Of the 16 cases of fatigue-type sacral stress previously reported in the literature, 9 occurred in runners, and 4 were found in military recruits. The runners are usually female with a history of amenorrhea and low bone density, suggesting that bone insufficiency may be a contributing factor.

Sacral stress fracture in a 22-year-old female distance runner. A, Axial T1-weighted image (TR = 520, TE = 14) shows hypointense edema signal in the left sacral ala (arrows). B, Axial T2-weighted image with fat suppression (TR = 5460, TE = 75) shows a subtle low signal line (arrowhead) centered in the area of marrow edema (arrows). C, Coronal T1-weighted image (TR = 500, TE = 14) again shows the marrow edema in the left sacrum (arrows), with a low signal line allowing the diagnosis of fracture. D, Coronal T2-weighted image with fat suppression (TR = 4666, TE = 105) better demonstrates the fracture line centered in the edema (arrows). E, Coronal T2-weighted scan inadvertently performed without fat suppression (TR = 4166, TE = 105) demonstrates the fracture line (arrow), but the extensive area of edema revealed with fat suppression (B and D) is barely detectable because of the bright marrow fat signal (arrowheads). Because of such diminished sensitivity for marrow changes, suppression of fat is considered mandatory for detection of stress injuries.

More recently, we have reported sacral stress fractures in 21 distance runners (12 women and 9 men), who had 22 fractures. Fifteen runners were on the Stanford cross-country and track teams, 5 were members of the local postcollege running club, and 1 was a longtime recreational runner. Nine of the women had a history of amenorrhea at the time of their injuries or in the past.67 This is in line with the work of Marx et al68 that a stress fracture in a cancellous bone such as the sacrum in a female athlete may be a warning sign of osteopenia. It is thus recommended that young women who have documented stress fractures of cancellous bone or cortical bone (with risk factors for osteopenia) undergo bone density evaluation.

The unilateral nature of sacral stress injuries also has been attributed to leg length discrepancy, with the longer side more commonly affected.69 Magnetic resonance imaging is the imaging modality of choice because plain-film findings are usually negative, and bone scan can be nonspecific. Indeed plain radiography of the sacrum may be not only unhelpful but misleading in many cases because of overlying bowel gas and fecal material.66

On MRIs, stress fractures in the sacrum show intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images in the anterior aspect of the sacral ala (Fig. 1), sometimes as a stress reaction without a linear fracture component, sometimes with a fracture line present.70

In the Stanford case series, 15 sacral stress fractures were confirmed by MRI, 9 by bone scan, and 2 by both imaging studies. Of the 15 who had MRI studies, 9 showed evidence of a discrete fracture with cortical disruption, and 6 had evidence of marrow edema without evidence of cortical involvement.67 When a fracture line is present, most often, the appearance is an oblique low-signal line surrounded by edema in the upper sacral ala, without displacement or visible fracture gap as may be seen in acute traumatic sacral fractures.

Treatment for both of the above pelvic stress fractures requires a period of rest and temporary use of crutches if there is any pain during ambulation. Symptoms usually resolve within several weeks, and a gradual return to running activity can typically be safely advised between 10 and 12 weeks.

Femoral Neck

Stress fractures of the femoral neck account for approximately 11% of stress fractures in athletes.71 These fractures should be considered in any athlete, especially a distance runner who presents with hip, thigh, or groin pain. Symptoms are worse with weight bearing, and there is often reduced range of movement in the hip, particularly internal rotation.72 A report by Shin et al73 suggests that MRI may be more specific than a bone scan in detecting stress fractures of the hip and in differentiating other causes of hip pain including synovial pit, iliopsoas muscle tear or tendinitis, obturator externus tendinitis, arthropathy, or focal bone abnormalities such as avascular necrosis or cysts.

There are 2 types of stress fracture of the femoral neck: the distraction or tension type and the compression type. Biomechanical studies have shown strain measurements higher in compression on the concave side of the calcar and neck as compared with the tension strains measured on the convex side.74 The distraction fractures are common in older patients and characteristically begin as cortical defects in the superior aspect of the femoral neck. Because this fracture develops perpendicular to the lines of stress, it is at higher risk for progression to complete fracture and displacement and must be detected early. An undisplaced distraction type fracture requires bed rest until passive movements of the hip are pain-free and radiographs show evidence of callus formation. A displaced fracture requires surgical reduction and internal fixation.17

Compression fractures are more common in younger athletic patients and are located at the cortex of the mid or lower medial margin of the femoral neck (Fig. 2). The early radiographic appearance of these fractures is subtle endosteal lysis or sclerosis along the inferior cortex of the femoral neck. This may be followed by progressive sclerosis of the region and appearance of a fracture line. If the radiographic findings are subtle or absent, MRI can be used to detect marrow edema and sometimes the presence of low-signal intensity fracture line that is often best seen on T2-weighted images, outlined by the high-signal intensity of adjacent bone marrow. The marrow edema can be subtle and occasionally is located low on the femoral neck, close to the lesser trochanter.70 An example of such an injury is shown in Fig. 3. In this anatomical area, it is important to be aware of a normal condensation of bone projecting into the medullary canal of the low femoral neck called the calcar femorale to avoid mistaking this finding for a fracture line on MRI.

Midfemoral neck stress fracture in a 20-year-old female collegiate basketball player. A, Coronal T1-weighted MRI (TR = 600, TE = 15) of the left hip shows extensive marrow edema (black arrows) and a low-signal fracture line (white arrow) along the medial compressive aspect of the femoral neck. B, Coronal T2-weighted MRI with fat suppression (TR = 4500, TE = 72) shows marrow edema (white arrows), partial fracture (black arrow), and periosteal edema.
Stress reaction at the level of the lesser trochanter in a 20-year-old female soccer player. A, Coronal T2-weighted scan with fat suppression (TR = 4650, TE = 54) shows marrow edema along the endosteal surface of the inferomedial femoral neck. B, Axial T1-weighted image (TR = 600, TE = 14) shows a normal low signal line (arrow) known as the calcar femorale, which should not be confused with a fracture line. C, Axial T2-weighted image with fat suppression (TR = 4266, TE = 64) shows that the marrow edema (arrows) is near the calcar femorale. D, Axial CT image in a different patient, showing that the calcar (arrow) is a normal dense condensation of bone, and not a fracture line.

If there is no fracture line present, treatment is conservative, with a period of non-weight-bearing to allow healing. Athletes are allowed to continue conditioning exercises such as swimming, or cycling during the period of rest for their injured femur. The return-to-play criteria are based on asymptomatic full weight bearing, no pain with passive range of motion of the hip, and usually follow-up imaging studies with signs of a healed fracture.71 As a rule, 2 to 3 months are required for complete healing of stress fractures of this type.

Surgical management of this injury is considered under the following circumstances: failure of nonoperative management, prophylactic stabilization of a fracture at high risk for displacement, any displaced femoral stress fracture, and malunion or nonunion.71

Femoral Shaft

The femur is a long bone that is tubular in shape with a thick cortex and an anterolateral bow in the proximal and middle third of the bone.75 These anatomical features help to accommodate stress placed on the femur during standing, walking, and running. Stresses applied to the femur during the running cycle can be estimated to approximate 3 times body weight.76 The bowed configuration of the femoral shaft dictates that during weight bearing, the medial side is under compression and the lateral side is under tension. In vitro biomechanical studies on loaded cadaver femurs using strain gauges applied to the cortex have shown that the posteromedial cortex of the proximal femur has the greatest strain and is particularly susceptible to repetitive submaximal stresses.74 In this region, there are also significant muscular forces related to the origin of the vastus medialis and the insertion of a large portion of the adductor muscle group.

Stress fractures of the femoral shaft have been documented in the literature with increasing frequency in recent years (Fig. 4). In 1990, an article by Volpin et al77 reported on 257 consecutive stress fractures in military recruits with 22.5% of these fractures found in the femoral shaft. In a smaller study, Johnson et al25 found a similar incidence of 20.6% femoral shaft stress fractures during a 2-year period for a varsity collegiate sports program. In their series of 34 stress fractures, 8 were in the femur, with 7 located in the femoral shaft, and 1 in the femoral neck. Kang et al78 also described 7 cases of stress fractures of the femoral shaft in women's college lacrosse.

Femoral diaphyseal stress fracture in a 21-year-old female basketball player. Patient had insidious onset of pain during the season. A, Coronal T1-weighted image (TR = 500, TE = 22) shows an essentially normal appearance of the proximal femoral shaft. B, Coronal T2-weighted image with fat suppression (TR = 4050, TE = 96) shows periosteal reaction (large arrows) as well as endosteal edema (small arrows). C, Axial T1-weighted image (TR = 583, TE = 22) shows thickening of the medial femoral cortex. D, Corresponding T2-weighted image with fat suppression (TR = 5050, TE = 96) shows periosteal reaction with a thin curvilinear area of intracortical signal as well as endosteal edema (arrowhead). E, Computed tomographic image (1.25 mm of section thickness, bone reconstruction kernel) performed on the same day as MRI shows periosteal reaction (white arrows) and intracortical lucency (black arrow) consistent with limited intracortical fracture.

We have described a series of 25 cases in our track-and-field varsity team members and recreational runners during a period of 10 years (1992-2002).79 In our retrospective review, all injuries except 2 involved the medial femoral cortex on the compressive side; the 2 exceptions involved the anterior and posterior cortices of proximal femoral diaphysis.79

Athletes with femoral shaft stress injuries typically complain of an insidious onset of vague poorly localized thigh pain that is activity related. In the initial stages, the pain is often attributed to a muscle strain or tear. If training continues after the onset of symptoms, the pain progresses to the point where it is experienced not only with running but also with ambulation and even during rest at night. Rarely, the athlete may experience little or no pain and seeks medical attention only after displacement of the fracture.80,81

Physical examination only rarely reveals swelling, limited range of motion, or pain with forced rotation.82 The "fulcrum test" can be helpful in localizing the anatomical site of involvement.25 For this test, the athlete is seated on the examining table with the lower legs dangling. The examiner's arm is used as a fulcrum under the thigh and is moved from distal to proximal thigh as gentle pressure is applied to the dorsum of the knee with the opposite hand. At the point of the fulcrum under the stress fracture, gentle pressure on the knee produces a sharper and more localized pain. The "hop" test may also be useful.72

Magnetic resonance imaging shows periosteal as well as bone marrow edema involving the medial aspect of the femur approximately at the junction of the proximal and middle thirds of the femoral diaphysis (Fig. 4), sometimes with a fracture line present as well.70 In the Stanford case series, 12 of 25 cases had both MRI and bone scan, and there was a close correlation between the 2 methods (91.7%, Spearman correlation coefficient). However, compared with scintigraphy, MRI had the capability to show more detailed anatomical information, such as periosteal edema, bone marrow edema, and fracture line.79

Provided there is no evidence of full cortical break or displacement, once the athlete can ambulate without pain, a cross-training program is appropriate. When the patient is pain-free with normal weight-bearing activities, a gradual return to athletics can begin. Typically, the athlete gradually returns to a running program at 8 to 12 weeks after the injury. Delayed union or nonunion of femoral diaphyseal stress fracture is rare after conservative therapy; if present, treatment with an intramedullary rod may be considered.79

Ivkovik et al83 proposed a new treatment algorithm to stress fractures of femoral shaft. It is carried out in 4 phases, each lasting 3 weeks, and the move to the next phase is based on the result of the tests (fulcrum and hop) carried out at the end of the previous phase. They treated 7 top-level athletes who were followed for 48 to 96 months. During follow-up, there was no recurrence of discomfort or pain, and all the athletes eventually returned to competition level.

Stress fractures of the distal femur are uncommon compared with femoral neck or diaphyseal lesions. An example of a stress fracture in the distal femoral metaphysis is shown in Fig. 5. Although most stress injuries are not immediately adjacent to the joint, it is increasingly suggested that lesions previously thought to represent spontaneous osteonecrosis of the knee or avascular necrosis may, in some cases, represent subchondral insufficiency fractures.84

Stress fracture of distal femoral metaphysis in a 19-year-old male recreational athlete. A, Coronal T1-weighted image (TR = 800, TE = 19) shows low signal line (arrows) in the medial femoral diaphysis. B, Sagittal proton density-weighted image (TR = 4000, TE = 18) shows fracture line (arrow). C, Sagittal fat-suppressed T2-weighted image (TR = 4000 TE 48) shows geographic marrow edema (arrows) surrounding area of fracture.


The patella is a rare site of stress fracture.85,86 Fractures here may appear as vertical or transverse fracture lines. The transverse fractures are prone to displacement, and immobilization is recommended.87 Longitudinal stress fractures can occur in the lateral patella facet. If healing does not occur and displacement creates incongruity of the articular surfaces, excision of the lateral fragment may be useful.88


Tibial Stress Injuries

Many athletes, particularly runners, commonly experience pain along the medial border of the tibia related to training. Orava and Puranen89 found that pain in this location from medial tibial stress syndrome, and tibial stress fractures accounted for 75% of 465 injuries causing exertional leg pain in a sports medicine clinic. It is often difficult to distinguish clinically between medial tibial stress syndrome (tibial periostitis) and the more severe tibial stress reaction or fracture.90,91

The physical examination with tibial periostitis reveals a diffuse area of tenderness over the posterior medial edge of the tibia. The pain is occasionally aggravated by testing muscle strength actively, particularly in those muscles that have origins on the posterior medial tibial border including the soleus (best tested by repetitive toe raises), posterior tibialis, and flexor digitorum longus.

The key symptoms that help distinguish tibial stress reaction and fracture from medial tibial stress syndrome are pain persisting after running and pain with daily ambulation. Physical examination findings such as localized tibial tenderness and pain with direct or indirect (at a distance from the site of tenderness) percussion over the bone also correlate with more extensive marrow involvement and cortical abnormalities on MRI.46 Additionally, pain in the proximal portion of the tibia is rare for shin splints but can be seen in approximately 25% to 43% of tibial stress fractures.46,56

Athletes prone to tibial stress injuries often have a tendency toward increased subtalar pronation because of a combination of factors including reduced ankle dorsiflexion secondary to tightness in the gastrocsoleus musculature, a standing foot angle less than 140 degrees (weight-bearing measurement of the angle between the medial malleolar-navicular prominence, the navicular prominence, and the head of the first metatarsal), a higher incidence of hindfoot and forefoot varus, and greater hindfoot movement during running than noninjured controls.6,92,93 It has been found that not only the degree of pronation but also the velocity of pronation are important discriminators between athletes with and without medial tibial stress syndrome.92 Thus, many athletes benefit from a foot orthosis to help control pronation and dissipate increased stress to the tibia and supporting musculature.

A study46 comparing bone scan and MRI to diagnose tibial stress injuries concluded that the periostitis (seen as periosteal edema on MRI) may be the initial injury on a spectrum that if allowed to progress may evolve into a more serious bone injury. Figure 6 shows an example of a tibial stress reaction.

Tibial stress reaction in a 22-year-old collegiate runner. A, Axial T1-weighted image (TR = 500, TE = 16) shows location of marker capsules at point of maximum pain (arrow). B, Axial T2-weighted image with fat suppression (TR = 4000, TE = 72) at same level demonstrates periosteal edema (large arrows) and endosteal edema (small arrows). C, Sagittal T1-weighted image (TR = 520, TE = 14) shows low signal in the marrow cavity (large arrows). Note presence of a normal nutrient vessel above this area (small arrow). D, Sagittal T2-weighted image with fat suppression (TR = 4200, TE = 54) shows extent of marrow edema (arrows).

Gaeta et al94 compared CT, MRI, and bone scan in 42 athletes with early tibial stress injuries with 10 asymptomatic athletes in the control group. Sensitivity of MRI, CT, and bone scintigraphy was 88%, 42%, and 74%, respectively. Specificity was 100% for MRI and CT. They concluded that MRI is the single best technique in assessing patients with suspected tibial stress injuries. Besides the fact of lacking specificity, bone scintigraphy failure in the identification of lesions in several cases maybe because of the absence of significant osteoblastic response in the early stress reactions. Computed tomography may have a role in early stage injuries, because it was found to be the best method in detecting osteopenia, the earliest sign of fatigue damage of the cortical bone.

The temporary cessation of running is essential to allow for bony remodeling and repair. This can range from a few days to 3 weeks for a minor injury to, albeit infrequently, 12 weeks for a severe injury with frank cortical fracture. If there is pain with daily activities, a pneumatic tibial brace can be used to immobilize distal and midtibial injuries.95,96

Atypical Stress Fractures of the Anterior Midtibia

Stress fractures of the anterior cortex of the midtibia are unique and require a different treatment regimen. These injuries occur most commonly in athletes performing jumping and leaping activities, accounting for their rare occurrence in distance runners.97,98 They are characterized by tenderness that may be more diffuse than local. Routine roentgenograms show a radiolucent cortical defect surrounded by sclerosis, known as the "dreaded black line" for its propensity to nonunion. In some cases, multiple such lines may be present (Fig. 7). Bone scans can be negative if the lesion is metabolically inactive (fibrous union) or can show linear uptake compatible with periostitis. Occurring on the tension side of bone, in a region of reduced vascularity, these are prone to delayed union or progression to complete fracture. These patients require treatment with non-weight-bearing immobilization for 6 to 8 weeks and also may benefit from electrical stimulation. Surgical excision and bone grafting or more definitive and aggressive placement of an intramedullary rod is indicated after 3 to 6 months of failed closed management.99-101

Dreaded black lines. Patient was a 21-year-old football player with 5 years of intermittent, but worsening, bilateral anterior shin pain. Lateral radiograph of the right tibia shows 4 transverse areas of intracortical lucency (arrows) as well as somewhat diffuse thickening of the anterior tibial cortex. Patient underwent intramedullary rod fixation to prevent progression to complete fracture during continued athletic activity.

Stress Fracture of the Medial Tibial Plateau

The medial tibial plateau is an unusual site of stress fracture.102,103 Tenderness is located along the anteromedial aspect of the proximal tibia just below the medial joint line. This injury is often misdiagnosed as pes anserinus tendinitis or bursitis (Fig 8). If radiographs are positive, they typically show a linear transverse region of sclerosis 2 to 3 mm thick in the medial tibial plateau on either side of the physeal scar. An MRI examination may demonstrate bone marrow edema of the medial tibial plateau before radiographic signs appear, with periosteal edema present as well and sometimes presence of fracture line.70 Use of a long-leg brace may be necessary for proper immobilization, especially for grade 4 injuries with a cortical break.

Proximal tibial stress fracture in a 21-year-old female basketball player. A, Coronal T1-weighted image (TR = 716, TE = 8) shows low signal partial fracture line in medial tibia (arrows). B, Coronal T2-weighted image with fat suppression (TR = 4916, TE = 50) shows extensive marrow edema in the medial tibial plateau and metaphysis (arrows). C, Axial proton density-weighted image with fat suppression (TR = 5100, TE = 11) shows medial tibial periosteal reaction (arrows). Such reactive changes from the osseous stress injury account for the difficulty in distinguishing this injury from soft tissue processes such as pes anserinus bursitis.

Differential Diagnosis

The differential diagnosis of tibial stress fractures should include periostitis, exertional compartment syndromes, particularly of the deep posterior compartment, and popliteal artery entrapment syndrome. An exertional compartment syndrome is suggested when patients complain of exertional aching or crampy leg pain, tightness, or even weakness. The symptoms are often bilateral, located along the muscle involved, and may be associated with numbness or tingling in the distribution of the involved compartment.30,104-108 Popliteal artery entrapment presents with symptoms of intermittent claudication including calf pain, cramping, coolness, and, at times, paresthesias into the foot.30


Fibular stress fractures are relatively common. Although fibular stress fractures can occur more proximally, the majority occur in the lower third of the fibula, just proximal to the tibiofibular ligament attachment.109,110 These athletes are often found to have a cavus-type foot. The subcutaneus location of the fibula makes it easy to recreate symptoms with direct palpation over the involved bone. Radiographs are often positive, although MR examination becomes positive earlier after injury, showing periosteal as well as bone marrow edema and often fracture line.70 If there are any neuritic components to the pain complaint, consideration should be given to anterior-lateral exertional compartment syndrome or peroneal nerve entrapment. Fibular stress fractures are noncritical injuries, and a gradual return to running can typically resume when local tenderness resolves.

Medial Malleolus

Stress fracture of the medial malleolus is an uncommon cause of medial ankle pain in athletes. The repetitive stress of running and jumping can create a vertical stress fracture starting at the junction of the medial malleolus and the tibial plafond and continuing proximally and slightly medially. Shelbourne et al111 in 1988 proposed that athletes with radiographic signs of a medial malleolar fracture, especially a displaced fracture, who desire early return to full participation should be treated by open reduction and internal fixation. Radiographs may be nondiagnostic, whereas MRI shows focal bone marrow edema and sometimes a well-defined vertical fracture line.70,112

Nonsurgical treatment is appropriate for essentially all stress fractures of the medial malleolus. Treatment involves modified rest for 3 to 8 weeks followed by a gradual return to elevated levels of activity. Complete rest is avoided, particularly in the high-level athlete, because of the adverse effects of atrophy and deconditioning. Pneumatic ankle braces have been used effectively. To return to activity in most cases can be expected in 6 to 8 weeks.

The presence of a radiographically detectable fracture line, particularly in a high-level or in-season athlete, or displacement of the fracture is reported as an indication for surgicalintervention, although these recommendations have been made based on small case series without control groups.112


Calcaneal stress fractures present as heel pain with localized tenderness over the bone, usually in the body of the calcaneus posterior to the talus.113 Pain elicited by squeezing the calcaneus from both sides simultaneously can usually differentiate this condition from retrocalcaneal bursitis, Achilles tendinitis, plantar nerve entrapment, subtalar arthritis, and radiculopathy. Radiographs generally become positive within the first month after pain presentation and show callus formation perpendicular to the trabecular axis of the calcaneus, usually located between the calcaneal tuberosity and the posterior facet of the subtalar joint. Magnetic resonance imaging demonstrates marrow edema and sometimes a fracture line in a distribution subjacent to the posterior subtalar joint or the calcaneal tuberosity.70 This is a noncritical stress fracture with rapid healing, and return to activity is usually possible by 4 to 6 weeks. A less common type of calcaneal stress lesion involves the anterior process of the calcaneus (Fig. 9).114

Stress reaction in the anterior process of the calcaneus in a 18-year-old female cross-country runner. A, Sagittal T1-weighted image (TR = 616, TE = 22) shows location of the calcaneal anterior process (arrow) and mild decreased marrow signal. B, Sagittal T2-weighted image with fat suppression (TR = 3500, TE = 78) shows marrow edema in the anterior process (large arrows) without a discrete fracture line. Patient also had marrow edema in the tarsal navicular as part of a navicular stress fracture (not fully shown; see Fig. 10).

Tarsal Bones

Various tarsal bones can develop stress fractures, including the navicular, the medial cuneiform, and the lateral process of the talus.115-118 Tarsal navicular stress fractures deserve special mention as they are particularly difficult to diagnose in their early stages and have a high risk of nonunion (Fig. 10). These fractures occur more frequently in basketball players and runners.101 Athletes often present with a history of vague activity-related midfoot pain with associated tenderness over the dorsal border of the navicular near the talonavicular joint (the "N" spot).118 The symptoms are often mistaken for an arch strain or inflammation of the posterior tibial tendon. These fractures have been seen in patients with all foot types.119,120 Anatomical foot abnormalities that might concentrate stress on the tarsal navicular include a short first metatarsal, metatarsal adductus, narrowing of the medial aspect of the talonavicular joint, plantarward displacement of the talus and navicular with respect to the cuneiforms, limited ankle dorsiflexion, limited subtalar motion, and talar beaking.119,121

Tarsal navicular stress fracture in an 19-year-old male basketball player. A, Axial T1-weighted image (TR = 600, TE = 17) shows low-signal fracture line in the proximal dorsal aspect of the navicular (arrow). Note curvilinear band of low signal along the proximal aspect of the navicular, which represents a normal area of dense cortical bone at this articulation. B, Fracture line (arrow) and surrounding edema are well seen on axial T2-weighted image with fat suppression (TR = 4500, TE = 54). C, Coronal T2-weighted image with fat suppression (TR = 4000 TE 72) shows that the fracture line (arrows) extends from dorsal to plantar approximately one third of the width of the bone. D, Computed tomographic image (1.25 mm of section thickness, bone reconstruction kernel) in the coronal plane, performed 4 weeks after MR study to assess for healing. Lucent fracture line is visible, and there is dorsal navicular callus formation, consistent with healing response. Note that the sclerosis adjacent to the fracture is often because of the normal cortical condensation of the proximal navicular as opposed to reactive sclerosis.

Plain radiographs are rarely helpful in detecting navicular stress fractures, particularly with an incomplete fracture. Special anteroposterior views of the foot are recommended with the foot supinated and the medial side of the forefoot elevated so that the dorsal surface is perpendicular to the radiograph.122 Marginal sclerosis is a normal finding in the proximal articular margin of the navicular.119,122 One also must be aware of a bipartite or accessory navicular bone, which is usually asymptomatic. It has a rounded appearance on radiograph, rather than the jagged appearance of a fracture.

Definitive diagnosis usually requires bone scan or MRI. Thin-section CT (0.5-1.25 mm) is also recommended in coronal and transaxial planes to the navicular to detect early separation of bone fragments, which may alter the treatment toward early internal fixation or at the very least indicate a more prolonged period of immobilization.28,118 In addition, CT is useful to evaluate for formation of callus along the dorsal surface of the navicular as healing proceeds (Fig. 10D).

The most common site of stress fracture within the navicular is the central third, which is an area of relative avascularity.119,121 Fractures tend to occur along the proximal dorsal aspect of the bone and have a sagittal or oblique sagittal orientation. Significant disability can result with delayed diagnosis or inadequate treatment. The protocol for treatment of an uncomplicated partial stress fracture or nondisplaced complete stress fracture of this bone (documented by CT scan) should include at least 6 weeks of non-weight-bearing cast immobilization until the navicular is no longer tender. This is followed by a further 6-week program of rehabilitation that should include joint mobilization, release of soft tissue tightness, and correction of muscle weakness as a residual of the prolonged immobilization. A semirigid custom orthotic can be used for foot control and arch support in the rehabilitation phase and after return to running. Displaced complete fractures and nonunion or delayed union of a nondisplaced fracture should be treated with internal fixation or bone grafting as necessary, followed by immobilization and non-weight-bearing until union has occurred.119 Conversely, treatment for bone scan or MRI positive and CT negative stress fractures of the tarsal bone is more liberal, with immobilization until clinical symptoms clear and then progressive return to activity as tolerated.

Burne et al123 conducted a retrospective study of 11 patients who received nonoperative treatment of navicular stress fractures, with a minimum follow-up of 1 year. They found that few patients received standard of care treatment with non-weight-bearing cast immobilization for 6 weeks, and the clinical results were disappointing. No particular imaging findings by MRI or CT, were associated with clinical outcome.

Saxena et al124 reviewed a treatment of 22 navicular stress fractures and used the CT fracture pattern to classify the lesions. Type 1 shows a cortical break, type 2 fractures propagate into the navicular body, and type 3 fractures propagate into the opposite cortex. This classification also includes modifiers A (avascular necrosis of a portion of the navicular), C (cystic changes of the fracture), and S (sclerosis of the margins of the fracture). Based on their findings, they recommend surgery for patients with these modifiers, particularly with type 2 and 3 injuries. These same authors in a prospective study compared 19 athletes to the previously treated group. They confirmed the findings that the more involved the fracture, in general, the longer the healing time. Also, they reaffirm the recommendation of early operative intervention for types 2 and 3 injuries. Return to activity for the all groups was approximately 4 months.125 Stress fractures of the talus, cuboid, and cuneiform bones are uncommon. A stress fracture of the cuboid is shown in Fig. 11. In general, joint involvement, displacement, and nonunion do not occur. Treatment can be the same as that for other noncritical stress fractures.115,126-129 Stress fractures of the body of the talus, however, can extend into the subtalar joint, which places them into the critical at-risk category and requires 4 to 6 weeks of cast immobilization and occasionally open reduction and internal fixation.116,130

Cuboid stress fracture in a 20-year-old runner. A, Axial T1-weighted image (TR = 600, TE = 14) shows partial fracture (white arrow) surrounded by low signal edema (black arrows). B, Axial T2-weighted image (TR = 4500, TE = 72) shows fracture line (black arrow) and edema (white arrows).


Stress fractures of the metatarsal bones were first described in military recruits and referred to as a "march fracture." They are less common in athletes, accounting for 9% of all stress fractures in a study of 320 stress fractures in athletes by Matheson et al.29 The fracture typically occurs in the neck or distal shaft, with the second and third metatarsals most commonly affected. The diagnosis is straightforward with point tenderness and often-local swelling over the bone. Radiographic examination shows periosteal bone formation, but in the very early stages, MRI often can show pronounced periosteal and marrow edema at the fracture site, and sometimes a well-defined fracture line.70Figure 12 illustrates the radiographic and Fig. 13 the MR appearance of a fourth metatarsal stress fracture in a male collegiate basketball player.

Stress fracture of the fourth metatarsal in a 20-year-old male basketball player. Sequence of radiographs shows normal findings at 1 week after onset of pain (A), with evolution to (B) an undisplaced transverse fracture 4 weeks later. C, Follow-up image 8 weeks after initial radiographs shows fairly mature callus formation but with fracture line remaining partially visible (arrow). At this point, the patient returned to practice and competition without pain or later recurrence.
Fourth metatarsal stress fracture on MRI (same patient as shown in Figure 12). A, Axial T1-weighted MRI (TR = 516, TE = 17) 2 weeks after the initial negative radiographs shows extensive low signal in the fourth metatarsal shaft (arrows) and transverse band of low signal across the middiaphysis. B, Corresponding T2-weighted image with fat suppression (TR = 3800 TE 52) shows extensive marrow edema, periosteal reaction, and a discrete band of low signal representing the fracture and early callus formation (arrows).

These are noncritical stress fractures, and cross-training can begin as soon as painful ambulation subsides. Six to 8 weeks is usually necessary to permit full healing and return to running. Initial management includes a metatarsal pad placed behind the area of the fracture to help dissipate the stress more evenly and some type of hard-soled shoe or walking cast. Because athletes prone to these stress fractures often have a rigid pes cavus foot type, an athletic shoe with extra cushioning or use of an orthotic insert made of a softer shock absorbing material can help prevent future injuries.

Two types of metatarsal fractures deserve special mention. The first is at the base of the second metatarsal and is known as the dancer's fracture. Pain is noted to be greatest when in the full en pointe position. During this maneuver, the foot is maximally plantarflexed, and weight is borne on the plantar aspect and tip of the first and second distal phalanges. The injury involves the volar and medial aspect of Lisfranc joint and should be recognized early and treated with at least 4 weeks of non-weight-bearing immobilization.17,131

Stress fractures of the proximal fifth metatarsal diaphysis that occur more than approximately 1.5 cm distal to the tuberosity are known as the Jones fracture.132,133 The chief symptom is pain and tenderness in and around the fifth metatarsal, sometimes accompanied by swelling. It is important to differentiate this fracture from the acute avulsion fracture of the tuberosity of the fifth metatarsal. The Jones fracture in the athlete often blurs the distinction between a classic stress fracture and a fracture from a single traumatic event (Fig. 14). Even when an athlete reports symptoms related to a single incident, repetitive microtrauma may have predisposed the bone toward injury. A review of 63 cases by Josefsson et al134 found that 59% could be classified as stress fractures. This was in line with the findings of Torg et al135 that of 46 patients, about half were stress fractures, whereas many that were not classified as pure stress fractures did show some evidence of stress reaction.

Fifth metatarsal fracture in a 19-year-old male basketball player. Oblique radiograph shows typical location of fracture in the proximal fifth metatarsal (arrow), often on the lateral and plantar aspect of the bone.

Careful review of radiographs, especially at the plantar lateral aspect of the fifth metatarsal, often reveal evidence of chronic stress reaction, showing this to be an acute-on-chronic phenomenon. Early radiographs can be unremarkable, and follow-up films may demonstrate callus formation or lucent fracture line.101

The stress fractures of the fifth metatarsal have a prolonged healing time and significant risk of refracture after nonoperative treatment. Consequently, there has been a trend toward primary surgical fixation.101,134,136

Surgical management of nondisplaced fracture is routinely uncomplicated. Postoperative care consists of early range of motion exercises and weight bearing as tolerated. Return to sports generally is permitted after healing, usually 6 to 8 weeks postoperatively. The displaced stress fractures can be more complicated and require reduction and internal fixation. The use of bone grafting is somewhat controversial. Postoperative care is generally more conservative compared with that after internal fixation of a nondisplaced fracture and thus has a longer time to return to play.101


Stress fracture of a sesamoid of the great toe can be particularly disabling and can result in delayed union or nonunion. Athletes typically present with the gradual development of unilateral plantar pain, the medial sesamoid being more frequently involved than the lateral. Passive distal push of the sesamoid, direct tenderness, and sesamoid area pain with stretch of the flexor hallucis suggest the diagnosis. Radiographic changes may be difficult to detect for months. Occasionally, axial views or magnification views can assist in the diagnosis. Separation of the sesamoid fragments and irregular edges suggest a stress fracture rather than a bipartite sesamoid. Because a bone scan is nonspecific, CT scan or MRI is often indicated to confirm the diagnosis. Oloff and Schulhofer137 recommends MRI to visualize the associated soft tissues and differentiate fractures from bipartite sesamoids, fracture partitions, nonunions, and avascular necrosis. Magnetic resosnace imaging can detect bone marrow edema, presence of fracture line, and joint effusion or synovitis.70

Rest from the offending activity is clearly advised. Treatment involves casting in a non-weight-bearing short-leg cast with specific prevention of dorsiflexion for 6 weeks. Surgical excision is advocated if conservative treatment fails and usually provides symptom relief. This should only be done as a last resort for the tibial sesamoid, because hallux abductus may develop.137


Stress fractures are relatively common overuse injuries seen in athletes, particularly in running athletes. Clearly, prevention or early intervention is the preferable course of action. The key to the evaluation is a thorough history and examination addressing all possible contributing factors including training errors, biomechanical predisposition, muscle and flexibility imbalances, and inappropriate footwear. Because these injuries are often insidious in nature, a strong index of suspicion is often necessary for prompt detection. Once the diagnosis is made, the sports medicine physician must then be able to classify the injury as critical, less critical, or noncritical to make appropriate treatment decisions. Plain radiography, MRI, and radionuclide bone scanning play key roles in the detection and staging of osseous stress injuries, whereas CT plays a supplemental role for confirmation of fracture lines and to assess healing in selected patients. Radiologists involved in sports imaging need to have an appreciation for the mechanisms and different types and locations of stress injuries to ensure athletes' uncomplicated and timely return to high-level activity.


1. Stanitski CL, McMaster JH, Scranton PE. On the nature of stress fractures. Am J Sports Med. 1978;6:391-396.
2. Li G, Zhang S, Chen C, et al. Radiologic and histologic analysis of stress fracture in rabbit tibias. Am J Sports Med. 1985;13:285-294.
3. Markey KL. Stress fractures. Clin Sports Med. 1987;6:405-425.
4. Daffner RH, Pavlov H. Stress fractures: current concepts. AJR Am J Roentgenol. 1992;159:245-252.
5. Brukner P, Bennel K, Gordon M. Stress Fractures. Malden, MA: Blackwell Science; 1999.
6. James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med. 1978;6:40-50.
7. Jones BH, Harris JM, Vinh TN, et al. Exercise induced stress fractures and stress reactions of bone: epidemiology, etiology and classification. Exerc Sport Sci Rev. 1989;17:379-422.
8. Johanson MA. Contributing factors in microtrauma injuries of the lower extremity. J Back Musculoskel Rehabil. 1992;2:12-25.
9. Macera CA. Lower extremity injuries in runners: advances in prediction. Sports Med. 1992;13:50-57.
10. Brubaker CE, James SL. Injuries to runners. J Sports Med. 1974; 2:189-198.
11. James SL, Jones DC. Biomechanical aspects of distance running injuries. In: Cavanagh PR, ed. Biomechanics of Distance Running. Champaign, IL: Human Kinetics Books; 1990:249-269.
12. Giladi M, Milgrom C, Stein M, et al. External rotation of the hip: a predictor of risk for stress fractures. Clin Orthop. 1987;216:131-134.
13. Bennell KL, Malcolm SA, Thomas PR, et al. Risk factors for stress fractures in female athletes: a twelve month prospective study. Am J Sports Med. 1996;24:810-818.
14. Garrett WE Jr, Safran MR, Seaber AV, et al. Biomechanical comparison of stimulated and nonstimulated skeletal muscle pulled to failure. Am J Sports Med. 1987;15:448-454.
15. Crossley K, Bennel K, Wrigley T, et al. Ground reaction forces, bone characteristics, and tibial stress fracture in male runners. Med Sci Sports Exerc. 1999;31:1088-1093.
16. Cleek TM, Whalen RT. Effect of activity and age on long bones using anew densitometric technique. Med Sci Sports Exerc. 2005;37:1806-1813.
17. Brukner PD, Bennell KL. Stress fractures in runners. J Back Musculoskel Rehabil. 1995;5:341-351.
18. Protzman RR, Griffs CG. Stress fractures in men and women undergoing military training. II. J Bone Joint Surg. 1977;59A:825.
19. Brudvig TJG, Gudjer TD, Obermeyer L. Stress fractures in 295 trainees. A one year study of incidence as related to age, sex and race. Mil Med. 1983;148:666-867.
20. Pester S, Smith PC. Stress fractures in the lower extremity of soldiers in basic training. Orthop Rev. 1992;21:297-303.
21. Kiuru MJ, Pihlajamaki HK, Ahovuo JA. Bone stress injuries. Acta Radiol. 2004;45:317-326.
22. Snyder RA, Koester MC, Dunn WR. Epidemiology of stress fractures. Clin Sports Med. 2006;25:37-52.
23. Brunet ME, Cook SD, Brinker MR, et al. A survey of running injuries in 1505 competitive and recreational runners. J Sports Med Phys Fit. 1990;30:307-315.
24. O'Toole ML. Prevention and treatment of injuries to runners. Med Sci Sports Exerc. 1992;24(suppl):360-363.
25. Johnson AW, Weiss CB, Wheeler DL. Stress fractures of the femoral shaft in athletes-more common than expected. Am J Sports Med. 1994;22:248-256.
26. Goldberg B, Pecora C. Stress fractures. A risk of increased training in freshmen. Phys Sports Med. 1994;22:68-78.
27. Brukner PD, Bradshaw C, Khan<given-names/>, et al. Stress fractures, a review of 180 cases. Clin J Sport Med. 1996;6:85-89.
28. McBryde AM. Stress fractures. In: Baxter DE, ed. The Foot and Ankle in Sport. St Louis, MO: Mosby-Year Book; 1995:81-93.
29. Matheson GO, Clement DB, Mckenzie DC, et al. Stress fractures in athletes: a study of 320 cases. Am J Sports Med. 1987;15:46-58.
30. Andrish JT. The leg. In: Delee JC, Drez D, Jr, eds. Orthopedic Sports Medicine: Principle and Practice. Philadelphia, PA: WB Saunders; 1994:1603-1631.
31. Khan K, Brown J, Way S, et al. Overuse injuries in classical ballet. Sports Med. 1995;19:341-357.
32. Mulligan EM. The "gray" cortex: an early sign of stress fracture. Skel Radiol. 1995;24:201-.
33. Geslin GE, Thrall JH, Espinosa JL, et al. Early detection of stress fractures using Tc-99m-polyphosphate. Radiology. 1976;121:683-687.
34. Prather JL, Nusynowitz ML, Snoudy HA, et al. Scintigraphic findings in stress fractures. J Bone Joint Surg. 1977;59:869-874.
35. Wilcox JR, Moniot AL, Green JP. Bone scanning in the evaluation of exercise related stress injuries. Radiology. 1977;123:699-703.
36. Zwas ST, Elkanovitch R, Frank G. Interpretation and classification of bone scintigraphic findings in stress fractures. J Nucl Med. 1987;28:452-457.
37. Roub LW, Gumerman LW, Hanley EN, et al. Bone stress: a radionuclide imaging prospective. Radiology. 1979;132:431-438.
38. Ammann W, Matheson GO. Radionuclide imaging in the detection of stress fractures. Clin J Sport Med. 1991;1:115-122.
39. Bergman AG, Fredericson M, Ho C, et al. Asymptomatic tibial stress reactions: MRI detection and clinical follow-up in distance runners. AJR Am J Roentgenol. 2004;183:635-638.
40. Milgrom C, Chisin R, Giladi M, et al. Negative bone scans in impending tibial stress fractures. Am J Sports Med. 1984;12:488-491.
41. Keen JS, Lash EG. Negative bone scan in a femoral neck stress fracture: a case report. Am J Sports Med. 1992;20:234-236.
42. Sterling JC, Webb RF, Meyers MC, et al. False negative bone scan in a female runner. Med Sci Sports Exerc. 1993;25:179-185.
43. Hoch AZ, Pepper M, Akuthota V. Stress fractures and knee injuries in runners. Phys Med Rehabil Clin N Am. 2005;16:749-777.
44. Stafford SA, Rosenthal DI, Gebhart MC, et al. MRI in stress fracture: a case report. AJR Am J Roentgenol. 1986;147:553-556.
45. Martin SD, Healy JH, Horowitz S. Stress fracture MRI. Orthopaedics. 1993;16:75-78.
46. Fredericson M, Bergman AG, Hoffman KL, et al. Tibial stress reaction in runners: correlation of clinical symptoms and scintigraphy with a new magnetic imaging grading system. Am J Sports Med. 1995;23:472-481.
47. Lee JK, Yao L. Stress fractures: MR imaging. Radiology. 1988;169: 217-220.
48. Anderson MW, Greenspan A. State of the art: stress fractures. Radiology. 1996;199:1-12.
49. Wilder RP, Brennan DK. Fundamentals and techniques of aqua running for athletic rehabilitation. J Back Musculoskel Rehabil. 1994;4:287-296.
50. Valmassy RL. Clinical Biomechanics of the Lower Extremities. St Louis, MO: Mosby-Year Book; 1996.
51. Cook SD, Brinker MR, Poche M. Running shoes: their relationship to running injuries. Sports Med. 1990;10:1-8.
52. Drinkwater BL, Nilson K, Chesnut CH III, et al. Bone mineral content of amenorrheic and eumenorrheic athletes. N Engl J Med. 1984;311:277-281.
53. Lloyd T, Trianatafyllou SJ, Baker ER, et al. Women athletes with menstrual irregularity have increased musculoskeletal injuries. Med Sci Sports Exerc. 1986;18:374-379.
54. Myburgh KH, Hutchins J, Fataar AB, et al. Low bone density is an etiologic factor for stress fractures in athletes. Ann Intern Med. 1990;113:754-759.
55. Bennell KL, Malcolm SA, Thomas <given-names/>, et al. Risk factors for stress fractures in female track and field athletes: a retrospective analysis. Clin J Sport Med. 1995;5:229-235.
56. Barrow GW, Saha S. Menstrual irregularity and stress fractures in collegiate female distance runners. Am J Sports Med. 1988;16:209-216.
57. Carbon R, Sambrook PN, Deakin V, et al. Bone density of elite female athletes with stress fractures. Med J Aust. 1990;153: 373-376.
58. Fredericson M, Kent K. Normalization of bone density in a previously amenorrheic runner with osteoporosis. Med Sci Sports Exerc. 2005; 37:1481-1486.
59. Stewart GW, Brunet ME, Manning MR, et al. Treatment of stress fractures in athletes with intravenous pamidronate. Clin J Sport Med. 2005;15:92-94.
60. Latshaw RF, Kantner TR, Kalenak A, et al. A pelvic stress fracture in a female jogger. Am J Sports Med. 1981;9:54-56.
61. Noakes TD, Smith JA, Lindenberg G, et al. Pelvic stress fractures in long distance runners. Am J Sports Med. 1985;13:120-123.
62. Marymount JV, Lynch MA, Henning CE. Exercise-related stress of the sacroiliac joint, an unusual cause of low back pain in athletes. Am J Sports Med. 1986;14:320-323.
63. Holtzhausen LM, Noakes TD. Stress fracture of the sacrum in two distance runners. Clin Sports Med. 1992;2:139-142.
64. Schils J, Hauzeur J. Stress fracture of the sacrum. Am J Sports Med. 1992;20:769-770.
65. Eller DJ, Katz DS, Bergman AG, et al. Sacral stress fractures in long-distance runners. Clin J Sport Med. 1997;7:222-225.
66. Featherstone T. Magnetic resonance imaging in the diagnosis of sacral stress fracture. Br J Sports Med. 1999;33:276-284.
67. Fredericson M, Salamancha L, Beaulieu C. Sacral stress fractures: tracking down nonspecific pain in distance runners. Phys Sports Med. 2003;31:31-42.
68. Marx RG, Saint-Phard D, Callahan LR, et al. Stress fractures sites related to underlying bone health in athletic females. Clin J Sport Med. 2001;11:73-76.
69. Friberg O. Leg length asymmetry in stress fractures: a clinical and radiological study. J Sports Med. 1982;22:485-488.
70. Bergman AG, Fredericson M. MR imaging of stress reactions, muscle injuries, and other overuse injuries in runners. Magn Reson Imaging Clin N Am. 1999;7:151-174.
71. DeFranco MJ, Recht M, Schils J, et al. Stress fractures of the femur in athletes. Clin Sports Med. 2006;25:89-103.
72. Clement DB, Ammann W, Taunton JE, et al. Exercise-induced stress injuries to the femur. Int J Sports Med. 1993;14:348-353.
73. Shin AY, Morin WD, Gorman JD, et al. The superiority of magnetic resonance imaging in differentiating the cause of hip pain in endurance athletes. Am J Sports Med. 1996;24:168-176.
74. Oh I, Harris WH. Proximal strain distribution in the loaded femur. J Bone Joint Surg. 1978;60A:75-85.
75. Brunet ME, Hontas RB. The thigh. In: Drez D, DeLee JC, eds. Orthopaedic Sports Medicine. Philadelphia, PA: WB Saunders; 1994:1087.
76. Sherman VM, Plyley MJ, Vogelgesand D, et al. Isokinetic strength during rehabilitation following arthrotomy: specificity of speed. Athl Train. 1981;18:138-141.
77. Volpin G, Hoerer D, Groisman G, et al. Stress fractures of the femoral neck following strenuous activity. J Orthop Trauma. 1990;4:394-398.
78. Kang L, Belcher D, Hulstyn MJ. Stress fractures of the femoral shaft in women's college lacrosse: a report of seven cases and review of the literature. Br J Sports Med. 2004;39:902-906.
79. Fredericson M, Jang KU, Bergman G, et al. Femoral diaphyseal stress fractures: results of a systematic bone scan and magnetic resonance imaging evaluation in 25 runners. Phys Ther Sport. 2004;5:188-193.
80. Provost RA, Morris JM. Fatigue fracture of the femoral shaft. J Bone Joint Surg. 1969;51:487-498.
81. Bargren JH, Tilson DH, Bridgeford OE. Prevention of displaced fatigue fractures of the femur. J Bone Joint Surg. 1971;53:1115-1117.
82. Butler JE, Brown SL, McConnell BG. Subtrochanteric stress fractures in runners. Am J Sports Med. 1982;10:228-232.
83. Ivkovic A, Bojanic I, Pecina M. Stress fractures of the femoral shaft in athletes: a new treatment algorithm. Br J Sports Med. 2006;40: 518-520.
84. Ramnath RR, Kattapuram SV. MR appearance of SONK-like subchondral abnormalities in the adult knee: SONK redefined. Skel Radiol. 2004;33:575-581.
85. Devas MB. Stress fractures of the patella. J Bone Joint Surg. 1960;42B:71-74.
86. Dickason JM, Fox JM. Fracture of the patella due to overuse syndrome in a child: a case report. Am J Sports Med. 1982;10:248-249.
87. Mata SG, Grande MM, Ovejero AH. Transverse stress fracture of the patella. Clin J Sport Med. 1996;6:259-261.
88. Hershman EB, Mailly T. Stress fractures. Clinics in Sports Med. 1990;9:183-214.
89. Orava S, Puranen J. Athlete's leg pains. Br J Sports Med. 1979;13: 92-97.
90. Jackson DW. Shinsplints: an update. Physician Sports Med. 1978;6:50-61.
91. Mubarak SJ, Guld RN, Lee YF, et al. The medial tibial stress syndrome. A cause of shin splints. Am J Sports Med. 1982;10:201-205.
92. Messier SP, Pittalla KA. Etiologic factors associated with selected running injuries. Med Sci Sports Exerc. 1988;20:501-505.
93. Sommer HM, Vallentyne SW. Effect of foot posture on the incidence ofmedial tibial stress syndrome. Med Sci Sports Exerc. 1995;27: 800-804.
94. Gaeta M, Minutoli F, Scribano E, et al. CT and MR imaging findings in athletes with early tibial stress injuries: comparison with bone scintigraphy findings and emphasis on cortical abnormalities. Radiology. 2005;235:553-561.
95. Whitlaw GP, Wetzler MJ, Levy AS, et al. A pneumatic leg brace for the treatment of tibial stress fractures. Clin Orthop. 1991;270:301-305.
96. Swenson JE, DeHaven KE, Sebastianelli WJ, et al. The effect of a pneumatic leg brace on return to play in athletes with tibial stress fractures. Am J Sports Med. 1997;25:322-328.
97. Orava S, Hulkko A. Stress fracture of the mid-tibial shaft. Acta Orthop Scand. 1984;55:35-37.
98. Kadel NJ, Teitz CC, Kronmal RA. Stress fractures in ballet dancers. Am J Sports Med. 1992;20:445-449.
99. Plasschaert VF, Johansson CG, Micheli LJ. Anterior tibial stress fracture treated with intramedullary nailing: a case report. Clin J Sport Med. 1995;5:58-62.
100. Brukner P, Fanton G, Bergman G, et al. Bilateral stress fractures of the anterior part of the tibial cortex. J Bone Joint Surg. 2000;82A:213-218.
101. Kaeding CC, Yu JR, Wright R, et al. Management and return to play of stress fractures. Clin J Sport Med. 2005;15:442-447.
102. Engber WD. Stress fractures of the medial tibial plateau. J Bone Joint Surg. 1977;59A:767-769.
103. Harolds JA. Fatigue fractures of the medial tibial plateau. South Med J. 1981;74:578-581.
104. Davey JR, Rorabeck CH, Fowler PJ. The tibialis posterior compartment syndrome: an unrecognized cause of exertional compartment syndrome. Am J Sports Med. 1984;12:391-396.
105. Fronek J, Mubarak SJ, Hargens AR, et al. Management of chronic exertional anterior compartment syndrome of the lower extremity. Clin Orthop Relat Res. 1987;220:217-227.
106. Jones DC, James SL. Overuse injuries of the lower extremity: shin splints, ilioitibial band friction syndrome, and exertional compartment syndromes. Clin Sports Med. 1987;6:273-290.
107. Bourne RB, Rorabeck CH. Compartment syndromes of the lower leg. Clin Orthop Relat Res. 1989;240:97-104.
108. Weinik MM, Falco FJ. Acute and chronic compartment syndromes of the lower leg. J Back Musculoskel Rehabil. 1992;2:17-25.
109. Burrows HJ. Fatigue fractures of the fibula. J Bone Joint Surg. 1948; 30B:266-279.
110. Blair WF, Manley SR. Stress fracture of the proximal fibula. Am J Sports Med. 1980;8:212-213.
111. Shelbourne K, Fisher D, Rettig A, et al. Stress fractures of the medial malleolus. Am J Sports Med. 1988;16:60-63.
112. Sherbondy PS, Sebastianelli WJ. Stress fractures of the medial malleolus and distal fibula. Clin Sports Med. 2006;25:129-137.
113. Pilgaard S. Stress fracture of the os calcis. Acta Orthop Scand. 1968;39:270-272.
114. Ouellette H, Salamipour H, Thomas BJ, et al. Incidence and MR imaging features of fractures of the anterior process of calcaneus in a consecutive patient population with ankle and foot symptoms. Skel Radiol. 2006;35:833-837.
115. Khan KM, Brukner PD, Bradshaw C. Stress fracture of the medial cuneiform bone in a runner. Clin Sports Med. 1993;3:262-264.
116. Motto SG. Stress fracture of the lateral process of the talus. J Sports Med Br. 1993;27:275-276.
117. Black KP, Ehlert KJ. Stress fracture of the lateral process of the talus in a runner. J Bone Joint Surg Am. 1994;3:441-443.
118. Khan KM, Brukner PD, Kearney C, et al. Tarsal navicular stress fracture in athletes. Sport Med. 1994;17:65-76.
119. Torg JS, Pavlov H, Cooley LH, et al. Stress fractures of the tarsal navicular. A retrospective review of 21 cases. J Bone Joint Surg. 1982;64A:700-712.
120. Hulko A, Orava S, Peltokallio P. Stress fracture of the navicular bone: nine cases in athletes. Acta Orthop Scand. 1985;56:503-505.
121. Fitch KD, Blackwell JD, Gilmour WN. Operation for non-union of navicular stress fracture of the tarsal navicular. J Bone Joint Surg. 1989;71B:105-110.
122. Pavlov H, Torg JS, Freiberger RH. Tarsal navicular stress fractures: radiographic evaluation. Radiology. 1983;148:641-645.
123. Burne SG, Mahoney CM, Forster BB, et al. Long-term outcome and clinicoradiological correlation using both computed tomography and magnetic resonance imaging. Am J Sports Med. 2005;33:1875-1881.
124. Saxena A, Fullem B, Hannaford D. Results of treatment of 22 navicular stress fractures and a new proposed radiographic classification system. J Foot Ankle Surg. 2000;39:96-103.
125. Saxena A, Fullem B. Navicular stress fractures: a prospective study on athletes. Foot Ankle Int. 2006;27:917-921.
126. Marymount JH, Mills GQ, Merritt WD, et al. Fractures of the lateral cuneiform bone in the absence of severe direct trauma. Am J Sports Med. 1980;8:135.
127. Meurman OA, Elving S. Case Reports. Stress fracture of the cuneiform bones. Br J Radiol. 1980;53:157.
128. Beaman DN, Roeser WM, Holmes JR, et al. Cuboid stress fractures: a report of two cases. Foot Ankle. 1993;14:525-528.
129. Chen JB. Cuboid stress fracture. A case report. J Am Podiatr Med Assoc. 1993;83:153-155.
130. Bradshaw C, Khan K, Brukner P. Stress fracture of the body of the talus in athletes demonstrated with computed tomography. Clin J Sport Med. 1996;6:48-51.
131. Micheli LJ, Sohn RS, Soloman R. Stress fractures of the second metatarsal involving Lisfranc's joint in ballet dancer: a new overuse injury of the foot. J Bone Joint Surg. 1985;67A:1372-1375.
132. Lehman R, Torg JS, Pavlov H, et al. Fractures of the base of the fifth metatarsal distal to the tuberosity: a review. Foot Ankle. 1987;7:245-252.
133. Lawrence SJ, Botte MJ. Jones' fractures and related fractures of the proximal fifth metatarsal. Foot Ankle. 1993;14:358-365.
134. Josefsson PO, Karlsson M, Redlund-Johnell, et al. Jones fracture: surgical versus nonsurgical treatment. Clin Orthop Relat Res. 1995;299:252-255.
135. Torg JS, Baulduini FC, Zelko RR, et al. Fractures of the base of the fifth metatarsal distal to the tuberosity: classification and guidelines for nonsurgical and surgical management. J Bone Joint Surg. 1984;66A:209-214.
136. Josefsson PO, Karlsson M, Redlund-Johnell, et al. Closed treatment of Jones fracture. Acta Orthop Scand. 1994;65:545-547.
137. Oloff LM, Schulhofer SD. Sesamoid complex disorders. Clin Podiatr Med Surg. 1996;13:497-513.

stress fracture; magnetic resonance imaging; athletic injury; overuse injury

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