Overview of stress fractures

INTRODUCTION — As defined below, stress fractures are overuse injuries to bones caused by repetitive stresses, either tensile or compressive. Stress fractures may be the result of a small number of repetitions with a relatively large load (eg, a military recruit marching for several miles with a heavy backpack), a large number of repetitions with a usual load (eg, an athlete training for a long-distance race), or a combination of increased load and increased repetitions.

An overview of the classification, risk factors, diagnosis, management, and prevention of stress fractures is presented here. Specific stress fractures are discussed separately:

●Foot and ankle stress fractures (see "Stress fractures of the metatarsal shaft" and "Proximal fifth metatarsal fractures", section on 'Stress fractures of proximal diaphysis: Zone 2 injury' and "Stress fractures of the tarsal (foot) navicular" and "Cuboid and cuneiform fractures" and "Calcaneus fractures", section on 'Stress fractures')

●Lower extremity stress fractures (see "Stress fractures of the tibia and fibula" and "Femoral stress fractures in adults")

●Upper extremity and torso stress fractures (see "Stress fractures of the humeral shaft" and "Initial evaluation and management of rib fractures")

DEFINITIONS

●Fracture – Fracture refers to the breaking of a bone. Complete fractures divide the affected bone into two or more pieces, while partial (incomplete) fractures do not extend through the cortex. An example of an incomplete fracture is the "greenstick" fracture, in which the convex side of a long bone is disrupted while the concave surface remains intact. These are most common in children.

●Stress fracture – A stress fracture occurs when a bone breaks after being subjected to repeated tensile or compressive stresses, none of which would be large enough individually to cause the bone to fail, in a person who is not known to have an underlying disease that would be expected to cause abnormal bone fragility.

●Stress reaction – A radiographic finding on computed tomography (CT), magnetic resonance imaging (MRI), or bone scan of increased metabolic activity at a site of bone turnover that does not yet show cortical disruption. Stress reactions are often asymptomatic but considered a precursor to a stress fracture.

●Bone stress injury – A term that includes all clinically symptomatic stress reactions and stress fractures.

●Insufficiency fracture – An insufficiency fracture occurs when the mechanical strength of a bone is reduced to the point at which a stress that would not fracture a healthy bone breaks the weak one. The condition that causes reduced bone strength typically does so throughout the skeleton (eg, osteoporosis, osteomalacia, or osteogenesis imperfecta) but may be more localized (eg, demineralization in a limb due to disuse).

Insufficiency fractures due to osteoporosis, pseudofractures, and radiolucent lines seen in the bones of patients with osteomalacia are reviewed elsewhere. (See "Clinical manifestations, diagnosis, and evaluation of osteoporosis in postmenopausal women" and "Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations and treatment" and "Epidemiology and etiology of osteomalacia".)

●Pathologic fracture – A pathologic fracture is due to a localized loss of strength in a bone from a disease process immediately underlying the bone. Examples of pathologic fractures include those that occur at sites of bone tumors (primary or metastatic), bone cysts, and infections.

PATHOPHYSIOLOGY — Bone remodels in response to a mechanical stress [1]. The rate and amount of remodeling depends upon the number and frequency of loading cycles a bone is subjected to (Wolff's law). An abrupt increase in the duration, intensity, or frequency of physical activity without adequate periods of rest may lead to pathologic changes in bone. These pathologic changes result from an imbalance between bone resorption and formation. During periods of intense exercise, bone formation lags behind bone resorption. This renders the bone susceptible to microfractures. Bone responds to this microscopic injury with a reparative response that includes edema, which can be visualized with magnetic resonance imaging (MRI). Some changes associated with stress fracture can appear on MRI before symptoms develop. (See 'Imaging studies' below.)

With continued overload, microfractures may propagate (symptoms generally develop during this process) and eventually coalesce into a discontinuity within the cortical bone (ie, a stress fracture). Continued overload can complete the fracture and result in displacement at the fracture site. In summary, stress fracture represents one point on a spectrum of stress-induced bone changes referred to as stress injury.

CLINICAL CLASSIFICATION (GRADING AND RISK OF COMPLICATIONS) — No gold-standard classification system has been developed for describing stress fractures [2]. Two clinically useful systems may be used: one describes severity based upon radiographic and clinical features, while another categorizes fractures as either high risk or low risk based upon location. Stress fractures have also been classified clinically on the basis of their risk of complications, such as fracture propagation or displacement, nonunion, persistent pain, avascular necrosis, reinjury, or inability to resume pre-injury level of activity [3,4]. A system involving magnetic resonance imaging (MRI) findings is described below. (See 'Magnetic resonance imaging' below.)

The distinction between "low-risk" and "high-risk" stress fractures is based primarily on the fracture site. Stress fractures at low-risk sites are unlikely to entail complications and are generally amenable to conservative management. In contrast, high-risk stress fractures are managed more aggressively, often surgically.

●Sites at high risk of complications:

•Spine – Pars interarticularis of the lumbar spine

•Hip and thigh – Femoral head, superior side of the femoral neck (ie, tension side)

•Knee and leg – Patella, anterior cortex of the tibia (ie, tension side)

•Multiple sites at ankle and foot – Medial malleolus, talus, tarsal navicular, proximal fifth and fourth metatarsals, base of the second metatarsal, great toe sesamoids

●Sites at low risk of complications:

•Second through fourth metatarsal shafts

•Posteromedial tibial shaft

•Proximal humerus or humeral shaft

•Ribs

•Sacrum

•Pubic ramus

EPIDEMIOLOGY — The incidence of stress fracture is less than 1 percent in the general population [5]. The incidence in athletic populations varies with the type of athlete; military recruits, runners, and gymnasts are considered the highest-risk populations. The incidence of lower extremity stress fracture in all United States military members between 2009 and 2012 was 5.69 per 1000 person-years [6].

The incidence of stress fractures among United States collegiate athletes was 5.70 per 100,000 athletic exposures (AEs) over a 10-year period [7]. In this study, the sports with the highest rates were women's cross country (28.6/100,000 AEs), women's gymnastics (25.6/100,000 AEs), and women's track (22.2/100,000 AEs). The metatarsals accounted for 38 percent of fractures, followed by the tibia (22 percent) and the low back and pelvis (12 percent). In sports with both female and male participants, the rate of stress fracture was over twice as high in females (9.13/100,000 AEs) as in males (4.44/100,000 AEs).

The incidence among United States high school athletes was 1.54 per 100,000 AEs over an eight-year period [8]. Again, rates were highest in girls' cross country (10.62), girls' gymnastics (7.43), and boys' cross country (5.42). The lower leg accounted for the most frequent site (40 percent), followed by the foot (35 percent) and low back and pelvis (15 percent), and the rate was higher in girls (2.22/100,000 AEs) than in boys (1.27/100,000 AEs).

RISK FACTORS — Important risk factors for developing stress fractures include a history of prior stress fracture, low level of physical fitness, increased volume and intensity of physical activity, menstrual irregularity, lower body mass index (BMI), diet poor in calcium, and low bone mineral density (table 1).

Those with the "female athlete triad" (low energy availability with or without an eating disorder, menstrual dysfunction, and low bone mineral density) are at high risk for stress fracture due to a combination of risk factors. The clinical syndrome "relative energy deficiency in sport" (RED-S) includes several features described below as risk factors. Some overlap with the female athlete triad, but this syndrome includes both males and females [9]. (See "Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations" and "Functional hypothalamic amenorrhea: Evaluation and management".)

Prior stress fracture — A history of stress fractures is a strong predictor of future stress fractures [10-15]. A systematic review of eight studies of stress fracture risk found that a prior history was the most significant risk factor (odds ratio [OR] 4.99, 95% CI 2.91-8.56) [13]. The relative risk (RR) is over sixfold in distance runners and military recruits with a history of at least one stress fracture [10,16]. Among track athletes, 60 percent of those who sustained a stress fracture had a history of stress fracture. The one-year recurrence rate in these athletes was 12.6 percent [11].

Activity-related factors

●Repetitive activities and high training volume – Specific repetitive activities predispose athletes to site-specific stress fractures. As examples, throwing athletes have an increased risk of humeral and scapular fractures, while runners are at increased risk for spine, pelvic, and lower extremity fractures, primarily of the tibia and metatarsals [5,8,10,17,18]. Gymnasts have an increased risk for stress fractures of the spine, wrist, and foot due to frequent loading of these areas. Stress fractures of the ribs may be seen in golfers and rowers. The following table lists the stress fractures associated with particular sports (table 2).

Time spent performing such activity is associated with increased risk. Among military trainees, higher total distance travelled on foot during training is associated with increased risk of bone stress injury [19]. Increased frequency of training is associated with greater risk of stress fracture in elite figure skaters, with those who train more than 12 times per week sustaining nearly double the incidence of ankle and tibia fractures as those who train less often [20].

Weightbearing bones, primarily those of the lower extremity, are at greatest risk for stress fracture. As an example, tibial fractures accounted for 49 percent of all stress fractures seen in athletes, followed in frequency by fractures of the metatarsals [17]. Greater than 12 hours of exercise per week is a risk factor for bone stress injury in females [21].

Non-athletes who abruptly increase their level of activity may also be at risk for stress fracture. An example would be the patient whose activity was restricted by the pain of arthritis who resumes walking after joint replacement surgery [22].

●Decreased physical fitness – Decreased muscle strength and endurance are associated with an increased incidence of stress fractures [23,24]. Muscles play a supportive role in bone health; when muscles are weak or fatigued, other musculoskeletal structures absorb greater impact. A dramatic increase in physical training may overwhelm the bones' capacity to compensate with normal remodeling. Specific factors associated with higher rates of stress fractures include >1 cm decrease in calf girth [5], less lean mass in the lower extremities [25], less than seven months of prior strength training [26], and poor lower extremity muscle strength [27]. Rowers with lower knee extensor to elbow extensor strength ratios also had a higher incidence of rib stress fractures in one retrospective case-control study [28].

Although muscle inflexibility has long been cited as a possible risk factor for stress fracture, its role remains unclear [23]. Among several prospective studies looking at ankle dorsiflexion, one found restricted flexibility to be associated with stress fractures [29] while two found no association [25,30]. One prospective study found decreased hamstring flexibility to be associated with tibial stress fractures in runners [31].

●Lower exercise levels prior to military training – Three prospective studies have reported that lower exercise levels (which are different than fitness levels) confer a higher risk of stress fracture [14,32,33]. Among United States Marine recruits, those who self-classified their activity level before basic training as "inactive" had a sixfold higher rate of stress fracture than those with "below average" or higher activity levels [32]. The incidence among Chinese military recruits with a history of fewer than seven hours per week of exercise before basic training was nearly twice that of recruits with more [14]. A study of Finnish military recruits found that those with a history of exercise more often than twice a week prior to the start of military training had a 60 percent lower incidence of stress fracture [33].

●Worn footwear – Recruits who begin basic training using old shoes have a higher incidence of stress fractures [32].

●Running surface – Two retrospective studies found no association between running surface and stress fractures [34,35], but one found that running on a treadmill reduced tibial strain compared with over-ground running [36].

Nutrition, bone health, and body composition

●Inadequate vitamin D and calcium – Vitamin D and calcium are essential for bone health and fracture prevention [37]. When the amounts of these nutrients are inadequate, bone is weakened and is potentially more susceptible to fractures of any kind.

A systematic review of eight observational studies, including 761 cases of stress fracture, reported an association between low serum 25-hydroxyvitamin D (25[OH]D) concentrations and lower extremity stress fractures among military personnel [38]. Two large retrospective studies of male and female United States Navy recruits reported a markedly higher incidence of stress fractures sustained during training among those with vitamin D deficiency [39,40]. Vitamin D deficiency and insufficiency were also seen in a high percentage (63 percent) of adolescents with pars interarticularis stress fractures [41]. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on 'Optimal intake to prevent deficiency'.)

Case-control studies show that lower calcium intake is associated with an increase in stress fracture incidence in females (RR 1.1 per 100 mg of decreased intake) [42,43].

●Disordered eating – Restricted caloric intake in female track and field athletes, gymnasts, and dancers correlates with an increased incidence of stress fracture [25,44]. Disordered eating deprives the body of the nutrients needed for bone and muscle metabolism in addition to contributing to other health risks. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis".)

●Decreased bone density – Lower bone mineral density, as assessed by quantitative ultrasonography or dual-energy x-ray absorptiometry (DEXA) scan, strongly correlates with an increased incidence of stress fractures in both males and females [10,25,42,45-48]. A family history of osteopenia or osteoporosis is associated with a threefold higher risk of stress fractures in adolescent female athletes [46].

●Nonsteroidal antiinflammatory drug (NSAID) use – In two large retrospective studies of active-duty United States military, use of NSAIDs in the prior 180 days was associated with an increased risk of stress fracture (RR 1.7 and 2.9). [49,50]. A possible mechanism involves interference with bone remodeling in response to a stress injury. (See "Nonselective NSAIDs: Overview of adverse effects", section on 'Healing of musculoskeletal injury'.)

●Extremes of body composition – Low BMI (less than about 21) is associated with increased risk of stress fractures in females [21,51] and males [51]. Among United States military recruits, males and females in the lowest deciles for body fat percentage had a slightly higher risk of stress fracture. In males, those with the highest body fat percentage were also at higher risk [52]. Among adolescents, lower BMI increases the risk of bone stress injury [53].

Anatomy and biomechanics

●Foot and hip anatomy – A systematic review found that extreme foot arch morphologies (pes planus or cavus) likely increase risk of tibial stress fractures, but no definitive conclusions could be drawn [54]. A prospective study of Royal Marine recruits showed a higher risk of second metatarsal stress fracture in those with pes cavus [55]. Radiographic findings of femoroacetabular impingement may be a risk factor for femoral neck stress fractures [56].

●Running biomechanics – A meta-analysis of 14 studies of limited quality in which runners with tibial stress fracture were compared with controls (ie, runners without fracture) failed to identify any association between tibial stress fractures and discrete ground reaction forces [57]. Findings from retrospective studies suggest that earlier hindfoot eversion [58] and shorter duration of foot pronation [59] are associated with higher tibial stress fracture rates. Delayed forefoot loading may be associated with metatarsal stress fractures [55].

Non-modifiable risk factors

●Female sex – Females are at greater risk than males of developing stress fractures. RR ranges from 1.2 to 10 depending upon the population studied (eg, athletes versus general population) and the fractures considered [5,6,8,13,15,51,60]. Females have 51 times the rate of sacral stress fractures but 3.4 times the rate of pubic ramus and proximal tibial stress fractures [27]. Although the reasons for this discrepancy remain unproven, higher rates of concomitant risk factors, such as decreased bone mineral density and disordered eating, likely contribute [5,61].

●Menstrual dysfunction – Amenorrhea is an independent risk factor for stress fractures in females [10,15,26,42,60,62,63].

The combination of low energy availability (with or without an eating disorder), menstrual irregularity, and low bone mineral density comprises the "female athlete triad" and places a female at greatly increased risk of stress fractures. Even those without the entire syndrome but with an elevated female athlete triad cumulative risk score demonstrate an increased risk for developing bone stress injuries [21,64,65]. This score is discussed further below. (See 'General guidelines' below and "Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations" and "Functional hypothalamic amenorrhea: Evaluation and management".)

Poor physical fitness may predispose some females to developing stress fractures. Studies of female military recruits show that many begin basic training at lower physical fitness levels than their male counterparts [66,67].

●Age – The incidence of stress fractures is greatest in patients aged 17 to 26 years, but this likely has more to do with increased activity than age. Two large prospective studies of military recruits found increased risk of stress fractures as age increased [27,51], and one reported a bimodal distribution with increased risk in those under 20 and over 40 [6].

●Race/ethnicity – In two large cohort studies [51,68] of United States military recruits, non-Hispanic Black Americans had the lowest risk of stress fracture. Non-Hispanic White Americans had the highest risk (RR 1.92), with other ethnicities at intermediate risk.

DIAGNOSIS

Overall approach — Early diagnosis is important for avoiding complications and a prolonged delay in return to activity. Key features include a history of localized pain of insidious onset that increases with activity and focal tenderness limited to the stress fracture site. While the history and physical examination findings are often sufficient for the diagnosis and management of low-risk stress fractures, their accuracy is limited. An algorithm summarizing our approach to the assessment of suspected stress fracture is provided (algorithm 1).

Plain radiographs are recommended initially, but advanced imaging may be helpful when high-risk stress fractures are suspected, early definitive diagnosis is necessary, or patients are not responding to usual treatment. Magnetic resonance imaging (MRI) is the best imaging technique to make a definitive diagnosis. (See 'Clinical classification (grading and risk of complications)' above and 'Imaging studies' below.)

The author treats clinically suspected low-risk stress fractures empirically and reserves advanced imaging for suspected high-risk stress fractures or low-risk fractures that are not responding after several weeks of treatment. In exceptional circumstances, such as elite athletes for whom early definitive treatment and prognostic information are more important, advanced imaging may be performed earlier.

History — A thorough history often provides the diagnosis. The clinician should inquire about likely risk factors and solicit a detailed description of the pain and any antecedent physical activity. Particularly important are recent changes in activity level and participation in athletic activities. Often, patients describe starting a new training program or significant changes in their training regimen (eg, boot camp, addition of hill runs, transition to a harder training surface). The following table lists the stress fractures associated with particular sports (table 2).

A dietary history is valuable for both males and females to exclude eating disorders and dietary deficiency of calcium or vitamin D. A menstrual history will help to screen for potential hormonal deficiencies.

Clinicians should look for risk factors by inquiring about the patient's general health, past and current medical conditions, medications, alcohol and tobacco use, occupation, previous injuries, and family history (especially of osteoporosis).

Pain description — Patients classically report the insidious onset of localized pain. The pain is initially related to activity and increases in severity with increased activity. If the patient continues in the inciting activity, symptoms worsen. Eventually, the pain is present during less strenuous activity and, ultimately, during rest. Occasionally, the patient experiences an abrupt increase in pain at the site of milder chronic symptoms, suggesting that a repeatedly stressed area of bone has completely fractured. Less frequently, a patient's initial presentation may involve the acute onset of severe pain resulting from a complete fracture at the site of a pre-existing stress fracture. (See 'Definitions' above.)

Physical examination — Focal tenderness of the affected bone is the most sensitive physical finding for diagnosing a stress fracture. Tenderness is usually limited to the site of injury unless a complete fracture is present, in which case the area of tenderness may be wider due to bleeding and inflammation.

Many stress fractures are preceded by a bone stress injury of lesser severity that may be more diffuse. As an example, shin splints often precede the development of a stress fracture of the medial tibial border, in which case tenderness may be present along several centimeters of the tibial shaft. However, once a fracture develops, the site of injury will likely demonstrate more focal tenderness. (See "Running injuries of the lower extremities: Patient evaluation and common conditions", section on 'Medial tibial stress syndrome (shin splints) and tibial stress fractures'.)

In areas where little soft tissue covers the injured bone, there may be subtle soft tissue swelling over the stress fracture and, occasionally, mild erythema. Bony callus may be palpable in chronic, severe cases. Defects of the cortical surface and bony crepitus are not present.

When the fracture site is not easily palpable, maneuvers to stress the bone at the area of pain may aid diagnosis. The fulcrum test may be useful when long bones are involved [69]. It is performed by placing one hand under the area that is painful and applying steady pressure while the other hand applies steady pressure at the end of the same bone. This creates a fulcrum effect that stresses the site of suspected injury. Increased pain at the area in question during the test is consistent with a stress fracture. The fulcrum test is neither sensitive nor specific, and imaging is needed to make a precise diagnosis. (See 'Imaging studies' below.)

Some clinicians use the hop test to help diagnose femoral neck stress fractures [17]. This test simply involves having the patient hop on the affected leg, which typically reproduces pain at the fracture site. The patient should stop hopping immediately if significant pain develops around the hip or groin while performing the test. While suggestive of injury, the hop test is nonspecific, and confirmatory imaging is necessary to make a definitive diagnosis. Some authors have expressed concern that repeated hopping risks converting the rare tension-side femoral neck stress fracture into a complete fracture, but we know of no actual cases where this has occurred. For patients who may have a femoral neck stress fracture and experience pain simply bearing weight, it is prudent to prescribe nonweightbearing status until appropriate imaging can be obtained.

The technique of placing a vibrating tuning fork directly over an area of injury to induce pain at a stress fracture site has shown widely disparate sensitivity and specificity in two studies and therefore cannot be recommended as a method to identify a stress fracture [70]. Therapeutic ultrasound placed in a similar manner had a pooled sensitivity of 64 percent and specificity of 63 percent for identifying stress fractures in one systematic review of seven studies, and thus, its usefulness for diagnosis is also limited [70]. Compared with bone scan, ultrasound demonstrated a sensitivity of 43 percent and specificity of 49 percent [71].

Biomechanical evaluation of the affected region should be done to identify factors that may have predisposed to injury or affect healing. In general, the entire affected limb and its attachments to the axial skeleton should be evaluated whenever a stress fracture is suspected. The examination should assess:

●Leg-length discrepancy (noted in 70 percent of patients with lower extremity stress fractures [25])

●Joint range of motion and ligamentous stability

●Muscle strength and flexibility

●Limb alignment (eg, genu varus or valgus)

●Foot type (eg, pes cavus or planus)

●Gait analysis in shoes worn during physical activity

●Core muscle strength (eg, abdominal, back, and hip musculature)

Imaging studies

Approach to stress fracture imaging — Often, history and examination provide the basis for clinicians to manage low-risk stress fractures without imaging studies (algorithm 1). Plain radiographs should be obtained initially and are helpful when positive due to their high specificity, but they are insensitive. If plain radiographs are negative but clinical suspicion remains high and a need for definitive diagnosis exists, MRI is recommended because it is both sensitive and specific. Bone scan is sensitive but nonspecific. Computed tomography (CT) is used as an adjunct if extensive bony injury is suspected because it provides greater anatomic detail of bone. Plain radiographs, MRI, and bone scan each have an associated injury severity grading system (table 3).

A systematic review of 21 studies, nearly all of high or moderate quality, of the diagnostic accuracy of imaging modalities for lower extremity stress fractures found MRI to be the most sensitive and most specific [72]. Bone scan was not recommended when MRI was available due to the former's low specificity (range 33 to 98 percent) and high ionizing radiation dose. CT was not recommended due to its high false-negative rate. The value of plain radiography lay in its specificity but was limited by a high false-negative rate.

Plain radiographs — Radiographs should be obtained but are typically normal for the first two to three weeks after the onset of symptoms, and findings may take months to appear [73]. Periosteal elevation, cortical thickening, sclerosis, and a true fracture line are all examples of positive findings (image 1 and image 2 and image 3). Severity grading based on appearance is described in the accompanying table (table 3). Although such findings are specific, plain radiographs have poor sensitivity in the detection of stress fractures [72]. Of note, periosteal elevation on plain radiograph correlates closely with high-grade stress fracture on MRI [74]. (See 'Magnetic resonance imaging' below.)

Magnetic resonance imaging — MRI is supplanting bone scan as the imaging study of choice for diagnosing bone stress injury. The systematic review of high- and moderate-quality studies discussed above found that MRI is as sensitive as bone scan and more specific [72], and it provides important prognostic information [75]. (See 'Approach to stress fracture imaging' above.)

MRI appears to be useful in determining the severity along the spectrum of bone stress injury and is better at differentiating pathologic fractures from stress fractures [76]. When an intraarticular stress fracture is suspected, MRI better distinguishes bone injury from ligament or cartilage injury. Additionally, MRI does not entail ionizing radiation, may be less expensive than a bone scan, and provides information about injury to surrounding soft tissues.

Though more specific than a bone scan, MRI findings must be interpreted with caution, especially when no clear fracture is present. Asymptomatic tibial stress reactions are seen in 43 percent of asymptomatic runners [77]. Findings such as isolated bone marrow edema are nonspecific and can occur with bone tumors, avascular necrosis, and osteomyelitis [78]. Correlation of MRI findings with the history and physical examination is critical for accurate diagnosis. MRI findings consistent with a stress fracture range from periosteal or bone marrow edema to frank cortical fracture lines [78,79].

A system to grade bone stress injury severity based on MRI findings has been developed (table 3) [80,81]:

●Grade 1 (mild) fractures show only periosteal edema (image 4)

●Grade 2 (moderate) fractures show bone marrow edema on T2-weighted images (image 5)

●Grade 3 (severe) fractures show marrow edema on both T1- and T2-weighted images (image 6)

●Grade 4 (severe) fractures show a cortical fracture line in addition to edema (image 7)

A simplified system has been proposed in which grades 1 and 2 are termed "low-grade" and grades 3 and 4 are termed "high-grade" fractures [82]. The use of these grading systems helps clinicians provide information about time to recovery. (See 'Return to activity' below.)

Bone scan — Radionuclide studies (three-phase bone scan) were traditionally used for diagnosis because they can show evidence of stress fracture within two to three days of injury and have high sensitivity (image 8). However, the specificity of bone scan is low [72]. Approximately 40 percent of positive findings occur at asymptomatic sites [60].

Bone scans can also be falsely positive with shin splints. Areas of increased uptake may represent subclinical sites of bone remodeling or stress reactions. Increased uptake can also appear in the setting of bone tumors, osteomyelitis, or avascular necrosis. Although rare, there are reports of false-negative bone scans [78,83]. Because of these limitations, MRI is supplanting bone scan as the diagnostic study of choice when plain radiographs are negative and confirmation of suspected stress fracture is needed. (See 'Magnetic resonance imaging' above.)

Acute stress fractures appear as discrete, localized, sometimes linear areas of increased uptake on all three phases (angiographic, soft tissue, and delayed phases) of a technetium-99 methylene diphosphonate bone scan. In contrast, shin splints are typically positive only during the delayed phase of the scan [84]. A system to grade stress fracture severity based on bone scan findings has been developed (table 3) [85].

Computed tomography — CT is limited as a primary diagnostic imaging modality by its high false-negative rate [72]. It can be considered if MRI is unavailable or inconclusive, but it is also useful as an adjunct study when plain films are positive and extensive bony injury is suspected because it provides greater anatomic detail of bone involvement (image 9). CT can also show fracture lines in long bones. In the setting of a negative plain radiograph and a positive bone scan, CT can differentiate between fracture and stress reaction or other conditions of the bone such as tumor or osteomyelitis [17].

Ultrasonography — Ultrasound continues to gain popularity as an imaging tool for musculoskeletal conditions, particularly as image resolution improves and clinicians gain experience. Ultrasound can display several findings suggestive of stress fracture, including hematoma, periosteal elevation, hypervascularity (image 10), and cortical defect over the area of tenderness (image 11) [86-89]. A systematic review of seven high-quality studies found ultrasound to be more sensitive than specific, signifying a low false-negative rate but a high false-positive rate in diagnosing tibia and metatarsal stress fractures, and concluded that it is best used (in trained hands) to rule out a stress fracture based on negative findings [72].

DIFFERENTIAL DIAGNOSIS — Several disorders can present with localized musculoskeletal pain. Tendinopathy, muscle strains, joint sprains, nerve entrapment syndromes, and compartment syndrome share some features with stress fractures. Bone stress reactions probably represent precursor lesions that will progress to stress fractures if the sites are not protected from further insults. Among runners, medial tibial stress syndrome (ie, "shin splints") is the most common example of this phenomenon. Neoplasm and infection represent the most worrisome diagnoses in the differential list. (See "Running injuries of the lower extremities: Patient evaluation and common conditions", section on 'Medial tibial stress syndrome (shin splints) and tibial stress fractures'.)

●Tendinopathy – Overuse syndromes frequently are due to tendinopathy, a condition characterized by chronic pain in the affected tendon. Onset is usually insidious. Tenderness is localized to the affected tendon, which can sometimes be difficult to distinguish from the underlying bones. Pain may be reproduced by passive stretch and resisted contraction of the affected tendon. (See "Overuse (persistent) tendinopathy: Overview of pathophysiology, epidemiology, and presentation".)

●Muscle strain – Localized pain may develop acutely or insidiously as a result of isolated trauma or repeated minor injuries to one or more muscles. Tenderness and pain with passive stretch or resisted contraction of the involved muscle are indicative of a muscle strain. A localized hematoma and/or palpable depression may develop at the site of a sizable muscle tear. Although radiographs do not reveal a fracture, this is also often true with stress fractures. (See "Running injuries of the lower extremities: Patient evaluation and common conditions", section on 'Labral tear'.)

●Ligament sprain – Ligamentous injuries are typically the result of a single episode of trauma, though repeated injury may lead to a subacute or chronic disorder that could raise suspicion for stress fracture. Tenderness with sprains is generally localized to the area of the affected ligaments. Stressing the ligaments reproduces or exacerbates the pain and may reveal ligamentous laxity.

●Nerve entrapment syndromes – In addition to pain, other neurologic symptoms, particularly paresthesia, numbness, and weakness, may be clues to the presence of a nerve entrapment syndrome of the upper or lower extremity. (See "Overview of upper extremity peripheral nerve syndromes" and "Overview of lower extremity peripheral nerve syndromes".)

●Exertional compartment syndrome – Compartment syndromes are caused by increased tissue pressure within a fascial compartment that compromises local circulation and neuromuscular function. In susceptible individuals, the compartment pressure increases with exercise, resulting in exercise-induced pain, tightness, distal paresthesia, muscle weakness, or numbness. Symptoms usually resolve within several minutes of rest. There may be no symptoms or diagnostic signs at rest; provocative testing and compartment pressure testing may be necessary. A more detailed discussion of exertional compartment syndrome is found separately. (See "Chronic exertional compartment syndrome".)

●Medial tibial stress syndrome (shin splints) – Shin splints are an inflammatory response of the connective tissue of the lower leg to repetitive loading. Unlike a stress fracture, the patient with shin splints has no discrete bone tenderness. Instead, diffuse tenderness over the middle to distal third of the tibial border (usually medial but sometimes lateral) is typically present. However, if overuse continues, shin splints may progress to a stress fracture without a clear demarcation of this change, and distinguishing between the two can sometimes be difficult clinically. Like stress fractures, shin splints develop in people who suddenly increase their level of physical activity. The change may be in intensity, frequency, or type of exercise. The most frequently associated exercise is running. Shin splints are discussed elsewhere. (See "Running injuries of the lower extremities: Patient evaluation and common conditions", section on 'Medial tibial stress syndrome (shin splints) and tibial stress fractures'.)

●Neoplasm – Bone pain due to neoplasm is generally characterized as being focal and constant. Painful benign and malignant neoplasms of bone can generally be differentiated from stress fractures by imaging studies. Lytic, blastic, and mixed lesions may be appreciated on plain radiographs. Malignant tumors may arise primarily from bone or be metastatic. The approach to the diagnosis of primary bone tumors and bone pain due to cancer, and the evaluation of a patient with a complete or impending pathologic fracture, are discussed separately. (See "Bone tumors: Diagnosis and biopsy techniques" and "Overview of cancer pain syndromes", section on 'Multifocal bone pain' and "Clinical presentation and evaluation of complete and impending pathologic fractures in patients with metastatic bone disease, multiple myeloma, and lymphoma".)

●Infection – Osteomyelitis can cause localized bone pain and tenderness. It can occur at any age and at different anatomic sites. Among adolescents and young adults, osteomyelitis of long bones is most prevalent and may present in similar fashion to a stress fracture. Bone infection that results from a contiguous soft tissue infection should be readily recognized in the extremities but may be more difficult to differentiate from a stress fracture in the bones of the pelvis.

Hematogenous seeding in older children and young adults generally affects the ends of long bones, while in skeletally mature adults, the vertebrae are most often affected. Laboratory tests and imaging studies may have some value, but it is not possible to exclude osteomyelitis on the basis of noninvasive studies. The clinical features and the approach to diagnosis of osteomyelitis are discussed elsewhere. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis" and "Hematogenous osteomyelitis in children: Clinical features and complications", section on 'Clinical features'.)

TREATMENT CONCEPTS

General approach — If a stress fracture is strongly suspected clinically or is confirmed with imaging, early intervention is needed to reduce pain, promote healing, and prevent further bone damage. The sooner treatment is begun, the quicker the patient returns to full activity [90]. Conservative management is recommended for low-risk fracture sites. Surgical consultation is necessary for patients with fractures at high-risk sites or for whom a lengthy rehabilitation process is untenable, such as some high-level athletes or laborers whose livelihoods depend upon a timely return to work.

Conservative management consists of the following:

●Acute pain control

●Protection of the fracture site with reduced weightbearing or splinting in selected stress fracture locations

●Reduction or modification of activities such that pain is not present

●Gradual resumption of activities if pain free

●Rehabilitative exercise to promote optimal biomechanics and fitness

●Risk factor reduction as indicated

●Proper nutrition, including additional calcium and vitamin D during treatment

Details about treatment are provided below and in reviews of specific fractures. (See "Stress fractures of the tibia and fibula" and "Stress fractures of the metatarsal shaft" and "Stress fractures of the humeral shaft" and "Proximal fifth metatarsal fractures", section on 'Stress fractures of proximal diaphysis: Zone 2 injury'.)

In some cases, the presence of a stress fracture may lead to diagnosis of relative energy deficiency in sport or the “female athlete triad." Management of these patients is discussed separately. (See "Functional hypothalamic amenorrhea: Evaluation and management".)

Low-risk sites — Fractures of the second and third metatarsal shafts, posteromedial tibial shaft, fibula, proximal humerus or humeral shaft, ribs, sacrum, and pubic rami are considered low risk for fracture propagation or nonunion [91]. These fractures usually heal with conservative treatment. (See 'Determining if conservative treatment is appropriate' below.)

As an example, tibia stress fractures commonly occur at the junction between the middle and distal thirds of the diaphysis on the compression side of the bone (posterior medial). In this case, a brief period of relative rest followed by gradual, progressive, nonpainful exercise over several weeks is appropriate therapy.

High-risk sites — Expert orthopedic or sports medicine consultation should be obtained for a stress fracture at any site with a high risk of complications, which may include fracture propagation or displacement, nonunion, avascular necrosis, need for surgery, persistent pain, or long-term disability. High-risk sites include the following:

●Pars interarticularis of the lumbar spine [92]

●Femoral head [93]

●Femoral neck [4,94]

●Patella

●Anterior cortex of the tibia (ie, tension side)

●Medial malleolus

●Talus

●Tarsal navicular

●Proximal fourth metatarsal

●Proximal fifth metatarsal shaft

●Great toe sesamoid

●Base of second metatarsal [3]

●Hallux sesamoids [4]

A systematic review and meta-analysis of 76 studies of bone stress injuries in athletes (n = 2974) found that these fractures were associated with higher complication rates, longer recovery times, and lower rates of return to full sport [4]. The following table summarizes the estimated time needed for return to full sport according to stress fracture location, radiographic severity, and risk classification (table 4). (See 'Return to activity' below.)

Determining if conservative treatment is appropriate — Although conservative treatment is generally preferred to surgical intervention in the management of stress fractures, each patient should be considered individually. An elite athlete or laborer may depend upon an early return to activity to remain competitive or earn their living. Such patients may benefit from more aggressive rehabilitation or from orthopedic consultation earlier in their course than those whose career or livelihood is not threatened by a longer period of rehabilitation. A patient may also require early surgical intervention if there is evidence of nonunion (ie, cyst formation or sclerosis surrounding the fracture) because such fractures are less likely to heal by conservative measures alone.

Elements of conservative care

Pain control — Ice (applied locally for 15 minutes every three hours as needed) and pain medication (acetaminophen or low-potency opiates) are used to control acute pain. The effect of nonsteroidal antiinflammatory drugs (NSAIDs) on fracture healing is discussed separately. (See "Nonselective NSAIDs: Overview of adverse effects", section on 'Possible effect on fracture healing'.)

Excessive analgesia may mask pain, making it difficult to gauge appropriate increases in physical activity during rehabilitation [95]. It is prudent to use as little analgesic medication as possible and to strongly discourage using analgesics as a means to increase pain-free activity.

Protection of the fracture site — The forces exerted on the injured bone must be reduced such that pain is eliminated in order to allow for bone remodeling and healing. As examples, high-risk femoral head and tension-side femoral neck stress fractures should be treated with crutches and complete nonweightbearing as soon as clinically suspected and continued until orthopedic consultation is obtained.

Other pelvic or lower extremity stress fractures should be treated with reduced weightbearing if walking causes persistent pain. In many foot stress fractures, protection with a controlled ankle motion (CAM) boot, hard-sole shoe, fracture boot, or leg splint eliminates pain with walking.

Bracing may be helpful in some instances, but studies may be limited depending on the type of stress fracture and clinical context. Use of a calf-length pneumatic brace for tibial stress fractures may reduce the time until pain-free return to play for some patients. Bracing of the spine may be indicated for some stress fractures of the pars interarticularis; orthopedic consultation is recommended for such injuries. (See "Stress fractures of the tibia and fibula".)

Activity modification — Modification of activities that place stress on the affected bones is critical to the successful treatment of stress fractures. Pain is typically used to judge the efficacy of activity modification. Simply put, activities should be limited to those that are pain free. Failure to do so may prolong healing time and increase the risk of completed fracture or nonunion.

Active individuals will not tolerate long periods of inactivity. It is mentally untenable and leads to cardiopulmonary deconditioning and muscle atrophy. Instead, patients should be encouraged to engage in activities that closely approximate their desired activity but are pain free. For instance, runners may walk briskly, use elliptical machines, perform shallow-end aquatic therapy or deep-water running, or run on a reduced-weightbearing treadmill machine. Cycling and swimming are excellent alternatives.

As healing progresses, exercises involving increasing amounts of bone stress can be added gradually as tolerated, using pain as a guide. Should the patient experience any pain at the fracture site, the activity should be replaced by an exercise that places less stress upon the healing bone.

Preventive measures should be considered, as discussed below, in order to reduce the risk of recurrence. (See 'Prevention' below.)

Rehabilitative exercise — Athletes, laborers, and patients with biomechanical problems predisposing to injury should participate in rehabilitation supervised by a knowledgeable physical therapist, athletic trainer, or comparable professional. The key principle during rehabilitation is protected, gradually progressive exercise that allows for adequate bone healing while promoting cardiorespiratory fitness, muscular strength, and flexibility. If supervised rehabilitation is not possible, education, home exercises, and close follow-up with the treating clinician are advisable.

Calcium and vitamin D — Although the evidence supporting these treatments is limited and based primarily upon studies of fracture prevention, throughout the course of treatment for a stress fracture, we suggest taking additional daily calcium (1500 mg) and vitamin D (800 to 2000 international units) to help ensure fracture healing. Calcium intake may be increased through dietary changes or supplementation; vitamin D intake is typically increased with oral supplements. (See 'Nutrition, bone health, and body composition' above.)

Therapies of uncertain benefit

●Therapeutic ultrasound – Multiple studies suggest that ultrasound accelerates the healing of acute fractures, but evidence for its efficacy in stress fractures is mixed. Several randomized trials have reported no clinical benefit in stress fractures treated with low-intensity pulsed ultrasound (LIPUS) [96-98]. However, two randomized trials, one blinded and one not, in Indian soldiers found that ultrasound treatment substantially reduced the time until return to full duty [99,100]. These protocols used 1 Watt/cm² of ultrasound energy for five minutes per day at the fracture site in addition to usual conservative therapy. LIPUS may be effective for particular types of stress fractures, but further analysis is needed to determine whether this is so and what protocols may be most effective.

●Extracorporeal shockwave therapy (ECSWT) – Reports of successful treatment of stress fracture with ECSWT in humans are limited, and further study is needed to determine effectiveness [101]. One randomized trial of fifth metatarsal stress fractures in football (soccer) players reported comparable outcomes from weekly ECSWT and surgery with intramedullary screw [102].

●Medications – A small retrospective cases series of subchondral stress fractures of the knee showed markedly faster healing by magnetic resonance imaging (MRI) assessment at 3 and 12 months in patients treated with the prostacyclin analogue iloprost compared with those treated with the analgesic tramadol [103]. Controlled trials are needed before the effectiveness of prostacyclin analogues for the treatment of stress fractures can be determined.

●Electrical stimulation – Capacitively coupled electric fields were not more effective than placebo in healing posteromedial tibial stress fractures in a randomized controlled trial [104].

FOLLOW-UP — The clinician should re-evaluate the patient every one to three weeks during the healing period. Those with high occupational or athletic demands warrant more frequent evaluation than recreational patients. Pain should progressively subside with treatment. If symptoms persist after several weeks, compliance with the treatment regimen should be ascertained. Compliant patients with persistent pain may need more restrictive activity modification, further protection of the bone, and a more gradual rehabilitation program. Imaging is needed if there is no clinical improvement despite six additional weeks of conservative management, including the additional measures described.

Once magnetic resonance imaging (MRI), radiographs, bone scan, or computed tomography (CT) confirms the diagnosis of stress fracture, the clinician rarely needs subsequent imaging. Radiographic healing lags behind clinical healing, and both bone scan and MRI may remain positive for up to 12 months following the original injury. Clinical response to treatment should suffice as confirmation of healing for almost all patients. Additional imaging plays a role only when the clinical response to treatment fails to progress appropriately. In this case, repeat imaging will determine if the fracture has extended or developed an area of nonunion. CT images the fracture line in long bones better than plain radiography, bone scan, or MRI. (See 'Imaging studies' above.)

ORTHOPEDIC CONSULTATION — Prompt surgical referral (within a few days) is recommended for high-risk fracture sites, which have higher rates of nonunion and progression to complete fracture. Orthopedic referral is appropriate for patients who cannot tolerate a lengthy rehabilitation process, such as some high-level athletes or laborers whose livelihoods depend upon a timely return to work. Should conservative treatment fail, surgical consultation should be obtained, generally after repeat imaging reveals that the fracture has extended or a nonunion has developed. Of note, evidence supporting the role of surgery in the treatment of stress fractures is limited [105]. (See 'High-risk sites' above.)

RETURN TO ACTIVITY — Athletes and laborers with a stress fracture often need to know their prognosis in terms of the time required until they can compete or resume work. This can be difficult to determine and involves multiple factors. The following table summarizes the estimated time needed for return to full sport according to stress fracture location, radiographic severity, and risk classification (table 4).

A systematic review of 76 studies involving 2974 cases, most retrospective and performed predominately in male athletes, provides some guidance about return to sport following stress fracture [4]. The lowest overall rate for return to sport was reported for injuries of the femoral neck (55 percent), talus (69 percent), anterior tibial shaft (76 percent), and tarsal navicular (83 percent). The longest average times for return to sport were reported for stress fractures of the tarsal navicular (127 days), femoral neck (107 days), and the medial malleolus (106 days). These figures are averages, and healing for individuals may vary substantially given the many factors involved, including location within the bone, radiologic grade, duration of symptoms, compliance with treatment, and underlying bone health.

Affected bone — Each stress fracture site has its own propensity to heal based on anatomic differences such as cortical- versus trabecular-predominant architecture, blood supply, stability provided by surrounding structures, and amount of weightbearing. The following table summarizes the time to return to sport for several stress fracture locations (table 4); the actual time required for full participation can vary substantially [4]. Relative bone health also plays a role in healing.

Whether the affected bone is primarily trabecular versus cortical in architecture may be an important predictor of healing time. Trabecular bone is more adversely affected by low bone mineral density, which is an independent risk factor for stress fracture. Thus, stress fractures in trabecular bone may take longer to heal.

In a prospective study of collegiate track and field athletes, those with fractures at trabecular predominant bones (eg, pelvis, sacrum, femoral neck, calcaneus) took significantly longer to return to sport (31.1 weeks) than athletes with fractures at cortex predominant sites (14.9 weeks for metatarsals, tibia, fibula, navicular, and great toe sesamoids) [81]. The role of trabecular architecture was confirmed in a meta-analysis of studies assessing the correlation between MRI fracture grade and healing time [75].

Bone mineral density is inversely correlated with stress fracture healing, with lower bone mineral density predicting a longer recovery [81].

Radiologic grade of fracture — A higher fracture grade as determined by MRI or bone scan is strongly predictive of a longer recovery time. A meta-analysis of 16 studies showed that higher MRI-based grading (table 3) was strongly associated with increased time to return to sport in athletes [75]. Combining all anatomic locations, athletes with grade 1 injuries took 41.7 days to return to sports, whereas those with grades 2, 3, and 4 injuries took 70.1, 84.3, and 98.5 days, respectively. Using a simplified grading system where fractures with MRI grades 1 and 2 were categorized as "low grade" and grades 3 and 4 fractures as "high grade," athletes with high-grade injuries took an average of 29.7 days longer to return to sports than those with low-grade injuries.

Duration of symptoms — One retrospective study found that athletes under 20 years of age who sought treatment within three weeks of symptom onset had a markedly quicker return to activity (10.4 weeks) compared with those who delayed treatment (18.4 weeks) [90].

Underlying bone health — A prospective study of stress fractures in collegiate athletes found that lower bone mineral density correlated strongly with prolonged return to sport [81].

PREVENTION

General guidelines — Based upon our knowledge of proven and possible risk factors, we suggest the following guidelines for preventing stress fractures:

●Patients must be educated in proper training techniques, especially avoiding the "too much, too soon" training errors. Athletes should increase the frequency and intensity of training in small, incremental steps. A rough guide is no more than 10 percent increase in volume or intensity per week.

●Prevention of osteoporosis is important. A well-balanced diet, adequate calcium and vitamin D, muscle strength and flexibility training, and regular weightbearing exercise should be encouraged in all patients. (See 'Nutrition, bone health, and body composition' above.)

●We suggest that young female athletes be assessed with the female athlete triad cumulative risk assessment tool (table 5) [64,65], and young male endurance athletes be assessed with a modified version of the same tool (excluding the questions about menarche and menstruation) [106]. This simple tool assesses several proven risk factors for stress fracture (low energy availability, low body mass index [BMI], delayed menarche, menstrual dysfunction, prior stress reaction/fracture, low bone mineral density) and places athletes into low-, moderate-, or high-risk categories. An elevated score is associated with an increased risk for bone stress injury (and other medical conditions).

A retrospective cohort study of 323 collegiate female athletes using the cumulative risk assessment tool found that moderate-risk athletes were 2.6 times more likely to develop a bone stress injury, and high-risk athletes were 3.8 times more likely [65]. In a prospective study of collegiate male endurance athletes, each one-point increase in the modified cumulative risk assessment tool score was associated with a 57 percent higher incidence in bone stress injury [106]. Athletes with moderate or high risk should be treated to improve energy availability and bone mineral density. (See 'Prevention in those with prior stress fracture (secondary prevention)' below and "Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations" and "Anorexia nervosa in adults: Clinical features, course of illness, assessment, and diagnosis" and "Bulimia nervosa in adults: Clinical features, course of illness, assessment, and diagnosis".)

Prevention in military, police, and first responders — Much of the research done on stress fracture risk factors and prevention has involved military recruits and first responders (eg, firefighters, police). This population is at greater risk of injury, particularly during the training of new recruits. In addition to the principles outlined above, the following factors and interventions may be associated with lower risk of injury:

●Physical fitness prior to enlistment ‒ General physical fitness may be protective. Prospective studies demonstrate that military recruits who participate in ball sports for at least two years prior to enlistment have a significantly lower risk of developing stress fractures during initial military service [45,107,108]. Conversely, in a meta-analysis of randomized trials assessing interventions to reduce lower extremity injury among first responders, analysis of eight trials involving 6,838 subjects found that programmed physical training (eg, lower extremity mobility and strength exercises, core stabilization exercises) did not reduce the incidence of stress fractures [109].

●Foot orthoses ‒ Data pertaining to the effectiveness of foot orthoses in reducing stress fracture incidence is mixed. Prefabricated or custom-made foot orthoses were effective for preventing lower limb stress fractures according to a meta-analysis of four trials, with a pooled relative risk (RR) of 0.59 (95% CI 0.45-0.76) [110]. Quality varied among studies. The RR was lowest for metatarsal stress fractures (RR 0.25, 95% CI 0.09-0.69), but the intervention was also effective for tibial shaft (RR 0.65, 95% CI 0.43-0.96) and femoral neck (RR 0.53, 95% CI 0.35-0.80) stress fractures. A subsequent meta-analysis (described just above) of eight randomized trials involving 3,792 first responders found that neither orthotics nor other footwear modifications reduced the incidence of lower extremity injury or stress fracture (odds ratio [OR] 0.76, 95% CI 0.45-1.28) [109].

●Physical training modifications ‒ Traditionally, military physical training has emphasized middle-distance running, but modifications to this approach have reduced stress fractures in military populations. Several observational studies report substantial reductions in lower extremity stress fracture rates among recruits and soldiers who follow modified physical training programs [111-113]. Modifications have included reduced running mileage, greater variety of exercises (eg, multiaxial movements, agility training), progressive and periodized training, and consuming nutrients soon after high-intensity exercise.

The incidence of pelvic stress fractures in female military recruits was reduced from 11.2 to 0.6 percent by lowering march speed from 7.5 to 5 km/hour, running on softer surfaces, encouraging individual step length and running speed rather than marching or running in step, and using interval training (eg, alternating sprints and jogging) instead of traditional middle-distance runs [114].

Rest from running for one week during the middle of an eight-week basic military training regimen did not reduce stress fracture rates [115].

●Vitamin D and calcium supplementation ‒ Daily vitamin D (800 international units) and calcium (2000 mg) supplementation decreased stress fracture rates in a randomized trial of female United States Navy recruits and in several other prospective observational studies [37,116]. Higher doses of vitamin D may be needed in persons diagnosed with vitamin D insufficiency or deficiency. The Female Athlete Triad Coalition recommends maintaining serum 25(OH)D levels between 32 and 50 ng/mL [64]. (See 'Non-modifiable risk factors' above and "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on 'Optimal intake to prevent deficiency'.)

Interventions for which research has shown borderline or no clear benefit include:

●Oral contraceptives – In one randomized trial, oral contraceptive use in female distance runners reduced stress fracture incidence, but the difference did not achieve statistical significance [43]. The study was underpowered due to medication noncompliance. Women with oligomenorrhea or amenorrhea who took oral contraceptives had a significant increase in their bone mineral density.

●Shock-absorbing insoles – A meta-analysis of seven studies found that flat-contour, shock-absorbing insoles were not effective in preventing stress fractures or other lower extremity injuries [110].

●Risedronate (bisphosphonate) – Treatment with risedronate for 12 weeks in military recruits deemed to be at high risk for stress fracture did not reduce injury rates [117].

PREVENTION IN THOSE WITH PRIOR STRESS FRACTURE (SECONDARY PREVENTION) — Underlying causes and risk factors for stress fractures must be addressed to optimize healing and prevent recurrent injury. Referral to a clinician with sports medicine training or experience managing stress fractures may be beneficial.

Disordered eating — Disordered eating must be addressed. A careful history and examination can identify patients whose eating habits predispose to injury. Those with the "female athlete triad" (low energy availability with or without an eating disorder, menstrual irregularity, and low bone mineral density) are at particularly high risk and should have treatment by a multidisciplinary team consisting of a mental health professional, nutritionist, and primary care clinician [118]. (See "Eating disorders: Overview of prevention and treatment".)

Evaluate for decreased bone density — Consideration of performing bone density testing using dual-energy x-ray absorptiometry (DEXA) should be made in patients with any of the following:

●Stress fractures unexplained by excessive activity

●Recurrent stress fractures

●Family history of osteoporosis

●Regular use of glucocorticoids

●Disordered eating

Those with low bone density values should be treated with weightbearing exercise (as part of a graded treatment plan), calcium, vitamin D, and other indicated medications. Additional laboratory testing may be needed. Secondary osteopenia and osteoporosis are discussed in detail separately. (See "Evaluation and treatment of premenopausal osteoporosis".)

Dietary habits that promote higher bone mineral density may decrease the risk of stress fractures in susceptible individuals. In a prospective observational study of 17 female runners, higher intake of calcium, skim milk, and dairy products was associated with lower rates of stress fracture and increased bone mineral density [119].

Evaluate for vitamin D insufficiency or deficiency — Low levels of 25-hydroxyvitamin D (25[OH]D) may be a precursor to or coincident with reduced bone mineral density. Optimal levels are somewhat controversial, but the Female Athlete Triad Coalition recommends maintaining serum (25[OH]D) levels between 32 and 50 ng/mL [64]. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on 'Optimal intake to prevent deficiency'.)

Improve physical fitness — An assessment of past physical activity, the activity that led to the stress fracture (frequency, intensity, exercise selection), and future activity needs can help patients develop a fitness plan that promotes health and fitness but avoids recurrence of stress fractures. Consultation with a knowledgeable fitness specialist may be helpful. (See "The benefits and risks of aerobic exercise".)

Evaluate for anatomical and biomechanical factors — Biomechanical evaluation for factors such as leg-length discrepancy, muscle inflexibility, excessive foot pronation during running, and pes cavus (high arch) or pes planus (flatfoot) should be performed. Runners should be counseled to replace running shoes before the tread becomes worn or cushioning is lost (approximately every 350 to 500 miles). Gait analysis in runners can help identify problems and assist in the selection of appropriate running shoes. Orthotic prescription may help in some patients. Consultation with a sports medicine specialist can be helpful. Running injuries are discussed in detail separately. (See "Running injuries of the lower extremities: Risk factors and prevention".)

ADDITIONAL INFORMATION — Several UpToDate topics provide additional information about fractures, including the physiology of fracture healing, how to describe radiographs of fractures to consultants, acute and definitive fracture care (including how to make a cast), and the complications associated with fractures. These topics can be accessed using the links below:

●(See "General principles of fracture management: Bone healing and fracture description".)

●(See "General principles of fracture management: Fracture patterns and description in children".)

●(See "General principles of definitive fracture management".)

●(See "General principles of acute fracture management".)

●(See "General principles of fracture management: Early and late complications".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General fracture and stress fracture management in adults" and "Society guideline links: Acute pain management".)

SUMMARY AND RECOMMENDATIONS

●Definitions – A stress fracture occurs when a bone breaks after being subjected to repeated tensile or compressive stresses, none of which would be large enough individually to cause the bone to fail, in a person who is not known to have an underlying disease that would be expected to cause abnormal bone fragility. Stress fracture is part of a spectrum of bone stress injury. (See 'Definitions' above.)

●High- and low-risk fracture sites – High-risk stress fractures are those at greater risk for displacement, nonunion, or fracture propagation. (See 'Clinical classification (grading and risk of complications)' above.)

•High-risk sites include:

-Pars interarticularis of the lumbar spine

-Femoral head

-Superior side of the femoral neck (ie, tension side)

-Patella

-Anterior cortex of the tibia (ie, tension side)

-Medial malleolus

-Talus

-Tarsal navicular

-Proximal fourth and fifth metatarsals

-Great toe sesamoids

-Base of the second metatarsal

•Low-risk sites include the second through fourth metatarsal shafts, posteromedial tibial shaft, proximal humerus or humeral shaft, ribs, sacrum, and pubic rami.

●Risk factors – Important risk factors for stress fractures include a history of prior stress fracture, low level of physical fitness, a sudden increase in the volume and intensity of physical activity, menstrual irregularity, diet poor in calcium and vitamin D, low bone mineral density, disordered eating, and increasing age (table 1 and table 2). (See 'Risk factors' above.)

●Diagnosis – Early diagnosis of stress fractures is essential to avoid complications. In most cases, the history and physical examination provide sufficient information to diagnose and manage low-risk stress fractures without imaging studies (algorithm 1). (See 'Diagnosis' above.)

●Clinical presentation – Many patients with stress fractures describe the insidious onset of localized pain within days to weeks of beginning a strenuous physical activity. Examination generally reveals focal tenderness at the fracture site. (See 'History' above and 'Pain description' above and 'Physical examination' above.)

●Diagnostic imaging – Imaging is needed when high-risk stress fractures are suspected or a definitive diagnosis is necessary. Plain radiographs should be obtained initially and are helpful when positive due to their high specificity, but they are insensitive. Magnetic resonance imaging (MRI) is recommended if plain radiographs are negative but clinical suspicion remains high and a need for definitive diagnosis exists. (See 'Imaging studies' above.)

●Differential diagnosis – The differential diagnosis for stress fracture includes tendinopathy, muscle strain, joint sprain, nerve entrapment, exertional compartment syndrome, neoplasm, and infection. (See 'Differential diagnosis' above.)

●Management of fractures at low-risk locations – Stress fractures at low-risk sites are managed conservatively with the following interventions (see 'Low-risk sites' above):

•Acute pain control as needed using ice and acetaminophen and/or low-potency opioids

•Protection of the fracture site with reduced weightbearing or splinting in selected stress fracture locations

•Reduction or modification of activities such that pain is not present

•Gradual resumption of activities if pain free

•Rehabilitative exercise to promote optimal biomechanics

•Risk factor reduction as indicated

•Proper nutrition, including additional calcium and vitamin D (see 'Treatment concepts' above)

●Indications for surgical referral – Orthopedic consultation is necessary for patients with fractures at high-risk sites or for whom a lengthy rehabilitation process is untenable, such as some high-level athletes or laborers whose livelihoods depend upon a timely return to work. (See 'High-risk sites' above.)

●Prevention – The following general guidelines are useful for preventing stress fractures (see 'Risk factors' above and 'Prevention' above and 'Prevention in those with prior stress fracture (secondary prevention)' above):

•Educate athletes about proper training. Increase training in small, incremental steps. A rough guide is no more than 10 percent increase in volume or intensity per week.

•Encourage a well-balanced diet (including adequate calcium and vitamin D), muscle strength and flexibility training, and regular weightbearing exercise in all patients, particularly those at risk for osteoporosis. (See 'Nutrition, bone health, and body composition' above.)

•Assess young female athletes for menstrual irregularities and signs and symptoms of eating disorders, and provide appropriate treatment to prevent the female athlete triad. (See "Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations" and "Anorexia nervosa in adults: Clinical features, course of illness, assessment, and diagnosis" and "Bulimia nervosa in adults: Clinical features, course of illness, assessment, and diagnosis".)