Stress Fracture of the Hip

Author(s): Laura Peter, MD

Originally published:11/15/2011

Last updated:05/05/2016



Stress fractures are common injuries that tend to occur in athletes or other people who participate in activities that place repetitive and excessive stress on bone. Stress fractures can be further broken down based upon whether they occur as the result of excessive and repetitive strain placed on structurally normal bone (fatigue reaction) or normal stress applied to structurally abnormal bone (insufficiency reaction).1-5 Locations where femoral and/or “hip” stress fractures occur include: femoral shaft, femoral diaphysis, femoral neck, pubic rami, and sacral ala.

Femoral neck stress fractures can be divided into those that occur on the tension side (superior aspect when standing) and those that occur on the compression side (inferior aspect when standing). Tension-sided fractures are considered high-risk due to their tendency to displace if they progress to complete fracture, which results in increased incidence of healing problems and increases risk of avascular necrosis.1-4 Stress fractures of the femoral shaft, pubic rami, sacral ala, and compression side of the femoral neck are considered low-risk fractures.1,3


Fatigue fractures occur when continued repetitive loading exceeds the process of remodeling.1,5 Insufficiency fractures occur when normal loading is applied to bone in which new bone formation is impaired, producing reduced mechanical strength.1-5 Insufficiency or pathological fractures include those that occur in bone weakened by infection, tumor, or various processes producing low bone mineral density.1,3,4-5

Epidemiology including risk factors and primary prevention

Stress fractures comprise between 1 and 20% of athletic injuries; and 80% of stress fractures occur in the lower limb.6 More specifically, femoral stress fractures account for 6.6% of all stress fractures, and pelvic stress fractures account for 1.6%.4 The incidence of sacral stress fracture is unknown.1

Risk factors for stress fracture are divided into intrinsic and extrinsic factors.1-2 Intrinsic factors are those related to the individual athlete, including anatomic alignment, other structural abnormalities, conditioning, insufficient blood supply, and endocrine and/or nutritional abnormalities.1-2,7Extrinsic factors are related to training variables and other components that affect how stresses are applied to bone. These include type of sport, training intensity/duration and technique, equipment utilized, environmental factors, and training surface.1-2

The role of gender, age, and race in determining risk of developing stress fractures has also been discussed.1-5 Pelvic stress fractures (pubic rami and sacral) often occur in female long distance runners.5 Tension-sided femoral neck stress fractures occur more commonly in older patients, whereas those that are compression-sided occur more often in younger patients.5

Biomechanical risk factors are related to the specific locations where stress fractures occur. For femoral neck stress fractures, these include pes cavus, limb length inequality, and coxa vara.1 Studies in military personnel and, more recently, in the general population have suggested pincer-type femoroacetabular impingement (FAI) as a risk factor for femoral neck stress fracture (FNSF).7 Femoral shaft stress fractures tend occur where the greatest compressive strain is applied – the proximal posteromedial shaft.1The sacrum acts as the keystone in the arch of the pelvis; it is subjected to multiple forces which can lead to stress fracture.1 Stress fractures of the pubic ramus occur at the site of attachment of the adductor magnus on the inferior pubic ramus, where repetitive tensile forces are applied.1


Wolff’s law states that normal stress placed on normal bone produces normal remodeling of the bone.1-2,5 If sufficient time is allowed for remodeling and the load applied does not exceed the strength of the bone structure, the bone becomes stronger.1,5

Remodeling begins with osteoclastic resorption of bone and is followed by osteoblastic new bone formation.1,5 Osteoclastic resorption weakens the bone; if insufficient time is allowed for new bone formation, microfractures occur which can progress to stress reaction and eventual fracture.1,3,4-5The resorption phase peaks at about 3 weeks; but the normal duration for the complete remodeling process is 3 months.5

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

  1. New onset/acute:
    Repetitive loading of bone in the context of insufficient time for new bone formation produces an environment in which resorption predominates, leading to weakening of the bone.5The process of fatigue fracture begins with crack initiation which progresses to crack propagation and eventual complete fracture unless the conditions which precipitated the problem are altered to allow resumption of normal remodeling of bone.2Pain related to stress fracture occurs in the groin region for pubic rami and femoral neck fractures, the anterior thigh for femoral shaft fractures, and the lower back and/or buttock for sacral fractures.4-5 The initial onset of pain is insidious. At first, mild pain occurs only after a certain amount of activity and improves or even resolves fairly quickly after the activity is discontinued.1-3,5
  2. Subacute:
    As the process of fatigue fracture continues, less activity is required to bring on symptoms until eventually pain occurs at rest.1-3,5 Often (especially in competitive athletes) patients will not seek medical care until symptoms begin to interfere with training and/or function.3



Common history factors in suspected stress fractures include pain characteristics, training regimen, footwear, medical history, medications, nutrition, lifestyle habits, and any previous history of injuries related to over-training of the area currently injured.1,3-4

Pain Location; onset; quality (aching); modifying factors; progression
Training Type of activity or sport; recent changes in regimen (especially increased intensity and/or duration), sport surface, equipment/shoes; timing of injury relative to athlete’s sport season
Footwear Sport-specific; how old?; fit; history of use of orthoses/inserts
Medical history Diseases that affect bone; menstrual history
Previous injury Previous stress fracture (same or different location); other injuries and/or treatment that may have changed biomechanics (laxity after joint sprain or poor flexibility after immobilization)
Medications Particularly medications that can alter bone density (corticosteroids or hormones)
Nutrition Intake of vitamin D, calcium, and calories
Lifestyle habits Smoking, ethanol intake, disordered eating

Physical examination

Key or classic physical examination findings include: focal bony tenderness, limp due to pain with ambulation, and swelling over the location of the stress fracture.4 In femoral neck stress fractures, pain is elicited at end ranges of hip rotation and with active straight leg raise, rather than tenderness to palpation.1,5

Pain elicited during a one-legged hop (particularly during landing) can aid in the diagnosis.

Pubic rami fractures tend to produce marked tenderness to palpation and pain can be reproduced with single leg stance.5 Sacral stress fractures are painful both to palpation and to stressing of the sacroiliac joint.5

Functional assessment

Treatment of stress fracture could include a period of protected weight bearing, thus compromising the functional state of the patient who may require full or partial assistance with some self-care activities for a limited time period.

Laboratory studies

For osteoporosis in males, testosterone levels.

For suspected cancers, PSA or SPEP.


Plain radiographs may aid in diagnosis by revealing subtle periosteal/cortical changes.1 In light of studies indicating an association between pincer-type FAI and increased risk for FNSF, findings of coxa profunda and/or acetabular retroversion should increase index of suspicion for occult FNSF; especially if other risk factors for stress fracture are present.7 False negative radiographs are common (especially in the first 2-3 weeks after onset of symptoms).1-5 Bone scan has high sensitivity but lower specificity so has fallen out of favor.1-5 MRI is considered the gold standard for imaging suspected stress fractures.1-5 CT (computed tomography) and/or SPECT (single positron emission CT) are helpful when imaging of bony detail is needed (e.g., determining whether fracture is complete or incomplete; or imaging of sacrum or pars interarticularis).1-5

Supplemental assessment tools

DEXA scan to assess for osteoporosis.

Early predictions of outcomes

Outcome depends upon anatomic location and grade of the injury. The grade of the injury (usually based upon MRI findings) indicates severity of injury, ranging from stress reaction to complete fracture.2 The grade of the injury has been found to be predictive of time to healing and return to play for athletes.2 Higher grade injuries carry a greater risk of developing complications and require longer to progress to healing.1,2


Environmental factors include: the terrain/surface upon which an activity is performed and the equipment used for the activity. More specifically, with reference to surfaces, activities performed on hard (unyielding) surfaces are at higher risk of producing stress fractures. Running on irregular terrain and/or hills also increases risk.6  Femoral neck1, sacral, and pubic rami1stress fractures occur more commonly in long distance runners.3,5 Femoral shaft fractures are more related to jumping.3

Social role and social support system

High-risk fractures like the tension-sided femoral neck fractures may require a lengthy period of non-weight-bearing, causing the patient to require assistance for certain activities (carrying things is difficult due to the need to use crutches). Athletes who are part of a team may have additional anxiety about inability to participate. Military recruits with stress fractures may have to delay training, or maybe medically discharged if complications like fracture completion and/or avascular necrosis occur.

Professional Issues

The evaluating and treating physiatrist should pay special attention to severe groin pain as there could be a stress fracture. Lack of identification of hip stress fracture could result in displaced fracture if left untreated.


Available or current treatment guidelines

A method has been proposed for grading stress fracture severity based upon MRI findings.2 The authors of the article in which the method is presented used this grading system to make recommendations for “duration of rest needed for healing” in weeks.2 Grade 1 injuries require only 3 weeks, while Grade 4 injuries require 16 weeks or more.2

A review article published in 2013 looked at evidence-based protocols for functional rehabilitation and resumption of running after stress fractures involving the lower limbs.8 The authors’ stated intent was to provide a practical resource for clinicians.8

At different disease stages

  1. New onset/acute
    If the fracture is high-risk and/or high-grade, the patient should be referred on for orthopaedic/sports medicine consultation. Acutely displaced femoral neck stress fractures should be treated ASAP with open reduction internal fixation (ORIF).5Modifying weight bearing status helps to protect the limb from progression of the fracture, but also decreases pain. Some advocate the use of acetaminophen or opioids (for severe pain) over NSAIDs for acute pain relief, due to the risk of delayed healing associated with the use of anti-inflammatory medication.2-3
  2. Subacute
    The keys to maximizing healing include restriction of activity as soon as stress fracture is suspected; and repeat evaluation to ensure pain-free function.4 As the fracture is healing, any contributing factors to the development of the fracture should be addressed (training/technique errors, equipment modification, modify nutrition, etc.).5 Deconditioning can be minimized by participation in activities with modified or minimal weight bearing.
  3. Chronic
    Fractures with nonunion or avascular necrosis (AVN) require surgical treatment. Nonunion requires debridement and bone grafting.5 AVN of the femoral head requires hemiarthroplasty or even total hip arthroplasty.

Coordination of care

Treatments for hip stress fracture span the full spectrum of treatment from plain rest to active medical/rehabilitative care under the direction of physical and occupational therapists to surgical. The physiatrist must coordinate the care of all these treatment professionals on the team.

Patient & family education

In the context of stress fractures in athletes, patients, family, and coaches may all benefit from education on prevention of stress fractures. Once the fracture has occurred, education can be provided on maximizing healing, maintenance of function, and prevention of recurrence. The website is a nice resource for patient education materials on numerous topics, including stress fracture of the hip.6

Emerging/unique Interventions

Function-based measures such as Oswestry or SF-36 can be used for research or clinical outcomes. VAS scales for pain may be useful.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Any lower extremity pain associated with increased activity that resolves with rest should result in stress fracture being considered in the differential diagnosis.


Cutting edge concepts and practice

Acuity of fracture can be assessed using Doppler to provide a semiquantitative estimate of bone turnover.3


Gaps in the evidence-based knowledge

More study on injury prevention and optimum treatment guidelines would be helpful.


  1. Harrast MA, Colonno D. Stress fractures in runners. Clin Sports Med. 2010;29:399-416.
  2. Kaeding CC, Najarian RG. Stress fractures: classification and management. Phys Sportsmed. 2010;38(3):45-54.
  3. Patel DR. Stress fractures: diagnosis and management in the primary care setting. Pediatr Clin N Am. 2010;57:819-827.
  4. Patel DS, Roth M, Kapil N. Stress fractures: diagnosis, treatment, and prevention. Am Fam Physician. 2011;83(1):39-46.
  5. Teague DC. Stress fractures. In: Bucholz RW, Court-Brown CM, Heckman JD, Tornetta P III, eds. Rockwood and Green’s Fractures in Adults. 7th ed. Philadephia, PA: Lippincott Williams & Wilkins; 2010: 518-530.
  6. Kahanov L, Eberman LE, Games KE, Wasik M. Diagnosis, treatment, and rehabilitation of stress fractures in the lower extremity in runners. Open Access Journal of Sports Medicine. 2015; 6: 87-95.
  7. Goldin M, Anderson CN, Fredericson M, et al. Femoral neck stress fractures and imaging features of femoroacetabular impingement. PM&R. 2015; 7(6): 584-592.
  8. Liem BC, Truswell HJ, Harrast MA. Rehabilitation and return to running after lower limb stress fractures. Curr Sports Med Rep. 2013 May-Jun; 12(3): 200-7.
  9. A Patient’s Guide to Stress Fractures of the Hip.;; Accessed August 12, 2011.

Original Version of the Topic:

Laura Peter, MD. Stress Fracture of the Hip. Publication Date: 2011/11/15.

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