Stress Fracture of the Hip

Disease/ Disorder

Definition

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. They are part of a continuum of injuries which is broadly classified as bone stress injury (BSI). BSI represents the inability of bone to withstand repetitive loading leading to structural fatigue and microarchitectural discontinuities. BSI initially starts as a stress reaction which can progress to stress fracture and finally a complete bone fracture. 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 ramus, and sacral ala. Early identification of femoral neck stress fracture (FNSF) in particular is important to avoid long-term complications of complete, displaced FNSF.^6,7

FNSFs can be divided into those that occur on the tension side (superior aspect) and more commonly those that occur on the compression side (inferior aspect).⁸Tension-sided fractures are considered high-risk due to their tendency to displace if they progress to complete fracture, which results in increased likelihood of delayed healing and complications including avascular necrosis.^1-4 Stress fractures of the femoral shaft, pubic ramus, sacral ala, and compression side of the femoral neck are considered lower risk fractures.^1,3,9

Etiology

Stress fractures are often multifactorial and common risk factors include high volume of activity, anatomic changes, poor preparticipation fitness, low bone mineral density, and prior history of stress fracture. ⁷ 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 up to 20% of athletic injuries; and 80% of stress fractures occur in the lower limb.^6,10 While stress fractures are typically more common in the distal lower extremities, stress fractures of the hip and pelvis are becoming increasingly recognized in the literature.⁷ They have been found to be most prevalent in military recruits and endurance runners.^6,7 More specifically, femoral stress fractures account for 2.5% to 5% of all BSIs. ⁷ The incidence of sacral or pubic stress fractures is unknown, however they may be under-recognized.^1,7

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, poor biomechanics, other structural variations (such as small tibial width), conditioning, insufficient blood supply, and endocrine (hypoestrogenism) and/or nutritional abnormalities (negative energy balance).^1,2,8-10 Extrinsic factors are related to training variables and other elements that affect how stresses are applied to bone including type of sport, training intensity/duration and technique, equipment utilized, training surface, and environmental factors.^1-2  Those most at risk for BSI include runners who rapidly increase mileage and duration and those who average over 30-40 miles per week, ballet dancers, military recruits, athletes who participate in track and field or gymnastics, and those who exercise for over five hours per day.^6,7,9

The role of gender, age, and race in determining risk of developing stress fractures has also been discussed.^1-7   In general, female sex has a higher incidence of BSIs; however, this appears to be more likely related to relative energy deficiency in sport (RED-S). This incorporates the previous terminology of the female athlete triad (the triad) composed of menstrual irregularities, disordered eating, and low bone mineral density.⁷ RED-S refers to the inadequate energy intake for optimal health and performance for either sex in sport.^11,12 Pelvic stress fractures (pubic rami and sacral) occur most commonly in female long distance runners.⁵ Tension-sided femoral neck stress fractures occur more commonly in older patients, whereas compression-sided stress fractures occur more often in younger patients.⁵ Biomechanical risk factors are related to the specific locations where stress fractures occur. For FNSFs, these include pes cavus, limb length inequality, and coxa vara.¹ Other specific risk factors for FNSF include femoroacetabular impingement (either pincer or CAM deformities), decreased femoral bone mineral density, poor entry fitness scores, female sex, and gluteus medius weakness.^6,7 Though not routinely tested, genetic factors including the loss of calcitonin receptor C allele or vitamin-D receptor C-A haplotype have been shown to have higher risk for FNSF.⁶ FNSFs tend to occur where the greatest compressive strain is applied – the proximal posteromedial shaft.¹

Although rare, endurance runners, military recruits, and patients with increased pelvic anteversion tend to be most vulnerable for development of sacral stress fractures.^7,13  The 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 sacrum tend to occur within Zone I of the sacral ala lateral to the foramina.⁷ They often are the result of repetitive axial loading and develop vertically medial to the sacroiliac joint.⁷ Stress fractures of the pubis are most common among runners and military recruits.⁷ These tend to occur at the site of attachment of the adductor magnus on the inferior pubic ramus, where repetitive tensile forces are applied.^1,7

Patho-anatomy/physiology

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.^1,3,4-5 The resorption phase peaks at about 3 weeks; but the normal duration for the complete remodeling process is 3 months.⁵ Regarding FNSFs, the femoral neck incurs 8.4 times an individual’s body weight when running which can overcome metabolic repair abilities and lead to microfractures. ⁶

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

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.⁵ The 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.² In athletes, manifestation of stress fracture symptoms are usually seen around two months after an abrupt and large increase in exercising. Pain 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 typically insidious. ⁶ At first, mild pain occurs only after a certain amount of activity and improves or resolves fairly quickly after the activity is discontinued.^1-3,5-7

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

Essentials of Assessment

History

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

Physical examination

Assessment should begin with alignment and symmetry of the legs, ankles, and feet, as these may affect biomechanical forces.¹⁰ Although often nonspecific, classic physical examination findings include focal bony tenderness, antalgic gait, and swelling over the location of the stress fracture.^4,6 Bony tenderness of the pelvis may be difficult to reproduce due to the presence of overlying soft tissues.⁷ In FNSFs, pain may be elicited at end ranges of hip motion and with active straight leg raise, rather than tenderness to palpation.^1,5 Sacral stress fractures tend to present as lumbar back or pelvic pain.¹³ Pain elicited during a one-legged hop (particularly during landing) can aid in the diagnosis. The fulcrum test has proven to be a useful tool if clinically suspicious for femoral shaft stress fracture.¹⁵ Pubic rami fractures tend to produce marked tenderness to palpation and pain can be reproduced with single leg stance.⁵ Sacral stress fractures may be painful to palpation or with stressing of the sacroiliac joint.^5,13  FABER and Gaenslen’s tests may reproduce pain.¹³ In addition to a thorough musculoskeletal exam it is important to document accurate height and weights on all patients with suspicion or confirmed stress fractures. Calculating body mass index (BMI) and tracking weight changes are important predictors of recovery and preventing future stress injuries.^8,14,16

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

When a pathology is thought to have a nutritional or metabolic cause, laboratory workup should be obtained. Work up can include vitamin D levels, complete blood cell count, thyroid function tests, magnesium, phosphorus, parathyroid hormone, and a complete chemistry panel in high risk individuals or those with recurrent stress fractures.⁸ In addition, iron deficiency often accompanies low energy intake, so an iron panel should be considered.¹⁷ Sex hormone levels can be tested including estradiol, luteinizing hormone, follicle stimulating hormone, urine pregnancy test in females and testosterone in males.¹⁸ PSA or SPEP can be ordered for suspected cancers. Albumin and prealbumin should also be considered.¹⁹

Imaging

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.^1-5,7 It can identify early signs of stress fracture (bony and/ or soft tissue edema) as early as one to two days after symptoms onset. ⁸ Compared to other diagnostic modalities, MRI has demonstrated to be more sensitive and specific in detecting FNSFs. ⁶ 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, imaging of sacrum or pars interarticularis), or when MRI is contraindicated.^1-5,8

Supplemental assessment tools

A DEXA scan can be used to assess for osteoporosis or low bone mineral density in individuals with recurrent or high risk stress fractures.¹⁴ There have been multiple proposed classification guidelines for FNSF which may be divided into types I-IV in order of increasing severity.⁶

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.^2,16 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 healing time.^1,2

Environmental

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 the risk.²⁰ Femoral neck,¹ sacral, and pubic ramus¹ stress 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

Tension-sided femoral neck fractures are classified as high-risk fractures and 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 may be medically discharged if complications such as fracture completion and/or avascular necrosis occur or if they are unable to return to pre-injury level of activity.

Professional issues

The evaluating and treating physiatrist should pay special attention to complaints of severe groin, leg or foot pain or findings of antalgic gait or pain with hopping as such findings could indicate the presence of a stress fracture. Failure to identify a stress fracture might result in a displaced fracture and less favorable outcome if left untreated.

Rehabilitation Management and Treatments 

Available or current treatment guidelines 

A method has been proposed for grading stress fracture severity based upon MRI findings^2,16 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 of rest, 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.²¹ The authors’ stated intent was to provide a practical resource for clinicians, which is summarized below.²¹ 

At different disease stages 

New onset/acute 
If the fracture is high-risk and/or high-grade, the patient should be referred for consultation with the appropriate orthopaedic/sports medicine/musculoskeletal specialist. Acutely displaced FNSFs should be treated emergently with open reduction internal fixation (ORIF).⁵ Modifying weight bearing status helps to protect the limb from progression of the fracture and 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.^2-3However, precaution should be taken when prescribing opioids and consideration given to multi-modality management of pain without use of opioids whenever possible. During this time, a very thorough history should be taken to evaluate for contributing factors that can be addressed to help with healing and prevention.

Subacute 
The keys to maximizing healing include restriction of activity as soon as a stress fracture is suspected; and repeat evaluation to ensure pain-free function.⁴As the fracture is healing, any contributing factors to the development of the fracture should be addressed (training/technique errors, equipment modification, nutrition modification, etc.).⁵ Deconditioning can be minimized by allowing participation in activities with modified or minimal weight bearing. Athletes can begin gradual return to sports activities after being asymptomatic with normal daily activities for 10 -14 days. Markers of recovery on imaging include bone callus formation and resolution of fracture line.⁸ 

Chronic 
Fractures with nonunion or avascular necrosis (AVN) require surgical treatment. Nonunion requires debridement and bone grafting.⁵AVN of the femoral head requires hemiarthroplasty or possibly total hip arthroplasty.

MRI Based Management  

An additional treatment algorithm based on MRI characteristics for FNSFs has been proposed by Bernstein et al. ¹⁰  

• Individuals with compression or tension-sided stress fracture with edema but without clear fracture line can be treated nonoperatively with non-weightbearing for 6 weeks and close monitoring.  
• Individuals with compression-sided stress fracture with fracture line < 50% of the femoral width can be managed nonoperatively with non-weight bearing for 6 weeks and close monitoring. Serial radiographs can be used every 2 weeks to assess fracture progression. 
• Compression-sided stress fracture with the fracture line > 50% of the femoral width or hip effusion should undergo prophylactic fixation to prevent progression of fracture and/or displacement.  
• Tension-sided stress fracture with clear fracture line should be treated with surgical fixation due to high risk of displacement. There have been reported cases of non-operative management of tension-side stress fracture without fracture line with 6 weeks of non-weightbearing.  

The non-operative treatment regimen should consist of rehabilitation and a running progression. Each BSI is different. Therefore, each protocol should be adjusted for the individual athlete. Pain during or after activity will dictate advancement or regression of the protocol. Rehabilitation should focus on assessing and improving the athlete’s strength, joint mobility, core and pelvic stabilization, and muscle endurance.²² Cardiovascular endurance can be maintained with swimming, stationary biking, aquajogging, and later, an anti-gravity treadmill. ²² After the athlete is pain-free with ambulation for 1-2 weeks they can begin to run every other day. Often this starts with an anti-gravity treadmill. This may allow for a gradual increase in bone loading and maintenance of cardiovascular endurance and muscle strength. ^23,24 If using an antigravity treadmill, an athlete can start at 50% body weight, running on nonconsecutive days, increasing body weight by 5-10% per run, and increasing duration of running. ^23,25 If an athlete does not have access to an antigravity treadmill, they can participate in a run/walk progression at approximately 50% of their pace and gradually increase the time jogging and decrease the time walking.²² Protocols for the gradual progression of a run/walk program usually occur over 3 to 6 weeks.²² The athlete should undergo a gait analysis to correct underlying biomechanics that could place excessive load on the bones.²² 

Prevention of recurrent stress fractures 

It is important to address not only the treatment of stress fractures but the prevention of future injuries, especially for those at risk. Stress fractures usually occur with normal loading on a weakened bone (termed insufficiency fracture) or with excessive loading on a normal bone (stress fracture). Understanding the etiology of the initial bone stress injury helps correct the underlying issue to prevent recurrence. While the data is not clear in relation to oral contraceptives and bone mineral density, multiple studies have shown that estrogen containing oral contraceptives may provide a protective effect in female athletes.^5,14 However, masking menstrual irregularities with hormonal contraceptives is not recommended as it can impair the ability to capture athletes with a component of the female athlete triad and the risk of bone stress injury. ²⁶ Due to the association between low energy intake and stress fractures, it is important to discuss good nutritional and training principles.¹⁴ Athletes should undergo a consult with a registered dietician in order to ensure a positive energy balance and maintenance of adequate body weight to reduce the risk of hormonal imbalances contributing to decreased bone mineral density. Recommendations can include increasing intake of dairy products in addition to adding supplements such as oral calcium and vitamin D.⁸ Stress placed upon the bones contributing to the bone stress injuries also needs to be corrected. This includes assessing the body for asymmetries in joint range of motion, flexibility, and strength that places excessive stress on an area of bone. In addition, it is necessary to assess the athlete’s gait and previous training program to determine areas for modifications to prevent future injuries.

Coordination of care 

Treatments for stress fractures require an interdisciplinary team throughout the continuum of the athlete’s progression from rest to active rehabilitation and return to sport. This team is comprised of multiple physicians (sports medicine, orthopedics, endocrinology, gynecology). The physiatrist or sports medicine physician is often the team leader coordinating the care of the other 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 management and prevention of stress fractures. Once the fracture has occurred, education can be provided on maximizing healing, maintenance of function, and prevention of recurrence. It is also necessary to educate the athlete about the relationship between BSI and the female or male athlete triad (triad) and the more encompassing RED-S. ¹² This helps develop a more comprehensive treatment approach for all of the systems that can be affected by BSI and the related conditions.

Emerging/unique interventions/assessments 

Function-based measures such as Oswestry or SF-36 can be used for research or clinical outcomes. VAS scales for pain may be useful. Acuity of fracture can be assessed using Doppler to provide a semiquantitative estimate of bone turnover.³

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

Progressive lower extremity pain that is worse with impact loading and tenderness over the bone should raise suspicion for a bone stress injury. Imaging, including plain radiographs and MRI, are necessary to confirm the diagnosis. Treatment is aimed at preventing progression and ensuring adequate healing in a timely manner. The severity and location of the stress fracture guides treatment including operative versus nonoperative management and the time required for resting and rehabilitation prior to returning to full sports participation

Cutting Edge/ Emerging and Unique Concepts and Practice 

Emerging data on utilization of modalities such as extracorporeal shockwave therapy and pulsed ultrasound bone stimulation for bone healing have yielded limited benefit. Medications to prevent bone remodeling such as bisphosphonates have reported mixed results. In addition, given the teratogenic affects of bisphosphonates, it is recommended to avoid these medications in women of child-bearing age when possible. Other pharmacological agents including the use of parathyroid analog teriparatide (Forteo), which stimulates osteoblast genesis and osteoblast survival, may accelerate fracture healing in patients with stress fractures or with delayed fracture healing.^1,8,25 

Gaps in the Evidence-Based Knowledge 

Currently there are no universal rehabilitation protocols, largely because no two bone stress injuries are the same. However, with increasing data collection, more general algorithms can be updated. In addition, researchers are continuing to study pharmacologic agents and modalities to enhance bone healing, limiting the athlete’s time away from physical activity. 

References

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. Bernstein EM, Kelsey TJ, Cochran GK, Deafenbaugh BK, Kuhn KM. Femoral Neck Stress Fractures: An Updated Review. J Am Acad Orthop Surg. 2022;30(7):302-311. doi:10.5435/JAAOS-D-21-00398
7. Dutton RA. Stress Fractures of the Hip and Pelvis. Clin Sports Med. 2021;40(2):363-374. doi:10.1016/j.csm.2020.11.007Robertson
8. Moriera A, Bilezikian J. Stress Fractures: Concepts and Therapeutics. Journal of Clinical Endocrinology and Metabolism. 2017; 102(2): 525-534.
9. 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.
10. Behrens SB, Deren ME, Matson A, Fadale PD, Monchik KO. Stress fractures of the pelvis and legs in athletes: a review. Sports Health. 2013 Mar;5(2):165-74. doi: 10.1177/1941738112467423. PMID: 24427386; PMCID: PMC3658382.
11. Lin CY, Casey E, Herman DC, Katz N, Tenforde AS. Sex Differences in Common Sports Injuries. PM R. 2018;10(10):1073-1082. doi:10.1016/j.pmrj.2018.03.008
12. Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the Female Athlete Triad–Relative Energy Deficiency in Sport (RED-S). Br J Sports Med. 2014;48(7):491-497. doi:10.1136/bjsports-2014-093502
13. Tsatsaragkou A, Vlasis K, Raptis K, et al. Fatigue sacral fractures: A case series and literature review. J Musculoskelet Neuronal Interact. 2022;22(3):385-392.
14. Joy EA. Address risk factors to prevent bone stress injuries in male and female athletes.  British Journal of Sports Medicine. 2019; 53(4): 205-206.
15. Johnson AW, Weiss CB, Wheeler DL. Stress fractures of the femoral shaft in athletes: more common than expected. A new clinical test. Am J Sports Med. 1994;22(2):248-256.
16. Ramey LN, McInnis KC, Palmer WE. Femoral neck stress fracture. The American journal of sports medicine. 2016. 44 (8) 2122-2129.
17. Petkus DL, Murray-Kolb LE, De Souza MJ. The Unexplored Crossroads of the Female Athlete Triad and Iron Deficiency: A Narrative Review. Sports Med. 2017 Sep;47(9):1721-1737. doi: 10.1007/s40279-017-0706-2. PMID: 28290159.
18. Dipla, K., Kraemer, R.R., Constantini, N.W. et al. Relative energy deficiency in sports (RED-S): elucidation of endocrine changes affecting the health of males and females.Hormones 20, 35–47 (2021). https://doi-org.proxy1.library.jhu.edu/10.1007/s42000-020-00214-w
19. (Kiuru, M. J., Pihlajamäki, H. K., & Ahovuo, J. A. (2004). Bone stress injuries. Acta Radiologica, 45(3), 000-000.)
20. 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.
21. 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.
22. Warden SJ, Davis IS, Fredericson M. Management and prevention of bone stress injuries in long-distance runners. J Orthop Sports Phys Ther. 2014 Oct;44(10):749-65. doi: 10.2519/jospt.2014.5334. Epub 2014 Aug 7. PMID: 25103133.
23. Tenforde AS, Watanabe LM, Moreno TJ, Fredericson M. Use of an antigravity treadmill for rehabilitation of a pelvic stress injury. PM R. 2012 Aug;4(8):629-31. doi: 10.1016/j.pmrj.2012.02.003. PMID: 22920318.
24. Vincent HK, Madsen A, Vincent KR. Role of Antigravity Training in Rehabilitation and Return to Sport After Running Injuries. Arthrosc Sports Med Rehabil. 2022 Jan 28;4(1):e141-e149. doi: 10.1016/j.asmr.2021.09.031. PMID: 35141546; PMCID: PMC8811491
25. Coslick AM, Lagaz SR, Deu RS. Protocol for 8-Week Return to Running after a Femoral Stress Reaction. PM R. 2019 Aug;11(8):904-907. doi: 10.1002/pmrj.12117. Epub 2019 Apr 16. PMID: 30719846.
26. Cheng J, Santiago KA, Abutalib Z, Temme KE, Hulme A, Goolsby MA, Esopenko CL, Casey EK. Menstrual Irregularity, Hormonal Contraceptive Use, and Bone Stress Injuries in Collegiate Female Athletes in the United States. PM R. 2021 Nov;13(11):1207-1215. doi: 10.1002/pmrj.12539. Epub 2021 Feb 3. PMID: 33340255; PMCID: PMC8262270.
27. A Patient’s Guide to Stress Fractures of the Hip. eOrthopod.com; http://www.eOrthopod.com/public; Accessed August 12, 2011.
28. Almirol EA, et al. Short term effects of teriparatide versus placebo on bone biomarkers, structure, and fracture healing in women with lower extremity-stress fractures: A pilot study. Journal of Clinical and Translational Endocrinology. 2016; 6: 7-14.

Original Version of the Topic

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

Previous Revision(s) of the Topic

Laura Peter, MD. Stress Fracture of the Hip. 5/05/2016.

Gregory Mulford, MD, Maria Janakos, MD. Stress Fracture of the Hip. 7/24/2020

Author Disclosure

Alexis Coslick, DO
Nothing to Disclose

Minh Quan Le, MD
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Stephen Ritter, DO
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Mohammed Emam, MD
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