Stress Fracture of the Hip

Disease/Disorder

Definition

Stress fractures represent the severe end of a spectrum of injuries referred to as bone stress injuries (BSI). These occur when bone is subjected to repetitive mechanical loading that exceeds its capacity for structural repair. This process typically begins as a stress reaction, seen radiographically as bone marrow and periosteal edema, and can progress to a complete cortical break¹. Stress fractures are commonly seen in athletes and individuals who participate in activities that place repetitive stress on the skeletal system. They can be further categorized as fatigue fractures, resulting from excessive strain on structurally normal bone, or insufficiency fractures, which occur when normal stress applied to structurally abnormal bone.²

Common locations of hip stress fractures include the femoral shaft, femoral diaphysis, and femoral neck, while nearby pelvic stress fractures can occur at the pubic ramus and sacral ala. Early identification of femoral neck stress fractures (FNSF) in particular is important to avoid long-term complications such as displacement.^3,4 FNSFs are classified based on their anatomic location into tension sided (superior aspect) and the more common compression sided (inferior aspect).⁵ Tension-sided fractures are considered high-risk due to their tendency to displace if they progress to a complete fracture, which results in increased likelihood of delayed healing and long term complications.^6-9 In comparison, stress fractures of the femoral shaft, pubic ramus, and sacral ala are considered lower risk fractures.^6,8,10

Etiology

Classically, stress fractures are overuse injuries secondary to repetitive mechanical stress on the affected bone. Etiology is often multifactorial, with key risk factors including a high training volume, anatomic changes, poor preparticipation fitness levels, low bone mineral density, and prior history of stress fracture.⁴ Fatigue fractures occur when continued repetitive loading exceeds the process of remodeling, while insufficiency fractures occur when normal loading is applied to structurally compromised bone, resulting in an area of weakened mechanical strength.⁵ Insufficiency or pathological fractures include those that occur in bone weakened by infection, tumor, or various processes resulting in low bone mineral density.

Epidemiology including risk factors and primary prevention

Stress fractures comprise up to 20% of athletic injuries; with 80% of stress fractures occur in the lower limb.^3,11 While stress fractures are more common in the distal lower extremities such as the tibia, fibula, and metatarsals, stress fractures of the hip and pelvis are becoming increasingly recognized in the literature.⁴ They have been found to be most prevalent in military recruits and endurance runners.^3,4 More specifically, femoral stress fractures account for 2.5% to 5% of all BSIs.^4,6

Risk factors for stress fracture can be divided into intrinsic and extrinsic factors.^6,7 Intrinsic factors include anatomic factors such as acetabular retroversion, poor biomechanics, other structural anatomic variations, low bone mineral density, and hormonal (hypoestrogenism) and/or nutritional abnormalities (negative energy balance).^5-7,10,11 Extrinsic factors include type of sport, training intensity/duration and technique, equipment utilized, training surface, and environmental factors.^6,7 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.^3,4,10

In general, female athletes have a higher incidence of BSIs. The risk increases in older adults, though in this age group, fractures are more commonly insufficiency fractures from compromised bone mineral density. Though more common in female athletes, relative energy deficiency in sport (REDs) is a risk factor for stress fractures in athletes of both genders. REDs is a multifactorial syndrome that encompasses a spectrum of sports performance impairments secondary to prolonged and/or severe low energy availability and disordered fueling.^12,13 Specifically, REDs has been shown to be substantially implicated in bone health and is therefore a major risk factor for the development of hip stress fractures.

When looking at FNSFs, tension-sided femoral neck stress fractures occur more commonly in older patients, whereas compression-sided stress fractures occur more often in younger patients.² Biomechanical risk factors are related to the anatomic location of specific fractures. For FNSFs, these include pes cavus, limb length inequality, and coxa vara.^6,14,15 Other specific risk factors for FNSF include femoroacetabular impingement (pincer or CAM deformities), poor entry fitness scores, female sex, and gluteus medius weakness.^3,4 Though not routinely tested, genetic factors including the loss of calcitonin receptor C allele or vitamin-D receptor C-A haplotype have been also been shown to have higher risk for FNSF.³

Patho-anatomy/physiology

Wolff’s law states that mechanical stress placed on normal bone will result in remodeling of that bone.^2,6,7 If sufficient time is allowed for remodeling and the load applied does not exceed the strength of the bone structure, the bone will adapt by becoming stronger.^2,6 This remodeling process begins with osteoclastic resorption, followed by osteoblastic new bone formation.^2,6 Osteoclastic resorption weakens the bone, and if sufficient time is not given for new bone to form, microfractures occur, which can progress from an initial stress reaction to a complete fracture.^2,6,8,9

The mechanical demands of the hip are particularly significant, especially during high-impact activity such as running, where the femoral neck incurs forces up to 8.4 times an individual’s body weight. When this extreme repetitive loading exceeds the bone’s capacity for metabolic repair, microfractures accumulate, which can eventually progress to a FNSF.³

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.² The fracture process begins with crack initiation, with eventual propagation and development of a complete fracture unless the precipitating conditions are altered to allow resumption of normal bone remodeling.⁷ Pain related to stress fractures typically presents in the groin region for pubic rami and femoral neck stress fractures and in the anterior thigh for femoral shaft fractures.^2,9 The initial onset of pain is typically insidious.³ At first, pain occurs primarily during activity and resolves fairly quickly after the activity is discontinued.^2-4,6-8

Subacute
As the process of fracture continues without intervention, less activity is required to bring on symptoms until eventually pain occurs at rest.^3-8 Athletes may describe a “throbbing” pain at night, long after they have been active. Patients (especially competitive athletes) may not seek medical care until symptoms begin to interfere with training and/or function.⁸

Essentials of Assessment

History

Taking a complete history for suspected stress fractures should include asking about pain characteristics, training regimens, footwear, medical history, medications, nutrition, lifestyle habits, and any previous history of injuries related to over-training in the injured area.^1,3,4

Physical examination

Assessment should begin with alignment and symmetry of the legs, ankles, and feet, as these may affect biomechanical forces.¹¹ Although often nonspecific, classic physical examination findings include focal bony tenderness, antalgic gait, and swelling over the location of the stress fracture.^3,9 In FNSFs, pain may be elicited at end ranges of hip motion and with active straight leg raise.^2,6 For evaluating stress fractures of the femur, the fulcrum test is a highly sensitive and relatively specific clinical maneuver.¹¹

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.^5,16,19

Functional assessment

In addition to orthopedic special tests, functional assessments have been shown to predict stress fractures in the hip. In post-menopausal women, the inability to balance on a single leg for greater than 10 seconds, inability to squat to touch the floor, and weakened grip strength were individual predictors of future hip stress fractures.²⁰ In young female runners, one study found that contralateral hip drop and weak hip abductor strength were found in 99% of the participants with a history of FNSF compared to 52.9% of participants in the control group.²¹ Rapid foot pronation in midstance phase as well as medial knee displacement were also noted to be twice the incidence rate in the previously injured participants group.²¹

Laboratory studies

Laboratory workup should be obtained when there is concern for nutritional or metabolic deficiencies. Work up can include vitamin D levels, complete blood cell count, iron panels, thyroid function tests, magnesium, phosphorus, parathyroid hormone, and a complete chemistry panel in high risk individuals or those with recurrent stress fractures.⁵ Sex hormone levels can be tested including estradiol, luteinizing hormone, follicle stimulating hormone, urine pregnancy test in females and testosterone in males.²² Albumin and prealbumin should also be considered.²³

Imaging

Plain radiographs may aid in diagnosis by revealing subtle periosteal/cortical changes.⁶ The 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.⁴ False negative radiographs are common (especially in the first 2-3 weeks after onset of symptoms).^2,6-9 Bone scans have high sensitivity but low specificity, and have fallen out of favor.^2,6-9 MRI is considered the gold standard for imaging suspected stress fractures, andcan identify signs of stress fracture (bony and/ or soft tissue edema) as early as one to two days after symptom onset.^2,4-9 CT 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.^2,4-9

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.¹⁶

Early predictions of outcomes

Outcomes are highly dependent upon anatomic location and grade of injury. The Fredericson criteria is a grading system that evaluates the level of severity of a bone stress injury on a scale of I-IV. ²⁴ The Fredericson criteria are as follows

• Grade 1: mild marrow edema or periosteal edema on fat-suppressed T2WI (but not on T1WI)
• Grade 2: moderate marrow edema or periosteal edema on fat-suppressed T2WI (but not on T1WI)
• Grade 3: severe marrow edema or periosteal edema on both fat-suppressed T2WI and T1WI, without a fracture line on T1WI or T2WI
• Grade 4: severe marrow edema or periosteal edema on both fat-suppressed T2WI and T1WI, with a fracture line on T1WI or T2WI

Return to sport for FNSF is variable based on grade but can take on average 107 days.²⁵

Environmental

Environmental factors include the terrain/surface upon which an activity is performed, and the equipment used for the activity. More specifically, activities performed on hard surfaces are at higher risk of producing stress fractures. Running on irregular terrain and/or hills also increases this risk.^6,7 Femoral neck, sacral, and pubic ramusstress fractures occur more commonly in long distance runners while femoral shaft fractures are often related to jumping.⁸

Social role and social support system

Stress fractures can lead to significant anxiety in athletes due to lengthy periods of recovery and absence from participation. Having a strong support system and a multidisciplinary approach involving psychology and dietary counseling can be beneficial in treatment and help in navigating the barriers for return to sport.

Professional issues

For collegiate and professional athletes, femoral neck stress fractures can be a significant occupational hazard. The cultural pressure to “play through” the pain may lead to delayed or underreporting. The professional impact of this type of injury can be substantial, due to significant time loss from sport, which may impact professional contract negotiations or even NIL deals for NCAA athletes.

Rehabilitation Management and Treatments 

Available or current treatment guidelines 

Management strategies for stress injuries should be guided by the specific location and severity of the fracture. MRI-based grading scales are often used to classify the severity of the injury and establish a timeline for recovery.^3,7,10,19 These systems generally categorize FNSFs on a grade from 1-4, with higher grades corresponding to more extensive severity and a longer duration of required rest. While Grade 1 injuries may require only 3 weeks of rest, Grade 4 injuries can require 16 weeks or more.⁷ 

At different disease stages 

New onset/acute 
If the fracture is high-risk and/or high-grade, the patient should be referred to the appropriate orthopaedic/sports medicine/musculoskeletal specialist. Acutely displaced FNSFs should be treated emergently with open reduction internal fixation (ORIF).² Modifying weight bearing status helps prevent fracture progression and also decreases pain. Some advocate the use of acetaminophen or opioids (for severe pain) instead of NSAIDs for acute pain relief, due to the risk of delayed healing associated with the use of anti-inflammatory medication.^7,8 During this time, a thorough history should be taken to evaluate for contributing factors that can be addressed to help optimize healing.

Subacute 
Treatment should include activity modification as soon as a stress fracture is suspected.⁹ Contributing factors should be continually addressed (training/technique errors, equipment modification, nutrition modification, etc.).² Deconditioning can be minimized by allowing participation in activities with modified weight bearing, and gradual return to activity can be initiated after symptoms resolve. Markers of recovery on imaging include bone callus formation and resolution of fracture line, though repeat imaging is often unnecessary.⁵ 

Chronic 
Fractures with nonunion or avascular necrosis (AVN) require surgical treatment. Nonunion requires debridement and bone grafting, while AVN of the femoral head often requires hemiarthroplasty or a total hip arthroplasty.²

MRI based management

An additional treatment algorithm based on MRI characteristics for FNSFs has been proposed by Bernstein et al. as below³

*If fracture progression or persistent symptoms, proceed with operative fixation
♱For moderate or low risk fractures that are asymptomatic after 6 weeks, progressive weight bearing can be initiated

The non-operative treatment regimen should consist of an individualized rehabilitation program that includes a graded return to pain free weight-bearing and running. Rehabilitation should focus on improving the athlete’s strength, joint mobility, core and pelvic stabilization, and muscle endurance.²⁶ It is important to rehabilitate both lower extremities. Activity progression is dictated by the athlete’s pain during or after activity. For lower-risk BSIs, many rehab professionals permit progression of this program if pain is reported as ≤ 3 out of 10 on a pain scale.¹⁴ Cardiovascular endurance can initially be maintained with swimming, stationary biking, and aqua jogging.²⁶ Anti-gravity treadmill running can allow for gradual increase in bone loading while maintaining cardiovascular endurance and muscle strength, and athletes can start with partial body weight running and gradually increase this over time.^27,28

Prevention of recurrent stress fractures

Prevention of stress fractures requires a multifactorial approach to address nutritional, biomechanical, and hormonal health. Due to the association between low energy intake and stress fractures, athletes should undergo nutrition counseling with a registered dietician to ensure proper fueling and maintenance of adequate body weight.¹⁶ Recommendations may include increasing intake of dairy products or taking calcium and vitamin D supplementation.⁵ In addition, gait and biomechanical analysis and careful review of training programs can help minimize excessive bone loading and prevent future injuries. Multiple studies have shown that estrogen-containing oral contraceptives may provide a protective effect on bone density in female athletes, though more data is still needed in this area.^2,16 Masking menstrual irregularities with hormonal contraceptives is not recommended as it can impair the ability to capture athletes with underlying menstrual dysfunction.²⁹

Coordination of care

Treatment of stress fractures requires an integrated approach with a multidisciplinary team throughout the continuum of an athlete’s progression from rest to active rehabilitation and return to sport. The physiatrist or sports medicine physician typically leads the team and coordinates care with other medical specialists such as orthopedics or endocrinology to address fracture healing and metabolic health. Athletic trainers provide daily oversight for functional rehabilitation and often serve as the primary link between the athlete, medical team, and coaching staff. Clear communication with coaches is necessary to ensure appropriate adjustment of training loads. Collaboration with a registered dietitian and a physical therapist can help further support the athlete by addressing underlying energy deficits and biomechanical risk factors. 

Patient & family education

Patients, family, and coaches may all benefit from education on the etiology and prevention of stress fractures in athletes. Education should be provided on how to maximize healing, maintain function, and prevent recurrence. It is also necessary to educate the athlete and coach about the relationship between BSI and under fueling or REDs.¹³ This helps develop a comprehensive treatment approach for all of the systems affected by BSI and related conditions.

Emerging/unique interventions/assessments

Teriparatide (Forteo^®), a parathyroid hormone analogue, is being increasingly used off label for non-union and high-grade fractures to accelerate healing, with emerging evidence suggesting that parathyroid hormone enhances bony callus formation.³¹

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

Progressive hip or groin pain in an athlete that worsens with impact loading should raise immediate suspicion for a bone stress injury. Because initial radiographs may be negative, MRI is the gold standard to confirm the diagnosis and provide accurate grading. Treatment plans are determined by fracture location and risk of progression and should be individualized to each patient based on the severity of their injury and individual metabolic and biomechanical risk factors.

Cutting Edge/Emerging and Unique Concepts and Practice 

The use of modalities such as extracorporeal shockwave therapy and low-intensity pulsed ultrasound for bone healing have yielded limited benefit to date for acute stress fractures, though pulsed electromagnetic fields (PEMF) bone stimulators may be more effective at reducing time to fracture union.³² Medications to prevent bone remodeling such as bisphosphonates have shown mixed results in stress fracture management and are generally avoided in women of child-bearing age due to their long half-life and potential teratogenic effects.^5,29 The use of orthobiologics, including bone marrow aspirate concentrate and platelet-rich plasma, are emerging as options to enhance the biologic environment at the fracture site, but human clinical evidence regarding their efficacy currently lacks enough evidence to be conclusive.³²

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. Further research is needed to evaluate the long-term efficacy of pharmacologic agents, orthobiologics, and modalities for the enhancement of fracture healing in athletes.

References

1. Fukushima Y, Ray J, Kraus E, Syrop IP, Fredericson M. A review and proposed rationale for the use of ultrasonography as a diagnostic modality in the identification of bone stress injuries. J Ultrasound Med 2018;37(10):2297-307.
2. 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
3. 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
4. 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
5. Moriera A, Bilezikian J. Stress Fractures: Concepts and Therapeutics. Journal of Clinical Endocrinology and Metabolism. 2017; 102(2): 525-534.
6. Harrast MA, Colonno D. Stress fractures in runners. Clin Sports Med. 2010;29:399-416.
7. Kaeding CC, Najarian RG. Stress fractures: classification and management. Phys Sportsmed. 2010;38(3):45-54.
8. Patel DR. Stress fractures: diagnosis and management in the primary care setting. Pediatr Clin N Am. 2010;57:819-827.
9. Patel DS, Roth M, Kapil N. Stress fractures: diagnosis, treatment, and prevention. Am Fam Physician. 2011;83(1):39-46.
10. 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.
11. 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.
12. 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
13. 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
14. Schroeder JD, Trigg SD, Capo Dosal GE. Bone Stress Injuries: Diagnosis and Management. Am Fam Physician. 2024 Dec;110(6):592-600. PMID: 39700362
15. Nye NS, Covey CJ, Pawlak M, Olsen C, Boden BP, Beutler AI. Evaluating an Algorithm and Clinical Prediction Rule for Diagnosis of Bone Stress Injuries. Sports Health: A Multidisciplinary Approach. 2020;12(5):449-455. doi:10.1177/1941738120943540
16. 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.
17. Fedgo AA, Stahlman S. Increased risk for stress fractures and delayed healing with NSAID receipt, U.S. Armed Forces, 2014-2018. MSMR. 2020 Feb;27(2):18-25. PMID: 32105494.
18. Hodge JM, Wang Y, Berk M, et al. Selective serotonin reuptake inhibitors inhibit human osteoclast and osteoblast formation and function. Biological Psychiatry. 2013 Jul;74(1):32-39. DOI: 10.1016/j.biopsych.2012.11.003. PMID: 23260229
19. Ramey LN, McInnis KC, Palmer WE. Femoral neck stress fracture. The American journal of sports medicine. 2016. 44 (8) 2122-2129.
20. Rikkonen T, Poole K, Sirola J, Sund R, Honkanen R, Kröger H. Long-term effects of functional impairment on fracture risk and mortality in postmenopausal women. Osteoporos Int. 2018 Sep;29(9):2111-2120. doi: 10.1007/s00198-018-4588-4. Epub 2018 Jun 2. PMID: 29860666.
21. Whitney KE, Chanchi ML, d’Hemecourt PA, Stracciolini A, Kocher M, Dawkins C, Willwerth S, DeJong Lempke AF. Association between running gait biomechanics and femoral neck bone stress injuries in female runners. PM R. 2025 Dec;17(12):1432-1442. doi: 10.1002/pmrj.13418. Epub 2025 Jun 17. PMID: 40525729.
22. 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
23. (Kiuru, M. J., Pihlajamäki, H. K., & Ahovuo, J. A. (2004). Bone stress injuries. Acta Radiologica, 45(3), 000-000.)
24. Bergman R, Kaiser K. Stress Reaction and Fractures. 2025 Apr 3. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan–. PMID: 29939612.
25. Hoenig T, Eissele J, Strahl A, et alReturn to sport following low-risk and high-risk bone stress injuries: a systematic review and meta-analysisBritish Journal of Sports Medicine 2023;57:427-432
26. 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.
27. 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.
28. 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
29. 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.
30. 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.
31. Anderson, Paul A. MD1,a; Kates, Stephen L. MD2; Watts, Nelson B. MD3. Update on Atypical Femoral Fractures. The Journal of Bone and Joint Surgery 106(19):p 1819-1828, October 2, 2024. | DOI: 10.2106/JBJS.23.01439
32. Grzeskiewicz, E., Miller, T.L. (2023). Biologic Advancements in the Treatment of Stress Fractures. In: Miller, T.L. (eds) Endurance Sports Medicine. Springer, Cham. https://doi.org/10.1007/978-3-031-26600-3_10

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

Alexis Coslick, DO, Minh Quan Le, MD, Stephen Ritter, DO, Mohammed Emam, MD. Stress Fracture of the Hip. 5/11/2023

Author Disclosure

Marlena Rose Mueller, DO
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Nirmal Maxwell, DO
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Eli Schmidt, MD
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Zach Turner, MA
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