Attended for you
published online on 06.03.2026https://doi.org/10.34045/SEMS/2026/8
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Speaker: Pr Rowena Johnson, Sports Medicine Imaging, Royal College of Radiologists MSK lead, Mayo Clinic, London, UK
Congress: Sport & Exercise Medicine Switzerland and Swiss Sport Physiotherapy Association joint conference: “Structure & Function”, Lausanne, October 30th and 31st 2025

The video recording for this presentation is not publically available online.

Introduction

Bone stress injuries represent a significant diagnostic and therapeutic challenge in sports medicine, accounting for approximately 10% of sports medicine clinical presentations. Accurate diagnosis requires integration of clinical presentation, understanding of underlying pathophysiology, and sophisticated imaging interpretation. This article synthesizes current evidence on bone stress injury classification, imaging strategies, and clinical management considerations, drawing from expertise presented by Professor Rowena Johnson, musculoskeletal radiologist at the Mayo Clinic, London.

Definitions and clinical presentation

Terminology and Classification

The term «stress fracture» describes fractures occurring after repetitive stress insufficient to cause acute fracture. Two distinct subtypes exist with different pathophysiological mechanisms:
• Fatigue fractures: Result from abnormal muscular stress or torque applied to bone with normal elastic resistance. These predominate in athletic populations.
• Insufficiency fractures: Represent pathological fractures in non-tumoral abnormal bone with reduced elastic resistance to normal stress, occurring in metabolic bone disease, osteoporosis, or other conditions compromising bone integrity.

Clinical Characteristics

Typical presentation involves insidious onset of activity-related, localized pain during weightbearing that intensifies with continued exercise, occurs earlier in exercise sessions as pathology progresses, and resolves with non-weightbearing. Depending on anatomical location, redness, swelling, and palpable periosteal reaction may occur. Most cases are diagnosed clinically, with imaging confirming diagnosis and guiding management.

Pathophysiology

Bone Remodeling Under Repetitive Load

Bone undergoes continuous resorption and regeneration cycles. Repetitive submaximal loading—the critical threshold below acute fracture but above physiological adaptation capacity—triggers stress responses involving both physiological and mechanical changes. This process involves failure of bone synthesis coupled with increased osteoclastic activity, creating a net catabolic state.
Surrounding muscle groups undergo hypertrophy and strengthening more rapidly than bone adaptation, contributing to periostitis. Progressive osteoclastic activity without adequate regeneration decreases overall bone ultimate strength, leading to microfracture and potential complete fracture.

Temporal Progression

Bone stress injury evolves through identifiable phases:
Days 5-14: Osteoclastic resorption following initial injury
Subsequent weeks: Increased vascularity with endosteal and periosteal callus formation
Progressive phase: Cortical or medullary fracture development if loading continues

Gender-Specific Considerations and RED-S

Female athletes demonstrate distinct susceptibility patterns related to the Female Athlete Triad—aggressive training, nutritional disorders, and menstrual irregularity. Contemporary understanding encompasses Relative Energy Deficiency in Sport (RED-S), recognizing broader physiological consequences of energy availability inadequacy beyond reproductive function.
Critical clinical principle: All female athletes presenting with bone stress injuries warrant screening for RED-S factors including energy availability, menstrual function, nutritional adequacy, and hormonal status. However, male athletes can also experience RED-S, requiring vigilance across genders.
Diagnostic caveat: Athletes should not be assumed to have purely mechanical stress injuries. Multiple factors including metabolic conditions, nutritional deficiencies, hormonal imbalances, and systemic diseases can alter bone resistance, favoring fracture development.

Imaging strategy and classification

MRI Sequences and Interpretation

MRI represents the imaging modality of choice for suspected bone stress injuries, particularly when radiographs are normal (common in early presentations). Optimal interpretation requires understanding sequence-specific information:
STIR/fluid-sensitive sequences: Optimally demonstrate marrow edema—the brightest signal indicating pathology T1-weighted sequences: Optimally visualize fracture lines within bone marrow
Critical interpretation principle: Marrow edema does not invariably indicate pathology. Adolescent athletes demonstrate physiological hematopoietic marrow that can mimic pathological edema. Diffusely abnormal marrow signal should prompt consideration of metabolic or systemic conditions (e.g., HIV, hematological disorders).

Classification Systems

The Fredericson classification evaluates signal characteristics on fluid-sensitive and T1-weighted sequences, progressing from early stress response to complete fracture. The Arendt classification provides alternative grading. However, descriptive reporting supersedes classification adherence—clinicians must visualize pathology mentally rather than depending solely on grading systems. Documentation should include edema extent, fracture line presence and orientation, periosteal reaction, and cortical involvement.

Anatomical locations and specific considerations

Femoral Neck Stress Fractures

Femoral neck injuries demonstrate concerning progression potential. Compression-side fractures (medial femoral neck) may appear initially as marrow edema with periosteal inflammation, progressing to intracortical signal abnormality and cortical fracture if loading continues despite medical advice. CT provides superior fracture line visualization and surgical planning when indicated.
Risk factor identification: Posterior acetabular stress fractures, particularly bilateral, may reflect underlying structural abnormalities (e.g., posterior hip dysplasia) or training surface changes (e.g., transition to artificial turf), requiring multifactorial intervention.

Tibial Stress Injuries

Medial tibial stress syndrome represents a spectrum from periosteal reaction to cortical stress fracture. Proximal tibial stress fractures can present with minimal symptoms despite significant imaging findings. Distal tibial fractures demonstrate characteristic serpiginous morphology on T1 sequences.
Differential diagnosis: Intracortical tibial abnormalities may represent osteoid osteoma—a benign bone tumor demonstrating characteristic central nidus on CT—rather than stress fracture, altering management entirely.

Fibular Stress Fractures

Distal fibular injuries demonstrate variable imaging characteristics reflecting chronicity. Chronic injuries show florid periosteal reaction with extensive bone remodeling. Acute injuries demonstrate marrow edema, fracture line, and periostitis without extensive periosteal new bone formation.

Navicular Stress Fractures

Navicular injuries present unique management challenges. Synovial fluid inhibits new bone formation, producing characteristic Y-shaped fracture morphology and prolonged imaging abnormality (months). These injuries predominate in track and field athletes. Initial radiographs are frequently normal, mandating low threshold for MRI when clinical suspicion exists.
Bilateral screening: Calcaneal stress fractures frequently occur bilaterally, warranting contralateral imaging when unilateral injury is identified.

Localized bone density assessment

Traditional dual-energy X-ray absorptiometry (DEXA) demonstrates limitations in athletic populations. The majority of DEXA scans done in the World look at the left hip and lumbar spine and claim that it is representative of the whole body’s bone density. Athletes exhibit asymmetric bone density reflecting sport-specific loading patterns. Impact sports (football, rugby, gymnastics) produce osteogenic responses with elevated bone mineral density compared to general populations, whereas unloaded sports (swimming, cycling) do not. Runners will exhibit increases in calcaneal bone density.
Small field-of-view DEXA (customized regions of interest) enables localized bone density assessment at specific anatomical sites (e.g., adductor longus insertion). Research in football and rugby populations establishes normative BMD values for specific sites. Symphyseal osteopenia represents a potential etiology of pubic-related groin pain independent of traditional overload mechanisms. In triathletes, different areas of the foot can be assessed.
Critical dissociation: Localized osteopenia does not necessarily correspond to marrow edema on MRI—these represent distinct pathophysiological processes requiring independent assessment and interpretation.

Diagnostic pitfalls

Infection Masquerading as Stress Injury

Pubic symphysis marrow edema may represent infectious processes rather than mechanical overload. Loss of cortical definition distinguishes pubic cleft infection from osteitis pubis, requiring entirely different therapeutic approaches including antimicrobial therapy.

Systemic Disease Presentation

Sacral stress fractures in young athletes warrant consideration of inflammatory spondyloarthropathies, particularly with HLA-B27 positivity and family history of ankylosing spondylitis. Bone stress injuries may represent initial presentation of systemic disease.

Conclusion

Bone stress injury management requires integration of clinical presentation, pathophysiological understanding, and sophisticated imaging interpretation. Marrow edema is not invariably pathological or pain-causing. MRI sequence optimization (for example T1-VIBE or “pseudo-CT” sequences) enables accurate diagnosis, while recognition of differential diagnoses prevents misattribution of symptoms to mechanical stress when systemic, infectious, or neoplastic processes exist. Localized bone density assessment represents an emerging tool for understanding chronic groin pain. The fundamental principle remains: treat the patient, not the picture.

References

  1. Pentecost RL, Murray RA, Brindley HH. Fatigue, insufficiency, and pathologic fractures. JAMA. 1964 Mar 28;187(13):1001–1004. doi:10.1001/jama.1964.03060260029006.
  2. Pepper M, Akuthota V, McCarty EC. The pathophysiology of stress fractures. Clin Sports Med. 2006 Jan;25(1):1–16, vii. doi:10.1016/j.csm.2005.08.010.
  3. Kim DR, Weber K. Relative energy deficiency in sport (RED-S) and bone stress injuries. Oper Tech Sports Med. 2023 Sep;31(3):151025. doi:10.1016/j.otsm.2023.151025.
  4. Fredericson M, Bergman AG, Hoffman KL, Dillingham MS. Tibial stress reaction in runners: correlation of clinical symptoms and scintigraphy with a new magnetic resonance imaging grading system. Am J Sports Med. 1995 Mar-Apr;23(4):472–481. doi:10.1177/036354659502300405.
  5. Arendt EA, Griffiths HJ. The use of MR imaging in the assessment and clinical management of stress reactions of bone in high-performance athletes. Clin Sports Med. 1997 Apr;16(2):291–306. doi:10.1016/S0278-5919(05)70203-0.
  6. Uzunca K, Birtane M, Durmus-Altun G, Ustun F. High bone mineral density in loaded skeletal regions of former professional football (soccer) players: what is the effect of time after active career? Br J Sports Med. 2005 Mar;39(3):154–157; discussion 154–157. doi:10.1136/bjsm.2003.011494.
  7. Fredericson M, Chew K, Ngo J, Cleek T, Kiratli J, Cobb K. Regional bone mineral density in male athletes: a comparison of soccer players, runners, and controls. Br J Sports Med. 2007 Oct;41(10):664–668; discussion 668. doi:10.1136/bjsm.2006.030783.
  8. Aparisi Gómez MP, Wáng YXJ, Yu JS, Johnson R, Chang CY. Dual-energy X-ray absorptiometry for osteoporosis screening: AJR Expert Panel narrative review. AJR Am J Roentgenol. 2025 Dec; 225(6):e2532802. doi:10.2214/AJR.25.32802.

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