Stress Reaction and Fractures

Etiology

Mechanism of Stress Fractures

Stress fractures result from repeated submaximal loading. Traditionally, engineers compare these failures to fatigue fractures in materials like bridges; however, human bone undergoes constant remodeling, adding complexity to this analogy.[5][6] An imbalance between osteoclast and osteoblast activity triggers microdamage accumulation. High-risk stress fractures—tension-sided femoral neck, anterior tibial cortex, talar neck, and navicular—are prone to displacement or nonunion, possibly requiring surgical intervention. Low-risk fractures, including those in the fibula, posteromedial tibia, and metatarsal shafts, typically respond to activity modification.[7]

Types of Activities Associated with Stress Fractures

Different sports predispose athletes to specific stress fractures. Runners frequently sustain tibial and metatarsal fractures, whereas hurdlers have a higher patella fracture risk. Gymnasts and weightlifters are prone to spondylolysis, which results from repeated spinal hyperextension.[8] March fractures usually affect the second and third metatarsals, due to repetitive weight-bearing forces on relatively rigid segments.

Stress reactions and fractures result from repetitive microtrauma rather than acute injuries.[9] Stress fractures are common among runners and military recruits, often associated with changes in training intensity, footwear, or surfaces. Rapid changes in training programs, including increased distance, pace, volume, or cross-training without adequate time for adaptation, can contribute. Failure to follow intense training days with easy ones for recovery can also contribute to injury.[10] Therefore, prevention strategies focus on gradual activity increases, proper footwear, and sufficient recovery time.

Additionally, weekly distances exceeding 32 km (20 miles) significantly increase stress fracture risk for runners. These injuries typically arise during basic training or increased running and marching among military recruits. Female athletes and those with a prior history of stress fractures are at higher risk, especially when subjected to the same training regimens as male counterparts.[11][12] The higher incidence in females may reflect hormonal influences, lower bone density, or anatomical differences.[13]

Biomechanical and Nutritional Factors of Stress Fractures

Certain structural or gait abnormalities (eg, cavovarus foot alignment or narrow tibial width) may increase stress on specific bones. Contrasting earlier beliefs, ground reaction forces alone do not consistently predict stress fracture risk; rather, the vertical loading rate during heel strikes appears to correlate with injury incidence. Smaller tibial cross-sectional areas and lower muscle mass in the lower leg have also been linked to higher risk.[14] 

Insufficient energy intake compromises recovery and bone health. In the female athlete triad (now often termed Relative Energy Deficiency in Sport, or RED-S), disordered eating, amenorrhea, and low bone mineral density can lead to recurrent fractures. Male endurance athletes with high training volumes and restricted caloric intake may experience decreased testosterone and subsequent osteopenia or osteoporosis. Vitamin D also appears critical: low levels correlate with higher stress fracture risk, and supplementation may prevent some fractures, especially in military recruits.[15]

Risk Factors for Stress Reaction and Fractures

The most common risk factor is a sudden increase in activity levels, with longitudinal studies showing that higher pretraining activity levels may confer some protection. Other risk factors for stress fractures include the following intrinsic and extrinsic elements:

• Intrinsic factors:
  • Poor physical conditioning
  • Female sex
  • Hormonal imbalances
  • Menstrual disorders
  • Low bone density
  • Reduced muscle mass
  • Anatomical variations, such as genu valgum or a short leg [13][10][2]
• Extrinsic factors:
  • High-impact activities (eg, running, jumping)
  • Abrupt increases in physical activity levels
  • Inadequate footwear
  • Irregular or angled training surfaces
  • Nutritional deficiencies, particularly low vitamin D and calcium
  • Smoking
  • Poorly conditioned muscles [13][10][2]

Epidemiology

Stress fractures represent up to 20% of sports medicine clinic visits and appear commonly in athletes and military recruits.[16][17] In high school sports, they account for 0.8% of all injuries, with cross-country runners experiencing the highest incidence.[18] Overall, 40% of athletes will sustain a stress fracture at some point in their careers.[19] The lower leg (40.3%) and foot (34.9%) represent the majority of stress injuries in this group. Up to 16% of running injuries are stress fractures, with those exceeding 25 miles per week at higher risk. Among military members, repetitive training activities led to a stress fracture rate of 5.69 per 1,000 person-years between 2009 and 2012. Metatarsal stress fractures are prevalent, representing 25% of all stress fractures and 20% of sports medicine visits, with the second metatarsal being the most frequently affected due to its limited motion and structural characteristics. Approximately 78% of elite soccer-related stress fractures involve the fifth metatarsal.[20] Military recruits show even higher rates, especially among women, who develop stress fractures at a ratio of roughly 4:1 compared to men in similar training.

Stress fractures are predominantly seen in weight-bearing limbs. The most common stress fractures, in decreasing order of occurrence, include the tibia (23.6%), tarsal navicular (17.6%), metatarsals (16.2%), femur (6.6%), and pelvis (1.6%).[21] Medial tibial stress syndrome, or shin splints, is the earliest manifestation of stress injuries and represents a spectrum of medial tibial pain that may progress to a fracture if not addressed. The specific location of stress fractures often varies by sport. For example, navicular, tibia, and metatarsal fractures are common in track athletes, while tibia and fibula fractures are prevalent among distance runners. Dancers predominantly suffer from metatarsal fractures, and military recruits often experience fractures in the calcaneus and metatarsals. The ulna is the most frequently affected upper extremity bone.[22] Despite generally favorable healing, recurrence rates can approach 60%, emphasizing the need for comprehensive prevention strategies.[23] 

Pathophysiology

Bone Remodeling Pathophysiologic Mechanisms

Stress injuries occur when a mismatch between the bone's innate strength and the mechanical load it endures is present, leading to a gradual weakening of the bone structure. This mismatch can result from 2 primary mechanisms: fatigue fractures, where abnormal stress is applied to healthy bone, and insufficiency fractures, where normal stress is exerted on a compromised bone, specifically at muscle insertion points where repetitive load and stress are highest.[9][24] Insufficiency fractures may sometimes be referred to as pathological fractures, though this term traditionally describes fractures arising from focal bony abnormalities.

In normal healthy bone, osteoblastic activity repairs microdamage caused by regular physical activity. A stress fracture occurs when osteoclastic resorption exceeds osteoblastic repair, causing structural weakness. According to Wolff's law, bone adapts to repetitive loads, but excessive loading can disrupt osteocyte signaling, which allows microdamage to accumulate.[17] When osteocyte signaling falters, bone repair mechanisms fail to keep pace. This imbalance leads to stress fractures because the typical 3- to 4-month bone remodeling cycle cannot handle chronic excessive stress.[25] 

Biomechanic Pathophysiologic Mechanisms

Biomechanical factors also influence stress fracture development. Compression fractures often run parallel to the bone's axis on the concave side, whereas tension fractures lie perpendicular on the convex side.[26] Foot biomechanics, with longer or more plantarflexed metatarsals bearing a disproportionate load, can significantly impact fracture risk. Certain foot types (eg, cavovarus) increase stress on the lateral column and predispose individuals to fractures of the fourth and fifth metatarsals.[27][28] External factors, including training type, intensity, environmental conditions, and footwear, all further contribute to stress fracture risk.

Histopathology

Animal studies reveal that, at the cellular level, stress fractures involve irregular bone changes. Histologic studies of stress fractures show that repetitive stress triggers increased osteoclastic activity that surpasses the rate of osteoblastic activity and new bone formation. As a result, the bone weakens. After 2 weeks, woven bone develops islands of cartilage and active resorption cavities along the periosteal margin. By 4 weeks, remodeling begins at the periosteal surface and continues along the fracture plane into the medullary cavity. The formation of a periosteal hard callus is a hallmark of healing.[29][30]

History and Physical

Clinical History

Patients typically report a gradual, dull ache that worsens with weight-bearing and often follows recent spikes in training intensity or changes in terrain or footwear.[31] Pain initially occurs only during exercise but can progress to discomfort during daily tasks and may persist upon waking.[32] Evaluating the past 6 to 8 weeks of training (changes in frequency, duration, or intensity), biomechanics, and intrinsic risk factors (eg, age, body composition, female athlete triad, or prior stress fractures) is critical. Certain medications (eg, glucocorticoids, bisphosphonates) also elevate fracture risk. Extrinsic contributors include dietary deficiencies and structural abnormalities in foot or gait mechanics.[19][33]

Physical Examination

Focal tenderness over the affected area is common and may be accompanied by soft tissue swelling. Differentiating muscle injury or early stress reactions from a true stress fracture is critical: soft tissue tenderness usually indicates strain or early reaction, whereas bony tenderness strongly suggests a fracture. Certain anatomical sites, eg, the pelvis and sacrum, can be diagnostically challenging due to their subtle presentations.[23] Several clinical tests aid in diagnosis, including:

• One-leg hop test: This test helps distinguish medial tibial stress syndrome from tibial stress fractures. Patients with fractures often cannot hop without pain, especially on landing.
• Fulcrum test: The fulcrum test evaluates possible femoral shaft stress fractures. The examiner places an arm under the thigh and applies pressure to the knee; pain or apprehension indicates a positive result.
• Lumbar extension or single-leg hyperextension (Stork test): This test assesses spondylolysis but has limited sensitivity and specificity. Spondylolysis may be asymptomatic and found incidentally on imaging, while spondylolisthesis involves anterior displacement of the vertebral body due to an unhealed pars defect.[34][8]

A biomechanical evaluation is also important; for instance, a supinated foot increases forefoot loading and the risk of second metatarsal fractures. Pain localization through palpation and assessing joint motion can guide diagnosis, and patients may exhibit a limping gait when weight-bearing if the joint is involved.[35]

Evaluation

Plain Radiographs

Plain radiographs are typically the first imaging modality for suspected stress injuries because they are widely available, affordable, and involve low radiation exposure. However, they frequently appear normal early in the injury process, resulting in low sensitivity.[11] Subtle signs—such as periosteal elevation, cortical thickening, sclerosis, or a fracture line—often take 2 to 3 weeks to become visible. A "dreaded black line" may signal a high-risk fracture in areas like the tibia or femur.[36][37] Spondylolysis poses an additional diagnostic challenge, sometimes requiring 5 specialized views to visualize the pars interarticularis properly.[34] Even with multiple views, early lesions can be missed, so further imaging, particularly MRI, is warranted if clinical suspicion remains high despite normal radiographs. 

Metatarsal stress fractures ("march fractures") require particular attention. Plain radiographs may initially be negative or show only subtle periosteal reactions or cortical blurring. The "gray cortex" sign—poorly defined cortical lucency—may indicate early stress fractures.[38] Over time, radiographic signs such as callus formation or cortical lucency may become apparent.[39]

Magnetic Resonance Imaging

MRI is the most sensitive (80%–100%) and specific (100%) imaging modality for diagnosing stress injuries and is thus considered the gold standard.[22] Typical MRI findings include periosteal and bone marrow edema, fracture lines extending into the medullary canal, and adjacent soft tissue involvement (see Image. Stress Fracture on MRI). MRI offers the advantage of evaluating concurrent injuries to muscles, ligaments, or cartilage without radiation exposure.[40][41]

Computed Tomography

Computed tomography (CT) imaging provides detailed visualization of sclerosis, new bone formation, periosteal reactions, or fracture lines. CT is particularly useful in evaluating occult fractures and distinguishing between healing bone and fibrous unions. However, it involves greater radiation exposure and lower sensitivity than MRI. 

Additional Imaging Studies

Other imaging techniques, such as single-photon emission computed tomography (SPECT) and 3-phase bone scans with technetium-99, are also used to detect early stress reactions not visible on plain radiographs.[2] Bone scintigraphy is moderately sensitive at 74%. These scans are highly sensitive but less specific, often showing increased uptake in areas of high bone turnover. Conditions like avascular necrosis, infections, or malignancies can also produce similar findings, limiting their diagnostic utility. These modalities are not typically used for follow-up imaging due to their lower specificity.

Laboratory Studies

Laboratory tests play a limited role in diagnosing stress fractures but are valuable in recurrent or frequent cases. Vitamin D deficiency (serum levels below 20 ng/mL) has been linked to higher stress fracture incidence.[40] In recurrent fracture scenarios, assessing thyroid-stimulating hormone, parathyroid hormone, and bone mineral density may be beneficial.[17] 

Classification Systems 

Stress fractures are broadly categorized into high-risk and low-risk injuries. Metatarsal stress fractures, for example, are classified as low-risk due to their generally favorable prognosis with activity modification and weight-bearing management.[24] Multiple imaging-based classification systems have been developed to define injury severity and prognosis more clearly.

Radiographic Grading System

The following 5-tiered grading system for stress fracture developed by Kaeding and Miller is associated with specific radiographic findings:

1. Asymptomatic radiographic findings
2. Pain with no fracture on imaging
3. Nondisplaced fracture on imaging
4. Displaced fracture on imaging
5. Sclerotic nonunion on imaging [42]

Magnetic Resonance Imaging Grading System

Nattiv et al developed a classification for stress fractures in athletes, similar to the grading system suggested by Fredericson et al, involving the evaluation of bone marrow edema and periosteal reaction in bone stress injuries on MRI (see Image. T1 and T2 Images of Stress Fracture).[21][43] The following findings are associated with each grade:

• 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 (see Image. Grade 4 Stress Fracture) 

Treatment / Management

The treatment of stress injuries depends on whether the lesion is a stress reaction or fracture, its anatomical location, and the potential for rehabilitation. Clinicians must identify fractures at risk for delayed union, nonunion, displacement, or intra-articular extension. General management principles include partial or nonweight-bearing for 2 to 6 weeks, followed by gradual activity resumption. Early detection is essential since prompt intervention facilitates quicker recovery.

Low-Risk Fracture Management

Low-risk stress fractures typically receive conservative treatment using a 2-phase approach. Low-risk locations include the posterior tibia, second to fourth metatarsals, femur, pubic rami, sacrum, and fibula. Phase 1 involves analgesia, modified weight-bearing, and cessation of inciting activities. Temporary immobilization is appropriate if ambulation is painful. Recommended alternative activities include water fitness, cycling, and elliptical training to preserve fitness and strength.[23][9][40] Phase 2 commences after a pain-free period and features a graduated return to activity supported by ongoing physical therapy. For instance, runners should initially resume running at a reduced pace and distance on alternating days. Patients gradually progress toward baseline intensity, frequency, and duration over several weeks. The length of each phase varies. A practical guideline is to match the duration of pain resolution with an equal duration of graduated return to activity. Footwear modifications and orthotics may benefit athletes with pronounced foot pronation or supination. Shoes should ideally provide adequate heel width, firm midsole support, and a straight last. Regular shoe replacement every 300 to 350 miles, along with gait analysis and running form adjustments, can further minimize reinjury risk.[44]

High-Risk Fracture Management

High-risk stress fractures occur at sites with poor vascular supply, maximal tensile loading, or a predisposition to nonunion.[21][45] These injuries require a high index of suspicion and can pose diagnostic challenges. High-risk locations include the femoral neck, anterior tibia, tarsal navicular, talus, sesamoids, and the first and fifth metatarsals. These fractures often fail conservative management and can cause significant morbidity due to the risk of displacement from tensile forces at muscular attachments, causing bony distraction.[45] Femoral neck fractures constitute a distinct subgroup. Magnetic resonance imaging is recommended due to low radiographic sensitivity. Superior (tension-sided) femoral neck stress fractures require surgical consultation, whereas inferior (compression-sided) fractures involving <50% bone width may initially receive conservative treatment with close monitoring. Increasing pain or fracture size necessitates orthopedic referral, and displacement requires immediate operative intervention to prevent femoral head avascular necrosis.[46]

Spondylolysis Management

Spondylolysis represents a unique stress injury, with limited clinical trial data guiding management.[8] Conservative treatment typically involves activity modification, core strengthening, and potentially bracing. Activity restriction ranges from 2 weeks to 6 months, depending on symptom resolution. The efficacy of bracing, while controversial, is supported by some evidence showing >80% pain-free return with rigid orthoses limiting lumbar extension, worn 23 hours daily for up to 6 months.[34][47] Persistent symptoms may necessitate surgical intervention, with several effective techniques described, though this is outside the scope of this review.(A1)

Nutritional Supplementation

Calcium and vitamin D supplementation may reduce stress fracture incidence, though evidence supporting faster healing is limited. A study of female United States Navy recruits found a 20% fracture rate reduction using daily supplements of 2000 mg of calcium and 800 IU of vitamin D.[48] Generalizability remains unclear, as other studies suggest increased fracture risk with supplementation.[12] Female athletes with delayed menarche, infrequent menstruation, or decreased bone mineral density warrant endocrine evaluation and targeted supplementation. Routine vitamin D and calcium supplementation should be restricted to athletes with documented deficiencies or repeated stress fractures. Evaluation for eating disorders, along with psychiatric and nutritional intervention, is recommended where indicated. Bisphosphonates show preliminary promise but require further research validation.(A1)

Bone Specific Management 

Recommendations for the management of specific types of stress fractures include:

• Rib: Managed nonoperatively with rest, analgesics, and training adjustments to correct mechanics.
• Pelvis: Conservatively treated with rest, protected weight bearing, and gradual activity resumption.
• Femoral neck: Compression-sided fractures with less than 50% bone width involvement receive conservative treatment with nonweight-bearing and activity restrictions. Tension-sided or extensive compression fractures (>50% width) typically require percutaneous screw fixation.
• Femoral shaft: Usually managed conservatively with rest, modified weight-bearing, and activity restriction. Surgical fixation with intramedullary nailing is indicated for fracture displacement, low bone density, or age over 60.
• Patella: Treated conservatively with immobilization followed by progressive activity.
• Tibia: Conservatively managed with protected weight-bearing and activity modification. The presence of an anterior cortical "dreaded black line" typically necessitates surgical intervention with intramedullary nailing or plating based on patient-specific considerations. Medial tibial plateau fractures usually receive conservative treatment. Medial malleolar fractures may require operative intervention depending on ankle stability.
• Fibula: Conservative management includes rest, immobilization, and progressive activity resumption.
• Tarsals: Calcaneal stress fractures generally heal rapidly with conservative treatment. Navicular fractures carry high nonunion risk, requiring nonweight-bearing for up to 12 weeks, with surgical fixation indicated for completed fracture lines. Talus and medial cuneiform fractures often respond to conservative management.
• Metatarsals: Typically conservatively managed, with metatarsal padding as necessary. Dancer fractures (base of the second metatarsal) require nonweight-bearing immobilization. Fifth metatarsal fractures carry significant nonunion risk, often requiring immobilization and surgical management. Sesamoid fractures necessitate rest, immobilization, and offloading from offending activities.

Differential Diagnosis

The differential diagnosis for stress reactions and fractures is broad but can be refined based on anatomical location and clinical features. Conditions with similar presentations include:

• Bone contusion: Typically related to acute trauma rather than repetitive loading.
• Cellulitis: Presents with superficial skin erythema, warmth, and significant soft tissue swelling.
• Osteomyelitis/infection: Often accompanied by systemic symptoms (eg, fever and elevated inflammatory markers).
• Tendonitis/tendinopathy: This condition usually presents as pain localized along the tendon and worsens with specific tendon loading rather than bone palpation.
• Bursitis: Localized tenderness over bursae, with pain exacerbated by direct pressure, is typical in this condition.
• Degenerative changes/arthropathy: Pain is often associated with joint stiffness and limited motion and worsens with joint use rather than weight-bearing on bone.
• Exertional compartment syndrome: This condition is characterized by progressive, activity-induced muscle tightness relieved quickly after cessation.
• Acute compartment syndrome: Presents acutely after trauma with severe pain disproportionate to exam findings and neurovascular compromise.
• Neuropathic pain: This type of pain is typically sharp, burning, or electric in nature and has sensory abnormalities.
• Complex regional pain syndrome (CRPS): CRPS is associated with abnormal skin changes, autonomic dysfunction, and severe disproportionate pain.
• Radiculopathy: Pain radiates along a dermatome and worsens with spinal movements rather than localized bone stress.
• Nerve entrapment: Pain accompanied by numbness or tingling in specific nerve distributions.
• Arterial entrapment: This condition is characterized by exertional limb pain with vascular symptoms (pallor, reduced pulses) during activity.
• Coagulation disorders: These conditions usually present with spontaneous or easy bruising and often systemic bleeding issues.
• Avascular necrosis: Avascular necrosis often involves deep, dull joint pain unrelated to repetitive loading, frequently with risk factors such as corticosteroid use.
• Benign or malignant bone tumors (osteosarcoma, Ewing sarcoma, metastasis): Often show progressive night pain, unrelieved by rest, possible palpable mass, and abnormal imaging appearance.

Depending on anatomical location, nonmusculoskeletal conditions (eg, dermatologic, vascular, neurologic, genitourinary, reproductive, and gastrointestinal) may also be considered, including:

• Pelvic or femoral stress injuries may mimic reproductive or gastrointestinal disorders.
• Tibial stress injuries require differentiation from chronic exertional compartment syndrome (CECS) and popliteal artery entrapment syndrome.

Advanced imaging (particularly MRI) is valuable in distinguishing stress fractures from malignancies, osteomyelitis, and osteoid osteomas, with reported accuracy between 93% and 98%.[24]

Prognosis

The prognosis for patients with stress reactions or fractures largely depends on early recognition, injury severity, anatomical location, and adherence to appropriate management strategies. Patients diagnosed in the stress reaction stage—defined by bone marrow edema without cortical disruption—typically experience favorable outcomes with conservative measures, such as activity modification, offloading, and nutritional optimization. Recovery generally occurs within 6 to 8 weeks if mechanical stress is adequately reduced. For patients whose injuries progress to stress fractures, the prognosis varies significantly according to the fracture site and displacement severity.

Low-risk fractures, eg, those involving the tibia, fibula, or metatarsals, usually heal well with conservative care, including protected weight-bearing and a gradual return to activity. These injuries typically resolve within 6 to 12 weeks, with most patients regaining full function.[49] In contrast, high-risk fractures—including those involving the femoral neck, anterior tibial cortex, and navicular bone—have a greater risk of delayed union, nonunion, or progression to complete fractures if managed inadequately. Such injuries often require prolonged immobilization or surgical intervention. Poor prognostic indicators include ongoing mechanical loading, inadequate nutritional status, osteoporosis, and conditions such as relative energy deficiency in sport (RED-S).[50]

Overall, long-term outcomes are generally favorable with timely intervention. However, recurrence is common if underlying biomechanical issues or training errors remain unaddressed. Preventive strategies such as progressive training schedules, optimized footwear, sufficient calcium and vitamin D intake, and patient education on symptom recognition are essential for reducing recurrence risk. With early diagnosis and appropriate evidence-based management, most patients can fully recover and resume prior activity levels without significant long-term impairment.

Complications

Stress reactions and fractures, if not identified and managed promptly, can lead to acute and chronic complications affecting long-term function. Complication risks depend on injury severity, location, and treatment adequacy. An interprofessional approach addressing biomechanics, nutrition, and training practices is essential to minimize these risks and ensure optimal musculoskeletal recovery.

Acute Complications

Progression to complete fracture

One of the most significant risks of untreated or poorly managed stress reactions is the progression to a complete fracture. Continued mechanical loading on an already weakened bone can result in a full-thickness cortical break, necessitating prolonged immobilization or surgical intervention. High-risk sites, such as the femoral neck, anterior tibia, and navicular bone, are particularly prone to this complication.

Delayed union

Stress fractures that fail to heal within the expected timeframe (typically 6–12 weeks) may be classified as delayed unions. This can occur due to inadequate immobilization, premature return to activity, poor nutritional status, or underlying metabolic conditions. Delayed healing prolongs recovery and increases the likelihood of chronic pain and dysfunction.

Soft tissue injury

Persistent stress on the affected bone may also lead to compensatory overuse injuries in surrounding muscles, tendons, or ligaments. This includes conditions such as tendinopathy, plantar fasciitis, or muscle strains.

Chronic Complications

Nonunion

Nonunion occurs when a stress fracture fails to heal completely, often requiring surgical intervention, including bone grafting or internal fixation. This is more common in high-risk fractures, particularly in locations with limited vascular supply, such as the navicular and anterior tibia.

Chronic pain and functional limitations

Despite radiographic healing, persistent pain can occur due to incomplete bone remodeling, residual biomechanical abnormalities, or secondary soft tissue dysfunction. This may lead to chronic activity restrictions and reduced athletic performance.

Recurrent stress fractures

Inadequate rehabilitation, improper return-to-sport protocols, or failure to address underlying biomechanical and nutritional factors can result in recurrent stress fractures. Individuals with poor bone mineral density or those engaged in high-impact sports are particularly susceptible.

Joint degeneration and osteoarthritis

Recurrent stress fractures, particularly in weight-bearing joints, may accelerate cartilage wear and contribute to early-onset osteoarthritis. This is especially concerning in fractures involving the femoral neck or tibial plateau.