- Stress fractures are overuse injuries caused by cumulative microdamage from repetitive bone loading.
- Stress fractures occur in different situations:
- Fatigue fracture: abnormal repetitive stress applied to normal bone (e.g., young college athletes or new military recruits with increased physical activity demands and inadequate conditioning). Common sites include tibia, fibula, metatarsals, femoral neck, and navicular.
- Insufficiency fracture: normal stress applied to structurally abnormal bone (e.g., femoral neck fracture in osteopenic bone, metabolic bone disease). Common sites include spine, sacrum, femoral neck, and medial femoral condyle.
- Combination fracture: abnormal stress applied to abnormal bone (e.g., female long-distance runners with premature osteoporosis from athletic triad)
- Weight-bearing bones of the lower extremity are most commonly affected at the following sites:
- Tibia/fibula (most common)
- Metatarsals (second most)
- Femoral neck
- Pars interarticularis
- High-risk stress fractures occur in zones of tension or areas with poor blood supply and are more likely to result in fracture displacement and/or nonunion. High-risk sites include the following:
- Femoral neck
- Anterior tibial diaphysis
- Pars interarticularis of lumbar spine (L4, L5)
- 5th metatarsal at metaphyseal–diaphyseal junction
- Proximal 2nd metatarsal
- Medial malleolus
- Tarsal navicular
- Talar neck
- Synonym(s): march fracture, fatigue fracture
- Greatest incidence in 15- to 27-year-olds
- Females > males
- Accounts for up to 20% of visits to sports medicine and orthopedic clinics
- Lifetime athletic stress fracture is 10% (1).
- Affects up to 6.9% of male and 21.0% of female military members
Etiology and Pathophysiology
- Bone is dynamic and constantly remodeling in response to applied physiologic stress.
- Repetitive loading or overuse causes microfractures that fail to heal due to imbalance between bone resorption and bone formation.
- If microdamage accumulates in excess of reparation, bony fatigue leads to stress fracture.
- Females are at 2.3 times higher risk than males.
- Female athlete triad
- Small tibial width
- Later menarche, amenorrhea, or irregular menses
- History of stress fracture
- History of osteoporosis, osteomalacia, rheumatoid arthritis, prolonged corticosteroid therapy
- BMI <19 kg/m2
- Skeletal malalignment: pes cavus/planus, leg length discrepancies, excessive forefoot varus, tarsal coalitions, prominent posterior calcaneal process, tight heel cords
- Biomechanical factors such as increased vertical loading rate (e.g., heel-to-toe running instead of forefoot striking)
- High-risk exercises—track and field, cross country
- Training regimen—running >20 miles/week or training >5 hr/day
- Nutritional—inadequate caloric intake or history of eating disorder
- Chronic low vitamin D
- Rapid increase in mileage, running pace, or training volume
- Inappropriate footwear
- Hard training/running surface
- Inadequate recovery or rest and training with fatigued muscle
- Lifestyle: high alcohol intake or smoking
- Meds: glucocorticoids, anticonvulsants, antidepressants, depot-medroxyprogesterone acetate (DMPA), methotrexate, antiretrovirals, chronic cannabis use, >5 years of bisphosphonate use
- Prevention is the key especially in adolescent athletes (1).
- Graduated increments in training load intensity: no more than 10% per week
- Optimize energy balance.
- Diversify sports participation (minimizing sports specialization).
- Reduce intensity and duration of activity if new-onset pain.
- Proper footwear (Athletes should have a gait analysis prior to training.)
- Increasing dynamic physical activity (jumping; plyometric training) increases bone density and resistance to mechanical stress.
- Decrease vertical loading rate either by switching to forefoot strike running or (if continuing with heel-to-toe strike) by using a heel pad insert.
- Vitamin D supplementation (800 IU/day) in combination with calcium (2,000 mg/day)
Commonly Associated Conditions
- Female athlete triad
- Metabolic bone disorders
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