Stress fracture in the world class athlete: a case study : Medicine & Science in Sports & Exercise

Journal Logo

Clinical Sciences: Case Study

Stress fracture in the world class athlete

a case study


Author Information
Medicine & Science in Sports & Exercise 30(6):p 783-787, June 1998.
  • Free


Stress fractures were first described by Breithaupt in German soldiers in 1855 (2). These fractures, also known as fatigue or marching fractures, typically occur in normal bone that has been subjected to repeated cyclic loading with loads normally less than those that cause spontaneous fracture. Stress fractures may be the result of excessive, repetitive tensile and compressive forces transmitted to the bone by the ligaments, tendons, and muscles during protracted activity (22). Bone may also experience brief periods of high strain of two to three times normal training loading values because of the peak activities of dismount in gymnasts and jumping in basketball players and ballet dancers. These high peak strain values, subjected to bone cyclically, produce microscopic fatigue damage quite readily and early in the training period (20,21). The three animal athletic groups in which stress fracture have been detected (thoroughbred racehorses (11), racing greyhounds (6) and the human), have been trained to produce the maximum in performance by repetitive training exercises. The requirement for constant training in the athlete does not provide sufficient time for the repair processes in bone to counteract the high forces inflicted by the rigorous training regime (22).

As in other pathologic bone conditions, stress injuries are detectable at an earlier time postinjury with scintigraphy (15,16,29) and magnetic resonance imaging than with plain radiographs (8). The 99mtechnetium-polyphosphate compounds, used in scintigraphy, accumulate in areas of high blood flow and metabolic activity and make the condition of stress fracture detectable earlier than the time at which radiographs can resolve the condition (8). Stress fractures of the mid-tibia are relatively rare compared with proximal and distal third fractures (12,13). They are also the most resistant to treatment. In general, the treatment of tibial stress fractures is rest, the removal of impact activity from the athlete's training regime, and cross training to maintain fitness. For mid-tibia fractures, Fredericson recommends a period of non-weight-bearing cast immobilization of 6-8 wk (8). Prolonged periods of rest may result in clinical symptomatic improvement, but the resumption of full activity may cause a reoccurrence of the problem (5). For the world class athlete, prolonged rest may be intolerable if the injury coincides with competitive opportunities such as the Olympic Summer Games.

Recently Heckman et al. (10), in a prospective, randomized, double-blind and placebo-controlled study of tibial diaphysis fracture healing, reported a significant acceleration of all phases of the healing process and demonstrated that placebo treated fractures took 60% longer to heal than fractures treated with pulsed low-intensity ultrasound (10). Prescription use by physicians, since the device was available for orthopaedic application, indicates a success rate of 96% and a treatment time of 104 ± 11.3 for all tibial stress fractures with a success rate of 90% and healing time of 113 ± 22.6 d for mid-tibial stress fractures. The 4% failure rate was in mid-tibial stress fractures.

Ultrasound is used for surgery with an intensity of 5 to 100 W·cm−2) and in conventional therapeutic applications at an intensity of 0.5 to 3 W·cm−2 Both uses achieve results by a considerable increase in the temperature of the exposed tissue (29). In conventional therapeutic uses, care providers use a stroking method to avoid excess temperature rises, thereby preventing cell necrosis, particularly in bone applications. In comparison, safe diagnostic imaging applications, such as fetal sonograms, employ much lower intensities of only 0.005 to 0.05 W·cm−2 and are considered nonthermal stimuli. The low-intensity ultrasound therapy device prescribed in this case study was the SAFHS (Sonic Accelerated Fracture Healing System, Exogen, Inc., Piscataway, NJ). The device applied an intensity of only 0.03 W·cm−2 which is in the range of diagnostic procedures. There are no known contraindications to the use of this low-intensity ultrasound device.

Ultrasound is acoustic radiation at frequencies above the limit of human hearing. This acoustic radiation provides micromechanical stresses and strains to the bone and surrounding tissue by pulses of high frequency sound waves. The literature reports that bone healing can be affected by mechanical forces such as early weight bearing, dynamic compression techniques, and impact loading. In addition, mechanical stimulation has been demonstrated to play a major regulatory role in bone physiology. Binderman (1) demonstrated effects of static mechanical input on bone cell regulation and correlated the results with clinical effectiveness in orthodontics (stress induced remodeling). Application of dynamic mechanical force by Buckley et al. (3) extended our knowledge of the mechanism involved in cellular response to stress and provided information under physiological loading regimens. The work of Rubin et al. (18) on inhibiting osteopenia provides information on strain levels required to regulate both resorption and new bone formation.

In animal studies Duarte (7) reported that the use of an early version of SAFHS resulted in a significant acceleration of healing as assessed by radiographs and histology in both a controlled fibular osteotomy and a femoral drill hole defect model. Pilla et al. (14), in a rabbit bilateral placebo-controlled study, reported a statistically significant 80% increase in the strength of the low-intensity ultrasound treated limb at postoperative day 14 and demonstrated that the treated limb reached intact bone strength levels 40% earlier than the contralateral control. Wang et al. (24) and Yang et al. (27) reported that low-intensity ultrasound produced a statistically significant increase in fracture callus amount and fracture stiffness and strength in a bilateral, placebo-controlled rat femoral model that used intramedullary rod fixation for immobilization. Yang et al. also reported that low-intensity ultrasound increased the soft callus on the treated side, altered the expression of cartilage related protein, and increased aggrecan expression early in the healing phase. These results suggest an effect on noncollagenous protein synthesis and expression of collagen phenotypes and are consistent with the subjective impression of increased cartilage and advanced endochondral ossification after low-intensity ultrasound treatment (26,27). Tanzer et al. (23) reported on the results of research investigating the effect of SAFHS treatment on the rate of bony ingrowth into porous coated metal implants in a bilateral femoral transcortical canine model with statistically significant effect of SAFHS on the amount and depth of bone ingrowth. Ryaby et al. (18,19), in in vitro studies, demonstrated that the SAFHS device has multifunctional cellular effects of direct relevance to bone formation and resorption such as increasing calcium uptake and modulating adenylate cyclase activity, TGF-beta synthesis, and PTH response.

In other clinical studies using low-intensity ultrasound, Xavier and Duarte (25) reported on the successful acceleration of healing in pseudarthroses with an average time from initial fracture to ultrasound treatment of 13 months (range 6-60 months) (25). Choffie and Duarte (4) studied the effect of low-intensity ultrasound in delayed and nonunions including ones with metal fixation. They reported an overall healing success rate of 91% (e.g., 93%, 87%, and 87% in the scaphoid, femur, and tibia, respectively).

The following case study reports on the use of pulsed, low-intensity ultrasound to accelerate the healing of mid-tibial stress fracture in a world class gymnast.


Patient is a 14-yr-old world-class gymnast (no menses), who came to the office on June 10, 1996, complaining of leg pain. The day before she had competed in the National Gymnastics Championships and developed pain. She was concerned that the injury would prevent her from competing in the Summer Olympics in Atlanta.

The physical examination revealed her to be limping, with difficulty in ambulation. There was tenderness over the gastroc/soleus junction. There was 2+ tenderness in the mid-aspect of the anterior tibia. Conventional thermal ultrasound had been applied to her leg in the gym, but this therapy had caused her significant pain and was discontinued. Past medical history is pertinent in that she had been experiencing some problems with both heels, and more recently, the problem involved the left heel. The diagnosis for her heel condition was mild Sever's disease condition and plantar fasciitis.

On June 10, 1996, radiographs were taken and were normal on assessment. An MRI was performed which showed a stress injury with a 3.5-cm area of edema in the midshaft bone marrow area of the tibia and some periosteal edema as well (see Fig. 1). A bone scan was performed which showed positive uptake in the immediate injection series of blood flow and an increase in osteoblastic activity at 2 h (see Figs. 2 and 3). The patient was advised to stop rigorous active gymnastic training that involved high impact loading such as dismounts but was allowed to continue with upper extremity workouts. An Aircast-type of brace (Aircast Inc., Summit, NJ) was prescribed for daily use. Her diet was evaluated and supplemental multivitamins were prescribed. A daily course of massage therapy was instituted.

Figure 1:
MRI scan: T1 coronal MR image of the right tibia shows abnormal marrow signal.
Figure 2:
AP bone scan: Delayed (2-h) images show correlative area of increased tibial osteoblastic activity.
Figure 3:
Lateral bone scan: Delayed (2-h) images also show corre lative area of increased tibial osteoblastic activity.

Although the nature of the injury was not severe at this point, the location of the injury created concern that any rest period and cessation of training activities would prevent the patient from participating in the Summer Olympics. The use of the low-intensity SAFHS device to facilitate fracture healing by augmenting the body's natural bone repair process at the cellular level was discussed with the patient and her trainer. It was important to accelerate the healing process to allow the patient to resume her normal training and retain her peak physical condition in preparation for the Olympic games. Based on the clinical results reported for the SAFHS device, there was confidence that low-intensity ultrasound therapy, combined with a structured rehabilitative and dietary regimen, would accelerate the healing process and strengthen the integrity of the bone at the fracture site. The SAFHS bone healing system was prescribed to be used at home for a 20-min period three times a day. The daily use of the device with the hypoallergenic coupling gel was explained to the patient and her parents. The exact position of treatment module placement over the injury site was marked on the anterior surface of the mid-tibia. The patient either secured the treatment module with a hook loop strap assembly or was treated for each session by her mother holding the treatment module in place over the injury site.

The patient returned 1 wk later and still complained of some pain with workout and exercise, but the level of pain had decreased from that experienced on June 10. A normal walking gait did not produce any pain. The patient did not like the Aircast brace. Upper extremity workouts such as bars was continued; however, no landings, dismounts, or tumbling were allowed. On June 21, 1996, there was continued mild improvement with some evidence of tenderness at the fracture site upon palpation. A week later she was markedly improved, with only minimal tenderness evident at the anterior fracture site and the posteromedial tibia. A cylindrical basket-weave-type tape was used for her leg, and the patient was allowed to begin use of the tumble track and trampoline. Some weight-bearing jumping in the pool, and mild weight-bearing landing-type of activities were also allowed.

On July 3, 1996, she showed continued improvement. Plain radiographs were assessed as normal. The patient had progressed to a full workout with mild to moderate intensity on landings. On July 13, 1996, 1 month after injury, she had progressed to full workouts and participated in a trial meet. A few days later, the patient started to participate in the Olympics. Examination at this time revealed only a trace tenderness with deep palpation. There was some discomfort with landings, but not of a significant degree.

The patient participated in a pre-Olympic meet and the Olympics with minimum discomfort. Her performance in the team competition was instrumental in the United States Women's Gymnastic Team winning a gold medal. The patient was next seen on August 9, 1996. The x-rays continued to be normal. The Exogen SAFHS system had been discontinued, and she was not having any pain or symptoms with weight-bearing activities. There was a slight amount of skin irritation in the mid-tibia that could have been a minor reaction to the coupling gel. The patient reported that she was doing the full range of gymnastic activities without discomfort.


This patient presented with stress fracture verified by bone scan and MRI in one of the most troublesome regions to treat, the mid-tibia. Normal therapy for a mid-tibia stress fracture would be rest and the cessation of exercise for a period of 6-8 wk with literature references suggesting a non-weight-bearing cast. The rest period is followed by a return to a graded workout program (5,8). Other authors have recommended longer periods of rest with mid-tibia injuries and reported periods averaging 5-6 months (9,12,13). The concomitant use of the low-intensity ultrasound system allowed the patient to resume full workouts in only 3 wk and engage in the trials for the Olympic competition in a period of only 33 d. A week later she assisted her team in capturing the gold medal in the rigorous competition of the Olympics.


The athlete's rapid return to full weight-bearing activities and a rigorous gymnastic schedule, resulting in competitive participation in one of the most demanding of world sports activity, may be attributable to the acceleration of healing effects of this new low-intensity ultrasound therapy. Continued use of this new treatment modality will define the treatment opportunities and allow it to be used in the most appropriate circumstances.


1. Binderman, I., U. Zor, A. M. Kaye, Z. Shimshoni, A. Harell, and D. Sömjen. The transduction of mechanical force into biomechanical events in bone cells may involve activation of phospholipase A2. Calcif. Tissue Int. 42:261-266, 1988.
2. Briethaupt, M. Zur Pathologic des Mensch Lichen Fusses. Med. Zeitung 24:169-171, 175-177, 1855.
3. Buckley, M. J., A. J. Banes, L. G. Levin, et al. Osteoblasts increase their rate of division and align in response to cyclic, mechanical tension in vitro. Bone Miner. 4:225-236, 1988.
4. Choffie, M. and L. R. Duarte. Low-intensity pulsed ultrasound and effects on ununited fractures. Orthopaedic Health Conference, University Hospital, University of Sao Paulo, Brazil, June, 1994.
5. Clanton, T., B. Solcher, and D. Baxter. Treatment of anterior mid-tibial stress fractures. Sports Med. Arthr. Rev. 2:293-300, 1994.
6. Devas, M. Compression stress fractures in man and the greyhound. J. Bone Joint Surg. Br. 43B:540-551, 1961.
7. Duarte, L. R. The stimulation of bone growth by ultrasound. Arch. Orthop. Trauma Surg. 101:153-159, 1983.
8. Fredericson, M., A. Bergman, K. Hoffman, and M. Dillingham. Tibial stress reaction in runners. Am. J. Sports Med. 23:472-481, 1995.
9. Green, N., R. Rogers, and A. Lipscomb. Nonunions of stress fractures of the tibia. Am. J. Sports Med. 13:171-176, 1985.
10. Heckman, J. D., J. P. Ryaby, J. McCabe, J. J. Frey, and R. F. Kilcoyne. Acceleration of tibial fracture healing by non-invasive low-intensity pulsed ultrasound. J. Bone Joint Surg. Am. 76A:26-34, 1994.
11. Nunamaker, D., D. Butterwick, and M. Provost. Fatigue fractures in thoroughbred racehorses: relationship with age, peak bone strain, and training. J. Orthop. Res. 8:604-611, 1990.
12. Orava, S. and A. Hulkko. Delayed unions and nonunions of stress fractures in athletes. Am. J. Sports Med. 16:378-382, 1988.
13. Orava, S. Diagnosis and treatment of stress fractures located at the mid-tibial shaft in athletes. Int. J. Sports Med. 12:419-422, 1991.
14. Pilla, A. A., M. Mont, P. R. Nasser, et al. Non-invasive low-intensity pulsed ultrasound accelerates bone healing in the rabbit. J. Orthop. Trauma 4:246-253, 1990.
15. Prather, J., M. Nusynowitz, and H. Snowdy. Scintigraphic findings in stress fractures. J. Bone Joint Surg. Am. 59A:869-874, 1987.
16. Roub, L., L. Gumerman, and E. Hanley. Bone stress: a radionuclide imaging perspective. Radiology 132:431-438, 1979.
17. Rubin, C. and K. McLeod. Inhibition of osteopenia by biophysical intervention. In: Osteoporosis, R. Marcus, J. Kelsey, and D. Feldman (Eds.). New York: Academic Press, 1996, pp. 351-371.
    18. Ryaby, J. T., E. J. Bachner, J. A. Bendo, P. F. Dalton, S. Tannenbaum and A. A. Pilla. Low-intensity pulsed ultrasound increases calcium incorporation in both differentiating cartilage and bone cell cultures. Trans. Orthop. Res. Soc. 14:15, 1989.
    19. Ryaby, J. T., J. Matthew, A. A. Pilla, and P. Duarte-Alves. Low-intensity pulsed ultrasound modulates adenylate cyclase activity and transforming growth factor beta synthesis. In: Electromagnetics in Biology and Medicine. C. T. Brighton and S. R. Pollock (Eds.) San Francisco: San Francisco Press, 1991, pp. 95-100.
    20. Schaffler, M., E. Radin, and D. Burr. Mechanical and morphological effects of strain rate on fatique of compact bone. Bone 10:207-214, 1989.
    21. Schaffler, M., E. Radin, and D. Burr. Long-term fatigue behaviour of compact bone at low strain magnitude and rate. Bone 11:321-326, 1990.
    22. Stanitski, C., J. McMaster, and P. Scranton. On the nature of stress fractures. Am. J. Sports Med. 6:391-396, 1978.
    23. Tanzer, M., E. Harvey, A. Kay, P. Morton, and J. D. Bobyn. Effect of noninvasive low-intensity ultrasound on bone growth porous-coated implants. J. Orthop. Res. 14:901-906, 1996.
    24. Wang, S. J., D. G. Lewallen, M. E. Bolander, E. Y. S. Chao, D. M. Ilstrup, and J. F. Greenleaf. Low-intensity ultrasound treatment increases strength in a rat femoral fracture model. J. Orthop. Res. 12:40-47, 1994.
    25. Xavier, C. A. M. and L. R. Duarte. Ultrasonic stimulation of bone callus: clinical application. Rev. Bras. Ortopedia 18:73-80, 1983.
    26. Yang, K. H., S. J. Wang, D. G. Lewallen, et al. Low-intensity ultrasound stimulates fracture healing in rat model: biomechanical and gene expression analysis. Trans. Orthop. Res. Soc. 19:519, 1994.
    27. Yang, K. H., J. Parvizi, S. J. Wange, et al. Exposure to lowintensity ultrasound increases aggregan gene expression in a rat femur fracture model. J. Orthop. Res. 14:802-809, 1996.
    28. Ziskin, M. C. Applications of ultrasound in medicine Comparison with other modalities. In: Ultrasound: Medical Applications, Biological Effects and Hazard Potential. M. H. Repacholi, M. Grandolfo, and A. Rindi (Eds.) New York: Plenum, 1987, pp. 49-61.
      29. Zwas, T., R. Elkabnovitch, and G. Frank. Interpretation and classification of bone scintographic findings in stress fractures. J. Nucl. Med. 28:452-457, 1987.


      © Williams & Wilkins 1998. All Rights Reserved.