Stress fracture

One in ten of all sports injuries is a stress fracture. Here’s how to break the pattern.

Stress fractures are partial or complete fractures of bone, often called fatigue fractures since they are caused by repetitive strain during sub-maximal activity. They result from the inability of the bone to react favourably to the stress imposed. There are two main types of stress fracture: ‘fatigue’ fracture and ‘insufficiency’ fracture. A fatigue fracture results from the application of abnormal muscle stress or torque to a bone with normal elastic resistance, and is associated with new or different activity, and strenuous or repeated activity. Insufficiency fractures result from normal muscular activity stressing the bone, and are commonly seen in post-menopausal and/or amenhorroeic women, whose bones are deficient in mineral or elastic resistance.

 Lower limbs tend to be the most common sites for stress fractures, although the specific anatomical site depends on the type of activity. Gymnasts and cricketers may develop fractures in the lumbar spine, while dancers develop them in the foot. Stress fractures have been reported to occur in almost all sports, including swimming and wrestling.

What causes them?
There are two theories about the origin of stress fractures. The ‘fatigue theory’ suggests that during repeated efforts (as in running), the muscles become unable to support the skeleton during impact as the foot strikes the ground. Instead of the muscles absorbing the shock, the load is transferred to the bone. As the loading surpasses the capacity of the bone to adapt, a fracture develops. The ‘overload theory’ suggests that certain muscle groups contract in such a way that they cause the attached bones to bend. After repeated contractions and bending, the bone breaks.
Stress fractures are probably preceded by periostitis (inflammation of connective tissue covering the surface of bone), causing bone pain and pain during exercise. Management of shin splints involves rest; if the symptoms still persist after two weeks, a stress fracture is suspected. When the pain has persisted for six weeks or more, a stress fracture is the likely cause. In about half of the cases, symptoms start appearing slowly, while in the other half they appear without warning. First, pain is felt during training but not at rest. With continued training, pain increases as the intensity increases. Pain will persist after exercise, and at some point localised swelling and tenderness are apparent at the fracture site. Stress fractures are not seen initially on X-ray, which makes diagnosis difficult. The treatment of stress fractures involves rest from usual weight-bearing activity for about four-to-eight weeks, and until the pain has gone.

How common are they?
In runners, stress fractures tend to be more common than in all the other sports put together. Stress fractures have been reported to comprise about 10 per cent of all sports injuries, and between 4.7 per cent and 15.6 per cent of all running injuries. Among women runners, some studies have found that the incidence of fracture was 49 per cent among those with very irregular menstruation and 39 per cent among those with irregular menstruation. In addition, runners with menstrual irregularities tended to suffer more from multiple stress fractures.

About 20-25 per cent of stress fractures occur in the fibula, the tibia and the metatarsal bones. Runners most frequently develop fractures of the tibia.

Bone facts
There are two types of bone. Cortical (hard, compact) bone is found in the shaft of the long bones. Trabecular (spongy, cancellous) bone is found at the end of the long bones.

Bone formation depends on a five-stage cycle resulting in ‘old’ bone being removed and ‘new’ bone being produced. Normally the amount being removed equals new bone formed. Osteoclasts are responsible for bone resorption (removal), while osteoblasts help in laying down new bone. The stimulus for osteoblast recruitment may include mechanical loading, muscular activity and gravity. Osteoblasts are responsible for the synthesis of collagen, the main component of new bone. The maturing process and final strength of the new bone depends on adequate calcium and phosphate supply. Finally, the mechanical strength of the bone also depends on the orientation of collagen fibrils within the bone. This scaffold-like arrangement is often interrupted in older individuals, resulting in a weaker bone structure despite normal bone mineral content.

Bone mass tends to increase until about the age of 35. The final bone mass is determined by three main factors: genetic endowment, environmental factors, including physical activity, diet (calcium) and the negative effects of cigarette smoking, caffeine and alcohol, and hormonal status (mainly oestrogen and progesterone in women and testosterone in men).

What are the risk factors?
There are a wide variety of factors commonly linked with the risk of stress injuries to the bone:
Age: The risk appears to grow with increasing age as the bone in older individuals is less resistant to fatigue. The risk is also linked to declining fitness.

Training errors: Commonly, stress fractures appear after a change in activity and an increase in running mileage and intensity. Excessive running on hard surfaces that absorb force poorly, and running on crowned roads which cause an unequal distribution of weight within the foot, have been implicated. If, after a lay-off, training is resumed at the same volume and intensity, the athlete will be at an increased risk of developing stress fractures. Beginners are similarly at risk.

Fitness history: It is suspected, though not proven, that the most sedentary and least fit people entering a sports programme are more likely to get stress fractures. Gradual increase in training loads is important.

Footwear: Gardner and colleagues (1988) reported that the cost of training shoes (expensive versus inexpensive) made no difference in the incidence of stress fractures in Marine recruits. The one significant factor linked with stress fractures during recruit training was the running shoe age. Those who wore newer shoes developed fewer fractures.

 Endocrine status: Peak bone mass may be jeopardised in prolonged amenorrhoea (absence of menstruation). Women athletes suffering from amenorrhoea are at especially high risk, more so if their diets are low in calcium. Although studies show that bone density in cortical bones tends to be normal among amenorrhoeic female athletes, these still remain the prime sites for stress fractures. Grimston and co-workers (1991) have shown that runners who began running training in close association with the age of menarche demonstrate a higher incidence of stress fractures than those commencing training at a later age. Heavy endurance training may also compromise androgen status in men, which may lead to lowered bone strength. At present, little is known about this relationship.

Nutritional factors: Training, nutritional and hormonal factors tend to be closely interlinked with stress fractures (see Peak Performance no. 59, 1995, pp 4-7). Recommended calcium intake in post-puberty is 800mg/day, whereas stress-fracture patients are encouraged to consume 1500mg of calcium daily.

Biomechanical factors: Most research has been done among military recruits, and the findings have shown that biomechanical factors, involving anatomical variation, have an important role in the development of stress fractures. Gilati and Abronson (1985) showed that tibial torsion (twisting/bending of the tibia) and the degree of external rotation at the hip were associated with the incidence of stress fractures. When neither were present, the incidence of stress fractures was 17 per cent, but when both were present, the incidence increased to 45 per cent. The assessment of these types of ‘faults’ generally requires sophisticated equipment which unfortunately is not readily available. Other factors linked with the occurrence of stress fractures include: high arched foot, excessive pronation (turning inward) or supination (turning outward) of the foot, longer second toe and bunion on the great toe. All of these will alter the mechanics of running and consequently impose abnormal stresses on adjacent structures and, eventually, the bone.

Although the occurrence of stress fractures and stress reactions on the bone is often multi-factorial and not very well understood, there are a number of important preventive measures an athlete can take.

1. Avoid abrupt increases in overall training load and intensity. Take adequate rest.

2. Buy less expensive shoes and change them frequently. As a general rule, running shoes tend to lose their shock-absorbing capacity by 400 miles.

3. Bony alignment may be modified to some extent by the use of orthotics in the shoes and taping the foot and/or ankle. Those with hyperpronating feet may choose shoes with maximally rigid heel counter. Expert advice is needed for correct choice of insoles and taping techniques.

4. Women athletes should pay careful attention to training, hormonal status and nutrition, and recognise any eating disorder.

Pirkko Korkia

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