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Low levels of physical and muscle conditioning are also an important risk factor for the genesis of this problem. 8, 10, 28 Inadequate nutritional intake may alter bone metabolism and predispose toward appearance of stress fractures. There is an inverse relationship between bone mineral density and the risk of stress fractures. This was attributed to bone density and its biomechanics. 11, 13 In a military population, the incidence among whites was twice as high as among blacks, without any difference between the sexes. 11, 23, 27 Studies conducted in the United States have attempted to evaluate the incidence of these injuries among white and black athletes, without observing any significant differences. 11, 24Īge also cannot be considered to be a risk factor in isolation for stress fractures. 11, 16, 26 In reality, hormonal, nutritional, biomechanical and anatomical alterations are the true factors that favor appearance of stress fractures in women. Many studies have mistakenly considered that only female gender is a risk factor for stress factors to appear. The intrinsic factors relate to possible anatomical variations, muscle conditions, hormonal states, gender, ethnicity or age. 17, 24 Lastly, if the athlete's fitness level is insufficient for the sports movement or functional technique, this may lead to injury, sometimes without the number of repetitions having been very high. 8, 23 The quality of the training track may also be a risk factor, when it is uneven, irregular or very rigid. 6, 9, 10, 11 Equipment such as footwear that has low impact absorption, is worn out (more than six months of use) or is a bad fit for the athlete's foot may cause injuries. 8, 9, 14, 20, 21, 22, 23Ībrupt increases in the intensity and volume of training are often enough for lesions to develop. 8, 9, 20, 21, 22, 23Extrinsic factors relate to sports movements, nutritional habits, equipment used and the type of ground. This makes stress fractures multifactorial and difficult to control. The factors associated with increased risk of development of stress fractures can be divided into extrinsic and intrinsic factors. 20 Therefore, when fatigue, weakness or muscle unpreparedness occur, this protective action is lost and the risk of bone tissue lesions increases. Markey also proposed that the muscle mass acts toward dispersing and sharing impact loads on the bone tissue. reabsorption of the injured cells and replacement with new bone tissue take place. 10 The bone repair process in stress fractures differs from the process in cases of common acute fractures and only takes place through bone remodeling, i.e.

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If this is not treated, it will evolve to complete fracturing of the bone affected. 11 Elastic deformation occurs initially, and this progresses to plastic deformity until it finally results in microfracturing.

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4, 5, 6, 10, 18, 19 The load applied is considered to be insufficient to cause an acute fracture, but the combination of overloading, repetitive movements and inadequate recovery time make this a chronic injury. Six to eight weeks after a sudden and non-gradual increase in the intensity of an athlete's or new patient's physical activity, this cyclical and repetitive physiological overloading may lead to the appearance of microfractures and may not allow the bone tissue to have sufficient time to undergo remodeling and adapt to the new condition, and thus to repair the microlesion. 7, 8 The aim here was to present an updating article on this topic and condense the main information obtained through the most important studies published over the last few years. 6 In both situations, imbalance between the bone that is formed and remodeled and the bone that it reabsorbed will result in discontinuity of the bone at the site affected. On the other hand, fractures resulting from bone insufficiency occur in bone that is mechanically compromised and generally presents low bone mineral density.

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6 Fatigue fractures occur after formation and accumulation of microfractures in normal bone trabeculae. These fractures may be the final stage of fatigue or insufficiency of the bone affected.

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This injury occurs as a result of high numbers of occurrences of cyclical overloading of intensity lower than the maximum bone strength, on non-pathological bone tissue. 1, 2 In 1958, Devas made the first report on stress fractures in athletes. 1, 2, 3 They were named “march fractures” and their characteristics were confirmed 40 years later with the advent of radiography. Stress fractures were first described in Prussian soldiers by Breithaupt in 1855.

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Tibia stress fracture treatment