In this study we did not find any statistically significant differences in the tibial BMDs between the athletes with MTSS (range duration symptoms, 3-10 weeks) and the control group. Magnusson et al., 2001 had measured BMDs in five different tibial areas in athletes diagnosed with MTSS. The mean duration of symptoms was 31 months (range, 5-120 months). They compared BMD in MTSS patients with a healthy athletic group and a healthy non-athletic group. In the MTSS group, the BMD in the region corresponding to the pain was 15 ± 9% and 23 ± 8% lower than those observed in the non-athletic control and the athletic control groups, respectively. In the MTSS group, BMD measurements of the other regions were mostly higher than the measurements of the control group (proximal tibia: 16 ± 14%, femoral neck: 9 ± 9%), but lower than the measurements of the athletic control group (proximal tibia: 13 ± 11%, femoral neck: 11 ± 8%). They speculated that reduced accrual during growth and in response to exercise, or excessive bone loss after the onset of symptoms, or combinations of these mechanisms might contribute to the deficit in bone mineral density. Three different areas of the tibia were measured in this study (Figure 1). These were not the same as in the Magnusson et al. study, which makes comparison between the studies hard. As the DXA device could not get a single shot for the whole tibia, we used metal marks for the before-mentioned three points and measured them separately. Magnusson et al., 2001 did not explain how they determined their five regions on the tibia. According to the figure in their study, our painful R2 area corresponds to theirs R4, and our R3 area corresponds to their R2 area. Our R1 area did not match any of the five regions of the Magnusson et al. study. Mechanical loading is known to stimulate bone formation (Carter, 1982; Waldorff et al., 2010). Frost, 2004 stated in his excellent review about bone physiology that repeated bone strains cause microdamage in the bone. This microdamage has an operational threshold strain range that lies above the bone’s modeling threshold. Normally, load bearing bones can detect and repair the little microdamage caused by strains that stay belove the microdamage threshold; remodeling basic multicellular units provide that repair and osteocytes may provide this detection. The diversity and daily repetition of stress stimulates bone remodeling up to a limit (Lanyon et al., 1982). During bone remodeling, while osteoclastic activity is completed within 2-3 weeks, the osteoblastic activity can continue up to 3 months. In our study, we did not find any statistically significant difference between the MTSS group and the control group regarding tibial BMD measurements. The average injury duration of the MTSS group was 5.0 weeks (range, 3-10 weeks). The mean injury duration in the Magnusson et al., 2001 study was 31 months. Probably due to repeated excessive stress for a long time, the repetitive osteoclastic stimulation and the slowly acting osteoblastic activity impair bone turnover during remodeling in favor to the destructive processes. This can be the reason why we could not find any change in the early period (5.0 ± 2.1 weeks), whereas Magnusson did measure significant differences in longstanding (31 month) MTSS patients. In a follow-up study, Magnusson et al., 2003 reported that after an average of 5.7 years, when the MTSS patients were totally free of complaints, bone mineral density in the former painful tibia area increased by 19 ± 11%. No statistically significant difference in BMD with the healthy athletes group was found in the follow-up measurements. They proposed that the deficit in bone density was in conjunction with the symptoms. Another finding of Magnusson et al., 2001 was that the femoral neck BMD and the lumbar BMD in the MTSS group were significantly lower than in the healthy athletes group. Myburgh et al., 1990 found a similar result in their study. They compared lumbar and femoral neck BMDs of 25 patients with stress fracture with those of healthy athletes. The stress fracture group displayed significantly lower BMD measurements. This may have various causes like an attainment of lower peak bone mineral density, a lower response to comparable exercise training, a marginally lower physical activity level, or bone loss associated with reduced activity during the MTSS (Magnusson et al., 2001). Our findings revealed no statistically significant differences between the groups regarding femoral and lumbar bone mineral densities. However, only with a controlled longitudinal study we would be able to assess whether it is developing later with MTSS. As the purpose of this study was to investigate regional BMD in the painful localization, we also assessed a possible change in BMD due to calcium intake via a dietary survey, too. In order to calculate monthly calcium intake, we asked for the monthly consumption of foods with the highest calcium content. In the inquiry, monthly consumption of milk, yoghurt, cheese, legumes and nuts were noted. There was no significant difference between groups in terms of dietary total calcium intake. Therefore, we cannot discuss the effect of relative calcium deficiency in the development of MTSS or decrease in tibial BMD. The subjects of both groups reported similar training characteristics. Many times, increases in training intensity, duration, or content have been associated with MTSS (Clement et al., 1981; Marti et al., 1988; Rudzki, 1997). In fact, in 81.8% of the patients in our study, MTSS developed following an increase in training intensity, duration, or content. |