With respect to the role of drinking water, changing of water sources to deep well water has been reported to decrease the X-ray metaphyseal detection rate in different settings. In general, the effect of preventive measures however remains controversial, due to methodological problems (no randomised controlled trials), lack of documentation, or, as discussed above, inconsistency of results. Treatment
Treatment of KBD is palliative. Surgical corrections have been made with success by Chinese and Russian orthopedists. By the end of 1992, Médecins Sans Frontières—Belgium started a physical therapy programme aiming at alleviating the symptoms of KBD patients with advanced joint impairment and pain (mainly adults), in Nyemo county, Lhasa prefecture. Physical therapy had significant effects on joint mobility and joint pain in KBD patients. Later on (1994–1996), the programme has been extended to several other counties and prefectures in Tibet. Epidemiology
Kashin–Beck disease occurrence is limited to 13 provinces and two autonomous regions of China. It has also been reported in Siberia and North Korea, but incidence in these regions is reported to have decreased with socio-economic development. In China, KBD is estimated to affect some 2 million to 3 million people across China, and 30 million are living in endemic areas. Life expectancy in KBD regions has been reported to be significantly decreased in relation to selenium deficiency and Keshan disease (endemic juvenile dilative cardiomyopathia). The prevalence of KBD in Tibet varies strongly from valley to valley, and village to village.
Kashin–Beck disease (KBD) is a chronic, endemic type of osteochondropathy (disease of the bone) that is mainly distributed from northeastern to southwestern China, including 15 provinces. As of 2011, Tibet has the highest incidence rate of KBD in China. Southeast Siberia and North Korea are other affected areas. KBD usually involves children ages 5–15. To date, more than a million individuals have had KBD. The symptoms of KBD include joint pain, morning stiffness in the joints, disturbances of flexion and extension in the elbows, enlarged inter-phalangeal joints, and limited motion in many joints of the body. Death of cartilage cells in the growth plate and articular surface is the basic pathologic feature; this can result in growth retardation and secondary osteoarthrosis. Histological diagnosis of KBD is particularly difficult; clinical and radiological examinations have proved to be the best means for identifying KBD. Little is known about the early stages of KBD before the visible appearance of the disease becomes evident in the destruction of the joints.This disease has been recognized for over 150 years but its cause has not yet been completely defined. Currently, the accepted potential causes of KBD include mycotoxins present in grain, trace mineral deficiency in nutrition, and high levels of fulvic acid in drinking water. Selenium and iodine have been considered the major deficiencies associated with KBD. Mycotoxins produced by fungi can contaminate grain, which may cause KBD because mycotoxins cause the production of free radicals. T-2 is the mycotoxin implicated with KBD, produced by members of several fungal genera.