Kaschin-Beck disease is an endemic condition prevalent in the northern regions of China. It was first discovered in the northeast and later identified in the northwest. In the northwest, it is also known as "Liu Guaizi disease." Cases are typically concentrated in specific areas, forming endemic zones. The disease primarily affects adolescents, with males being more commonly affected. Those who leave endemic areas during childhood rarely develop the disease, while those who leave after the age of 12 may still contract it, though onset tends to occur later.

bubble_chart Etiology

The cause of Kashin-Beck disease remains unknown. It was once suspected to be caused by chronic oral poisoning, but this has not been confirmed. Most researchers believe it may be related to pathogenic fungi in grains. Animal experiments have shown that when animals are fed grains contaminated with pathogenic fungi, the pathological changes observed in their bones closely resemble those of Kashin-Beck disease. The pathogenic fungus may be Fusarium sporotrichioides, but this has not been fully confirmed.

bubble_chart Pathological Changes

The main pathological changes involve early ossification of the epiphysis. It can be divided into the late stage [third stage]: ① Premature ossification of the epiphyseal plate: This causes the epiphyseal plate to lose its normal shape, becoming uneven. The ossification of the epiphyseal plate may be inconsistent, leading to variations in plate thickness; the rate of ossification may also vary, resulting in varus or valgus deformities of the joint. The cortical bone on the diaphyseal side of the epiphyseal plate forms an acute angle. ② Early fusion of the epiphysis and metaphysis. The central cartilage of the epiphysis undergoes premature ossification and expands outward. Sometimes, the central cartilage ruptures, causing the metaphysis to develop a linear depression, eventually leading to complete fusion. ③ Premature disappearance of the epiphysis and epiphyseal plate, cessation of bone growth, and the bone ends becoming enlarged and twisted.

If the disease occurs during adolescence, premature ossification of the epiphyseal plate leads to developmental disorders, manifesting as the dwarfism type. The patient has a short stature, enlarged joints, and experiences pain and limited mobility, with the ankle joint being the first affected, followed sequentially by the finger joints, knees, elbows, wrists, toe joints, and hips. Due to uneven fusion rates of the epiphyseal plates, the lower limbs often develop genu varum, genu valgum, or hip varus deformities. The fingers are short and stubby, and the feet are flat. The younger the age of onset, the more severe the deformity.

If the disease occurs in the late stage [third stage] of adolescence, the deformity is less noticeable. The main symptoms are those of osteoarthritis, including joint swelling, slight effusion, a grating sensation during movement, and occasional locking symptoms. Sometimes, loose bodies can be detected within the joint. In adults, the lower limbs are more commonly affected, with swelling and pain in the ankles and knees making walking very difficult.

X-ray findings closely resemble those of osteoarthritis, with the ankle joint being the most severely affected. In the early stages, widening of the joint space and severe irregularity can be observed, along with loose bodies within the joint. Subsequently, the cortical bone density of the joint surface increases, and the joint space tends to narrow. Prominent osteophytes develop at the joint margins, often accompanied by subchondral cystic changes. The talus body is frequently flattened, with dense bone and a flattened shape resembling ischemic necrosis. Later, osteophytes, increased bone density, and subchondral cysts may form in the talonavicular and subtalar joints. The patellofemoral joint of the knee may also become uneven, with numerous osteophytes at the margins, enlarged joint ends, and loose bodies within the joint. Over time, the joint collapses. The hip joint undergoes similar changes, with the femoral head appearing ischemic and necrotic, possibly accompanied by hip varus deformity. In the fingers, the joint ends are enlarged, the joint surfaces are uneven, the joint space is narrowed, bone density is increased, and the phalanges are shortened.

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Large joint disease cannot be cured, nor can the progression of the disease be suppressed. Symptomatic treatment can alleviate pain. For those with obvious joint deformities, surgical treatment may be used. If loose bodies cause locking and pain, the loose bodies can be removed. If excessive or oversized osteophytes affect joint movement, the osteophytes can be excised to improve function. For those with joint varus or valgus, osteotomy can be performed. Since most cases are bilateral or involve multiple sexually transmitted diseases, joint fusion surgery is not advisable.

bubble_chart Prevention

Strengthening food storage and handling in epidemic areas, or transporting food from outside the epidemic area, can significantly reduce disease.