Abstract
BackgroundKashin–Beck disease (KBD) is a chronic, deforming, endemic osteochondropathy that begins in patients as young as 2–3 years of age. The pathogenesis of KBD remains unclear, although selenium (Se) deficiency and T-2 toxin food contamination are both linked to the disease. In the present study, we evaluated transforming growth factor-β receptor (TGF-βR I and II) levels in clinical samples of KBD and in pre-clinical disease models.MethodsHuman specimens were obtained from the hand phalanges of eight donors with KBD and eight control donors. Animal models of the disease were established using Sprague–Dawley rats, which were fed an Se-deficient diet for 4 weeks and later administered the T-2 toxin. Cartilage cellularity and morphology were examined by hematoxylin and eosin staining. Expression and localization of TGF-βRI and II were evaluated using immunohistochemical staining and western blotting.ResultsIn the KBD samples, chondral necrosis was detected based on cartilage cell disappearance and alkalinity loss in the matrix ground substance. In the necrotic areas, TGF-βRI and II staining were strong. Positive percentages of TGF-βRI and II staining were higher in the cartilage samples of KBD donors than in those of control donors. TGF-βRI and II staining was also increased in cartilage samples from rats administered T-2 toxin or fed on Se-deficient plus T-2 toxin diets.ConclusionTGF-βRI and II may be involved in the pathophysiology of KBD. This study provides new insights into the pathways that contribute to KBD development.
Highlights
Kashin–Beck disease (KBD) is a chronic, deforming, endemic osteochondropathy that begins in patients as young as 2–3 years of age
Necrotic fields were characteristically observed at the zones of the maturing cartilage and extended to the transition region between the hypertrophic and proliferative zones of growth plate cartilage, or to the middle and deep zones of the articular cartilages
In donors with KBD, chondral necrosis was established based on cartilage cell disappearance, whereby only red outlines of chondrocytes remained, accompanied by alkalinity loss in the matrix ground substance, which exhibited a lighter blue color upon hematoxylin and eosin (H&E) staining
Summary
Kashin–Beck disease (KBD) is a chronic, deforming, endemic osteochondropathy that begins in patients as young as 2–3 years of age. We evaluated transforming growth factor-β receptor (TGF-βR I and II) levels in clinical samples of KBD and in pre-clinical disease models. In KBDendemic areas, Se levels in serum and food are significantly lower than in non-KBD-endemic areas [7,8,9,10]. KBD rat models were established by administering T-2 toxin to rats fed a diet low in Se [14]. This model effectively initiated chondrocyte apoptosis within the articular cartilage deep zone, comparable to KBD [15].
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