Last update 01 Nov 2024

Kashin-Beck Disease

Last update 01 Nov 2024

Basic Info

Synonyms

Disease, Kashin-Beck, Endemic polyarthritis, Kaschin-Beck

+ [21]

Introduction

Disabling osteochondrodysplasia with OSTEOSCLEROSIS, cone-shaped METAPHYSIS, and shortening of the DIAPHYSIS. It is endemic in parts of Siberia and northern China. Mineral deficiencies (e.g., selenium, iodine), fungal cereal contamination, and water contamination may be contributing factors in its etiology.

Drugs associated with Kashin-Beck Disease

TengHuangJianGu

Target-

Mechanism-

Active Org.

Hunan Fangsheng Pharmaceutical Co., Ltd.

Originator Org.

Hunan Fangsheng Pharmaceutical Co., Ltd.

Active Indication

Hyperostosis [+3]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date31 Mar 2009

Clinical Trials associated with Kashin-Beck Disease

ChiCTR2400090676 / SuspendedNot ApplicableIIT

Prospective Multi-Center Study on the Microbiome of different joint diseases

Start Date14 Oct 2024

Sponsor / Collaborator-

ChiCTR2400090655 / SuspendedNot ApplicableIIT

Effects of perioperative procedures on skin microbial composition in patients undergoing hip or knee surgery

Start Date14 Oct 2024

Sponsor / Collaborator-

ChiCTR2300076470 / SuspendedPhase 1IIT

Evaluation of the clinical efficacy of Zhengqing Fengtongning sustained release tablets in the treatment of kaschin-beck disease

Start Date01 Nov 2023

Sponsor / Collaborator-

100 Clinical Results associated with Kashin-Beck Disease

100 Translational Medicine associated with Kashin-Beck Disease

0 Patents (Medical) associated with Kashin-Beck Disease

589

Literatures (Medical) associated with Kashin-Beck Disease

01 Dec 2024·International Immunopharmacology

T-2 toxin induces chondrocyte extracellular matrix degradation by regulating the METTL3-mediated Ctsk m6A modification

Article

Author: Dong, Hexuan ; Li, Haonan ; Qi, Fang ; Yu, Qian ; Yu, Jun ; Jiang, Hong ; Li, Hongzhi ; Zhang, Bing ; Lin, Buyi

T-2 toxin is a major cause of Kashin-Beck disease (KBD), which is characterised by cartilage damage. N6-adenosine-methyltransferase-like 3 (METTL3) regulates cartilage injury; however, its role in T-2 toxin-induced cartilage injury remains elusive. Herein, we investigated the involvement of METTL3-mediated m6A modification in T-2 toxin-induced cartilage damage. METTL3-mediated m6A methylation levels were correlated with cartilage extracellular matrix (ECM) degradation, which was exacerbated following METTL3 silencing. Cathepsin K (Ctsk) was identified as a downstream target of METTL3 using m6A-methylated RNA immunoprecipitation（MeRIP）sequencing and RNA sequencing. Silencing Ctsk aggravated HT-2 toxin-induced ECM degradation. Increasing the m6A methylation levels in vivo via dietary methionine supplementation mitigated cartilage damage. In summary, HT-2 toxin induced cartilage ECM degradation by regulating the METTL3-mediated m6A modification of Ctsk. These findings highlight the METTL3/m6A/Ctsk axis as a potential therapeutic target for the treatment of KBD and other cartilage-associated diseases.

01 Nov 2024·Toxicon

Effects of T-2 and deoxynivalenol mycotoxins on mouse spinal bone growth and integrity

Article

Author: Liu, Li ; Meng, Peilin ; Yao, Cong ; Liu, li ; Hao, Shuichu ; Jia, Yumen ; Zhang, Chun

Kashin-Beck Disease (KBD), an osteoarticular disorder, is influenced by various factors, including exposure to Deoxynivalenol (DON) and T-2 mycotoxins. This study systematically explored the impact of these mycotoxins on the development and structural resilience of spinal structures in mice, examining both isolated and combined effects. The experiment involved 72 male mice divided into nine groups, each subjected to varying concentrations of T-2, DON, or their combinations over four weeks. Rigorous monitoring included body weight, key indicators of bone metabolism, and cellular activities essential to bone health. Comprehensive evaluations using biomechanical analysis, x-ray, and micro-computed tomography (micro-CT) were conducted to assess alterations in spinal structure. The findings revealed a pivotal aspect: mice exhibited a dose-dependent decline in body weight when exposed to individual mycotoxins, while simultaneous exposure produced an unanticipated antagonistic effect. Moreover, decreases were noted in levels of calcium, phosphorus, and vitamin D, coupled with changes in the activities of osteoblasts (increased) and osteoclasts (decreased), all intricately tied to the toxins' dosages and combinations. Notably, variations in the biomechanical properties corresponded with the mycotoxin dosage and blend, showing a decline in biomechanical strength. Micro-CT analyses further substantiated the profound toxic impact of the toxin dosage and mixtures on both the cortical and trabecular components of the spinal structures. In summary, this investigation unequivocally illuminates the dose- and ratio-dependent deleterious impacts of DON and T-2 mycotoxins on the growth and structural soundness of spinal structures in mice. These findings highlight the urgent need for a comprehensive understanding of the potential hazards these toxins pose to bone health, providing invaluable guidance for future toxicological research and public health strategies.

01 Oct 2024·Osteoarthritis and Cartilage

Chondrocyte autophagy mediated by T-2 toxin via AKT/TSC/Rheb/mTOR signaling pathway and protective effect of CSA-SeNP

Article

Author: Deng, Huan ; Liu, Haobiao ; He, Yujie ; Yang, Zhihao ; Han, Jing ; Qiao, Lichun ; He, Huifang ; Bao, Miaoye ; Xiang, Rongqi ; Lin, Xue

OBJECTIVEKashin-Beck disease (KBD) is an endemic, degenerative, and cartilage-damaging disease for which low selenium and T-2 toxins are considered environmental pathogenic factors. This study aimed to investigate the molecular mechanisms of autophagy in cartilage damage caused by T-2 toxin and the protective effect of chondroitin sulfate A nano-elemental selenium (CSA-SeNP) on the cartilage.METHODSKBD chondrocytes and C28/I2 human chondrocyte cell lines were used. T-2 toxin, AKT inhibitor, and CSA-SeNP treatment experiments were conducted separately, with a treatment time of 24 h. Autophagy was monitored using MDC staining, and mRFP-GFP-LC3 adenovirus, respectively. RT-qPCR and western blotting were used to detect the expression of the relevant genes and proteins.RESULTSThe suppression of autophagy observed in KBD chondrocytes was replicated by applying 10 ng/mL T-2 toxin to C28/I2 chondrocytes for 24 h. The AKT/TSCR/Rheb/mTOR signaling pathway was activated by T-2 toxin, which inhibits autophagy. The supplementation with CSA-SeNP alleviated the inhibition of autophagy by T-2 toxin through the AKT/TSCR/Rheb/mTOR signaling pathway.CONCLUSIONSLoss of autophagy regulated by the AKT/TSCR/Rheb/mTOR signaling pathway plays an important role in cartilage damage caused by T-2 toxin. CSA-SeNP supplementation attenuated inhibition of autophagy in chondrocytes by T-2 toxin by modulating this signaling pathway. These findings provide promising new targets for the prevention and treatment of cartilage disease.

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