Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (700 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
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.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Disease, Kashin-Beck; Kashin Beck Disease.
Where it fits in the MeSH classification
- Broader topics
- Osteochondrodysplasias
Related concepts
- Osteosclerosis
- Metaphysis
- Diaphysis
Research landscape
PubMed indexes 346 records tagged with the MeSH heading “Kashin-Beck Disease” (counts retrieved 2026-11-04). 141 of them (40.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 202 records.
Reviews account for 30 records (8.7%) and meta-analyses for 15. Randomized controlled trials number 8 (2.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3 |
| 2000-2009 | 0 |
| 2010-2019 | 202 |
| 2020 onward | 141 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 30 | 8.7% |
| Meta-analyses | 15 | 4.3% |
| Randomized controlled trials | 8 | 2.3% |
Method: PubMed query "Kashin-Beck Disease"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in bones, joints, muscles and skin
Joint, bone, muscle and skin conditions are often judged by pain scores, function questionnaires, imaging or photographs, and symptoms can fluctuate, so placebo response and natural improvement matter. Imaging changes are common in people without symptoms. Nothing on this page is advice about treatment. Check how outcomes were measured, whether the comparison group received a placebo or usual care, and how long the benefit lasted.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Comparison of the major cell populations among osteoarthritis, Kashin-Beck disease and healthy chondrocytes by single-cell RNA-seq analysis | 2021 | Research article Design not recorded in structured metadata | 81 | cc by PMID 34045450 · DOI · PMC8160352 |
| Research Progress of Selenium-Enriched Foods | 2023 | Review article Design not recorded in structured metadata | 46 | cc by PMID 37836473 · DOI · PMC10574215 |
| Proteoglycan metabolism, cell death and Kashin-Beck disease | 2012 | Review article Design not recorded in structured metadata | 35 | cc by PMID 22733148 · DOI · PMC3423566 |
| Magnetofection-mediated siRNA delivery ameliorates cartilage damage in Kashin-Beck disease via targeting SIRT3 and protecting primary cilia | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42559309 · DOI · PMC13440625 |
Comparison of the major cell populations among osteoarthritis, Kashin-Beck disease and healthy chondrocytes by single-cell RNA-seq analysis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Chondrocytes are the key target cells of the cartilage degeneration that occurs in Kashin-Beck disease (KBD) and osteoarthritis (OA).
- Closing excerpt
- Our study allows us to better understand the heterogeneity of chondrocytes in KBD and OA and provides new evidence of differences in the pathogenetic mechanisms between these two diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (254 words)
Chondrocytes are the key target cells of the cartilage degeneration that occurs in Kashin-Beck disease (KBD) and osteoarthritis (OA). However, the heterogeneity of articular cartilage cell types present in KBD and OA patients and healthy controls is still unknown, which has prevented the study of the pathophysiology of the mechanisms underlying the roles of different populations of chondrocytes in the processes leading to KBD and OA. Here, we aimed to identify the transcriptional programmes and all major cell populations in patients with KBD, patients with OA and healthy controls to identify the markers that discriminate among chondrocytes in these three groups. Single-cell RNA sequencing was performed to identify chondrocyte populations and their gene signatures in KBD, OA and healthy cells to investigate their differences as related to the pathogenetic mechanisms of these two osteochondral diseases. We performed immunohistochemistry and quantitative reverse-transcription PCR (qRT-PCR) assays to validate the markers for chondrocyte population. Ten clusters were labelled by cell type according to the expression of previously described markers, and one novel population was identified according to the expression of a new set of markers. The homeostatic and mitochondrial chondrocyte populations, which were identified by the expression of the unknown markers MT1X and MT2A and MT-ND1 and MT-ATP6, were markedly expanded in KBD. The regulatory chondrocyte population, identified by the expression of CHI3L1, was markedly expanded in OA. Our study allows us to better understand the heterogeneity of chondrocytes in KBD and OA and provides new evidence of differences in the pathogenetic mechanisms between these two diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34045450 · DOI · PMC8160352
Research Progress of Selenium-Enriched Foods [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Selenium is an essential micronutrient that plays a crucial role in maintaining human health.
- Closing excerpt
- This review summarizes the physiological role and metabolism of selenium, the development of selenium-enriched foods, the physiological functions of selenium-enriched foods, and provides an analysis of total selenium and its species in selenium-enriched foods, with a view to laying the foundation for selenium-enriched food development.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (131 words)
Selenium is an essential micronutrient that plays a crucial role in maintaining human health. Selenium deficiency is seriously associated with various diseases such as Keshan disease, Kashin-Beck disease, cataracts, and others. Conversely, selenium supplementation has been found to have multiple effects, including antioxidant, anti-inflammatory, and anticancer functions. Compared with inorganic selenium, organic selenium exhibits higher bioactivities and a wider range of safe concentrations. Consequently, there has been a significant development of selenium-enriched foods which contain large amounts of organic selenium in order to improve human health. This review summarizes the physiological role and metabolism of selenium, the development of selenium-enriched foods, the physiological functions of selenium-enriched foods, and provides an analysis of total selenium and its species in selenium-enriched foods, with a view to laying the foundation for selenium-enriched food development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37836473 · DOI · PMC10574215
Proteoglycan metabolism, cell death and Kashin-Beck disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Kashin-Beck Disease (KBD) is an endemic, chronic and degenerative osteoarthropathy principally occurring in children.
- Closing excerpt
- In this mini-review, we discuss the close relationship between chondrocyte death including necrosis and loss of proteoglycan, and its potential mechanism during KBD onset and development, which may provide new clues for KBD research.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (92 words)
Kashin-Beck Disease (KBD) is an endemic, chronic and degenerative osteoarthropathy principally occurring in children. The characteristic pathological change of KBD is chondrocyte necrosis in hyaline articular cartilage. Proteoglycans are one of the major components in the extracellular matrix of articular cartilage, and disrupted proteoglycan metabolism and loss of proteoglycans in articular cartilage from KBD patients has been observed. In this mini-review, we discuss the close relationship between chondrocyte death including necrosis and loss of proteoglycan, and its potential mechanism during KBD onset and development, which may provide new clues for KBD research.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 22733148 · DOI · PMC3423566
Magnetofection-mediated siRNA delivery ameliorates cartilage damage in Kashin-Beck disease via targeting SIRT3 and protecting primary cilia [4]
Abstract reading summary — source excerpts
- Opening excerpt
- RationaleKashin-Beck disease (KBD) is an endemic osteochondropathy caused by T-2 toxin, however, the molecular mechanism underlying T-2 toxin-induced chondrocyte damage remains unclear.
- Closing excerpt
- The EMF-augmented si-SIRT3@SPIONs therapy can effectively protect T-2 toxin-induced primary cilia damage and cartilage degeneration, thus providing a promising therapeutic modality for KBD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (223 words)
RationaleKashin-Beck disease (KBD) is an endemic osteochondropathy caused by T-2 toxin, however, the molecular mechanism underlying T-2 toxin-induced chondrocyte damage remains unclear. This study aimed to elucidate the pathogenic role of T-2 toxin in KBD and develop an EMF-augmented nanotherapy for KBD-related cartilage damage.MethodsThis study investigated T-2 toxin-induced chondrocyte damage by evaluating protein acetylation, primary cilia integrity and the levels of chondrogenic markers (Sox9, Col2a1). In vitro experiments were performed via pharmacological and genetic SIRT3 inhibition. To protect chondrocytes, si-SIRT3@SPIONs were fabricated, and EMF was applied to improve cell transfection and silencing efficiency. A KBD model in SD rats was used to validate the in vivo therapeutic effect; immunohistochemical staining and micro-CT scanning and reconstruction were performed to comprehensively evaluate in vivo treatment efficacy.ResultsPathological SIRT3 overexpression induced by T-2 toxin disrupted chondrocyte protein acetylation, impaired primary cilia integrity, and suppressed the gene expression of chondrogenic markers. SIRT3 inhibition efficiently protected T-2 toxin-induced chondrocyte cytotoxicity in vitro. Furthermore, EMF-augmented si-SIRT3@SPIONs treatment ameliorated cartilage damage, preserved matrix composition and restored normal chondrocyte phenotype in KBD model rats.ConclusionsT-2 toxin induces chondrocyte injury and promotes KBD progression mainly by disrupting primary cilia integrity and protein acetylation, with SIRT3 overexpression acting as a mediating factor. The EMF-augmented si-SIRT3@SPIONs therapy can effectively protect T-2 toxin-induced primary cilia damage and cartilage degeneration, thus providing a promising therapeutic modality for KBD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42559309 · DOI · PMC13440625
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Selenium, iodine, and the relation with Kashin-Beck disease [5]
- Research article Endemic Kashin-Beck disease: A food-sourced osteoarthropathy [6]
- Research article Sodium selenite for treatment of Kashin-Beck disease in children: a systematic review of randomised controlled trials [7]
- Research article Effects of five types of selenium supplementation for treatment of Kashin-Beck disease in children: a systematic review and network meta-analysis [8]
- Research article Role of inflammation in the process of clinical Kashin-Beck disease: latest findings and interpretations [9]
- Research article Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease [10]
References
- Wang X, Ning Y, Zhang P, Poulet B, Huang R, Gong Y, et al.. Comparison of the major cell populations among osteoarthritis, Kashin-Beck disease and healthy chondrocytes by single-cell RNA-seq analysis. . 2021. PMID 34045450 · DOI · PMC8160352
- Chen Z, Lu Y, Dun X, Wang X, Wang H. Research Progress of Selenium-Enriched Foods. . 2023. PMID 37836473 · DOI · PMC10574215
- Li S, Cao J, Caterson B, Hughes CE. Proteoglycan metabolism, cell death and Kashin-Beck disease. . 2012. PMID 22733148 · DOI · PMC3423566
- Chen Y, Wang D, Zhang Y, Liu X, Du Z, Chen X, et al.. Magnetofection-mediated siRNA delivery ameliorates cartilage damage in Kashin-Beck disease via targeting SIRT3 and protecting primary cilia. . 2026. PMID 42559309 · DOI · PMC13440625
- Yao Y, Pei F, Kang P. Selenium, iodine, and the relation with Kashin-Beck disease. Nutrition. 2011. PMID 21967994 · DOI
- Wang K, Yu J, Liu H, Liu Y, Liu N, Cao Y, et al.. Endemic Kashin-Beck disease: A food-sourced osteoarthropathy. Semin Arthritis Rheum. 2020. PMID 31548049 · DOI
- Jirong Y, Huiyun P, Zhongzhe Y, Birong D, Weimin L, Ming Y, et al.. Sodium selenite for treatment of Kashin-Beck disease in children: a systematic review of randomised controlled trials. Osteoarthritis Cartilage. 2012. PMID 22370124 · DOI
- Xie D, Liao Y, Yue J, Zhang C, Wang Y, Deng C, et al.. Effects of five types of selenium supplementation for treatment of Kashin-Beck disease in children: a systematic review and network meta-analysis. BMJ Open. 2018. PMID 29511006 · DOI · PMC5855457
- Han J, Wang W, Qu C, Liu R, Li W, Gao Z, et al.. Role of inflammation in the process of clinical Kashin-Beck disease: latest findings and interpretations. Inflamm Res. 2015. PMID 26261076 · DOI
- Yu FF, Zhang YX, Zhang LH, Li WR, Guo X, Lammi MJ. Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease. Medicine (Baltimore). 2016. PMID 28033256 · DOI · PMC5207552
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.