Kashin-Beck Disease Research Articles

Polymorphism of MMP-3 gene and imbalance expression of MMP-3 / TIMP-1 in articular cartilage are associated with an endemic osteochondropathy, Kashin- Beck disease

BackgroundThe etiology of Kashin-Beck disease (KBD), an endemic osteochondropathy, is largely unknown. Matrix metalloproteinase-3 (MMP-3) plays a central role in the initiation and progression of cartilage destruction, however, no study has reported on the relationship between KBD and MMP-3. The objective of this study was to explore the polymorphism of MMP-3 gene and expression of MMP-3 / TIMP-1(Tissue inhibitors of matrixmetalloproteinases-1) in the pathogenesis of KBD.MethodsSingle nucleotide polymorphism (SNP) genotyping was conducted in 274 KBD cases and 248 healthy controls for eight SNPs in MMP-3 using the Sequenom MassARRAY system. Additionally, the expression of MMP-3、TIMP-1 in different layers of the articular cartilage was analyzed by immunohistochemistry for 22 KBD patients, 15 osteoarthritis (OA) patients and 21 controls.ResultsThe results showed that six SNPs (rs520540、rs591058、rs679620、rs602128、rs639752 and rs678815) in MMP-3 were associated with the increased risk of KBD, however, after Bonferroni correction, only the SNP rs679620 in the recessive model remained significant difference (OR = 2.31, 95%CI = 1.29–4.14, P = 0.0039), homozygous for “T” allele have a risk for KBD than “C” allele carriers. Moreover, the percentages of cells expressing MMP-3 in articular cartilage were significantly higher in the KBD and OA groups than in the controls (t = 5.37 and 4.19, P<0.01). While the KBD and OA groups had lower levels of TIMP-1 positive staining compared with the controls (t = 5.23and 5.06, P<0.01). And there was no significant different between KBD and OA for the levels of MMP-3 and TIMP-1 positive staining (t = 0.05and 0.28, P>0.05).ConclusionsMMP-3 is associated with the susceptibility of KBD, and the imbalance expression of MMPs / TIMPs leading to cartilage degradation may play an important role in cartilage degradation and osteoarthritis formation in OA and KBD.

Serum proteomic analysis of differentially expressed proteins and pathways involved in the mechanism of endemic osteoarthritis.

Kashin-Beck disease (KBD) is a chronic and endemic osteochondral disease and the etiology and pathogenic mechanism of KBD are still unknown. This study aimed to elucidate and screen KBD-associated proteins, which were differentially expressed between KBD patients and healthy controls. We combined protein fractionation and liquid chromatography-tandem mass spectrometry (LC-MS/MS) with a high-resolution mass spectrometer coupled with tandem mass tags (TMTs) to quantitatively analyze and screen KBD-associated proteins, which were differentially expressed between KBD patients and healthy controls. In addition, we used parallel reaction monitoring (PRM) to quantify proteins in serum from patients with KBD and healthy controls in order to verify the differentially expressed proteins in patients with KBD. We identified 224 differentially expressed proteins, including 11 up-regulated and 213 down-regulated proteins. Catalase (CAT) was observed to be significantly elevated in patients with KBD compared with control patients. Further, the fold difference of CAT is significantly elevated in PRM compared with label-free quantification. The results in this study suggest that CAT may be the reflection of the dynamic nature of KBD and could be considered as a novel pathogenic indicator for patients with KBD.

Comprehensive expression profiles of mRNAs, lncRNAs and miRNAs in Kashin-Beck disease identified by RNA-sequencing.

Kashin-Beck disease (KBD) is a chronic, endemic and deforming osteochondropathy, whose basic pathological alterations include apoptosis and necrosis of chondrocytes in articular cartilage and growth plates and imbalanced extracellular matrix metabolism. Numerous studies have reported that long noncoding RNAs (lncRNAs) and microRNA (miRNAs) are aberrantly expressed in KBD. Our study was comprised of 5 KBD patients and 5 healthy individuals and we compared the expression profiles of mRNAs, lncRNAs and miRNAs through RNA-sequencing (RNA-seq). Bioinformatic analysis of GO and KEGG was employed to conduct functional annotation and pathway enriched analysis. In total, 3194 mRNAs, 4103 lncRNAs and 1550 miRNAs were detected to be differentially expressed by RNA-seq (P < 0.05; |log2FC| ≥1). The lysosome pathway, Wnt signaling pathway, TNF signaling pathway, endocytosis and mTOR signaling pathway were identified to be involved in the KBD development according to the result of the KEGG analysis. In addition, a ceRNA network based on lncRNA-miRNA-mRNA was constructed to probe the intricate regulatory mechanism and interaction between transcripts, which was visualized using the Cytoscape software. The ce-lncRNAs of four aberrantly expressed genes, FOSB, EGR3, BCAM and SOX6, were determined through the network. Among the identified DElncRNAs, we selected 8 differentially expressed lncRNAs to confirm the reliability of RNA-seq data by qRT-PCR in 11 KBD patients and 11 healthy individuals. We aimed to provide a comprehensive understanding ofmRNA, lncRNA and miRNA alterations between KBD patients and healthy individuals, and meanwhile reveal several potential causative molecular and signaling pathways involved in KBD.

Altered Expression of the Hedgehog Pathway Proteins BMP2, BMP4, SHH, and IHH Involved in Knee Cartilage Damage of Patients With Osteoarthritis and Kashin-Beck Disease

ObjectiveTo investigate the expression of Hedgehog (HH) signaling pathway proteins in knee articular cartilage from Kashin-Beck disease (KBD) and osteoarthritis (OA) patients.MethodsKnee articular cartilage samples were collected from normal (N), OA, and KBD adults (aged 38-60 years) and divided into 3 groups with 6 subjects in each group. The localization of the HH pathway proteins bone morphogenetic protein 2 (BMP2), bone morphogenetic protein 4 (BMP4), Sonic hedgehog (SHH), and Indian hedgehog (IHH) was observed with the microscope after immunohistochemical (IHC) staining. Positive staining cell rates of each proteins were compared.ResultsThe strongest stainings of all proteins were observed in the middle zones of all 3 groups. The positive staining rates of BMP4 and IHH were significantly lower in the OA and KBD groups than those in the N group in all 3 zones. The positive staining rates of BMP2 and SHH tend to be lower in the OA and KBD groups than those in the N group in the deep zone, while higher in the OA and KBD groups than those in the N group in superficial and middle zones.ConclusionsAltered expression of the HH pathway proteins BMP2, BMP4, SHH, and IHH was found in OA and KBD articular cartilage. There seemed to be a compensatory effect between SHH and IHH in cartilage damage. Further studies on the pathogenesis of OA and KBD may be carried out from these aspects in the future.

Crosstalk between CpG Methylation and Polymorphisms (CpG-SNPs) in the Promotor Region of DIO2 in Kashin-Beck Disease

ObjectiveThis study was designed to determine the methylation profile of four CpGs and the genotypes of two CpG-SNPs located in promoter region of DIO2 in patients with Kashin-Beck disease (KBD). We also analyzed the interaction between the CpGs methylations and CpG-SNPs. MethodsWhole blood specimens were collected from 16 KBD patients and 16 healthy subjects. Four CpGs and two CpG-SNPs in the promoter regions of DIO2 were detected using matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS). The CpGs methylation levels were compared between samples from KBD patients and healthy subjects. The methylation levels were also analyzed in KBD patients with different CpG-SNP genotypes. ResultsThe mRNA expression of DIO2 in whole blood of KBD patients was significnatly lower than in healthy controls (P “0.05). The methylation levels of DIO2-1_CpG_3 in KBD patients were significantly higher than those in healthy controls (P <0.05). The methylation levels of four CpGs were not significantly different between KBD patients and healthy controls. The methylation level of DIO2-1_CpG_3 in the promoter region of DIO2 in KBD patients with GA/AA genotype was significantly higher than that of KBD patients with GG genotype (P <0.05). ConclusionThe methylation level of DIO2 increases in KBD patients. Similar trends exist in KBD carriers of variant genotypes of CpG-SNPs DIO2 rs955849187.

T-2 toxin induces articular cartilage damage by increasing the expression of MMP-13 via the TGF-β receptor pathway.

T-2 toxin pre-disposes individuals to osteoarthritis, Kashin-Beck disease (KBD). The major pathological change associated with KBD is the degradation of the articular cartilage matrix. Herein, we investigated the key molecules that regulate T-2 toxin-mediated cartilage degradation. Potential KBD treatments were also investigated. Sprague Dawley rats were divided into the T-2 toxin group and the control group. The T-2 toxin group received 100ng/g BW/day, whereas the control group received a similar dose of PBS. The expression of matrix metalloproteinase-13 (MMP-13) and TGF-β receptor I/II (TGF-βRI/II) was analyzed using immunohistochemical staining. C28/I2 chondrocytes were exposed to TGF-βRI/II binding inhibitor (GW788388) for 24h before incubation in different T-2 toxin concentrations (0, 6, 12, and 24ng/mL for 72h). The expression of mRNA for TGF-βRI/II, MMP-13 and proteins for MMP-13, and Smad-2 in chondrocytes were analyzed using RT-PCR and western blot, respectively. Safranin O staining revealed that T-2 toxin treatment modulated the expression of articular cartilage matrix. On the other hand, T-2 toxin treatment sharply increased the expression of MMP-13, TGF-βRI, and TGF-βRII in the rat cartilages. Interestingly, blocking the TGF-βRs-smad 2 signaling pathway using GW788388 abrogated the effect of T-2 toxin on upregulating MMP-13 expression. The expression of MMP-13 in chondrocytes induced with T-2 toxin is regulated via the TGF-βRs signaling pathway. As such, inhibiting the expression of TGF-βRs is a potential KBD treatment.

Research Progress of Fibroblast Growth Factor 8's Role in the Regulation of Bone Development and Homeostasis

The proper development and the homeostasis maintenance of bones are important prerequisites for the normal functioning of the human body. Bone developmental deformities or homeostasis disorders, such as Kashin-Beck disease, craniosynostosis, cleft palate and osteoarthritis, severely affect the life of patients, causing significant stress to the family and the society. Fibroblast growth factor 8 (FGF8) plays multiple functions through the course of the life of organisms. Abnormal expression of FGF8 may cause disorders of bone homeostasis and developmental abnormalities of bones. More and more studies have found that FGF8 may play an important role in bone development and may become a potential therapeutic target. Herein, we reviewed the role of FGF8 in a variety of skeletal abnormalities, intending to provide new perspectives for the prevention and treatment of related diseases in the future.

Selen - uloga u očuvanju i unapređenju zdravlja i sprečavanju bolesti

Introduction: Selenium is a trace element whose importance for the functioning of the organism in health and disease is very intensively studied in modern research. This scientific evidence is constantly being supplemented, which requires monitoring and evaluation. Aim: The aim of this review paper is to systematize the results of relevant scientific research on the role of selenium in health preservation and promotion and the prevention of disease. Method: Available literature in English from the PubMed database was searched using the keywords "selenium"; "health"; "disease"; "toxicity"; "food"; "deficiency"; "cancer" and "diabetes mellitus". Results: Selenium is a microelement that manifests a powerful antioxidant effect within the enzyme phospholipid hydroperoxide glutathione peroxidase, while as a part of the enzyme deiodinase plays a role in the transformation of thyroxine into triiodothyronine. Brazilian nut is a food with an extremely high concentration of selenium, followed by tuna and oysters. Selenium deficiency in the body manifests as cardiomyopathy (Keshan disease) or osteoarthritis (Kashin-Beck's disease). Selenium poisoning is characterized by gastrointestinal and neurological symptoms, changes in the skin, on nails and garlic breath. Although a negative correlation has been observed between selenium concentration and the risk of carcinoma (breast, prostate, cervical, liver, gastric, thyroid, colorectal and bladder), studies have not shown so far a significant effect of selenium nutritional intake or supplementation in the prevention of cancer. Selenium concentrations are significantly lower in hepatitis, cirrhosis of the liver, obesity, autoimmune diseases (Hashimoto's disease, psoriasis, rheumatoid arthritis, ulcerous colitis, Crohn's disease), AIDS, and COVID-19, compared to healthy people. On the other hand, excessive selenium intake can increase the risk of diabetes mellitus type 2. Conclusion: Selenium has a significant physiological role in preserving health, primarily as an antioxidant and in the functioning of the thyroid gland, while selenium deficiency can be manifested by cardiomyopathy and osteoarthritis. Low concentrations of selenium in the body may increase the risk of several diseases: cancer, autoimmune diseases, AIDS and COVID-19. On the other hand, excessively high doses of selenium may increase the risk of diabetes mellitus or even poisoning - selenosis.

成人大骨节病的手术治疗进展

成人大骨节病的手术治疗进展

Mechanism of DNA methylation-mediated downregulation of O6-methylguanine-DNA methyltransferase in cartilage injury of Kashin-Beck disease.

Kashin-Beck disease (KBD) is an endemic osteoarthropathy, in which excessive apoptosis of chondrocytes occurs. O6-methylguanine-DNA methyltransferase (MGMT), a DNA damage repair gene, plays an important role in apoptosis, but the mechanism is unclear in KBD cartilage injury. This study was to investigate the expression and promoter methylation of MGMT in KBD patients and its role in DNA damage and apoptosis of chondrocytes. MGMT mRNA and protein level were detected by quantitative real-time PCR and immunohistochemistry. Demethylation of MGMT was carried out using 5-Aza-2'-deoxycytidine, and the methylation level of MGMT promoter was measured by quantitative methylation specific PCR. Next, small hairpin RNA was used to knockdown the expression of MGMT. Cell viability, apoptosis and DNA damage were determined by MTT assay, flow cytometry, Hoechst 33342 staining and alkaline comet assay following T-2 toxin and selenium treatment. MGMT protein expression and mRNA levels were decreased (P = 0.02, P = 0.007) and promoter methylation was increased (P = 0.008) in KBD patients. Meanwhile, MGMT level was upregulated by 5-Aza-2'-deoxycytidine in chondrocytes (P = 0.0002). DNA damage and apoptosis rates were increased in MGMT-silenced chondrocytes (all P < 0.0001). Furthermore, DNA damage and apoptosis were increased in chondrocytes treated with T-2 toxin (all P < 0.0001), but were decreased after selenium treatment (P < 0.0001, P = 0.01). Decreased mRNA level and increased methylation of MGMT were found in the T-2 toxin group (P = 0.005, P = 0.002), while selenium reversed it (P = 0.02, P = 0.004). MGMT might play a crucial part in the pathogenesis of KBD cartilage injury, which could provide a therapeutic target for KBD.

Research advance on the important role of selenoproteinin human health

<p indent=0mm>Selenium (Se) is an essential trace element for animal and human health. Se deficiency and Se excessive intake can lead to severe symptoms and are related to diseases. Se is mainly combined with protein in the form of selenocysteine (Sec) and selenomethionine (Se-Met) in the human body. Generally, proteins formed by incorporating Sec into them are called selenoproteins, while proteins bound in other forms are called Se-containing proteins. Selenoprotein is the main form of Se to exert its biological functions in the human body, and Se deficiency could reduce the content and activity of selenoproteins and disturb the normal physiological function. Researches on the relationship between selenoproteins and human health have received increasing attention, and a comprehensive understanding of the function of selenoproteins is helpful to explain the effects of Se on human health. Although the functions of selenoproteins are not yet fully understood, the critical role of many selenoproteins in human health has been revealed increasingly. So far, 25 kinds of selenoproteins have been found in the human body, and this review focuses on the structure and biological function of glutathione peroxidase (GPX), thioredoxin reductase (TrxR) and iodothyronine deiodinase (ID) families and their relationship with diseases. It shows that selenoproteins such as GPX, TrxR and ID families have biological functions of regulating cell oxidative stress, endoplasmic reticulum stress, antioxidant defense, immune response and inflammatory response. The single nucleotide polymorphism (SNP) and DNA methylation in the promoter region of selenoprotein are related to the risk of diseases. Selenoproteins play a vital role in the pathogenesis and prevention of diseases such as tumors, cardiovascular diseases, osteoarthritis (OA), Keshan disease (KSD), Kashin-Beck disease (KBD), and corona virus disease 2019 (COVID-19) through their genetic and epigenetic forms. This research will provide clues and basis for further revealing the role of Se and selenoprotein in human health and screening to prevent disease targets. However, due to the complexity and unknown biological functions of selenoproteins, the mechanism of selenoproteins in resisting diseases and promoting human health is still worthy of further exploration and research.

Progress of Selenium Deficiency in the Pathogenesis of Arthropathies and Selenium Supplement for Their Treatment.

Selenium, an essential trace element for human health, exerts an indispensable effect in maintaining physiological homeostasis and functions in the body. Selenium deficiency is associated with arthropathies, such as Kashin-Beck disease, rheumatoid arthritis, osteoarthritis, and osteoporosis. Selenium deficiency mainly affects the normal physiological state of bone and cartilage through oxidative stress reaction and immune reaction. This review aims to explore the role of selenium deficiency and its mechanisms existed in the pathogenesis of arthropathies. Meanwhile, this review also summarized various experiments to highlight the crucial functions of selenium in maintaining the homeostasis of bone and cartilage.

Integrative pharmacology powers the detection of active components and mechanism underlying Wang Bi granules in rheumatoid arthritis

In China, Wang Bi Granule (WBG)2, composed of 16 herbal and 1 animal-based compounds, is used for clinical treatment of the "Wang Bi" syndrome, commonly referred to as later rheumatoid arthritis (RA) in modern medicine. It is also used in the treatment of ankylosing spondylitis, tuberculous arthritis, and Kashin-Beck disease, which are characterized by joint pain and swelling deformation. However, its pharmacological mechanisms remain unknown. We aimed to characterize the chemical components in WBG and examine the underlying mechanism for RA treatment using integrative pharmacological strategy, including chemical composition detection, efficacy evaluation, and mechanism exploration. We employed UPLC-QTOF-MS/MS to describe the chemical profile of WBG. TNF-α-stimulated RAW264.7 cells were used to simulate the inflammatory processes in RA and evaluate the anti-inflammatory effects of WBG. Network pharmacology was used to determine the mechanism underlying WBG action in RA. A total of 278 chemical components were identified or tentatively characterized. The water extract of WBG improved the imbalance in inflammation in TNF-α-stimulated RAW264.7 cells by regulating 179 differential genes. 55 key active constituents were obtained based on the interactions among "components" targets, RA-related genes, and differential genes (WBG vs TNF-α group) which may ameliorate RA by regulating 161 hub genes primarily involved in inflammation-related pathways. The present study, for the first time, employed integrative pharmacology to characterize the chemical profile of WBG and elucidate its mechanism of action against RA through an inflammation-immune regulatory system.

The WNT/β-catenin signalling pathway induces chondrocyte apoptosis in the cartilage injury caused by T-2 toxin in rats

We investigated whether the WNT/β-catenin signalling pathway is involved in paediatric Kashin–Beck disease (KBD) and T-2-toxin-induced cartilage injury in rats to better understand the mechanism of KBD. One hundred twenty-two children were selected and assigned to the case (31), internal control (41), and external control (50) groups. The serum β-catenin and bone morphogenetic protein 2（BMP2）levels in each group were measured and compared. Thirty-six rats were randomly assigned to three groups, which received no intervention, T-2 toxin, or solvent. After 18 weeks, the expression of LDL receptor related proteins 5 (LRP5), β-catenin, BMP2, BAX, BCL2, APAF1, and caspase 9 was measured and compared. The serum BMP2 levels were significantly elevated in the children with KBD and in the rats treated with T-2 toxin. In the T-2 toxin group, LRP5 and β-catenin expression was reduced, whereas BAX, APAF1, and caspase 9 expression was increased. In conclusion, the WNT/β-catenin signalling pathway is suppressed in KBD, which induces chondrocyte apoptosis, leading to cartilage injury. Therefore, BMP2 may play a role in the pathogenesis of KBD.

Supplementary files of a manuscript entiled "Comprehensive expression profiles of mRNAs, lncRNAs and miRNAs in Kashin-Beck Disease identified by RNA-sequencing"

Supplementary files of a manuscript entiled "Comprehensive expression profiles of mRNAs, lncRNAs and miRNAs in Kashin-Beck Disease identified by RNA-sequencing"

Alterations in the gut microbiota and metabolite profiles of patients with Kashin-Beck disease, an endemic osteoarthritis in China

Kashin-Beck disease (KBD) is a severe osteochondral disorder that may be driven by the interaction between genetic and environmental factors. We aimed to improve our understanding of the gut microbiota structure in KBD patients of different grades and the relationship between the gut microbiota and serum metabolites. Fecal and serum samples collected from KBD patients and normal controls (NCs) were used to characterize the gut microbiota using 16S rDNA gene and metabolomic sequencing via liquid chromatography-mass spectrometry (LC/MS). To identify whether gut microbial changes at the species level are associated with the genes or functions of the gut bacteria in the KBD patients, metagenomic sequencing of fecal samples from grade I KBD, grade II KBD and NC subjects was performed. The KBD group was characterized by elevated levels of Fusobacteria and Bacteroidetes. A total of 56 genera were identified to be significantly differentially abundant between the two groups. The genera Alloprevotella, Robinsoniella, Megamonas, and Escherichia_Shigella were more abundant in the KBD group. Consistent with the 16S rDNA analysis at the genus level, most of the differentially abundant species in KBD subjects belonged to the genus Prevotella according to metagenomic sequencing. Serum metabolomic analysis identified some differentially abundant metabolites among the grade I and II KBD and NC groups that were involved in lipid metabolism metabolic networks, such as that for unsaturated fatty acids and glycerophospholipids. Furthermore, we found that these differences in metabolite levels were associated with altered abundances of specific species. Our study provides a comprehensive landscape of the gut microbiota and metabolites in KBD patients and provides substantial evidence of a novel interplay between the gut microbiome and metabolome in KBD pathogenesis.

Differences of selenium and other trace elements abundances between the Kaschin-Beck disease area and nearby non-Kaschin-Beck disease area, Shaanxi Province, China

In order to find out the environmental geochemical characteristics of KBD affected area, KBD and non-KBD villages in KBD Counties, Weibei KBD area, Shaanxi Province, China were studied. Contents of Se and other elements in soil, wheat, maize and drinking water were analyzed. The results show that soil of Weibei KBD area is deficient in trace elements comparing with BSC and non-KBD area. Wheat of Weibei KBD area is deficient both in major elements and trace elements comparing with REC. Wheat of KBD village is especially deficient in Cr, Co, Se, Mo and Mg. Contents of Sr, Li and Mo in wheat of KBD village are significantly lower than nearby non-KBD village, but the average Se content is slightly higher. The deficiency of trace elements, especially Se, Sr, Li and Mo in staple food and trace elements in soil, is the main characteristic for the environment of KBD area.

Endoplasmic reticulum stress pathway mediates T-2 toxin-induced chondrocyte apoptosis

T-2 toxin leads to chondrocyte apoptosis and excessive extracellular matrix degradation. The aim of this study is to investigate if endoplasmic reticulum stress (ERS) – initiated apoptosis is involved in the chondrocyte damage induced by T-2 toxin. In vivo, rats were divided into a control group, T-2 toxin 200 ng/g BW/d group, the protein levels of GRP78, CHOP, and caspase-12 were detected using immunohistochemistry in articular cartilage tissues. In vitro, C28/I2 and ATDC5 chondrocytes were treated with various concentrations of T-2 toxin. For the salubrinal protection assay, cells were pretreated with 20 μM salubrinal for 1 h, and treated with and without T-2 toxin for 24 h. The cell viability was determined using the MTT assay; and the cell apoptosis was determined using the Flow Cytometry Assay; the mRNA and protein levels of the ERS markers and ECM were determined using RT-PCR and western blotting. This study found that the expressions of GRP78, CHOP, and caspase-12 is higher in T-2 toxin group than in control group both in vivo and in vitro, and the T-2 toxin administration promoted chondrocyte apoptosis, suppressed matrix synthesis, and accelerated cellular catabolism via the ERS signaling pathway. In addition, this study found that salubrinal prevented chondrocyte injury by inhibiting ERS-mediated apoptosis via the PERK-eIF2α-ATF4-CHOP signaling pathway. Collectively, this study provides a new clue to elucidate the mechanism of T-2 toxin-induced chondrocyte damage, and presents a novel therapeutic possibility of salubrinal for Osteoarthropathy such as osteoarthritis (OA) and Kaschin-Beck disease (KBD).

Impressions of the interdepartmental expedition to study Urov disease and goiter in August-October 1932

The problem of Trans-Baikal endemic polyarthritis or Kashin-Beck's disease, and in the language of the local population of the Urovka disease, is so urgent that the organs of the People's Commissariat of Agriculture, the People's Commissariat of Heavy Industry, the People's Commissariat of Railways, Tsustrakh and other branches of the national economy and industry are interested in studying it.

Long-term outcomes of arthroscopic debridement of the knee in adults with Kashin-Beck disease: an 18-year follow-up.

ObjectiveKashin–Beck disease (KBD) is an endemic degenerative joint disease with a high disability rate. We retrospectively evaluated the 18-year clinical follow-up outcomes of adult patients with KBD who underwent arthroscopic debridement for knee osteoarthritis.MethodsThirty-one patients with KBD (31 knees) underwent arthroscopy for knee osteoarthritis. The visual analog scale (VAS) score, walking distance, knee mobility, and patients’ self-evaluated improvement in clinical symptoms were retrospectively evaluated before and 18 years after the operation.ResultsThe patients’ self-evaluated clinical symptoms showed considerable improvement at 2, 6, and 8 years after surgery but deteriorated at 10 and 18 years after surgery. Knee mobility was greater after than before arthroscopy but decreased from 6 to 18 years postoperatively. The VAS score for knee pain was high before the operation, decreased at 2 years postoperatively, increased at 6 years postoperatively, and was significantly lower at 18 years postoperatively than before surgery. The walking distance was significantly longer at 2, 6, and 8 years postoperatively than preoperatively.ConclusionsArthroscopic treatment may be an effective therapy for adult patients with KBD who develop knee osteoarthritis. In this study, arthroscopy had a long-term effect on patients with KBD who had Kellgren–Lawrence grade <IV osteoarthritis.