TCF12 regulates the TGF-ß/Smad2/3 signaling pathway to accelerate the progression of osteoarthritis by targeting CXCR4.

Objective: Osteoarthritis (OA), which involves total joint damage and dysfunction, is a leading cause of disability worldwide. However, its exact pathogenesis remains unclear. Here, we identified TCF12 as an important regulator of the progression of OA. Methods: qRT-PCR, immunoblotting and immunohistochemistry (IHC) were used to detect the expression level of TCF12. The interaction of TCF12 with its downstream factor CXCR4 was assessed by Western blotting, immunofluorescence, qRT-PCR and luciferase assays. A mouse model was generated to examine the functions and mechanism of TCF12 in vivo. Result: TCF12 expression was upregulated in chondrocytes stimulated with IL-1ß and osteoarthritic chondrocytes. TCF12 upregulates the expression of CXCR4 and leads to dysfunction of the TGF-ß signaling pathway. Furthermore, knockdown of TCF12 alleviated cartilage damage in a mouse model generated by destabilization of the medial meniscus (DMM). Conclusion: TCF12 aggravates the progression of OA by targeting CXCR4 and then activating the TGF-ß signaling pathway, suggesting that TCF12 may be a new target for the treatment of OA. The translational potential of this article: Transcription Factor 12(TCF12), is known to regulate cell development and differentiation, It has been widely studied in various organs and diseases, but its role in OA remains unclear. Here, we identified Transcription Factor 12(TCF12) as an important regulator mediating chondrocyte senescence and cartilage extracellular matrix degradation indicating its role in OA. We found that TCF12 expression was upregulated both locally and systemically as OA advanced in patients with OA, and in mice after DMM surgery to induce OA. TCF12 expression caused striking progressive articular cartilage damage, synovial hyperplasia in OA mice, and remarkably, it was relieved by intra-articular administration of mutant mouse TCF12 lentiviral vector (shTCF12). Furthermore, TCF12 upregulated the expression of CXCR4, leading to exacerbation of experimental OA partially through activation of TGF-ß signaling in chondrocytes. TCF12 expression was upregulated in chondrocytes treated with IL-1ß and osteoarthritic chondrocytes. Our findings established an essential role of TCF12 in chondrocyte senescence and cartilage extracellular matrix degradation during OA, and identified intra-articular injection of TCF12 as a potential therapeutic strategy for OA prevention and treatment.

Novel resorbable bone wax containing ß-TCP and starch microspheres for accelerating bone hemostasis and promoting regeneration.

Traditional non-resorbable bone wax has been used in clinical surgery for more than 100 years. However, residual bone wax has been proven to cause numerous complications. In this study, a novel resorbable bone wax was designed to overcome the disadvantages of traditional non-resorbable bone wax. Alkylene oxide copolymers were used as the main component of resorbable bone wax; additionally, ß-tricalcium phosphate and starch microspheres were added to enhance bone regeneration and hemostatic ability. This novel resorbable bone wax has a high potential for clinical translation and is expected to be developed as a substitute for traditional bone wax.

The Modified Longitudinal Capsulotomy by Outside-In Approach in Hip Arthroscopy for Femoroplasty and Acetabular Labrum Repair-A Cohort Study.

Hip arthroscopy is difficult to perform due to the limited arthroscopic view. To solve this problem, the capsulotomy is an important technique. However, the existing capsulotomy approaches were not perfect in the surgical practice. Thus, this study aimed to propose a modified longitudinal capsulotomy by outside-in approach and demonstrate its feasibility and efficacy in arthroscopic femoroplasty and acetabular labrum repair. A retrospective cohort study was performed and twenty-two postoperative patients who underwent hip arthroscopy in our hospital from January 2019 to December 2021 were involved in this study. The patients (14 females and 8 males) had a mean age of 38.26 ± 12.82 years old. All patients were diagnosed cam deformity and labrum tear in the operation and underwent arthroscopic femoroplasty and labrum repair by the modified longitudinal capsulotomy. The mean follow-up time was 10.4 months with a range of 6−12 months. There were no major complications, including infection, neurapraxias, hip instability or revision in any patients. The average mHHS were 74.4 ± 15.2, 78.2 ± 13.7 and 85.7 ± 14.5 in 3 months, 6 months and 12 months after surgery, respectively, which were all better than that before surgery (44.9 ± 8.6) (p < 0.05). The average VAS were 2.8 ± 1.2, 1.5 ± 0.6 and 1.2 ± 0.7 in 3 months, 6 months and 12 months after surgery, respectively, which were all lower than that before surgery (5.5 ± 2.0) (p < 0.05). The modified longitudinal capsulotomy by outside-in approach is proved to be a safe and feasible method for hip arthroscopy considering to the feasibility, efficacy and security. The arthroscopic femoroplasty and labrum repair can be performed conveniently by this approach and the patient reported outcomes after surgery were better that before surgery in short-term follow-up. This new method is promising and suggested to be widely used clinically.

N6-methyladenosine (m6A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m6A/SIRT1 manner.

Increasing evidence suggest the biological roles of N6-methyladenosine (m6A) and long noncoding RNAs (lncRNAs) in the bone disease, especially osteoarthritis (OA). However, the interaction of m6A and lncRNA in osteoarthritis is still unclear. Here, we found that a m6A-related lncRNA LINC00680 upregulated in the OA tissue and IL-1ß-induced isolated primary chondrocytes. Functionally, in IL-1ß-induced chondrocytes, silencing of LINC00680 recovered the proliferation and repressed the extracellular matrix (ECM) degradation. Mechanistically, m6A methyltransferase METTL3 combined tithe the m6A site of LINC00680 to up-regulate its expression. Moreover, LINC00680 interacted with SIRT1 mRNA through binding at m6A site on SIRT1 mRNA 3'-UTR, thereby enhancing the stability of SIRT1 mRNA. Overall, these findings exhibited a role of LINC00680/m6A/SIRT1 mRNA complex in chondrocytes. Taken together, the present study intends to uncover the mechanism by which METTL3-mediated LINC00680 accelerates OA progression, which may provide novel insight for OA.

Value of 3D preoperative planning for primary total hip arthroplasty based on artificial intelligence technology.

BACKGROUND: Accurate preoperative planning is an important step for accurate reconstruction in total hip arthroplasty (THA). Presently, preoperative planning is completed using either a two-dimensional (2D) template or three-dimensional (3D) mimics software. With the development of artificial intelligence (AI) technology, AI HIP, a planning software based on AI technology, can quickly and automatically identify acetabular and femur morphology, and automatically match the optimal prosthesis size. However, the accuracy and feasibility of its clinical application still needs to be further verified. The purposes of this study were to investigate the accuracy and time efficiency of AI HIP in preoperative planning for primary THA, compared with 3D mimics software and 2D digital template, and further analyze the factors that influence the accuracy of AI HIP. METHODS: A prospective study was conducted on 53 consecutive patients (59 hips) undergoing primary THA with cementless prostheses in our department. All preoperative planning was completed using AI HIP as well as 3D mimics and 2D digital template. The predicted component size and the actual implantation results were compared to determine the accuracy. The templating time was compared to determine the efficiency. Furthermore, the potential factors influencing the accuracy of AI HIP were analyzed including sex, body mass index (BMI), and hip dysplasia. RESULTS: The accuracy of predicting the size of acetabular cup and femoral stem was 74.58% and 71.19%, respectively, for AI HIP; 71.19% (P = 0.743) and 76.27% (P = 0.468), respectively, for 3D mimics; and 40.68% (P < 0.001) and 49.15% (P = 0.021), respectively, for 2D digital templating. The templating time using AI HIP was 3.91 ± 0.64 min, which was equivalent to 2D digital templates (2.96 ± 0.48 min, P < 0.001), but shorter than 3D mimics (32.07 ± 2.41 min, P < 0.001). Acetabular dysplasia (P = 0.021), rather than sex and BMI, was an influential factor in the accuracy of AI HIP templating. Compared to patients with developmental dysplasia of the hip (DDH), the accuracy of acetabular cup in the non-DDH group was better (P = 0.021), but the difference in the accuracy of the femoral stem between the two groups was statistically insignificant (P = 0.062). CONCLUSION: AI HIP showed excellent reliability for component size in THA. Acetabular dysplasia may affect the accuracy of AI HIP templating.

Characterization of exosomal long non-coding RNAs in chondrogenic differentiation of human adipose-derived stem cells.

The exosomes derived from chondrogenic stem cells and long non-coding RNAs (lncRNAs) play a key role in cartilage regeneration. Here, we investigated the expression profile of exosomal lncRNAs in chondrogenesis of human adipose derived stem cells (hADSCs). hADSCs were induced to differentiate into chondrocytes in vitro. Exosomes from undifferentiated hADSCs and chondrogenic hADSCs were isolated. LncRNA and mRNA expression profiles in the isolated exosomes were analyzed by RNA sequencing. The resultant data were subjected to gene ontology (GO) terms and KEGG pathway analysis to identify differentially expressed lncRNAs. We identified 23 upregulated and 163 downregulated lncRNAs in exosomes derived from chondrogenic hADSCs compared to that in exosomes from undifferentiated hADSCs. In addition, analysis of mRNA expression data revealed 968 upregulated genes and 572 downregulated genes in exosomes of chondrogenic hADSCs. Lncrna and mRNA expression levels were further validated by qRT-PCR. Differentially expressed lncRNAs and mRNAs were utilized to construct a coding-non-coding gene co-expression network (CNC network). GO terms and KEGG pathway enrichment analysis revealed several significant processes differentially regulated between undifferentiated hADSCs and chondrogenic hADSCs. Taken together, this study revealed the differential expression of exosomal lncRNAs of chondrogenic hADSCs and provided a foundation for future study on the cartilage recovery mechanism of exosomes derived from chondrogenic stem cells.

Exosomal transfer of osteoclast-derived miRNAs to chondrocytes contributes to osteoarthritis progression.

Osteoarthritis (OA) is a prevalent aging-related joint disease lacking disease-modifying therapies. Here, we identified an upregulation of circulating exosomal osteoclast (OC)-derived microRNAs (OC-miRNAs) during the progression of surgery-induced OA in mice. We found that reducing OC-miRNAs by Cre-mediated excision of the key miRNA-processing enzyme Dicer or blocking the secretion of OC-originated exosomes by short interfering RNA-mediated silencing of Rab27a substantially delayed the progression of surgery-induced OA in mice. Mechanistically, the exosomal transfer of OC-miRNAs to chondrocytes reduced the resistance of cartilage to matrix degeneration, osteochondral angiogenesis and sensory innervation during OA progression by suppressing tissue inhibitor of metalloproteinase-2 (TIMP-2) and TIMP-3. Furthermore, systemic administration of a new OC-targeted exosome inhibitor (OCExoInhib) blunted the progression of surgery-induced OA in mice. We suggest that targeting the exosomal transfer of OC-miRNAs to chondrocytes represents a potential therapeutic avenue to tackle OA progression.

Identification and Characterization of Long Non-Coding RNAs in Osteogenic Differentiation of Human Adipose-Derived Stem Cells.

BACKGROUND/AIMS: Long noncoding RNAs (lncRNAs) play important roles in stem cell differentiation. However, their role in osteogenesis of human adipose-derived stem cells (ASCs), a promising cell source for bone regeneration, remains unknown. Here, we investigated the expression profile and potential roles of lncRNAs in osteogenic differentiation of human ASCs. METHODS: Human ASCs were induced to differentiate into osteoblasts in vitro, and the expression profiles of lncRNAs and mRNAs in undifferentiated and osteogenic differentiated ASCs were obtained by microarray. Bioinformatics analyses including subgroup analysis, gene ontology analysis, pathway analysis and co-expression network analysis were performed. The function of lncRNA H19 was determined by in vitro knockdown and overexpression. Quantitative reverse transcription polymerase chain reaction was utilized to examine the expression of selected genes. RESULTS: We identified 1,460 upregulated and 1,112 downregulated lncRNAs in osteogenic differentiated human ASCs as compared with those of undifferentiated cells (Fold change ≥ 2.0, P < 0.05). Among these, 94 antisense lncRNAs, 85 enhancer-like lncRNAs and 160 lincRNAs were further recognized. We used 12 lncRNAs and 157 mRNAs to comprise a coding-non-coding gene expression network. Additionally, silencing of H19 caused a significantly increase in expression of osteogenesis-related genes, including ALPL and RUNX2, while a decrease was observed after H19 overexpression. CONCLUSION: This study revealed for the first time the global expression profile of lncRNAs involved in osteogenic differentiation of human ASCs and provided a foundation for future investigations of lncRNA regulation of human ASC osteogenesis.

MicroRNA-455-3p modulates cartilage development and degeneration through modification of histone H3 acetylation.

Histone acetylation regulated by class I histone deacetylases (HDACs) plays a pivotal role in matrix-specific gene transcription and cartilage development. While we previously demonstrated that microRNA (miR)-455-3p is upregulated during chondrogenesis and can enhance early chondrogenesis, the mechanism underlying this process remains largely unclear. In this study, we characterized the effect of miR-455-3p on histone H3 acetylation and its role during cartilage development and degeneration. We observed that miR-455-3p was highly expressed in proliferating and pre-hypertrophic chondrocytes, while HDAC2 and HDAC8 were primarily expressed in hypertrophic chondrocytes. Meanwhile, miR-455-3p suppressed the activity of reporter constructs containing the 3'-untranslated regions of HDAC2/8, inhibited HDAC2/8 expression and promoted histone H3 acetylation at the collagen 2 (COL2A1) promoter in human SW1353 chondrocyte-like cells. Treatment with the HDAC inhibitor trichostatin A (TSA) resulted in increased expression of cartilage-specific genes and promoted glycosaminoglycan deposition. Moreover, TSA inhibited matrix metalloproteinase 13 (Mmp13) expression and promoted nuclear translocation of SOX9 in interleukin-1-treated primary mouse chondrocytes. Lastly, knockdown of HDAC2/3/8 increased SRY (sex-determining region Y)-box 9 (SOX9) and decreased Runt-related transcription factor 2 (RUNX2) expression. Taken together, these findings suggest that miR-455-3p plays a critical role during chondrogenesis by directly targeting HDAC2/8 and promoting histone H3 acetylation, which raises possibilities of using miR-455-3p to influence chondrogenesis and cartilage degeneration.

MicroRNA-381 Regulates Chondrocyte Hypertrophy by Inhibiting Histone Deacetylase 4 Expression.

Chondrocyte hypertrophy, regulated by Runt-related transcription factor 2 (RUNX2) and matrix metalloproteinase 13 (MMP13), is a crucial step in cartilage degeneration and osteoarthritis (OA) pathogenesis. We previously demonstrated that microRNA-381 (miR-381) promotes MMP13 expression during chondrogenesis and contributes to cartilage degeneration; however, the mechanism underlying this process remained unclear. In this study, we observed divergent expression of miR-381 and histone deacetylase 4 (HDAC4), an enzyme that directly inhibits RUNX2 and MMP13 expression, during late-stage chondrogenesis of ATDC5 cells, as well as in prehypertrophic and hypertrophic chondrocytes during long bone development in E16.5 mouse embryos. We therefore investigated whether this miRNA regulates HDAC4 expression during chondrogenesis. Notably, overexpression of miR-381 inhibited HDAC4 expression but promoted RUNX2 expression. Moreover, transfection of SW1353 cells with an miR-381 mimic suppressed the activity of a reporter construct containing the 3'-untranslated region (3'-UTR) of HDAC4. Conversely, treatment with a miR-381 inhibitor yielded increased HDAC4 expression and decreased RUNX2 expression. Lastly, knockdown of HDAC4 expression resulted in increased RUNX2 and MMP13 expression in SW1353 cells. Collectively, our results indicate that miR-381 epigenetically regulates MMP13 and RUNX2 expression via targeting of HDAC4, thereby suggesting the possibilities of inhibiting miR-381 to control chondrocyte hypertrophy and cartilage degeneration.

miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.

Increasing evidence has reported the significant roles of lncRNA or miRNAs in the biology of various diseases. This study was aimed to elucidate the potential roles of miR-141 and lncRNA H19 and H19-derived miR-675 in regulating osteoblasts proliferation and apoptosis and to explore its potential mechanism. miR-141 mimic or miR-141 inhibitor or siRNA-H19 or miR-675 inhibitor was transfected into human hFOB1.19 cells. The effects or miR-141 expression on H19 or miR-675 expression, on osteoblasts proliferation and apoptosis were analyzed. Moreover, effects of H19 and miR-675 expression on cell proliferation were also analyzed. The results showed that miR-141 was down-regulated in both hFOB1.19 cells and osteosarcoma tissues. The overexpressed miR-141 suppressed H19 and miR-675 expression in hFOB1.19 cells. Besides, miR-141 suppression significantly increased cell viability but this effect was blocked by silencing H19 or miR-675 inhibitor, which is similar to the effects on VEGF and IGF2 expression. Furthermore, miR-141 overexpression induced osteoblasts apoptosis, but decreased the levels of caspase-3 and the Bcl-2/Bax ratio. Taken together, our study revealed that tumor-suppressor miR-141 overexpression suppressed osteoblasts proliferation but induced apoptosis through down-regulating H19 or miR-675 in osteosarcoma. This study may provide theoretical basis for illustrating the interaction between lncRNA and miRNAs in osteosarcoma and for the therapeutic target of miR-141 in osteosarcoma treatment.

Characterization of long non-coding RNA expression profiles in lymph node metastasis of early-stage cervical cancer.

Pelvic lymph node metastasis (PLNM) is an independent prognostic parameter and determines the treatment strategies of cervical cancer. Increasing evidence indicates that long non-coding RNAs (lncRNAs) play a crucial role in the process of tumor biological functions. This study aimed to mine lymph node metastasis-associated lncRNAs and investigate their potential pathophysiological mechanism in cervical cancer lymph node metastasis. We applied the lncRNA-mining approach to identify lncRNA transcripts represented on Affymetrix human genome U133 plus 2.0 microarrays from Gene Expression Omnibus (GEO) and then by validation in clinical specimens. The biological role and molecular mechanism of these lncRNAs were predicted by bioinformatic analysis. Subsequently, a receiver operating characteristic (ROC) curve and survival curve were conducted to evaluate the diagnostic and prognostic value of candidate lncRNAs. In total, 234 differentially expressed lncRNAs were identified to significantly associate with pelvic lymph node metastasis in early-stage cervical cancer. Our qRT-PCR results were consistent with the mining analysis (P<0.05). The functional enrichment analysis suggested that these lncRNAs may be involved in the biological process of lymph node metastasis. The ROC curves demonstrated satisfactory discrimination power of MIR100HG and AC024560.2 with areas under the curve of 0.801 and 0.837, respectively. Survival curve also indicated that patients with high MIR100HG expression had a tendency of poor prognosis. This is the first study to successfully mine the lncRNA expression patterns in PLNM of early-stage cervical cancer. MIR100HG and AC024560.2 may be a potential biomarkers of PLNM and these lncRNAs may provide broader perspective for combating cervical cancer metastasis.

MiR-455-3p regulates early chondrogenic differentiation via inhibiting Runx2.

The expression of miR-455-3p has been shown to be up-regulated in chondrogenesis of mesenchymal stem cell, but its role in different stages during chondrogenesis remains unknown. Here, we show that miR-455-3p is increased in ATDC5 cells from 0 d to 21 d, but rapidly decreases at 28 d, and a similar expression kinetic is detected in the development of mouse embryos. We show that miR-455-3p functions as an activator for early chondrogenic differentiation, most likely by inhibiting the expression of Runt-related transcription factor 2 (Runx2) as indicated by luciferase reporter assays. In conclusion, miR-455-3p may activate early chondrogenesis by directly targeting Runx2.

[EXPRESSIONS OF CARTILAGE DEGENERATIVE RELATED GENES AND microRNAs IN TORN MENISCUS].

OBJECTIVE: To investigate the expressions of cartilage degenerative related genes in meniscus, and to evaluate the potential effect of meniscal damage on cartilage degeneration, and to analyze the relationship between microRNAs (miRNAs) expression and cartilage degeneration. METHODS: Meniscal tissue was collected from 5 patients undergoing partial meniscectomy between September 2012 and October 2013 (experimental group), and normally meniscal tissue without tearing from amputees was used as controls (control group). Pathological changes of menisci were observed; and real-time fluorescent quatitative PCR was performed to examine the relative expression levels of cartilage degenerative related genes and miRNAs: Aggrecan (ACAN), type X collagen (COL10A1), matrix metalloproteinases 13 (MMP-13), CCAAT enhancer binding protein ß (CEBP-ß), a disintegrin and metalloproteinase with thrombospondinmotif 5 (ADAMTS-5), miR-193b, miR-92a, and miR-455-3p in meniscus. RESULTS: There were varying degrees of degenerative pathological changes in torn meniscus of experimental group. Compared with normal meniscus of control group, the expression of ACAN was decreased, while the expressions of COL10A1, CEBP-ß, ADAMTS-5, and MMP-13 were increased in torn meniscus of experimental group; and significant difference was found (P < 0.05) except ACAN and MMP-13 (P > 0.05). The expressions of miR-92a, miR-455-3p, and miR-193b in torn meniscus of experimental group were significantly higher than those in normal meniscus of control group (P < 0.05). CONCLUSION: Meniscal tissue has the intrinsic tendency of degeration after meniscus tear. The torn meniscus has greater stimulative impact on cartilage degeneration than normally morphological meniscus without tearing. The cartilage degenerative related miRNAs, including miR-193b, miR-92a, and miR-455-3p may contribute to the up-regulation of osteoarthritis.

The Role of MicroRNA-381 in Chondrogenesis and Interleukin-1-ß Induced Chondrocyte Responses.

AIM: The molecular pathways regulating cartilage degradation are unclear. miR-381 was identified as a putative regulator of chondrogenesis related genes. Here, we examined its role in chondrogenesis and osteoarthritic cartilage degeneration. METHODS: miR-381 expression was assessed in vitro in response to IL-1ß stimulation in primary human (PHC) and mouse (PMC) chondrocytes, and ATDC5 derived chondrocytes; and in vivo in mouse embryos and human osteoarthritic cartilage. The effects of miR-381 on chondrogenesis and NF-kB signaling were assessed using a synthetic RNA mimic or inhibitor and luciferase assay, respectively. Upstream regulators of miR381 were probed using siRNA or overexpression plasmids for Sox9 and Runx2. RESULTS: miR-381 expression was elevated in chondrogenic and hypertrophic ATDC5 cells. miR-381 was induced in vitro by IL-1ß in ATDC5 cells, PMCs, and PHCs, and was expressed in areas of cartilage degradation or absorption in vivo. Overexpression of Runx2 or Sox9 increased miR-381 expression in ATDC5 cells. miR-381 suppressed expression of collagen, type II, alpha 1, and enhanced expression of metalloproteinase-13 (MMP-13), but did not regulate NFKBIA and NKRF activity. CONCLUSION: miR-381 was highly expressed during chondrogenesis and in arthritic cartilage. It may contribute to absorption of the cartilage matrix by repressing type II collagen and inducing MMP-13.

Impaired ossification coupled with accelerated cartilage degeneration in developmental dysplasia of the hip: evidences from µCT arthrography in a rat model.

BACKGROUND: Developmental dysplasia of the hip (DDH) always leads to cartilage degeneration and osteoarthritis of the hip joint. However, the diagnosis of early cartilage degeneration in DDH is still a clinical challenge. This study aims to investigate the dynamic changes of bone and cartilage in the hip of a rat model of DDH and to explore the potential application of microcomputed tomography (µCT) arthrography to detect early cartilage degeneration in DDH. METHODS: Newborn Wistar rats were used to induce DDH by hindlimb swaddling. The bone and cartilage of the hip in model and control group were analyzed by µCT arthrography and histology examination at postnatal day 10, week 4, 6 and 8. RESULTS: Hip dysplasia developed with age, became obvious at postnatal week 6 and further progressed at week 8. µCT analysis showed that bone mineral density (BMD) and bone volume density (bone volume over total volume, BV/TV) of the femoral head and neck region (FHNR) in model group were both significantly lower than those in control group, and they increased dramatically from postnatal week 4 to week 6 but maintained at a similar level at week 8. Contrast-enhanced µCT (CE-µCT) arthrography and histology data showed age-dependent increase in cartilage attenuation (CA) and decrease in safranin O staining intensity (SI) in model group, respectively. Moreover, the model group revealed remarkably higher CA and lower SI than control group, respectively. In addition, significant changes of CA and SI were both observed from postnatal week 6 to week 8 in model group. A strong linear correlation (r2=0.789, P <0.001) was found between CA and SI in model group. Furthermore, BMD was negatively correlated with SI (t=-2.683, P <0.05), whereas specific bone surface (bone surface over bone volume, BS/BV) was positively correlated with SI (t =4.501, P <0.01), in model group. CONCLUSIONS: Impaired ossification coupled with continuous loss of sGAG in cartilage matrix was found in the dysplasia hip during the disease progression of DDH. Cartilage degeneration in the dysplasia hip may occur early at childhood, accelerated with age and become irreversible at young adult stage. All these abnormal changes could be quantitatively assessed by µCT arthrography.

The biomechanical differences of rotational acetabular osteotomy, Chiari osteotomy and shelf procedure in developmental dysplasia of hip.

BACKGROUND: Rotational acetabular osteotomy (RAO), Chiari osteotomy and shelf procedure are important treatments to delay the progression of osteoarthritis in developmental dysplasia of hip (DDH) patients, but their biomechanical differences are still unknown. This study was to evaluate the different biomechanical changes of hip joint after these three surgeries. METHODS: Sixteen DDH models of 8 human cadaver specimens were reconstructed, and treated by different surgeries, and then strain around femoral head was evaluated by strain gauges. RESULTS: Hip strain value of DDH model was decreased after treated by shelf procedure (Pleft = 0.016 and Pright = 0.021) and rotational acetabular osteotomy (P = 0.004), but not in Chiari osteotomy (P = 0.856). Moreover, the improved ratio of RAO treatment was better than shelf procedure (P = 0.015) and Chiari osteotomy (P = 0.0007), and the descendent range of shelf procedure was greater than Chiari osteotomy (P = 0.018). CONCLUSIONS: From biomechanics points, RAO was more effective in relieving hip joint stress compared with shelf procedure and Chiari osteotomy.

An iterative algorithm for the reflexive solution of the general coupled matrix equations.

The general coupled matrix equations (including the generalized coupled Sylvester matrix equations as special cases) have numerous applications in control and system theory. In this paper, an iterative algorithm is constructed to solve the general coupled matrix equations over reflexive matrix solution. When the general coupled matrix equations are consistent over reflexive matrices, the reflexive solution can be determined automatically by the iterative algorithm within finite iterative steps in the absence of round-off errors. The least Frobenius norm reflexive solution of the general coupled matrix equations can be derived when an appropriate initial matrix is chosen. Furthermore, the unique optimal approximation reflexive solution to a given matrix group in Frobenius norm can be derived by finding the least-norm reflexive solution of the corresponding general coupled matrix equations. A numerical example is given to illustrate the effectiveness of the proposed iterative algorithm.

[A survey on adolescent scoliosis in Guangzhou].

OBJECTIVE: To investigate the prevalence of adolescent scoliosis in Guangzhou for development of effective prevention and treatment program to the disease. METHODS: From November 2007 to July 2009, 30 142 students between 7 to 20 years old in primary and junior middle schools received physical check-up for detection of scoliosis through physical and radiographic examination. RESULTS: 211 cases were diagnosed as scoliosis (Cobb angle ≥ 10°), with the prevalence rate as 0.70%. 192 patients with idiopathic scoliosis (IS) were detected, accounting for 91.00%. There were 19 cases of congenital scoliosis, accounting for 9.00%. Sex ratio of scoliosis was 180/31. The prevalence of scoliosis was significantly lower in boys than that in girls (χ(2) = 112.332, P < 0.001). CONCLUSION: The crude prevalence of adolescent scoliosis was 0.70% in Guangzhou with majority of idiopathic scoliosis. Investigation on scoliosis among school-age population seemed to be important for the purposes of early diagnosis, selection of effective prevention and treatment.