Bone marrow edema at ligament insertion is an accurate MRI sign of deltoid ligament injury.

BACKGROUND: Magnetic resonance imaging (MRI) is effective in diagnosing deltoid ligament (DL) injury but its sensitivity in chronic cases is low. Additional diagnostic signs are required to reduce the risk of a false negative diagnosis. PURPOSE: To evaluate the added diagnostic value of bone marrow edema at the ligament insertion (BMELI) of DL to the MRI assessment of chronic DL injury. MATERIAL AND METHODS: One hundred patients who consecutively came to our institution between November 2018 and December 2021 and underwent arthroscopic surgery for chronic ankle instability (CAI) were enrolled in the present study. Preoperative MR images were retrospectively reviewed by two orthopedic surgeons to evaluate the sensitivity, specificity and interobserver reliability of three MRI signs in diagnosing chronic DL injury, namely, abnormal ligamentous morphological characteristics (ALMC), BMELI and medial clear space (MCS). RESULTS: Taking arthroscopy as the reference standard, there were 34 patients with and 66 without DL injury. ALMC had 64.71% (22/34; 46.47-79.70) sensitivity and 83.33% (55/66; 71.71-91.00) specificity, BMELI had 70.59% (24/34; 52.33-84.29) sensitivity and 95.45% (63/66; 86.44-98.82) specificity and MCS had 26.47% (9/34; 13.51-44.65) sensitivity and 92.42% (61/66; 82.50-97.18) specificity. Compared with ALMC, BMELI had similar efficacy in superficial cases (P = 0.06) and greater efficacy in deep cases (P = 0.04). All three signs showed good interobserver agreement (kappa values all above 0.7). CONCLUSION: BMELI can reliably indicate concomitant injury to the DL in CAI patients. Using BMELI as a sign of chronic DL injury when ALMC is unclear may reduce the risk of a false negative diagnosis.

Outcomes comparison of elastic bandage versus lower-leg cast immobilization after anterior talofibular ligament repair.

PURPOSE: The aim of this study was to compare the clinical outcomes between patients with chronic ankle instability (CAI) undergoing arthroscopic anterior talofibular ligament (ATFL) repair who received elastic bandage treatment and those who received lower-leg cast immobilization. METHODS: CAI patients with isolated ATFL injury undergoing arthroscopic ATFL repair from January 2017 and August 2019 were included in the study. The visual analogue scale (VAS) at rest and during activities, American Orthopedic Foot and Ankle Society (AOFAS) score, Karlsson Ankle Functional Score (Karlsson score), and time of returning to walk, walk normally, work and sports were evaluated preoperatively, and at 6 months and 12 months follow-up. RESULTS: A total of 41 patients were included in this study. Among them, 24 patients accepted lower-leg cast fixation, and the other 17 patients were immobilized with elastic bandage. Compared to patients with lower-leg immobilization, patients with elastic bandage fixation had significantly lower VAS during activities (P = 0.021) and higher AOFAS score (P = 0.015) at 12 months follow-up. The Karlsson score at 6 months follow-up were significantly higher in elastic bandage group than those in lower-leg group (P = 0.011). However, no significant difference was observed in time of returning to walk, work and sports between the two groups. CONCLUSION: Elastic bandage treatment was better than lower-leg cast immobilization in terms of eliminating pain symptom at 12 months follow-up, and improving ankle functional outcome at 6 months follow-up. Moreover, the present study emphasized that lower-leg cast immobilization offered no advantages in arthroscopic ATFL repair postoperative immobilization. STUDY DESIGN: Cohort study; Level of evidence, 3.

Prevalence and Injury Patterns of CFL Injury in Chronic Lateral Ankle Instability: An Observational Cross-Sectional Study Using Ultrasound.

The purpose of this paper is to assess the prevalence and injury patterns of the calcaneofibular ligament (CFL) in chronic lateral ankle instability (CAI) patients using ultrasound imaging. This retrospective study included 938 ankle ultrasound images from January 2016 to May 2018. The patients' demographic data and the injury pattern classified by the injury location and the remnant quality were recorded and correlated using t tests, Fisher's exact tests, and post hoc tests accordingly. Of the 938 CAI patients, CFL injury was found in 408/938 (44%). Among the 408 anterior talofibular ligament (ATFL) and CFL complex injury patients, 71/408 (17%) presented with a completely absorbed ATFL, whereas 13/71 (18%) presented with an absorbed CFL. The total CFL absorption proportion in all patients was relatively low (30/938 = 3%). Post hoc tests indicated a negative association between thickened ATFLs and complex injuries. In addition, a positive association existed between absorbed ATFLs and complex injuries as well as absorbed ATFLs and absorbed CFLs. Thus, the results indicated that total tearing and absorption injury patterns of the CFL in CAI are not common. Even when the ATFL is absorbed, only approximately one-fifth (13/71 = 18%) of CFLs require reconstruction, suggesting that it is unnecessary to routinely repair or reconstruct CFLs in all lateral ligament surgeries.

Metabolic Regulation of Immune Response and Tissue Remodeling in Gouty Arthritis (Review).

Gouty arthritis (GA), one of the most common forms of inflammatory arthritis, is characterized by elevated serum uric acid concentrations and the consequent deposition of monosodium urate crystals. Under low-grade inflammatory stress, cells tend to adapt to the microenvironment by reprogramming their metabolic pathways. Here we review the aberrant metabolic responses to the inflammatory environment in immune and tissue cells in distinct phases of GA. Regulation of these pathways is implicated in metabolic alterations including mitochondrial dysfunction, changes in the glycolytic pathway, and alteration of lipid, uric acid, and bone metabolism among others. Investigations of how these alterations lead to proinflammatory and anti-inflammatory effects in each period of GA have revealed links to its pathogenesis. Knowledge gained may open up new opportunities for diagnosis, treatment and prognosis of GA and offer rationale for further investigation into the mechanisms underlying the progression of the disease.

Contributions of joint damage-related events to gout pathogenesis: new insights from laboratory research.

Epidemiological and imaging findings indicate that gout frequently affects damaged joints. Recent studies suggest that the relationship between gout and joint damage may be more complex than a simple unidirectional link and that joint damage may promote the development of gout at affected sites. In this article, we review the clinical associations and recent laboratory research identifying events in the setting of osteoarthritis or joint injury that can alter the intraarticular microenvironment and locally regulate monosodium urate crystallisation and deposition or amplify the inflammatory response to deposited crystals. This includes cartilage matrix proteins or fibres released into the articular space that accelerates the crystallisation process, as well as the lack of lubricin and fibroblast priming that enhances the immune response towards the deposited crystals. These findings provide new insights into gout pathogenesis and offer a possible explanation for the site preference of gout in the damaged joint.

Type II collagen facilitates gouty arthritis by regulating MSU crystallisation and inflammatory cell recruitment.

OBJECTIVE: Increasing evidence suggests that impaired cartilage is a substantial risk factor for the progression from hyperuricaemia to gout. Since the relationship between cartilage matrix protein and gout flares remains unclear, we investigated its role in monosodium urate (MSU) crystallisation and following inflammation. METHODS: Briefly, we screened for cartilage matrix in synovial fluid from gouty arthritis patients with cartilage injuries. After identifying a correlation between crystals and matrix molecules, we conducted image analysis and classification of crystal phenotypes according to their morphology. We then evaluated the differences between the cartilage matrix protein-MSU complex and the pure MSU crystal in their interaction with immune cells and identified the related signalling pathway. RESULTS: Type II collagen (CII) was found to be enriched around MSU crystals in synovial fluid after cartilage injury. Imaging analysis revealed that CII regulated the morphology of single crystals and the alignment of crystal bows in the co-crystalline system, leading to greater phagocytosis and oxidative stress in macrophages. Furthermore, CII upregulated MSU-induced chemokine and proinflammatory cytokine expression in macrophages, thereby promoting the recruitment of leucocytes. Mechanistically, CII enhanced MSU-mediated inflammation by activating the integrin ß1(ITGB1)-dependent TLR2/4-NF-κB signal pathway. CONCLUSION: Our study demonstrates that the release of CII and protein-crystal adsorption modifies the crystal profile and promotes the early immune response in MSU-mediated inflammation. These findings open up a new path for understanding the relationship between cartilage injuries and the early immune response in gout flares.

Identification of m7G-related hub biomarkers and m7G regulator expression pattern in immune landscape during the progression of osteoarthritis.

BACKGROUND: Accumulating evidence has shown that aberrant N7-methylguanosine (m7G) RNA methylation played an important role in the occurrence and development of cancer. However, knowledge of m7G modifications in inflammatory diseases is limited. Osteoarthritis (OA) is the most common arthritic disease with poor prognosis. Our research aimed to identify m7G-related hub biomarkers and investigate m7G regulator expression pattern in immune landscape of OA patients. METHODS: Gene expression profiles and their clinical information were obtained from the Gene Expression Omnibus (GEO) database, and differential analysis of 14 m7G-related regulators between elective OA and normal samples was performed. M7G-related hub genes for OA were mined based on single-sample gene set enrichment analysis (ssGSEA) and the random forest (RF) algorithm, and qRT-PCR was performed to confirm the abnormal expression of hub genes. Enrichment, protein-protein interaction (PPI), transcription factor (TF)-gene interaction and microRNA (miRNA)-gene coregulatory analysis based on m7G hub genes were performed. Then we predicted several candidate drugs related to m7G hub genes using DSigDB database. Moreover, we comprehensively evaluated m7G methylation patterns in OA samples and systematically correlated these modification patterns with the characteristics of immune cell infiltration. The m7G score was generated to quantify m7G methylation patterns for individual OA patients by the application of principal component analysis (PCA) algorithm. RESULTS: We constructed an OA predictive model based on 4 m7G hub genes (SNUPN, METTL1, EIF4E2 and CYFIP1). Two m7G methylation patterns in OA were discovered to show distinct biological characteristics, and an m7G score were generated. M7G cluster A and a higher m7G score were found to be related to an inflamed phenotype. CONCLUSIONS: Our study was the first to comprehensively investigate the m7G methylation dysregulations in immune landscape during the progression of OA. These 4 m7G gene-related signatures can be used as novel OA biomarkers to predict the occurrence of OA. Evaluating the m7G methylation patterns of OA individuals will contribute to enhancing our cognition of immune infiltration characterization and guiding more effective immunotherapy strategies.

Gene signature based on glycolysis is closely related to immune infiltration of patients with osteoarthritis.

BACKGROUND: Osteoarthritis (OA) is a degenerative arthritis with high levels of clinical heterogeneity. Aberrant metabolism such as shifting from oxidative phosphorylation to glycolysis is a response to changes in the inflammatory microenvironment of OA. Therefore, there is a pressing need to identify novel glycolysis regulators during OA progression. METHODS: We systematically studied glycolysis patterns mediated by 141 glycolysis regulators in 74 human synovial samples and discussed the characteristics of the immune microenvironment modified by glycolysis. The random forest (RF) method was applied to screen candidate hub glycolysis regulators in OA. RT-qPCR was performed to validate these key regulators. Then distinct glycolysis patterns were identified, and systematic correlation between these glycolysis patterns and immune cell infiltration was analyzed. The glycolysis score was constructed to quantify glycolysis patterns together with immune infiltration of individual OA patient. RESULTS: 56 glycolysis-related differentially expressed genes (DEGs) were identified between OA and non-OA samples. STC1, VEGFA, KDELR3, DDIT4 and PGAM1 were selected as candidate genes to predict the probability of OA. Two glycolysis patterns in OA were identified. Glycolysis cluster A with higher glycolysis score was related to an inflamed phenotype. CONCLUSIONS: Taken together, our results established a glycolysis-based genetic signature for OA, guided in-depth studies on the metabolic mechanism of OA, and facilitated to explore new clinical treatment strategies.

Identification of four-gene signature to diagnose osteoarthritis through bioinformatics and machine learning methods.

BACKGROUND: Although osteoarthritis (OA) is one of the most prevalent joint disorders, effective biomarkers to diagnose OA are still unavailable. This study aimed to acquire some key synovial biomarkers (hub genes) and analyze their correlation with immune infiltration in OA. METHODS: Gene expression profiles and clinical characteristics of OA and healthy synovial samples were retrieved from the Gene Expression Omnibus (GEO) database. Hub genes for OA were mined based on a combination of weighted gene co-expression network analysis (WGCNA), the least absolute shrinkage and selection operator (LASSO), support vector machine recursive feature elimination (SVM-RFE), and random forest (RF) algorithms. A diagnostic nomogram model for OA prediction was developed based on the hub genes. Receiver operating characteristic curves (ROC) were performed to confirm the abnormal expression of hub genes in the experimemtal and validation datasets. qRT-PCR using patients' samples were conducted as well. In addition, the infiltration level of 28 immune cells in the expression profile and their relationship with hub genes were analyzed using single-sample GSEA (ssGSEA). RESULTS: 4 hub genes (ZBTB16, TNFSF11, SCRG1 and KDELR3) were obtained by WGCNA, lasso, SVM-RFE, RF algorithms as potential biomarkers for OA. The immune infiltration analyses revealed that hub genes were most correlated with regulatory T cell and natural killer cell. CONCLUSION: A machine learning model to diagnose OA based on ZBTB16, TNFSF11, SCRG1 and KDELR3 using synovial tissue was constructed, providing theoretical foundation and guideline for diagnostic and treatment targets in OA.

Deltoid ligament (DL) repair produced better results than DL nonrepair for the treatment for rotational ankle instability.

PURPOSE: To compare the clinical and magnetic resonance imaging (MRI) results after arthroscopic deltoid ligament (DL) repair versus DL nonrepair in patients with rotational ankle instability. METHODS: All patients with rotational ankle instability were enrolled in this retrospective cohort study. Clinical evaluation was performed by the American Orthopedic Foot and Ankle Society (AOFAS) score, Karlsson Ankle Functional Score (KAFS), and Tegner activity score preoperatively and at a minimum follow-up of 2 years. MRI at follow-up was performed to evaluate the DL morphology. RESULTS: A total of 50 patients were enrolled in this study. Among them, 24 patients received DL repair (the repair group), whereas 26 patients did not (the nonrepair group). No significant difference was found in the AOFAS score (98 ± 4 vs. 97 ± 4; n.s.), KAFS (94 ± 7 vs. 93 ± 9; n.s.), or Tegner activity score (5 ± 2 vs. 5 ± 1; n.s.) between the repair group and the nonrepair group at the final follow-up. However, the repair group had a significantly shorter return-to-sport time than the nonrepair group (4.6 ± 1.6 mo vs. 6.0 ± 2.5 mo; p = 0.03). Comparison of the postoperative deltoid ligament showed that the repair group had a lower signal intensity than the nonrepair group. CONCLUSION: Arthroscopic treatment of rotational ankle instability revealed good to excellent clinical results. However, patients who underwent DL repair had a significantly earlier return to sports as well as a lower signal intensity of DL than those who did not undergo DL repair. LEVEL OF EVIDENCE: Level III.

The application of a novel hydrodynamic cavitation device to debride intra-articular monosodium urate crystals.

INTRODUCTION: Efficient and complete debridement of intra-articular deposits of monosodium urate crystals is rarely achieved by existing arthroscopic tools such as shavers or radiofrequency ablation, while cavitation technology represents a prospective solution for the non-invasive clearance of adhesions at intra-articular interfaces. METHODS: Simulation modeling was conducted to identify the optimal parameters for the device, including nozzle diameters and jet pressures. Gouty arthritis model was established in twelve rats that were equally and randomly allocated into a cavitation debridement group or a curette debridement group. A direct injection nozzle was designed and then applied on animal model to verify the effect of the cavitation jet device on the removal of crystal deposits. Image analysis was performed to evaluate the clearance efficiency of the cavitation device and the pathological features of surrounding tissue were collected in all groups. RESULTS: To maximize cavitation with the practical requirements of the operation, an experimental rig was applied, including a 1 mm direct injection nozzle with a jet pressure of 2.0 MPa at a distance of 20 mm and a nitrogen bottle as high-pressure gas source. With regards to feasibility of the device, the clearance rates in the cavitation group were over 97% and were significantly different from the control group. Pathological examination showed that the deposition of monosodium urate crystals was removed completely while preserving the normal structure of the collagen fibers. CONCLUSIONS: We developed a promising surgical device to efficiently remove intra-articular deposits of monosodium urate crystals. The feasibility and safety profile of the device were also verified in a rat model. Our findings provide a non-invasive method for the intraoperative treatment of refractory gouty arthritis.

Outcomes of a novel all-inside arthroscopic anterior talofibular ligament repair for chronic ankle instability.

PURPOSE: This study aimed to introduce a novel all-inside arthroscopic anterior talofibular ligament (ATFL) repair for chronic ankle instability (CAI) with a knotless suture anchor technique-Hugging Repair, evaluate clinical outcomes, and analyze the associated risk factors. METHODS: A total of 84 patients (42 males and 42 females, mean age: 36.1 ± 11.2 years, range: 19-68 years) who underwent Hugging Repair from January 1, 2016 to December 31, 2018, were enrolled in this retrospective study. The American Orthopedic Foot and Ankle Society (AOFAS) score, Karlsson Ankle Functional Score (KAFS), Foot and Ankle Outcome Score (FAOS), Tegner score, and Numerical Rating Scale (NRS) were evaluated pre-operatively and at final follow-up. The potential risk factors such as age, body mass index (BMI), sex, post-injury duration (time from injury to surgery), follow-up time, number of anchors, concomitant injuries [e.g., osteochondral defects (OCD), sinus tarsi syndrome (STS), anterior ankle impingement (AAI)], first-time treatment, and number of ankle sprains were also analyzed through multiple regression analysis. RESULTS: There were 68 (81%) patients followed up for a mean time of 42 (range: 35-50) months. The median AOFAS score increased from 65 (35-72) to 90 (77-100), KAFS increased from 64 (38-71) to 90 (62-100), FAOS increased from 68 (50-70) to 97 (68-100), Tegner score increased from 1 (1-3) to 4 (2-7), and NRS increased from 3.5 (2-5) to 1 (0-3). No correlation was found between the functional scores and risk factors mentioned above. In the multivariate model, age was significantly negatively associated with KAFS, FAOS, and Tegner activity scale (P = 0.013; P = 0.002; P = 0.000); female was significantly associated with poorer Tegner activity scale (P = 0.004); and the presence of concomitant injuries was significantly negatively associated with AOFAS score (P = 0.033). CONCLUSION: The novel all-inside arthroscopic ATFL repair for CAI with a knotless suture anchor technique-Hugging Repair is a safe and suitable technique that achieves satisfactory clinical outcomes and provides an effective option for the treatment of CAI. Risk factors for patients who underwent all-inside ATFL repair were older age, female sex, and concomitant injuries.

Does radiofrequency application improve function and reduce pain in patients with insertional Achilles tendinopathy? A retrospective study with a minimum 2-year follow-up.

This case series study aimed to investigate patients with insertional Achilles tendinopathy (IAT) who underwent radiofrequency (RF), how much do their patient-reported outcomes scores improve and what percentage return to sport, and what patient-related factors are associated with improved scores and increased odds of return to sport, at a minimum of 2-year follow-up. Between 2012 and 2018, 41 patients were followed up. The median Victorian Institute of Sports Assessment-Achilles (VISA-A) score increased from 20 (range, 3-62) to 97 (range, 53-100), the median 11-point visual analogue scale (VAS) reduced from 8 (range, 1-10) to 0 (range, 0-3) and the median Tenger score increased from 1 (range, 0-1) to 3 (range, 2-8). Thirty-eight (92.7%) patients returned to sports with a mean time of 11 ± 4.8 months. In linear regression analysis, age was significantly associated with return-to-sports outcome (b = -0.07, 95% CI = -0.13 to -0.02, p = 0.02), while in logistic regression, symptoms duration revealed a significant impact on pain presence (OR = 1.07, 95% CI = 1.01 to 1.14, p = 0.02). In summary, RF for IAT had a 68.7 ± 14.5 VISA-A improvement at 5.4 years of follow-up regarding reliable functional restoration and pain reduction; however, the current evidence remains insufficient to support RF as an effective treatment for IAT.

Distinct macrophage polarization in acute and chronic gout.

Macrophage polarization mediates the development of inflammatory diseases. However, the polarization status at various stages of gout is not fully understood. Our study aimed to define the evolution of macrophage polarization in acute and chronic gout. Normal human synovium and synovium with tophi were collected for immunofluorescence (IF). Rat gouty joints were collected for joint thickness assessment and pathological evaluation. Tissue mRNA expression of inducible nitric oxide synthase (iNOS) and arginase-1 (Arg-1) were evaluated. Mouse peritoneal macrophages and THP-1 derived macrophages were stimulated by monosodium urate (MSU) crystals and were collected for detection of interleukin (IL) -1ß and IL-37 levels and iNOS/Arg-1 ratio. Arg-1 and IL-37 were highly expressed in normal synovium and synovium with tophi. In rat gouty joints, the inflammatory cell counts and ankle thickness began to increase at 2 h, peaked at 24 h, and was decreased spontaneously. An increase in macrophages preceded the neutrophils infiltration. Infiltration of M1 was positively related with the severity of arthritis. M2 appeared in an early stage (at 2 h) of inflammation. The number of M1 macrophages was comparable to that of M2 from 2 to 12 h and exceeded M2 number at 18 h and 24 h. The ratios of M2/M1 reversed at 48 h and remained reversed until 120 h. In mice gouty joints, iNOS/Arg-1 mRNA ratio was significantly higher than the that in control group at 8 h. The proportion of neutrophils and M1-macrophages reached peak at 4 h in mice model with peritoneal gout. Concentration of IL-1ß and ratio of iNOS/Arg-1 were increased at 6 h, peaked at 48 h, and were then decreased at 72 h in vitro, while the concentration of IL-37 peaked at 2 h and then decreased. In summary, altered macrophage polarization was observed in various stages of gouty inflammation. Macrophages in acute gout were polarized into M1 at early stage and into M2 at later stage while the macrophages in chronic gout mainly were only polarized towards M2. The number of M1 rose with the progression of inflammation. Early increase of M2 was observed, which might be generated directly from M0.

IL-37 blocks gouty inflammation by shaping macrophages into a non-inflammatory phagocytic phenotype.

OBJECTIVE: Interleukin (IL)-37 is a natural suppressor of inflammation. Macrophages play an important role in acute gout flare by dominating the inflammation and spontaneous relief. We have reported that IL-37 could limit runaway inflammation in gout. Here we focus on whether IL-37 inhibits gouty inflammation by altering macrophage functions, and how it does so. METHODS: Macrophage functions were evaluated in terms of phagocytosis, pyroptosis, polarization and metabolism. Phagocytosis and polarization of macrophages were detected by side scattering and double-labelling induced nitrogen monoxide synthase (iNOS)/arginase-1 (Arg-1) using flow cytometry, respectively. Transcription of pyroptosis-related molecules was detected by qPCR. Metabolomics was performed by liquid chromatograph mass spectrometer. Human IL-37 knock-in mice and a model with point mutation (S9A) at mouse Gsk3b locus were created by CRISPR/Cas-mediated genome engineering. MSU was injected into the paws and peritoneal cavity to model acute gout. Vernier calliper was used to measure the thickness of the paws. The mice paws and human synovium tissues or tophi were collected for pathological staining. Peritoneal fluid of mice was used to enrich macrophages to detect polarization. RESULTS: IL-37 promoted non-inflammatory phagocytic activity of macrophages by enhancing phagocytosis of MSU, reducing transcription of pyroptosis-related proteins and release of inflammatory cytokines, protecting mitochondrial function, and mediating metabolic reprogramming in MSU-treated THP-1 cells. These multifaceted roles of IL-37 were partly depended on the mediation of glycogen synthase kinase-3ß (GSK-3ß). CONCLUSIONS: Our study revealed that IL-37 could shape macrophages into a 'silent' non-inflammatory phagocytic fashion. IL-37 may become a potentially valuable treatment option for patients of chronic gout, especially for those with tophi.

Cartilage Matrix Changes in Hindfoot Joints in Chronic Ankle Instability Patients After Anatomic Repair Using T2-Mapping: Initial Experience With 3-Year Follow-Up.

BACKGROUND: Anatomic repair is widely accepted as the primary surgical treatment for chronic lateral ankle instability (CLAI). T2-mapping is a powerful tool for quantitative assessment of biochemical changes in cartilage matrix. PURPOSE: To longitudinally evaluate cartilage matrix changes in the hindfoot joints of CLAI patients before and after anatomic repair by using T2-mapping with magnetic resonance imaging (MRI). STUDY TYPE: Prospective. SUBJECTS: Thirty-two CLAI patients (males/females = 20/12) and 21 healthy controls (males/females = 13/7). FIELD STRENGTH/SEQUENCE: 3 T; sagittal multi-echo spin-echo technique (T2-mapping), coronal, sagittal, and axial spin-echo PD-FS, and sagittal T1WI sequences. ASSESSMENT: MRI examinations were performed in CLAI patients at baseline (prior to surgery) and 3 years after anatomic repair and in healthy controls. On T2-maps, the hindfoot joints were segmented into 16 cartilage subregions. The T2 value of each subregion was measured. All patients were evaluated with the American Orthopedic Foot and Ankle Society (AOFAS) scale at baseline and after surgery. STATISTICAL TESTS: Analysis of variance (ANOVA) and Student's t-test were used. The differences corresponding to P < 0.05 were considered statistically significant. RESULTS: At baseline, the T2 values in most cartilage subregions of talar dome and medial posterior subtalar joint (pSTJ) were higher in CLAI patients than in healthy controls. After surgery, only the T2 value of anteriomedial talar dome decreased from that at baseline (31.11 ± 3.88 msec vs. 34.27 ± 5.30 msec). The T2 values of other subregions with elevated T2 values remained higher than healthy controls. There were no significant differences in T2 values in the midtarsal joints between CLAI patients and healthy controls (P = 0.262, 0.104, 0.169, 0.103). Postoperatively, the patients' AOFAS scores improved significantly from 67.81 to 89.13. DATA CONCLUSION: CLAI patients exhibited elevated T2 values in most subregions of talar dome and medial pSTJ. After anatomic repair, although the patients exhibited good clinical outcomes, the elevated T2 values could not be fully recovered. LEVEL OF EVIDENCE: 2 TECHNICAL EFFICACY STAGE: 4.

The anterior talofibular ligament-posterior talofibular ligament angle decreased after ankle lateral stabilization surgery.

PURPOSE: The angle between the anterior talofibular ligament (ATFL) and the posterior talofibular ligament (PTFL) is increased in patients with chronic ATFL injury. This study aimed to compare the AFTL-PTFL angle before versus after ankle lateral stabilization surgery, and to evaluate whether the ATFL-PTFL angle correlates with the ligament injury severity. METHODS: This retrospective study included 48 patients with mechanical ankle instability treated between 2016 and 2018. After arthroscopic evaluation, all patients underwent ankle lateral stabilization surgery comprising ligament repair (n = 28) or reconstruction (n = 20). The ATFL-PTFL angle was measured in the axial plane on pre- and postoperative MRI. Comparisons were made of the pre- versus postoperative ATFL-PTFL angles, and the ATFL-PTFL angle of the repair versus reconstruction groups. Receiver operating characteristic (ROC) curve analysis was used to assess the diagnostic performance of the ATFL-PTFL angle in selecting the surgical technique. RESULTS: The postoperative ATFL-PTFL angle was significantly decreased compared with preoperatively. The ATFL-PTFL angle was significantly smaller in the repair group than the reconstruction group preoperatively and postoperatively. The area under the ROC curve was 0.741 (P < 0.01). The optimal cutoff point for the selection of ligament reconstruction was an ATFL-PTFL angle of 89.4° (sensitivity 0.85, specificity 0.61). CONCLUSION: The ATFL-PTFL angle decreases after ankle lateral stabilization surgery. The ATFL-PTFL angle is related to the severity of the ATFL injury. Ankle lateral ligament reconstruction should be considered when the ATFL-PTFL angle is > 89.4°. LEVEL OF EVIDENCE: Level III.

Knotless anchor repair produced similarly favourable outcomes as knot anchor repair for anterior talofibular ligament repair.

PURPOSE: To compare clinical function after knot anchor versus knotless anchor repair of the anterior talofibular ligament (ATFL) in patients with chronic lateral ankle instability. METHODS: All patients who underwent arthroscopic surgical ATFL repair using knot or knotless suture anchors were included in this study. Functional scores (American Orthopedic Foot and Ankle Society (AOFAS), Karlsson score and Tegner activity scores) and magnetic resonance imaging (MRI) were used to evaluate the ankle with a follow-up of at least 2 years. RESULTS: A total of 52 patients with chronic ankle instability were included in this study. Among these patients, 23 patients underwent one knot anchor repair procedure (Group A), and the other 29 patients underwent one knotless anchor repair procedure (Group B). At the final follow-up, there were no significant differences between Group A and Group B regarding the AOFAS score (89 ± 9 vs 84 ± 11; ns), Karlsson score (82 ± 14 vs 75 ± 18; ns), or Tegner activity score (4 ± 1 vs 4 ± 2; ns). There also were no significant differences in the mean ATFL signal-noise ratio (SNR) value (7.5 ± 4.4 vs 7.3 ± 2.9; ns) or ATFL angle (82° ± 7° vs 84° ± 9°; ns) between the groups. CONCLUSION: When compared with knot repair, knotless repair of the lateral ankle ligament produced similar functional outcomes. LEVEL OF EVIDENCE: III.

Anterior talofibular ligament (ATFL) repair using two suture anchors produced better functional outcomes than using one suture anchor for the treatment of chronic lateral ankle instability.

PURPOSE: To compare the function and activity level after one-anchor repair versus two-anchor repair of the anterior talofibular ligament (ATFL) in patients with chronic lateral ankle instability. METHODS: All patients who underwent arthroscopic surgical ATFL repair using suture anchors were included in this study. The American Orthopedic Foot and Ankle Society (AOFAS) score, Karlsson Ankle Functional Score (Karlsson score) and Tegner activity score were used to evaluate ankle function at a follow-up of a minimum of 2 years. A magnetic resonance imaging (MRI) scan was performed to evaluate the repaired ATFL. RESULTS: A total of 51 patients with chronic ankle instability were included in this study. Among them, 20 patients accepted a one-anchor repair procedure (one-anchor group), and the other 31 patients accepted a two-anchor repair procedure (two-anchor group). At the final follow-up, there was no significant difference in the AOFAS score between the one-anchor group and the two-anchor group (90 ± 9 vs 91 ± 10; ns). However, the mean Karlsson score of the two-anchor group (88 ± 12) was significantly higher than that of the one-anchor group (80 ± 14) (p = 0.04). There was a significant difference in activity level as measured by the Tegner activity score (5 ± 1 vs 4 ± 1; p < 0.001) between the two-anchor group and the one-anchor group after surgery. Patients in the two-anchor group (68%) had a significantly higher percentage of sport participation compared to those in the one-anchor group (30%) (p = 0.01). CONCLUSION: Compared with a one-anchor repair, a two-anchor repair of the lateral ankle ligament produced better functional outcomes. Arthroscopic ATFL repair with two anchors provided a minimally invasive technique with a higher rate of return to sports than repair with one anchor. The present study showed its clinical relevance by maintaining the advantage of ATFL repair using two anchors regarding the clinical function. LEVEL OF EVIDENCE: III.

Increased ATFL-PTFL angle could be an indirect MRI sign in diagnosis of chronic ATFL injury.

PURPOSE: Magnetic resonance imaging (MRI) has relatively low accuracy in diagnosing chronic anterior talofibular ligament (ATFL) injury. This study's purpose was to evaluate the angle between the ATFL and posterior talofibular ligament (PTFL) as a new indirect MRI sign of chronic ATFL injury in patients with mechanical ankle instability (MAI). METHODS: This study included 200 participants: 105 patients with MAI and 95 patients seen at our institution for reasons unrelated to ankle instability. MR images of all 200 participants were reviewed. The ATFL-PTFL angle in the axial plane was measured and compared between groups. Receiver operating characteristic curves (ROC) were used to analyze ATFL-PTFL angles in participants with and without ATFL injury. The sensitivity and specificity of this method for diagnosing ATFL injury were calculated. RESULTS: The mean ATFL-PTFL angle was significantly larger among MAI patients than among control patients (81.5° ± 9.8° vs 75.2° ± 8.9°, respectively; P < 0.01). The area under the ROC was 0.789 (P < 0.01). The optimal cut-off point for diagnosing ATFL injury on the basis of the ATFL-PTFL angle was 79.0° (sensitivity 0.89, specificity 0.67). CONCLUSION: The ATFL-PTFL angle was significantly larger among MAI patients than among those without MAI. Increased ATFL-PTFL angle offers a new indirect MRI sign for diagnosing chronic ATFL injury. The ATFL-PTFL angle can be used not only to improve the accuracy of diagnosis of chronic ATFL injury, but also to evaluate the restoration of normal ankle joint geometry after lateral ligament reconstruction. LEVEL OF EVIDENCE: III.