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Mesenchymal stem cells (MSCs) are expected to be useful therapeutics in osteoarthritis (OA), the most common joint disorder characterized by cartilage degradation. However, evidence is limited with regard to cartilage repair in clinical trials because of the uncontrolled differentiation and weak cartilage-targeting ability of MSCs after injection. To overcome these drawbacks, here we synthesized CuO@MSN nanoparticles (NPs) to deliver Sox9 plasmid DNA (favoring chondrogenesis) and recombinant protein Bmp7 (inhibiting hypertrophy). After taking up CuO@MSN/Sox9/Bmp7 (CSB NPs), the expressions of chondrogenic markers were enhanced while hypertrophic markers were decreased in response to these CSB-engineered MSCs. Moreover, a cartilage-targeted peptide (designated as peptide W) was conjugated onto the surface of MSCs via a click chemistry reaction, thereby prolonging the residence time of MSCs in both the knee joint cavity of mice and human-derived cartilage. In a surgery-induced OA mouse model, the NP and peptide dual-modified W-CSB-MSCs showed an enhancing therapeutic effect on cartilage repair in knee joints compared with other engineered MSCs after intra-articular injection. Most importantly, W-CSB-MSCs accelerated cartilage regeneration in damaged cartilage explants derived from OA patients. Thus, this new peptide and NPs dual engineering strategy shows potential for clinical applications to boost cartilage repair in OA using MSC therapy.

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Use of SPECT/CT (Single Photon Emission Computed Tomography/Computed Tomography) is increasing providing additional information in patients with inconclusive clinical examination and unremarkable imaging findings presenting with chronic pain after total ankle arthroplasty. To differentiate the cause of pain after total ankle arthroplasty can be challenging. SPECT/CT combines structural and metabolic imaging as a hybrid tool leading to higher specificity and overall diagnostic accuracy presumably in cases of gutter impingement, prosthetic loosening, and osteoarthritis of adjacent joints. Moreover, SPECT/CT can complement diagnostic work up in periprosthetic joint infections. Basal tracer enhancement has to be considered for the interpretation of imaging findings.

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Weight-bearing computed tomography has multiple advantages in evaluating the hindfoot and ankle. It can assess hindfoot and ankle alignment, pathology in ankle arthritis, and complications related to total ankle replacements. It is an essential tool in ankle osteoarthritis diagnostic, preoperative planning, and total ankle replacement outcomes. It allows for better accuracy and reproducibility of alignment and implant size. In addition, it has the potential to more assertively detect complications related to weight bearing.

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BACKGROUND: This study aimed to explore the awareness, experiences, and beliefs of individuals with osteoarthritis (OA) regarding their healthcare management, along with assessing their overall satisfaction levels. METHODS: A cross-sectional online survey was conducted in Italy, Sweden, and Russia, rigorously developed based on OA international guidelines in collaboration with healthcare professionals and individuals with OA. Participants over 40 years of age with self-reported hip and/or knee OA were eligible. The analytical framework included descriptive analysis (assessment of awareness levels for 'recommended', 'optional', and 'not recommended' treatments), analysis of suggested treatments and taken treatments, exploration of beliefs, barriers and satisfaction analysis (0-100 scale). RESULTS: A total of 401 participants (mean age: 59.7, 78.3% female, 28% Italian, 49% Swedish, 23% Russian) contributed to the study. In Sweden, 57%-72% accurately identified recommended treatments, while in Russia, the range was 34%-91%, and in Italy, it was 35%-73%. The predominant suggested and taken treatments were oral anti-inflammatory drugs in Italy (87/81%) and Russia (97/97%) and specific exercise in Sweden (84/79%). Notably, only Sweden reached a consensus on the effectiveness of exercise for everyone, while Russia and Italy insisted on radiographic findings as a prerequisite for exercise. Mean satisfaction levels were 59.7 (Italy), 47.4 (Sweden), and 35.2 (Russia). CONCLUSIONS: This study uncovered variations in awareness, treatment preferences, and beliefs among the three countries, underscoring the necessity for tailored education on OA management that accounts for regional differences across Europe.

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Recent evidence indicates that the damaged regions in osteoarthritis are accompanied by the accumulation of iron ions. Ferroptosis, as an iron-dependent form of cell death, holds significant implications in osteoarthritis. Melatonin, a natural product with strong scavenging abilities against reactive oxygen species and lipid peroxidation, plays a crucial role in the treatment of osteoarthritis. This study aims to demonstrate the existence of ferroptosis in osteoarthritis and explore the specific mechanism of melatonin in suppressing ferroptosis and alleviating osteoarthritis. Our findings reveal that melatonin reverses inflammation-induced oxidative stress and lipid peroxidation while promoting the expression of extracellular matrix components in chondrocytes, safeguarding the cells. Our research has revealed that NADPH oxidase 4 (NOX4) serves as a crucial molecule in the ferroptosis process of osteoarthritis. Specifically, NOX4 is located on mitochondria in chondrocytes, which can induce disorders in mitochondrial energy metabolism and dysfunction, thereby intensifying oxidative stress and lipid peroxidation. LC-MS analysis further uncovered that GRP78 is a downstream binding protein of NOX4. NOX4 induces ferroptosis by weakening GRP78's protective effect on GPX4 and reducing its expression. Melatonin can inhibit the upregulation of NOX4 on mitochondria and mitigate mitochondrial dysfunction, effectively suppressing ferroptosis and alleviating osteoarthritis. This suggests that melatonin therapy represents a promising new approach for the treatment of osteoarthritis.

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The role of mitochondria in the pathogenesis of osteoarthritis (OA) is significant. In this study, we aimed to identify diagnostic signature genes associated with OA from a set of mitochondria-related genes (MRGs). First, the gene expression profiles of OA cartilage GSE114007 and GSE57218 were obtained from the Gene Expression Omnibus. And the limma method was used to detect differentially expressed genes (DEGs). Second, the biological functions of the DEGs in OA were investigated using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Wayne plots were employed to visualize the differentially expressed mitochondrial genes (MDEGs) in OA. Subsequently, the LASSO and SVM-RFE algorithms were employed to elucidate potential OA signature genes within the set of MDEGs. As a result, GRPEL and MTFP1 were identified as signature genes. Notably, GRPEL1 exhibited low expression levels in OA samples from both experimental and test group datasets, demonstrating high diagnostic efficacy. Furthermore, RT-qPCR analysis confirmed the reduced expression of Grpel1 in an in vitro OA model. Lastly, ssGSEA analysis revealed alterations in the infiltration abundance of several immune cells in OA cartilage tissue, which exhibited correlation with GRPEL1 expression. Altogether, this study has revealed that GRPEL1 functions as a novel and significant diagnostic indicator for OA by employing two machine learning methodologies. Furthermore, these findings provide fresh perspectives on potential targeted therapeutic interventions in the future.

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The rapid advancement of cell therapies underscores the importance of understanding fundamental cellular attributes. Among these, cell fitness-how transplanted cells adapt to new microenvironments and maintain functional stability in vivo-is crucial. This study identifies a chemical compound, FPH2, that enhances the fitness of human chondrocytes and the repair of articular cartilage, which is typically nonregenerative. Through drug screening, FPH2 was shown to broadly improve cell performance, especially in maintaining chondrocyte phenotype and enhancing migration. Single-cell transcriptomics indicated that FPH2 induced a super-fit cell state. The mechanism primarily involves the inhibition of carnitine palmitoyl transferase I and the optimization of metabolic homeostasis. In animal models, FPH2-treated human chondrocytes substantially improved cartilage regeneration, demonstrating well-integrated tissue interfaces in rats. In addition, an acellular FPH2-loaded hydrogel proved effective in preventing the onset of osteoarthritis. This research provides a viable and safe method to enhance chondrocyte fitness, offering insights into the self-regulatory mechanisms of cell fitness.

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BACKGROUND: The pathogenesis of osteoarthritis (OA) involves the progressive degradation of articular cartilage. Exosomes derived from mesenchymal stem cells (MSC-EXOs) have been shown to mitigate joint pathological injury by attenuating cartilage destruction. Optimization the yield and therapeutic efficacy of exosomes derived from MSCs is crucial for promoting their clinical translation. The preconditioning of MSCs enhances the therapeutic potential of engineered exosomes, offering promising prospects for application by enabling controlled and quantifiable external stimulation. This study aims to address these issues by employing pro-inflammatory preconditioning of MSCs to enhance exosome production and augment their therapeutic efficacy for OA. METHODS: The exosomes were isolated from the supernatant of infrapatellar fat pad (IPFP)-MSCs preconditioned with a pro-inflammatory factor, TNF-α, and their production was subsequently quantified. The exosome secretion-related pathways in IPFP-MSCs were evaluated through high-throughput transcriptome sequencing analysis, q-PCR and western blot analysis before and after TNF-α preconditioning. Furthermore, exosomes derived from TNF-α preconditioned IPFP-MSCs (IPFP-MSC-EXOsTNF-α) were administered intra-articularly in an OA mouse model, and subsequent evaluations were conducted to assess joint pathology and gait alterations. The expression of proteins involved in the maintenance of cartilage homeostasis within the exosomes was determined through proteomic analysis. RESULTS: The preconditioning with TNF-α significantly enhanced the exosome secretion of IPFP-MSCs compared to unpreconditioned MSCs. The potential mechanism involved the activation of the PI3K/AKT signaling pathway in IPFP-MSCs by TNF-α precondition, leading to an up-regulation of autophagy-related protein 16 like 1(ATG16L1) levels, which subsequently facilitated exosome secretion. The intra-articular administration of IPFP-MSC-EXOsTNF-α demonstrated superior efficacy in ameliorating pathological changes in the joints of OA mice. The preconditioning of TNF-α enhanced the up-regulation of low-density lipoprotein receptor-related protein 1 (LRP1) levels in IPFP-MSC-EXOsTNF-α, thereby exerting chondroprotective effects. CONCLUSION: TNF-α preconditioning constitutes an effective and promising method for optimizing the therapeutic effects of IPFP-MSCs derived exosomes in the treatment of OA.

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BACKGROUND: Osteoarthritis (OA) is a degenerative osteoarticular disease, involving genetic predisposition. How the risk variants confer the risk of OA through their effects on proteins remains largely unknown. Therefore, we aimed to discover new and effective drug targets for OA and its subtypes. METHODS: A proteome-wide association study (PWAS) was performed based on OA and its subtypes genome-wide association studies (GWAS) summary datasets and the protein quantitative trait loci (pQTL) data. Subsequently, Mendelian randomization (MR) and colocalization analysis was conducted to estimate the associations between protein and OA risk. The replication analysis was performed in an independent dataset of human plasma pQTL data. RESULTS: The abundance of seven proteins was causally related to OA, two proteins to knee OA and six proteins to hip OA, respectively. We replicated 2 of these proteins using an independent pQTL dataset. With the further support of colocalization, and higher ECM1 level was causally associated with a higher risk of OA and hip OA. Higher PCSK1 level was causally associated with a lower risk of OA. And higher levels of ITIH1, EFEMP1, and ERLEC1 were associated with decreased risk of hip OA. CONCLUSION: Our study provides new insights into the genetic component of protein abundance in OA and a promising therapeutic target for future drug development.

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Osteoarthritis (OA) is a complex and common condition, especially affecting the knees due to their weight-bearing role. Traditionally seen as a degenerative disease, OA is now understood to have both mechanical and inflammatory causes. Despite its increasing prevalence, there is limited data on OA in Indonesia, resulting in low awareness among clinicians and the public. The aim of this study was to describe the OA burden in Indonesia, focusing on its prevalence, incidence, and years lived with disability (YLD) from 1990 to 2019, using data from the Global Burden of Disease (GBD) study 2019. A descriptive cross-sectional study was conducted to examine the prevalence, incidence, and YLD of OA in Indonesia from the GBD study 2019. OA prevalence and YLD were compared to other countries according to similar social demographics and geographical proximity. OA YLD was also compared to the top causes of death and disability YLD in Indonesia. The study found that OA cases in Indonesia more than doubled from 1990 to 2019, with increases of 153.12% in males and 143.36% in females. Similar trends were observed for knee OA. The age-standardized prevalence rate in Indonesia increased by 11.03% in males and 8.42% in females, and these were higher compared to China, India, Singapore, and the global average. Younger people had a higher OA prevalence rate growth than older groups. The incidence rate for OA also rose significantly, with males seeing a 10.89% increase to 290 per 100,000 people and females with an 8.57% increase to 384 per 100,000 people. Despite lower overall burden rates compared to some countries, Indonesia experienced significant growth in YLD due to OA (12.16% in males and 9.65% in females) since 1990. Although OA was less burdensome than stroke, diabetes, low back pain, and chronic obstructive pulmonary disease (COPD), its YLD growth rate was higher. In conclusion, OA prevalence and incidence in Indonesia significantly increased from 1990 to 2019, with a notable rise among younger populations. OA had a higher YLD growth compared to several other major diseases in Indonesia, highlighting the need for early detection and preventive measures, particularly for the younger population.

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BACKGROUND: It is currently unknown to what degree surgical or nonoperative treatment of acromioclavicular (AC) dislocation influences the development of osteoarthritis (OA). The aim of this study was to evaluate AC OA after surgical and nonoperative treatment for AC dislocations, compare OA prevalence between treatment options, and compare OA prevalence between the injured and contralateral shoulder. METHODS: Articles reporting on the prevalence of OA after surgical or nonoperative treatment of an AC dislocation with a minimal 2-year follow-up were included. AC OA presence was extracted for the injured and contralateral shoulder. Treatment categories were defined based on anatomical variation in the reattachment of ligaments: AC fixation, coracoclavicular (CC) fixation, AC and CC fixation, Bosworth screw synthetic graft, tendon graft, and conservative. Study quality was assessed using the Methodological Index for Non-Randomized Studies (MINORS) criteria. RESULTS: Ninety-four articles were included for qualitative analysis, and 7 articles were included for meta-analysis (n = 3,812; follow-up = 2.0-24.2 years; mean age 37.6 ± 10.4 years). A total of 3,483 patients underwent surgical treatment, and 329 patients underwent conservative treatment. OA prevalence ranged from 6.7%-29.3% between 7 pooled treatment categories. Most included studies had a follow-up <10 years (94%) and OA prevalence increased with time, regardless of treatment option. There was no difference in OA prevalence between the injured and contralateral shoulder (p = 0.120). MINORS scores were varied, ranging from poor to very good. CONCLUSION: The pooled AC OA prevalence of the 7 treatment categories ranged from 6.7% for the CC fixation surgical group to 29.3% for the conservative treatment group. However, the included studies were predominantly of low quality and had varying follow-up periods, with most having relatively short follow-up durations. No difference in AC OA prevalence was found between the injured and contralateral shoulder. Based on the available evidence, treatment choice for AC dislocation should not be influenced by the potential development of AC AO. LEVEL OF EVIDENCE: Level IV. See Instructions for Authors for a complete description of levels of evidence.

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INTRODUCTION: Osteoarthritis (OA) is a progressive degenerative disease characterized by the gradual degradation of cartilage, remodeling of subchondral bone, synovitis, and chronic pain. This condition impacts various large and small joints, including the temporomandibular joint (TMJ). However, addressing OA, particularly in impeding or reducing disease progression, is challenging due to its clinical and imaging heterogeneity. Authors are increasingly suggesting that this heterogeneity involves different phenotypes or subpopulations, discernible by variations in the disease's pathophysiology and structural manifestations. Even within the TMJ, these phenotypes may display distinct clinical features, laboratory parameters, biochemical markers, and imaging criteria. Recent research has proposed MRI as a reference standard for TMJ OA, highlighting its substantial agreement with histopathological changes. MRI-based phenotypes offer a promising avenue for understanding disease progression and treatment response, potentially providing valuable insights for prognosis and treatment planning. OBJECTIVE: This article introduces the ROAMES-TMJ (Rapid OsteoArthritis MRI Eligibility Score for TMJ) to assess the structural eligibility of individuals for inclusion in TMJ OA clinical trials.

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Articular cartilage phenotypic homeostasis is crucial for life-long joint function, but the underlying cellular and molecular mechanisms governing chondrocyte stability remain poorly understood. Here, we show that the protein tyrosine phosphatase SHP2 is differentially expressed in articular cartilage (AC) and growth plate cartilage (GPC) and that it negatively regulates cell proliferation and cartilage phenotypic program. Postnatal SHP2 deletion in Prg4+ AC chondrocytes increased articular cellularity and thickness, whereas SHP2 deletion in Acan+ pan-chondrocytes caused excessive GPC chondrocyte proliferation and led to joint malformation post-puberty. These observations were verified in mice and in cultured chondrocytes following treatment with the SHP2 PROTAC inhibitor SHP2D26. Further mechanistic studies indicated that SHP2 negatively regulates SOX9 stability and transcriptional activity by influencing SOX9 phosphorylation and promoting its proteasome degradation. In contrast to published work, SHP2 ablation in chondrocytes did not impact IL-1-evoked inflammation responses, and SHP2's negative regulation of SOX9 could be curtailed by genetic or chemical SHP2 inhibition, suggesting that manipulating SHP2 signaling has translational potential for diseases of cartilage dyshomeostasis.

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The extracellular matrix of cartilage primarily constitutes of collagen and aggrecan. Cartilage degradation starts with aggrecan loss in osteoarthritis (OA). Vitamin D (VD) plays an essential role in several inflammation-related diseases and can protect the collagen in cartilage during OA. The present study focused on the role of VD in aggrecan turnover of human articular chondrocytes treated with tumor necrosis factor α (TNF-α) and the possible mechanism. Treatment with different doses of VD and different periods of intervention with TNF-α and TGF-ß1 receptor (TGFßR1) inhibitor SB525334 were investigated. The viability of human chondrocytes and extracellular secretion of TGF-ß1 were measured. The expression of intracellular TGFßR1 and VD receptor was examined. Transcriptional and translational levels of aggrecan and the related metabolic factors were analyzed. The results showed that TNF-α markedly reduced the viability, TGFßR1 expressions and aggrecan levels of human chondrocytes, and increased disintegrin and metalloproteinase with thrombospondin motifs. The alterations were partially inhibited by VD treatment. Furthermore, the effects of VD were blocked by the TGFßR1 inhibitor SB525334 in TNF-α-treated cells. VD may prevent proteoglycan loss due to TNF-α via TGF-ß1 signaling in human chondrocytes.

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The management of rheumatic diseases has noticeably changed in recent years with the development of targeted therapeutic agents, namely, biological disease-modifying antirheumatic drugs. Identifying essential signaling pathways and factors crucial for the development and progression of these diseases remains a significant challenge. Therapy could be used to delay the onset or reduce harm. The endocannabinoid system's presence within the synovium can be identified as a suggested target for therapeutic interventions due to its role in modulating pain, inflammation, and joint metabolism. This review brings together the most pertinent information concerning the actions of the endocannabinoid system present in inflamed synovial tissue and its interaction with phytocannabinoids and synthetic cannabinoids, which can be used from a therapeutic perspective to minimize the inflammatory and pain processes typical of osteoarthritis and rheumatoid arthritis.

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Articular cartilage receives nutrients and oxygen from the synovial fluid to maintain homeostasis. However, compared to tissues with abundant blood flow, articular cartilage is exposed to a hypoxic environment (i.e., physioxia) and has an enhanced hypoxic stress response. Hypoxia-inducible factors (HIFs) play a pivotal role in this physioxic environment. In normoxic conditions, HIFs are downregulated, whereas in physioxic conditions, they are upregulated. The HIF-α family comprises three members: HIF-1α, HIF-2α, and HIF-3α. Each member has a distinct function in articular cartilage. In osteoarthritis, which is primarily caused by degeneration of articular cartilage, HIF-1α is upregulated in chondrocytes and is believed to protect articular cartilage by acting anabolically on it. Conversely, in contrast to HIF-1α, HIF-2α exerts a catabolic influence on articular cartilage. It may therefore be possible to develop a new treatment for OA by controlling the expression of HIF-1α and HIF-2α with drugs or by altering the oxygen environment in the joints.

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Osteoarthritis (OA) is an age-related disease characterized by inflammation, pain, articular cartilage damage, synovitis, and irreversible disability. Gynostemma pentaphyllum (Thunb.) Makino (GP), a herbal medicine traditionally used in East Asia for its anti-inflammatory properties, was investigated for its potential to modulate OA pathology and symptoms. This study evaluated GP's efficacy in inhibiting pain, functional decline, and cartilage destruction in monosodium iodoacetate-induced OA and acetic acid-induced writhing models. Additionally, the effects of GP on OA-related inflammatory targets were assessed via mRNA and protein expression in rat knee cartilage and lipopolysaccharide-induced RAW 264.7 cells. The GP group demonstrated significant pain relief, functional improvement, and cartilage protection. Notably, GP inhibited key inflammatory mediators, including interleukin (IL)-1ß, IL-6, matrix metalloproteinases (MMP)-3 and MMP-13, cyclooxygenase-2, and prostaglandin E receptor 2, surpassing the effects of active controls. These findings suggest that GP is a promising candidate for disease-modifying OA drugs and warrants further comprehensive studies.

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BACKGROUND: Despite improved visualization, the use of arthroscopic surgery to perform the Latarjet procedure has not decreased the rates of complications and glenohumeral osteoarthritis (OA) in the long term. Many of the reported complications are related to the use of screws for bone block fixation with freehand drilling. PURPOSE: To evaluate the long-term (at a minimum 10-year follow-up) clinical and radiological outcomes of the arthroscopic Bristow-Latarjet procedure using a posterior guided drilling technique and suture button for coracoid bone graft fixation. STUDY DESIGN: Case series; Level of evidence, 4. METHODS: Consecutive patients who underwent the arthroscopic Bristow-Latarjet procedure with suture button fixation between 2011 and 2013 were reviewed by 2 independent evaluators. Complications and revision surgery were recorded, and we evaluated patient-reported outcomes including subjective scores, recurrence of shoulder instability (dislocation or subluxation), range of motion limitations, and return to sports. Patients had radiographs taken at least 10 years after surgery to assess glenohumeral OA according to the Samilson-Prieto classification system and computed tomography scans to assess bone block positioning and healing. RESULTS: A total of 65 consecutive patients (68 shoulders) with a mean follow-up of 135 months (range, 120-156 months) were included. The mean age at the time of surgery was 25 ± 8 years; 7 patients had previous failed Bankart repair. At follow-up, 94% (64/68) of the shoulders had no recurrence of instability. The 4 cases of instability recurrence were traumatic and occurred at 3 weeks (a fall), 4 months, 2 years, and 7 years after surgery. No hardware failures, coracoid fractures, or neurological complications were observed. Overall, 61 patients (94%) were still participating in sports, with 44 (68%) at the same or higher level. Range of motion showed nonsignificant restrictions in external rotation with the arm at the side (7° ± 9°) and with the arm at 90° of abduction (9° ± 10°) compared with the contralateral side. Additionally, 11 shoulders (16%) had some residual anterior apprehension on clinical examination. At last follow-up, 77% (47/61) of the shoulders had no OA development or progression. Previous failed Bankart repair was a risk factor for the development of OA. Patients with OA had significantly lower Subjective Shoulder Value scores (79% vs 91%, respectively; P = .01) and decreased external rotation with the arm at the side (40° vs 65°, respectively; P = .001) compared with patients with no or little OA. CONCLUSION: The arthroscopically guided Bristow-Latarjet procedure with suture button fixation is a safe and durable surgical treatment method for recurrent anterior shoulder instability, allowing a high rate of return to sports without significant motion restrictions and no or little OA in the long term.

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BACKGROUND: High ankle sprains are common athletic injuries and can be associated with long-term sequelae. Regardless of operative or nonoperative treatment, there is a paucity of data in the literature about the long-term outcomes of high ankle sprains. HYPOTHESIS: Nonoperative treatment of high ankle sprains utilizing a standardized protocol will result in good long-term outcomes. STUDY DESIGN: Case series; Level of evidence, 4. METHODS: Patients who experienced a high ankle sprain without radiographic diastasis of the syndesmosis were identified from a previous study database and contacted for long-term follow-up. All patients were high school or National Collegiate Athletic Association Division IA athletes at initial injury and were treated nonoperatively with the same standardized protocol. Patients completed a questionnaire that included documentation of any interim ankle injuries, 2 different patient-reported outcome scores, and ankle radiographs to conduct Kellgren-Lawrence scoring for ankle osteoarthritis. RESULTS: In total, 76 cases in 74 patients were identified in the database. A total of 40 patients were successfully contacted, and 31 patients (24 collegiate and 7 high school athletes) with 33 high ankle sprains completed the survey (31/40; 77.5%). The mean age at follow-up was 45 years (range, 34-50 years), with a mean time from injury to follow-up of 25 years. Overall, 93.5% (n = 29) of the respondents were male, and 42% (n = 13) of the respondents reported an ipsilateral ankle injury since their initial injury, with 16% (n = 5) having ankle or Achilles surgery. The mean Patient-Reported Outcomes Measurement Information System-10 score was 53.4 (SD, 8.3; range, 37.4-67.7), PROMIS median (IQR), 54.1 (39.9, 68.3), and the mean Self-reported Foot and Ankle Score score was 42.7 (SD, 5.86). Follow-up ankle radiographs were obtained in 11 (35%) of the respondents; 27% had Kellgren-Lawrence grade >2 osteoarthritis, and 36% had signs of heterotopic ossification on imaging. The mean tibiofibular clear space was 4.5 mm, and the mean tibiofibular overlap was 7.15 mm, with 27% of patients demonstrating some tibiotalar narrowing. CONCLUSION: At long-term follow-up, nonoperative management of high ankle sprains without diastasis on imaging was associated with acceptable patient-reported functional outcomes and low rates of subsequent ankle injuries. There was a high incidence of arthritis, but most cases were not clinically significant. This case series shows the natural history of nonoperatively treated high ankle sprains and may serve as a comparison for different management techniques in the future.

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