We retrospectively reviewed 21 patients (22 shoulders) who presented with deep infection after surgery to the shoulder, 17 having previously undergone hemiarthroplasty and five open repair of the rotator cuff. Nine shoulders had undergone previous surgical attempts to eradicate their infection. The diagnosis of infection was based on a combination of clinical suspicion (16 shoulders), positive frozen sections (> 5 polymorphonuclear leukocytes per high-power field) at the time of revision (15 shoulders), positive intra-operative cultures (18 shoulders) or the pre-operative radiological appearances. The patients were treated by an extensive debridement, intravenous antibiotics, and conversion to a reverse shoulder prosthesis in either a single- (10 shoulders) or a two-stage (12 shoulders) procedure. At a mean follow-up of 43 months (25 to 66) there was no evidence of recurrent infection. All outcome measures showed statistically significant improvements. Mean abduction improved from 36.1° (. sd. 27.8) pre-operatively to 75.7° (. sd. 36.0) (p < 0.0001), the mean forward flexion from 43.1° (. sd. 33.5) to 79.5° (. sd. 43.2) (p = 0.0003), and mean external rotation from 10.2° (. sd. 18.7) to 25.4° (. sd. 23.5) (p = 0.0037). There was no statistically significant difference in any outcome between the single-stage and the two-stage group

Aims. Radiostereometric analysis (RSA) studies of vitamin E-doped, highly crosslinked polyethylene (VEPE) liners show low head penetration rates in cementless acetabular components. There is, however, currently no data on cemented VEPE acetabular components in total hip arthroplasty (THA). The aim of this study was to evaluate the safety of a new cemented VEPE component, compared with a conventional polyethylene (PE) component regarding migration, head penetration, and clinical results. Patients and Methods. We enrolled 42 patients (21 male, 21 female) with osteoarthritis and a mean age of 67 years (. sd. 5), in a double-blinded, noninferiority, randomized controlled trial. The subjects were randomized in a 1:1 ratio to receive a reverse hybrid THA with a cemented component of either argon-gas gamma-sterilized PE component (controls) or VEPE, with identical geometry. The primary endpoint was proximal implant migration of the component at two years postoperatively measured with RSA. Secondary endpoints included total migration of the component, penetration of the femoral head into the component, and patient-reported outcome measurements. Results. In total, 19 control implants and 18 implants in the VEPE group were analyzed for the primary endpoint. We found a continuous proximal migration of the component in the VEPE group that was significantly higher with a difference at two years of a mean 0.21 mm (95% confidence interval (CI) 0.05 to 0.37; p = 0.013). The total migration was also significantly higher in the VEPE group, but femoral head penetration was lower. We found no difference in clinical outcomes between the groups. Conclusion. At two years, this cemented VEPE component, although having a low head penetration and excellent clinical results, failed to meet noninferiority compared with the conventional implant by a proximal migration above the proposed safety threshold of RSA. The early proximal migration pattern of the VEPE component is a reason for continued monitoring, although a specific threshold for proximal migration and risk for later failure cannot be defined and needs further study. Cite this article: Bone Joint J 2019;101-B:1192–1198

Although success has been achieved with implantation of bone marrow mesenchymal stem cells (bMSCs) in degenerative discs, its full potential may not be achieved if the harsh environment of the degenerative disc remains. Axial distraction has been shown to increase hydration and nutrition. Combining both therapies may have a synergistic effect in reversing degenerative disc disease. In order to evaluate the effect of bMSC implantation, axial distraction and combination therapy in stimulating regeneration and retarding degeneration in degenerative discs, we first induced disc degeneration by axial loading in a rabbit model. The rabbits in the intervention groups performed better with respect to disc height, morphological grading, histological scoring and average dead cell count. The groups with distraction performed better than those without on all criteria except the average dead cell count. Our findings suggest that bMSC implantation and distraction stimulate regenerative changes in degenerative discs in a rabbit model

Periprosthetic bone loss after total joint arthroplasty is a major clinical problem resulting in aseptic loosening of the implant. Among many cell types, osteoblasts play a crucial role in the development of peri-implant osteolysis. In this study, we tested the effects of calcitriol (1α,25-dihydroxy-vitamin-D. 3. ) and the bisphosphonate pamidronate on titanium-particle- and TNF-α-induced release of interleukin-6 and suppression of osteoblast-specific gene expressions in bone-marrow-derived stromal cells with an osteoblastic phenotype. We monitored the expression of procollagen α1[1], osteocalcin, osteonectin and alkaline phosphatase mRNAs by Northern blots and real-time reverse transcription and polymerase chain reaction analyses. The release of various cytokines was also analysed by ELISA. We found that calcitriol or pamidronate could only partially recover the altered functions of osteoblasts when added alone. Only a combination of these compounds restored all the tested functions of osteoblasts. The local delivery of these drugs may have therapeutic potential to prevent or to treat periprosthetic osteolysis and aseptic loosening of implants

We describe a congenital deformity of the foot which is characterised by calcaneus at the ankle and valgus at the subtalar joint; spontaneous improvement does not occur and serial casting results in incomplete or impermanent correction of the deformities. Experience with five feet in four children indicates that release of the ligaments and tendons anterior and lateral to the ankle and lateral to the subtalar joint is the minimum surgery necessary; subtalar arthrodesis may be required in addition. The foot deformity described may occur as an isolated condition or in association with multiple congenital anomalies. The possibility of a neurological deficit should always be excluded.

Aims. The aim of this study is to evaluate the change in incidence rate of shoulder arthroplasty, indications, and surgeon volume trends associated with these procedures between January 2003 and April 2021 in the province of Nova Scotia, Canada. Methods. A total of 1,545 patients between 2005 and 2021 were analyzed. Patients operated on between 2003 and 2004 were excluded due to a lack of electronic records. Overall, 84.1% of the surgeries (n = 1,299) were performed by two fellowship-trained upper limb surgeons, with the remainder performed by one of the 14 orthopaedic surgeons working in the province. Results. Total shoulder arthroplasty (TSA) was the most frequent procedure (32.17%; n = 497), followed by stemmed hemiarthroplasty (SHA) (27.7%; n = 428). The most frequent indication for primary shoulder arthroplasty was degenerative osteoarthritis (58.1%; n = 882), followed by acute proximal humerus fracture in 15.11% (n = 245), and rotator cuff arthropathy in 14.18% (n = 220). The overall rate of revision was 7.7% (2.8% to 11.2%). The number of TSAs and reverse shoulder arthroplasties (RSAs) has been increasing since 2016. The amount of revision cases is proportional to the number of operations performed in the same year throughout the study period. Conclusion. The incidence of shoulder arthroplasty in the Maritime Provinces has increased over the last 16 years. Revision rates are similar the those found in other large database registries. Reverse shoulder arthroplasty prevalence has increased since 2016. Cite this article: Bone Jt Open 2023;4(8):567–572

Aims. Astragalus polysaccharide (APS) participates in various processes, such as the enhancement of immunity and inhibition of tumours. APS can affect osteoporosis (OP) by regulating the osteogenic differentiation of human bone mesenchymal stem cells (hBMSCs). This study was designed to elucidate the mechanism of APS in hBMSC proliferation and osteoblast differentiation. Methods. Reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting were performed to determine the expression of microRNA (miR)-760 and ankyrin repeat and FYVE domain containing 1 (ANKFY1) in OP tissues and hBMSCs. Cell viability was measured using the Cell Counting Kit-8 assay. The expression of cyclin D1 and osteogenic marker genes (osteocalcin (OCN), alkaline phosphatase (ALP), and runt-related transcription factor 2 (RUNX2)) was evaluated using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Mineral deposits were detected through Alizarin Red S staining. In addition, Western blotting was performed to detect the ANKFY1 protein levels following the regulation of miR-760. The relationship between miR-760 and ANKFY1 was determined using a luciferase reporter assay. Results. The expression of miR-760 was upregulated in OP tissues, whereas ANKFY1 expression was downregulated. APS stimulated the differentiation and proliferation of hBMSCs by: increasing their viability; upregulating the expression levels of cyclin D1, ALP, OCN, and RUNX2; and inducing osteoblast mineralization. Moreover, APS downregulated the expression of miR-760. Overexpression of miR-760 was found to inhibit the promotive effect of APS on hBMSC differentiation and proliferation, while knockdown of miR-760 had the opposite effect. ANKFY1 was found to be the direct target of miR-760. Additionally, ANKFY1 participated in the APS-mediated regulation of miR-760 function in hBMSCs. Conclusion. APS promotes the osteogenic differentiation and proliferation of hBMSCs. Moreover, APS alleviates the effects of OP by downregulating miR-760 and upregulating ANKFY1 expression. Cite this article: Bone Joint Res 2023;12(8):476–485

Aims. The aim of this study was to compare the clinical and radiological outcomes of reverse shoulder arthroplasty (RSA) using small and standard baseplates in Asian patients, and to investigate the impact of a mismatch in the sizes of the glenoid and the baseplate on the outcomes. Methods. This was retrospective analysis of 50 and 33 RSAs using a standard (33.8 mm, ST group) and a small (29.5 mm, SM group) baseplate of the Equinoxe reverse shoulder system, which were undertaken between January 2017 and March 2021. Radiological evaluations included the size of the glenoid, the β-angle, the inclination of the glenoid component, inferior overhang, scapular notching, the location of the central cage in the baseplate within the vault and the mismatch in size between the glenoid and baseplate. Clinical evaluations included the range of motion (ROM) and functional scores. In subgroup analysis, comparisons were performed between those in whom the vault of the glenoid was perforated (VP group) and those in whom it was not perforated (VNP group). Results. Perforation of the vault of the glenoid (p = 0.018) and size mismatch in height (p < 0.001) and width (p = 0.013) were significantly more frequent in the ST group than in the SM group. There was no significant difference in the clinical scores and ROM in the two groups, two years postoperatively (all p > 0.05). In subgroup analysis, the VP group had significantly less inferior overhang (p = 0.009), more scapular notching (p = 0.018), and more size mismatch in height (p < 0.001) and width (p = 0.025) than the VNP group. Conclusion. In Asian patients with a small glenoid, using a 29.5 mm small baseplate at the time of RSA was more effective in reducing size mismatch between the glenoid and the baseplate, decreasing the incidence of perforation of the glenoid vault, and achieving optimal positioning of the baseplate compared with the use of a 33.8 mm standard baseplate. However, longer follow-up is required to assess the impact of these findings on the clinical outcomes. Cite this article: Bone Joint J 2023;105-B(11):1189–1195

Aims. Autologous chondrocyte implantation (ACI) is a promising treatment for articular cartilage degeneration and injury; however, it requires a large number of human hyaline chondrocytes, which often undergo dedifferentiation during in vitro expansion. This study aimed to investigate the effect of suramin on chondrocyte differentiation and its underlying mechanism. Methods. Porcine chondrocytes were treated with vehicle or various doses of suramin. The expression of collagen, type II, alpha 1 (COL2A1), aggrecan (ACAN); COL1A1; COL10A1; SRY-box transcription factor 9 (SOX9); nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX); interleukin (IL)-1β; tumour necrosis factor alpha (TNFα); IL-8; and matrix metallopeptidase 13 (MMP-13) in chondrocytes at both messenger RNA (mRNA) and protein levels was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot. In addition, the supplementation of suramin to redifferentiation medium for the culture of expanded chondrocytes in 3D pellets was evaluated. Glycosaminoglycan (GAG) and collagen production were evaluated by biochemical analyses and immunofluorescence, as well as by immunohistochemistry. The expression of reactive oxygen species (ROS) and NOX activity were assessed by luciferase reporter gene assay, immunofluorescence analysis, and flow cytometry. Mutagenesis analysis, Alcian blue staining, reverse transcriptase polymerase chain reaction (RT-PCR), and western blot assay were used to determine whether p67. phox. was involved in suramin-enhanced chondrocyte phenotype maintenance. Results. Suramin enhanced the COL2A1 and ACAN expression and lowered COL1A1 synthesis. Also, in 3D pellet culture GAG and COL2A1 production was significantly higher in pellets consisting of chondrocytes expanded with suramin compared to controls. Surprisingly, suramin also increased ROS generation, which is largely caused by enhanced NOX (p67. phox. ) activity and membrane translocation. Overexpression of p67. phox. but not p67. phox. AD (deleting amino acid (a.a) 199 to 212) mutant, which does not support ROS production in chondrocytes, significantly enhanced chondrocyte phenotype maintenance, SOX9 expression, and AKT (S473) phosphorylation. Knockdown of p67. phox. with its specific short hairpin (sh) RNA (shRNA) abolished the suramin-induced effects. Moreover, when these cells were treated with the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) inhibitor LY294002 or shRNA of AKT1, p67. phox. -induced COL2A1 and ACAN expression was significantly inhibited. Conclusion. Suramin could redifferentiate dedifferentiated chondrocytes dependent on p67. phox. activation, which is mediated by the PI3K/AKT/SOX9 signalling pathway. Cite this article: Bone Joint Res 2022;11(10):723–738

Aims. To draw a comparison of the pullout strengths of buttress thread, barb thread, and reverse buttress thread bone screws. Methods. Buttress thread, barb thread, and reverse buttress thread bone screws were inserted into synthetic cancellous bone blocks. Five screw-block constructs per group were tested to failure in an axial pullout test. The pullout strengths were calculated and compared. A finite element analysis (FEA) was performed to explore the underlying failure mechanisms. FEA models of the three different screw-bone constructs were developed. A pullout force of 250 N was applied to the screw head with a fixed bone model. The compressive and tensile strain contours of the midsagittal plane of the three bone models were plotted and compared. Results. The barb thread demonstrated the lowest pullout strength (mean 176.16 N (SD 3.10)) among the three thread types. It formed a considerably larger region with high tensile strains and a slightly smaller region with high compressive strains within the surrounding bone structure. The reverse buttress thread demonstrated the highest pullout strength (mean 254.69 N (SD 4.15)) among the three types of thread. It formed a considerably larger region with high compressive strains and a slightly smaller region with high tensile strains within the surrounding bone structure. Conclusion. Bone screws with a reverse buttress thread design will significantly increase the pullout strength. Cite this article: Bone Joint Res 2021;10(2):105–112

Aims. The role of N,N-dimethylformamide (DMF) in diabetes-induced osteoporosis (DM-OS) progression remains unclear. Here, we aimed to explore the effect of DMF on DM-OS development. Methods. Diabetic models of mice, RAW 264.7 cells, and bone marrow macrophages (BMMs) were established by streptozotocin stimulation, high glucose treatment, and receptor activator of nuclear factor-κB ligand (RANKL) treatment, respectively. The effects of DMF on DM-OS development in these models were examined by micro-CT analysis, haematoxylin and eosin (H&E) staining, osteoclast differentiation of RAW 264.7 cells and BMMs, H&E and tartrate-resistant acid phosphatase (TRAP) staining, enzyme-linked immunosorbent assay (ELISA) of TRAP5b and c-terminal telopeptides of type 1 (CTX1) analyses, reactive oxygen species (ROS) analysis, quantitative reverse transcription polymerase chain reaction (qRT-PCR), Cell Counting Kit-8 (CCK-8) assay, and Western blot. Results. The established diabetic mice were more sensitive to ovariectomy (OVX)-induced osteoporosis, and DMF treatment inhibited the sensitivity. OVX-treated diabetic mice exhibited higher TRAP5b and c-terminal telopeptides of type 1 (CTX1) levels, and DMF treatment inhibited the enhancement. DMF reduced RAW 264.7 cell viability. Glucose treatment enhanced the levels of TRAP5b, cathepsin K, Atp6v0d2, and H. +. -ATPase, ROS, while DMF reversed this phenotype. The glucose-increased protein levels were inhibited by DMF in cells treated with RANKL. The expression levels of antioxidant enzymes Gclc, Gclm, Ho-1, and Nqo1 were upregulated by DMF. DMF attenuated high glucose-caused osteoclast differentiation by targeting mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signalling in BMMs. Conclusion. DMF inhibits high glucose-induced osteoporosis by targeting MAPK and NF-κB signalling. Cite this article: Bone Joint Res 2022;11(4):200–209

The June 2023 Shoulder & Elbow Roundup. 360. looks at: Proximal humerus fractures: what does the literature say now?; Infection risk of steroid injections and subsequent reverse shoulder arthroplasty; Surgical versus non-surgical management of humeral shaft fractures; Core outcome set needed for elbow arthroplasty; Minimally invasive approaches to locating radial nerve in the posterior humeral approach; Predictors of bone loss in anterior glenohumeral instability; Does the addition of motor control or strengthening exercises improve rotator cuff-related shoulder pain?; Terminology and diagnostic criteria used in patients with subacromial pain syndrome

The February 2023 Shoulder & Elbow Roundup. 360. looks at: Arthroscopic capsular release or manipulation under anaesthesia for frozen shoulder?; Distal biceps repair through a single incision?; Distal biceps tendon ruptures: diagnostic strategy through physical examination; Postoperative multimodal opioid-sparing protocol vs standard opioid prescribing after knee or shoulder arthroscopy: a randomized clinical trial; Graft healing is more important than graft technique in massive rotator cuff tear; Subscapularis tenotomy versus peel after anatomic shoulder arthroplasty; Previous rotator cuff repair increases the risk of revision surgery for periprosthetic joint infection after reverse shoulder arthroplasty; Conservative versus operative treatment of acromial and scapular spine fractures following reverse total shoulder arthroplasty

The October 2024 Shoulder & Elbow Roundup360 looks at: Proximal humeral fractures with vascular compromise; Outcomes and challenges of revision arthroscopic rotator cuff repair: a systematic review; Evaluating treatment effectiveness for lateral elbow tendinopathy: a systematic review and network meta-analysis; Tendon transfer techniques for irreparable subscapularis tears: a comparative review; Impact of subscapularis repair in reverse shoulder arthroplasty; Isolated subscapularis tears strongly linked to shoulder pseudoparesis; Nexel and Coonrad-Morrey total elbow arthroplasties show comparable revision rates in New Zealand study; 3D MRI matches 3D CT in assessing bone loss and shoulder morphology in dislocation cases

Aims. Osteoarthritis (OA) is the most common chronic pathema of human joints. The pathogenesis is complex, involving physiological and mechanical factors. In previous studies, we found that ferroptosis is intimately related to OA, while the role of Sat1 in chondrocyte ferroptosis and OA, as well as the underlying mechanism, remains unclear. Methods. In this study, interleukin-1β (IL-1β) was used to simulate inflammation and Erastin was used to simulate ferroptosis in vitro. We used small interfering RNA (siRNA) to knock down the spermidine/spermine N1-acetyltransferase 1 (Sat1) and arachidonate 15-lipoxygenase (Alox15), and examined damage-associated events including inflammation, ferroptosis, and oxidative stress of chondrocytes. In addition, a destabilization of the medial meniscus (DMM) mouse model of OA induced by surgery was established to investigate the role of Sat1 inhibition in OA progression. Results. The results showed that inhibition of Sat1 expression can reduce inflammation, ferroptosis changes, reactive oxygen species (ROS) level, and lipid-ROS accumulation induced by IL-1β and Erastin. Knockdown of Sat1 promotes nuclear factor-E2-related factor 2 (Nrf2) signalling. Additionally, knockdown Alox15 can alleviate the inflammation-related protein expression induced by IL-1β and ferroptosis-related protein expression induced by Erastin. Furthermore, knockdown Nrf2 can reverse these protein expression alterations. Finally, intra-articular injection of diminazene aceturate (DA), an inhibitor of Sat1, enhanced type II collagen (collagen II) and increased Sat1 and Alox15 expression. Conclusion. Our results demonstrate that inhibition of Sat1 could alleviate chondrocyte ferroptosis and inflammation by downregulating Alox15 activating the Nrf2 system, and delaying the progression of OA. These findings suggest that Sat1 provides a new approach for studying and treating OA. Cite this article: Bone Joint Res 2024;13(3):110–123

Aims. It is important to understand the rate of complications associated with the increasing burden of revision shoulder arthroplasty. Currently, this has not been well quantified. This review aims to address that deficiency with a focus on complication and reoperation rates, shoulder outcome scores, and comparison of anatomical and reverse prostheses when used in revision surgery. Methods. A Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) systematic review was performed to identify clinical data for patients undergoing revision shoulder arthroplasty. Data were extracted from the literature and pooled for analysis. Complication and reoperation rates were analyzed using a meta-analysis of proportion, and continuous variables underwent comparative subgroup analysis. Results. A total of 112 studies (5,379 shoulders) were eligible for inclusion, although complete clinical data was not ubiquitous. Indications for revision included component loosening 20% (601/3,041), instability 19% (577/3,041), rotator cuff failure 17% (528/3,041), and infection 16% (490/3,041). Intraoperative complication and postoperative complication and reoperation rates were 8% (230/2,915), 22% (825/3,843), and 13% (584/3,843) respectively. Intraoperative and postoperative complications included iatrogenic humeral fractures (91/230, 40%) and instability (215/825, 26%). Revision to reverse total shoulder arthroplasty (TSA), rather than revision to anatomical TSA from any index prosthesis, resulted in lower complication rates and superior Constant scores, although there was no difference in American Shoulder and Elbow Surgeons scores. Conclusion. Satisfactory improvement in patient-reported outcome measures are reported following revision shoulder arthroplasty; however, revision surgery is associated with high complication rates and better outcomes may be evident following revision to reverse TSA. Cite this article: Bone Jt Open 2021;2(8):618–630

Aims. Myokine developmental endothelial locus-1 (DEL-1) has been documented to alleviate inflammation and endoplasmic reticulum (ER) stress in various cell types. However, the effects of DEL-1 on inflammation, ER stress, and apoptosis in tenocytes remain unclear. Methods. Human primary tenocytes were cultured in palmitate (400 μM) and palmitate plus DEL-1 (0 to 2 μg/ml) conditions for 24 hours. The expression levels of ER stress markers and cleaved caspase 3, as well as phosphorylated 5' adenosine monophosphate-activated protein kinase (AMPK) and autophagy markers, were assessed by Western blotting. Autophagosome formation was measured by staining with monodansylcadaverine, and apoptosis was determined by cell viability assay and caspase 3 activity assay. Results. We found that treatment with DEL-1 suppressed palmitate-induced inflammation, ER stress, and apoptosis in human primary tenocytes. DEL-1 treatment augmented LC3 conversion and p62 degradation as well as AMPK phosphorylation. Moreover, small interfering RNA for AMPK or 3-methyladenine (3-MA), an autophagy inhibitor, abolished the suppressive effects of DEL-1 on inflammation, ER stress, and apoptosis in tenocytes. Similar to DEL-1, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), an activator of AMPK, also attenuated palmitate-induced inflammation, ER stress, and apoptosis in tenocytes, which 3-MA reversed. Conclusion. These results revealed that DEL-1 suppresses inflammation and ER stress, thereby attenuating tenocyte apoptosis through AMPK/autophagy-mediated signalling. Thus, regular exercise or administration of DEL-1 may directly contribute to improving tendinitis exacerbated by obesity and insulin resistance. Cite this article: Bone Joint Res 2022;11(12):854–861

Aims. After a few passages of in vitro culture, primary human articular chondrocytes undergo senescence and loss of their phenotype. Most of the available chondrocyte cell lines have been obtained from cartilage tissues different from diarthrodial joints, and their utility for osteoarthritis (OA) research is reduced. Thus, the goal of this research was the development of immortalized chondrocyte cell lines proceeded from the articular cartilage of patients with and without OA. Methods. Using telomerase reverse transcriptase (hTERT) and SV40 large T antigen (SV40LT), we transduced primary OA articular chondrocytes. Proliferative capacity, degree of senescence, and chondrocyte surface antigen expression in transduced chondrocytes were evaluated. In addition, the capacity of transduced chondrocytes to synthesize a tissue similar to cartilage and to respond to interleukin (IL)-1β was assessed. Results. Coexpression of both transgenes (SV40 and hTERT) were observed in the nuclei of transduced chondrocytes. Generated chondrocyte cell lines showed a high proliferation capacity and less than 2% of senescent cells. These cell lines were able to form 3D aggregates analogous to those generated by primary articular chondrocytes, but were unsuccessful in synthesizing cartilage-like tissue when seeded on type I collagen sponges. However, generated chondrocyte cell lines maintained the potential to respond to IL-1β stimulation. Conclusion. Through SV40LT and hTERT transduction, we successfully immortalized chondrocytes. These immortalized chondrocytes were able to overcome senescence in vitro, but were incapable of synthesizing cartilage-like tissue under the experimental conditions. Nonetheless, these chondrocyte cell lines could be advantageous for OA investigation since, similarly to primary articular chondrocytes, they showed capacity to upregulate inflammatory mediators in response to the IL-1β cytokine. Cite this article: Bone Joint Res 2023;12(1):46–57