Dagneaux, Louis

Aims An angular proximal femoral deformity, in association with osteoarthritis (OA) of the hip, considerably increases the technical complexity of primary total hip arthroplasty (THA). The aims of this study were to determine the long-term implant survival, the risk factors for failure, complications, and clinical outcomes of contemporary primary THA in this difficult group of patients. Methods Our institutional total joint registry was used to identify 119 primary THAs performed in 108 patients with an angular proximal femoral deformity, between January 1997 and September 2017. The deformity was related to a previous femoral osteotomy in 102 THAs (86%), and developmental or metabolic disorders in 17 THAs (14%). A total of 62 hips (53%) had a predominantly varus deformity. The mean age of the patients was 44 years (SD 13), their mean BMI was 29 kg/m 2 (SD 6), and 70 (59%) were female. An uncemented femoral component with metaphyseal fixation was used in 35 THAs (30%), an uncemented femoral component with diaphyseal fixation in 34 (29%), an uncemented modular femoral component with a metaphyseal fixation sleeve in 29 (24%), and a cemented femoral component in 21 (18%). Simultaneous corrective femoral osteotomy was performed in 22 THAs (18%). Kaplan-Meier survival and Harris Hip Scores (HHSs) were reported. The mean follow-up was eight years (2 to 22). Results The ten-year survival free of femoral loosening, any femoral revision, any revision and any reoperation was 95%, 93%, 90%, and 88%, respectively. A total of 13 revisions were undertaken, for aseptic femoral loosening in three, fracture of the femoral component in two, dislocation in two, aseptic acetabular loosening in two, polyethylene liner exchange in two, and infection in two. A preoperative varus deformity was associated with a higher risk of any revision (hazard ratio (HR) 12.5, p = 0.020), and those with a simultaneous osteotomy had a higher risk of any reoperation (HR 3.6, p = 0.023). The mean HHSs improved significantly from 52 preoperatively to 82 at ten years (p < 0.001). Conclusion In the largest series to date of primary THAs in patients with hip OA and an angular proximal femoral deformity, we found a good ten-year survival free from any revision. Varus deformities, particularly those treated with a simultaneous osteotomy due to the magnitude or location of the deformity, had a higher rate of further surgery. Cite this article: Bone Joint J 2025;107-B(6 Supple B):101–108.

Angular proximal femoral deformities increase the technical complexity of primary total hip arthroplasties (THAs). The goals were to determine the long-term implant survivorship, risk factors, complications, and clinical outcomes of contemporary primary THAs in this difficult cohort.Our institutional total joint registry was used to identify 119 primary THAs performed in 109 patients with an angular proximal femoral deformity between 1997 and 2017. The deformity was related to previous femoral osteotomy in 85%, and developmental or metabolic disorders in 15%. 53% had a predominantly varus angular deformity. The mean age was 44 years, mean BMI was 29 kg/m2, and 59% were female. An uncemented metaphyseal fixation stem was used in 30%, an uncemented diaphyseal fixation stem in 28%, an uncemented modular body stem with metaphyseal fixation sleeve in 24%, and a cemented stem in 18%. Simultaneous corrective femoral osteotomy was performed in 18%. Kaplan-Meier survivorships and Harris hip scores were reported. Mean follow-up was 8 years.The 10-year survivorships free of femoral loosening, aseptic femoral revision, any revision, and any reoperation were 95%, 93%, 90% and 88%, respectively. Revisions occurred in 13 hips for: aseptic femoral component loosening (3), stem fracture (2), dislocation (2), aseptic acetabular loosening (2), polyethylene liner exchange (2), and infection (2). Preoperative varus angular deformities were associated with a higher risk of any revision (HR 10, p=0.03), and simultaneous osteotomies with a higher risk of any reoperation (HR 3.6, p=0.02). Mean Harris hip scores improved from 52 preoperatively to 82 at 10 years (p<0.001).In the largest series to date of primary THAs in patients with angular proximal femoral deformities, we found a good 10-year survivorship free from any revision. Varus angular deformities, particularly those treated with a simultaneous osteotomy due to the magnitude or location of the deformity, had a higher reoperation rate.Keywords: Proximal femoral deformity; dysplasia; femoral osteotomy; survivorship; revisionLevel of evidence: Level III, comparative retrospective cohort

AimsNonagenarians (aged 90 to 99 years) have experienced the fastest percent decile population growth in the USA recently, with a consequent increase in the prevalence of nonagenarians living with joint arthroplasties. As such, the number of revision total hip arthroplasties (THAs) and total knee arthroplasties (TKAs) in nonagenarians is expected to increase. We aimed to determine the mortality rate, implant survivorship, and complications of nonagenarians undergoing aseptic revision THAs and revision TKAs.MethodsOur institutional total joint registry was used to identify 96 nonagenarians who underwent 97 aseptic revisions (78 hips and 19 knees) between 1997 and 2018. The most common indications were aseptic loosening and periprosthetic fracture for both revision THAs and revision TKAs. Mean age at revision was 92 years (90 to 98), mean BMI was 27 kg/m2 (16 to 47), and 67% (n = 65) were female. Mean time between primary and revision was 18 years (SD 9). Kaplan-Meier survival was used for patient mortality, and compared to age- and sex-matched control populations. Reoperation risk was assessed using cumulative incidence with death as a competing risk. Mean follow-up was five years.ResultsMortality rates were 9%, 18%, 26%, and 62% at 90 days, one year, two years, and five years, respectively, but similar to control populations. There were 43 surgical complications and five reoperations, resulting in a cumulative incidence of reoperation of 4% at five years. Medical complications were common, with a cumulative incidence of 65% at 90 days. Revisions for periprosthetic fractures were associated with higher mortality and higher 90-day risk of medical complications compared to revisions for aseptic loosening.ConclusionContemporary revision THAs and TKAs appeared to be relatively safe in selected nonagenarians managed with multidisciplinary teams. Cause of revision affected morbidity and mortality risks. While early medical and surgical complications were frequent, they seldom resulted in reoperation.Cite this article: Bone Joint J 2023;105-B(6):649–656.

Aims As has been shown in larger animal models, knee immobilization can lead to arthrofibrotic phenotypes. Our study included 168 C57BL/6J female mice, with 24 serving as controls, and 144 undergoing a knee procedure to induce a contracture without osteoarthritis (OA). Methods Experimental knees were immobilized for either four weeks (72 mice) or eight weeks (72 mice), followed by a remobilization period of zero weeks (24 mice), two weeks (24 mice), or four weeks (24 mice) after suture removal. Half of the experimental knees also received an intra-articular injury. Biomechanical data were collected to measure passive extension angle (PEA). Histological data measuring area and thickness of posterior and anterior knee capsules were collected from knee sections. Results Experimental knees immobilized for four weeks demonstrated mean PEAs of 141°, 72°, and 79° after zero, two, and four weeks of remobilization (n = 6 per group), respectively. Experimental knees demonstrated reduced PEAs after two weeks (p < 0.001) and four weeks (p < 0.0001) of remobilization compared to controls. Following eight weeks of immobilization, experimental knees exhibited mean PEAs of 82°, 73°, and 72° after zero, two, and four weeks of remobilization, respectively. Histological analysis demonstrated no cartilage degeneration. Similar trends in biomechanical and histological properties were observed when intra-articular violation was introduced. Conclusion This study established a novel mouse model of robust knee contracture without evidence of OA. This was appreciated consistently after eight weeks of immobilization and was irrespective of length of remobilization. As such, this arthrofibrotic model provides opportunities to investigate molecular pathways and therapeutic strategies. Cite this article: Bone Joint Res 2023;12(1):58–71.

AbstractExperimental analyses of posttraumatic knee arthrofibrosis utilize a rabbit model as a gold standard. However, a rodent model of arthrofibrosis offers many advantages including reduced cost and comparison with other models of organ fibrosis. This study aimed to characterize the biomechanical, histological, and molecular features of a novel posttraumatic model of arthrofibrosis in rats. Forty eight rats were divided into two equal groups. An immobilization procedure was performed on the right hind limbs of experimental rats. One group was immobilized for 4 weeks and the other for 8 weeks. Both groups were remobilized for 4 weeks. Limbs were studied biomechanically via assessment of torque versus degree of extension, histologically via whole knee specimen, and molecularly via gene expression of posterior capsular tissues. Significant differences were observed between experimental and control limbs at 4 N‐cm of torque in the 4‐week (knee extension: 115° ± 8° vs. 169° ± 17°, respectively; p = 0.007) and 8‐week immobilization groups (knee extension: 99° ± 12° vs. 174° ± 9°, respectively; p = 0.008). Histologically, in each group experimental limbs demonstrated increased posterior capsular thickness and total area of tissue when compared to control limbs (p < 0.05). Gene expression values evaluated in each group were comparable. This study presents a novel rat model of arthrofibrosis with severe and persistent knee contractures demonstrated biomechanically and histologically. Statement of clinical significance: Arthrofibrosis is a common complication following contemporary total knee arthroplasties. The proposed model is reproducible, cost‐effective, and can be employed for translational investigations studying the pathogenesis of arthrofibrosis and efficacy of neoadjuvant pharmacologic agents.

Background: Two-stage exchange arthroplasty with a high-dose antibiotic-loaded bone cement (ALBC) spacer and intravenous or oral antibiotics is the most common method of managing a periprosthetic joint infection (PJI) after a total knee arthroplasty (TKA). However, little is known about the contemporary incidence, the risk factors, and the outcomes of acute kidney injuries (AKIs) in this cohort. Methods: We identified 424 patients who had been treated with 455 ALBC spacers after resection of a PJI following a primary TKA from 2000 to 2017. The mean age at resection was 67 years, the mean body mass index (BMI) was 33 kg/m 2 , 47% of the patients were women, and 15% had preexisting chronic kidney disease (CKD). The spacers (87% nonarticulating) contained a mean of 8 g of vancomycin and 9 g of an aminoglycoside per construct (in situ for a mean of 11 weeks). Eighty-six spacers also had amphotericin B (mean, 412 mg). All of the patients were concomitantly treated with systemic antibiotics for a mean of 6 weeks. An AKI was defined as a creatinine level of ≥1.5 times the baseline or an increase of ≥0.3 mg/dL within any 48-hour period. The mean follow-up was 6 years (range, 2 to 17 years). Results: Fifty-four AKIs occurred in 52 (14%) of the 359 patients without preexisting CKD versus 32 AKIs in 29 (45%) of the 65 patients with CKD (odds ratio [OR], 5; p = 0.0001); none required acute dialysis. Overall, when the vancomycin concentration or aminoglycoside concentration was >3.6 g/batch of cement, the risk of AKI increased (OR, 1.9 and 1.8, respectively; p = 0.02 for both). Hypertension (β = 0.17; p = 0.002), perioperative hypovolemia (β = 0.28; p = 0.0001), and acute atrial fibrillation (β = 0.13; p = 0.009) were independent predictors for AKI in patients without preexisting CKD. At the last follow-up, 8 patients who had sustained an AKI had progressed to CKD, 4 of whom received dialysis. Conclusions: In our study, the largest series to date that we are aware of regarding this issue, AKI occurred in 14% of patients with normal renal function at baseline, and 2% developed CKD after undergoing a 2-stage exchange arthroplasty for a PJI after TKA. However, the risk of AKI was fivefold greater in those with preexisting CKD. The causes of acute renal blood flow impairment were independent predictors for AKI. Level of Evidence: Therapeutic Level IV . See Instructions for Authors for a complete description of levels of evidence.

(1) Background: Arthrofibrosis is a common cause of patient debility and dissatisfaction after total knee arthroplasty (TKA). The diversity of molecular pathways involved in arthrofibrosis disease progression suggest that effective treatments for arthrofibrosis may require a multimodal approach to counter the complex cellular mechanisms that direct disease pathogenesis. In this study, we leveraged RNA-seq data to define genes that are suppressed in arthrofibrosis patients and identified adiponectin (ADIPOQ) as a potential candidate. We hypothesized that signaling pathways activated by ADIPOQ and the cognate receptors ADIPOR1 and ADIPOR2 may prevent fibrosis-related events that contribute to arthrofibrosis. (2) Methods: Therefore, ADIPOR1 and ADIPOR2 were analyzed in a TGFβ1 inducible cell model for human myofibroblastogenesis by both loss- and gain-of-function experiments. (3) Results: Treatment with AdipoRon, which is a small molecule agonist of ADIPOR1 and ADIPOR2, decreased expression of collagens (COL1A1, COL3A1, and COL6A1) and the myofibroblast marker smooth muscle α-actin (ACTA2) at both mRNA and protein levels in basal and TGFβ1-induced cells. (4) Conclusions: Thus, ADIPOR1 and ADIPOR2 represent potential drug targets that may attenuate the pathogenesis of arthrofibrosis by suppressing TGFβ-dependent induction of myofibroblasts. These findings also suggest that AdipoRon therapy may reduce the development of arthrofibrosis by mediating anti-fibrotic effects in joint capsular tissues.