Background: Stiffness is a common reason for suboptimal clinical outcomes after primary total knee arthroplasty (pTKA).There is a lack of consensus regarding its definition, which is often conflated with its histopathologic subcategory-i.e., arthrofibrosis. There is value in refining the definition of acquired idiopathic stiffness in an effort to select for patients with arthrofibrosis. We conducted a systematic review and meta-analysis to establish a consensus definition of acquired idiopathic stiffness, determine its prevalence after pTKA, and identify potential risk factors for its development.Methods: MEDLINE, Embase, Cochrane Controlled Register of Trials (CENTRAL), and Scopus databases were searched from 2002 to 2017. Studies that included patients with stiffness after pTKA were screened with strict inclusion and exclusion criteria to isolate the subset of patients with acquired idiopathic stiffness unrelated to known extrinsic or surgical causes. Three authors independently assessed study eligibility and risk of bias and collected data. Outcomes of interest were then analyzed according to age, sex, and body mass index (BMI).Results: In the 35 included studies (48,873 pTKAs), the mean patient age was 66 years. In 63% of the studies, stiffness was defined as a range of motion of <90°or a flexion contracture of >5°at 6 to 12 weeks postoperatively. The prevalence of acquired idiopathic stiffness after pTKA was 4%, and this did not differ according to age (4%, I 2 = 95%, among patients <65 years old and 5%, I 2 = 96%, among those ‡65 years old; p = 0.238). The prevalence of acquired idiopathic stiffness was significantly lower in males (1%, I 2 = 85%) than females (3%, I 2 = 95%) (p < 0.0001) as well as in patients with a BMI of <30 kg/m 2 (2%, I 2 = 94%) compared with those with a BMI of ‡30 kg/m 2 (5%, I 2 = 97%) (p = 0.027).Conclusions: Contemporary literature supports the following definition for acquired idiopathic stiffness: a range of motion of <90°persisting for >12 weeks after pTKA in patients in the absence of complicating factors including preexisting stiffness. The mean prevalence of acquired idiopathic stiffness after pTKA was 4%; females and obese patients were at increased risk.Level of Evidence: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence. Stiffness is a common reason for failure of primary total knee arthroplasty (pTKA), contributing to up to 58% of reoperations or repeat interventions (such as manipulation under anesthesia) and >25% of 90-day hospital readmissions in some series [1][2][3] . Patients who develop this complication have poor functional outcomes and increased rates of knee pain, and their symptoms often are refractory to nonoperative and even oper-ative management 4,5 . The incidence of TKA increased from 31.2 per 100,000 person-years from 1971 to 1976 to 220.9 per 100,000 person-years from 2005 to 2008 6 . This trend, compounded by an increasing prevalence of obesity and a decreasing mean age of patients undergoing pTKA, wil...

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Arthrofibrosis is a common complication following total knee arthroplasty caused by pathologic fibroblast activation and excessive collagen deposition around a synovial joint leading to debilitating loss of motion. Treatment options are limited because the pathologic mechanisms remain to be characterized. Dysregulation of the inflammatory cascade may lead to communication between myofibroblasts and immune cells triggering tissue metaplasia, and excessive collagen deposition described clinically as arthrofibrosis. We explored the novel use of celecoxib (selective cyclooxygenase-2 [COX-2] inhibitor) to disrupt the downstream effects of the post-traumatic inflammatory cascade and inhibit scar tissue formation in a validated rabbit model of arthrofibrosis combined with new parameters for quantifying the stiffness of the posterior capsule. Biomechanical and molecular analyses, of contracted rabbit knee posterior capsule tissue after COX-2 inhibition revealed increased maximal passive extension and down-regulation of collagen messenger RNA compared with controls. Histopathologic examination suggested a trend of decreased quantities of dense fibrous connective tissue with COX-2 inhibition. These data may suggest that inhibiting the inflammatory cascade could potentially reduce pathologic myofibroblast activation, thereby reducing scar tissue formation and increasing the range of motion in arthrofibrotic joints. Implementing a multi-modal pharmacologic approach may simultaneously target numerous cellular components contributing to the complex process of arthrofibrogenesis.

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 (b = 0.17; p = 0.002), perioperative hypovolemia (b = 0.28; p = 0.0001), and acute atrial fibrillation (b = 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. P eriprosthetic joint infection (PJI) continues to be one of the most common failure mechanisms after primary total knee arthroplasty (TKA), resulting in high mor-bidity 1-4 and mortality 5 . In North America, the management of chronic PJIs after TKA most commonly consists of a 2-stage exchange arthroplasty with a high-dose antibiotic-loaded bone Disclosure: The authors indicated that no external funding was received for any aspect of this work. On the Disclosure of Potential Conflicts of Interest forms, which are provided with the online version of the article, one or more of the authors checked "yes" to ind...

Background: Some prior reports of total knee arthroplasty after high tibial osteotomy have shown high rates of aseptic loosening. As such, the goal of this study was to analyze the outcomes of contemporary total knee arthroplasty after high tibial osteotomy, with particular emphasis on survivorship free from aseptic loosening, any revision, and any reoperation; complications; radiographic results; and clinical outcomes. Methods: We retrospectively reviewed 207 patients who underwent 231 total knee arthroplasties using cemented prostheses after high tibial osteotomy from 2000 to 2012 through our total joint registry: 87% were after a closing-wedge osteotomy and 13% were after an opening-wedge osteotomy. The mean follow-up from total knee arthroplasty was 8 years. At the time of the total knee arthroplasty, the mean age was 64 years and the mean body mass index was 31 kg/m2. The majority of total knee arthroplasties had a posterior-stabilized design (93%), and 4% had a varus-valgus constraint design. Tibial stems were utilized in 8% of cases. Bivariate and multivariate Cox regression analyses were utilized to analyze risk factors for poorer survival. Results: At 10 years, survivorship free from aseptic loosening was 97%, survivorship free from any revision was 90%, and survivorship free from any reoperation was 85%. Fifteen patients (15 total knee arthroplasties [6%]) underwent aseptic revision, most commonly for instability (3%), aseptic loosening (2%), and periprosthetic fracture (1%). On bivariate analysis, patient age of <60 years was a significant risk factor for poorer revision-free survival (hazard ratio, 2.9; p = 0.02); on multivariate analysis, younger age was the only significant risk factor for revision (p = 0.04). There were 14 complications (6%), the most common being a manipulation under anesthesia in 9 cases (4%). No unrevised total knee arthroplasties had definitive radiographic evidence of loosening. Knee Society scores improved from a mean preoperative score of 59 points to a mean postoperative score of 93 points (p < 0.001). Conclusions: Contemporary total knee arthroplasty with a cemented prosthesis after high tibial osteotomy demonstrated excellent long-term durability, with 10-year survivorship free from aseptic loosening of 97%. There was reliable improvement in clinical outcomes, but perfect knee balance was sometimes challenging, as reflected by a 4% prevalence of manipulation under anesthesia and a 3% prevalence of revision for instability. Level of Evidence: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.

Aims Arthrofibrosis is a relatively common complication after joint injuries and surgery, particularly in the knee. The present study used a previously described and validated rabbit model to assess the biomechanical, histopathological, and molecular effects of the mast cell stabilizer ketotifen on surgically induced knee joint contractures in female rabbits. Methods A group of 12 skeletally mature rabbits were randomly divided into two groups. One group received subcutaneous (SQ) saline, and a second group received SQ ketotifen injections. Biomechanical data were collected at eight, ten, 16, and 24 weeks. At the time of necropsy, posterior capsule tissue was collected for histopathological and gene expression analyses (messenger RNA (mRNA) and protein). Results At the 24-week timepoint, there was a statistically significant increase in passive extension among rabbits treated with ketotifen compared to those treated with saline (p = 0.03). However, no difference in capsular stiffness was detected. Histopathological data failed to demonstrate a decrease in the density of fibrous tissue or a decrease in α-smooth muscle actin (α-SMA) staining with ketotifen treatment. In contrast, tryptase and α-SMA protein expression in the ketotifen group were decreased when compared to saline controls (p = 0.007 and p = 0.01, respectively). Furthermore, there was a significant decrease in α-SMA (ACTA2) gene expression in the ketotifen group compared to the control group (p < 0.001). Conclusion Collectively, these data suggest that ketotifen mitigates the severity of contracture formation in a rabbit model of arthrofibrosis. Cite this article: Bone Joint Res 2020;9(6):302–310.

Experimental 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.