Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.

AimsConcurrent hip and spine pathologies can alter the biomechanics of spinopelvic mobility in primary total hip arthroplasty (THA). This study examines how differences in pelvic orientation of patients with spine fusions can increase the risk of dislocation risk after THA.Patients and MethodsWe identified 84 patients (97 THAs) between 1998 and 2015 who had undergone spinal fusion prior to primary THA. Patients were stratified into three groups depending on the length of lumbar fusion and whether or not the sacrum was involved. Mean age was 71 years (40 to 87) and 54 patients (56%) were female. The mean body mass index (BMI) was 30 kg/m2(19 to 45). Mean follow-up was six years (2 to 17). Patients were 1:2 matched to patients with primary THAs without spine fusion. Hazard ratios (HR) were calculated.ResultsDislocation in the fusion group was 5.2% at one year versus 1.7% in controls but this did not reach statistical significance (HR 1.9; p = 0.33). Compared with controls, there was no significant difference in rate of dislocation in patients without a sacral fusion. When the sacrum was involved, the rate of dislocation was significantly higher than in controls (HR 4.5; p = 0.03), with a trend to more dislocations in longer lumbosacral fusions. Patient demographics and surgical characteristics of THA (i.e. surgical approach and femoral head diameter) did not significantly impact risk of dislocation (p > 0.05). Significant radiological differences were measured in mean anterior pelvic tilt between the one-level lumbar fusion group (22°), the multiple-level fusion group (27°), and the sacral fusion group (32°; p < 0.01). Ten-year survival was 93% in the fusion group and 95% in controls (HR 1.2; p = 0.8).ConclusionLumbosacral spinal fusions prior to THA increase the risk of dislocation within the first six months. Fusions involving the sacrum with multiple levels of lumbar involvement notably increased the risk of postoperative dislocation compared with a control group and other lumbar fusions. Surgeons should take care with component positioning and may consider higher stability implants in this high-risk cohort.

Both the rate of complications and mortality are high following resection of oncological periacetabular lesions and reconstruction. Many types of reconstruction have been used with unique challenges and complications for each technique. Newer prostheses, including custom-made prostheses and porous tantalum implants and augments, have shown promising early functional and radiographic outcomes. Cite this article: 2018;100-B(1 Supple A):22-30.

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.

We evaluated recently published articles relevant to the biological effects of titanium dioxide (TiO2) particles on local endogenous cells required for normal bone homeostasis, repair, and implant osseointegration. Structural characteristics, size, stability, and agglomeration of TiO2 particles alter the viability and behavior of multiple bone-related cell types. Resulting shifts in bone homeostasis may increase bone resorption and lead to clinical incidents of osteolysis, implant loosening, and joint pain. TiO2 particles that enter cells (through endocytosis or Trojan horse mechanism) may further disrupt implant retention. We propose that cellular responses to titanium-based nanoparticles contribute to pathological mechanisms underlying the aseptic loosening of titanium-based metal implants.

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.