Total Knee Arthroplasty in the Osteoporotic Tibia: A Biomechanical Evaluation of the Role of Stem Extensions and Cementing Techniques.

INTRODUCTION: Poor functional outcomes and aseptic loosening increase when total knee arthroplasty is performed on osteoporotic patients. This biomechanical study evaluated the effect of stem extension on the stability of tibial fixation using different cementing techniques. METHODS: A standard design tibial tray was implanted in a replica of a male osteoporotic tibia. Twenty-four implantations were performed using three variations of implant and cementing, and then mounted on a material testing machine load frame at 500 cycles of multiaxial loading simulating walking. The three-dimensional components of tray-tibia micromotion were measured. RESULTS: The primary implant total interface motion with surface cementing was 25.9 µm ± 14.7 µm and 10.6 µm ± 7.6 µm with full cementing (P = 0.001). The three-dimensional motion of fully cemented primary implants with stem extension was 4.4 µm ± 3.9 µm, which represents a decrease in micromotion of 83% in surface cemented primary implants (P < 0.0001) and 58% in the fully cemented components without stem extension (P < 0.009). CONCLUSION: Fully cemented primary implants with stem extensions demonstrated decreased micromotion and should be considered for use in osteoporotic total knee arthroplasty patients.

Antibiotic impregnated total femur spacers: a technical tip.

Simultaneous prosthetic joint infection of ipsilateral hip and knee arthroplasties is often accompanied by significant bone loss and presents a challenging reconstructive problem. Two-stage reconstruction is favored and requires the placement of a total femur spacer, which is not a commercially available device. We describe a surgical technique, reporting on 2 cases in which a customized total femur antibiotic impregnated spacer was created by combining an articulating knee spacer and an articulating hip spacer with a reinforced cement dowel construct connecting the 2 spacers. Custom total femoral spacers are useful in the management of infected femoral megaprostheses and cases with ipsilateral injected hip and knee arthroplasties and severe femoral bone loss.

MRI Findings Associated with Recalled Modular Femoral Neck Rejuvenate and ABG Implants.

MARS-MRI is suggested for the diagnosis of adverse local tissue reactions (ALTR) in patients with recalled femoral stems with modular necks, but there has been no major study looking at MARS-MRI findings in this population. A retrospective review was performed on 312 patients who received a modular neck hip implant between October 2007 and February 2012. 62% of patients had intra-articular effusions, with 27% containing debris. Extra-capsular effusions were present in 35% of hips. 54% had synovitis and 5.4% had osteolysis. Tendinopathy and tendon disruption was present in the gluteus medius (58%/12%), hamstring (56%/12%), gluteus minimus (38%/7.7%) and iliopsoas (7.1%/4.8%). Abnormal MARS-MRI findings are associated with modular neck femoral components and can suggest underlying ALTR. MARS-MRI abnormalities merit serious consideration in this population.

Revision of Recalled Modular Neck Rejuvenate and ABG Femoral Implants.

Modular neck femoral stems have been associated with adverse local tissue reactions (ALTR), leading to a voluntary recall, but these effects have not been well-characterized. A retrospective review of intraoperative findings and cobalt/chromium levels was performed in 103 hips undergoing revision for ALTR. The average preoperative serum cobalt level was 7.6 µg/L (range 1.1-23 µg/L) and chromium level was 1.8 µg/L (range 0.1-6.8 µg/L). Metallic sludge was noted in 100%, synovitis in 98%, pericapsular rind in 82%, and calcar erosion in 85%. An osteotomy was required for removal in 44%. We concluded that revision of modular neck femoral stems is associated with increased preoperative metal ion levels and stem-neck corrosion. Despite advanced stem explantation techniques, osteotomy was frequently required, leading to increased morbidity.

Tendon Contraction After Cyclic Elongation Is an Age-Dependent Phenomenon: In Vitro and In Vivo Comparisons.

BACKGROUND: Tendons are viscoelastic tissues that deform (elongate) in response to cyclic loading. However, the ability of a tendon to recover this elongation is unknown. HYPOTHESIS: Tendon length significantly increases after in vivo or in vitro cyclic loading, and the ability to return to its original length through a cell-mediated contraction mechanism is an age-dependent phenomenon. STUDY DESIGN: Controlled laboratory study. METHODS: In vitro, rat tail tendon fascicles (RTTfs) from Sprague-Dawley rats of 3 age groups (1, 3, and 12 months) underwent 2% cyclic strain at 0.17 Hz for 2 hours, and the percentages of elongation were determined. After loading, the RTTfs were suspended for 3 days under tissue culture conditions and photographed daily to determine the amount of length contraction. In vivo, healthy male participants (n = 29; age, 19-49 years) had lateral, single-legged weightbearing radiographs taken of the knee at 60° of flexion immediately before, immediately after, and 24 hours after completing eccentric quadriceps loading exercises on the dominant leg to fatigue. Measurements of patellar tendon length were taken from the radiographs, and the percentages of tendon elongation and subsequent contraction were calculated. RESULTS: In vitro, cyclic loading increased the length of all RTTfs, with specimens from younger (1 and 3 months) rats demonstrating significantly greater elongation than those from older (12 months) rats (P = .009). The RTTfs contracted to their original length significantly faster (P < .001) and in an age-dependent fashion, with younger animals contracting faster. In vivo, repetitive eccentric loading exercises significantly increased patellar tendon length (P < .001). Patellar tendon length decreased 24 hours after exercises (P < .001) but did not recover completely (P < .001). There was a weak but significant (R (2) = 0.203, P = .014) linear correlation between the amount of tendon contraction and age, with younger participants (<30 years) demonstrating significantly more contraction (P = .014) at 24 hours than older participants (>30 years). CONCLUSION: Cyclic tendon loading results in a significant increase in tendon elongation under both in vitro and in vivo conditions. Tendons in both conditions demonstrated an incomplete return to their original length after 24 hours, and the extent of this return was age dependent. CLINICAL RELEVANCE: The age- and time-dependent contraction of tendons, elongated after repetitive loading, could result in transient alterations in the mechanobiological environment of tendon cells. This, in turn, could induce the onset of catabolic changes associated with the pathogenesis of tendinopathy. These results suggest the importance of allowing time for contraction between bouts of repetitive exercise and may explain why age is a predisposing factor in tendinopathy.

Regulation of reactive oxygen species by p53: implications for nitric oxide-mediated apoptosis.

Nitric oxide (NO) induces vascular smooth muscle cell (VSMC) apoptosis in part through activation of p53. Traditionally, p53 has been thought of as the gatekeeper, determining if a cell should undergo arrest and repair or apoptosis following exposure to DNA-damaging agents, depending on the severity of the damage. However, our laboratory previously demonstrated that NO induces apoptosis to a much greater extent in p53(-/-) compared with p53(+/+) VSMC. Increased reactive oxygen species (ROS) within VSMC has been shown to induce VSMC apoptosis, and recently it was found that the absence of, or lack of, functional p53 leads to increased ROS and oxidative stress within different cell types. This study investigated the differences in intracellular ROS levels between p53(-/-) and p53(+/+) VSMC and examined if these differences were responsible for the increased susceptibility to NO-induced apoptosis observed in p53(-/-) VSMC. We found that p53 actually protects VSMC from NO-induced apoptosis by increasing antioxidant protein expression [i.e., peroxiredoxin-3 (PRx-3)], thereby reducing ROS levels and cellular oxidative stress. We also observed that the NO-induced apoptosis in p53(-/-) VSMC was largely abrogated by pretreatment with catalase. Furthermore, when the antioxidant protein PRx-3 and its specific electron acceptor thioredoxin-2 were silenced within p53(+/+) VSMC with small-interfering RNA, not only did these cells exhibit greater ROS production, but they also exhibited increased NO-induced apoptosis similar to that observed in p53(-/-) VSMC. These findings suggest that ROS mediate NO-induced VSMC apoptosis and that p53 protects VSMC from NO-induced apoptosis by decreasing intracellular ROS. This research demonstrates that p53 has antioxidant functions in stressed cells and also suggests that p53 has antiapoptotic properties.