Aims. The conventionally described mechanism of distal biceps tendon rupture (DBTR) is of a ‘considerable extension force suddenly applied to a resisting, actively flexed forearm’. This has been commonly paraphrased as an ‘eccentric contracture to a flexed elbow’. Both definitions have been frequently used in the literature with little objective analysis or citation. The aim of the present study was to use video footage of real time distal biceps ruptures to revisit and objectively define the mechanism of injury. Methods. An online search identified 61 videos reporting a DBTR. Videos were independently reviewed by three surgeons to assess forearm rotation, elbow flexion, shoulder position, and type of muscle contraction being exerted at the time of rupture. Prospective data on mechanism of injury and arm position was also collected concurrently for 22 consecutive patients diagnosed with an acute DBTR in order to corroborate the video analysis. Results. Four videos were excluded, leaving 57 for final analysis. Mechanisms of injury included deadlift, bicep curls, calisthenics, arm wrestling, heavy lifting, and boxing. In all, 98% of ruptures occurred with the arm in supination and 89% occurred at 0° to 10° of elbow flexion. Regarding muscle activity, 88% occurred during isometric contraction, 7% during eccentric contraction, and 5% during concentric contraction. Interobserver correlation scores were calculated as 0.66 to 0.89 using the free-marginal Fleiss Kappa tool. The prospectively collected patient data was consistent with the video analysis, with 82% of injuries occurring in supination and 95% in relative elbow extension. Conclusion. Contrary to the classically described injury mechanism, in this study the usual arm position during DBTR was forearm supination and elbow extension, and the muscle contraction was typically isometric. This was demonstrated for both video analysis and ‘real’ patients across a range of activities leading to rupture. Cite this article: Bone Jt Open 2022;3(10):826–831

Aims. This study aimed to demonstrate the promoting effect of elastic fixation on fracture, and further explore its mechanism at the gene and protein expression levels. Methods. A closed tibial fracture model was established using 12 male Japanese white rabbits, and divided into elastic and stiff fixation groups based on different fixation methods. Two weeks after the operation, a radiograph and pathological examination of callus tissue were used to evaluate fracture healing. Then, the differentially expressed proteins (DEPs) were examined in the callus using proteomics. Finally, in vitro cell experiments were conducted to investigate hub proteins involved in this process. Results. Mean callus volume was larger in the elastic fixation group (1,755 mm. 3. (standard error of the mean (SEM) 297)) than in the stiff fixation group (258 mm. 3. (SEM 65)). Pathological observation found that the expression levels of osterix (OSX), collagen, type I, alpha 1 (COL1α1), and alkaline phosphatase (ALP) in the callus of the elastic fixation group were higher than those of the stiff fixation group. The protein sequence of the callus revealed 199 DEPs, 124 of which were highly expressed in the elastic fixation group. In the in vitro study, it was observed that a stress of 200 g led to upregulation of thrombospondin 1 (THBS1) and osteoglycin (OGN) expression in bone marrow mesenchymal stem cells (BMSCs). Additionally, these genes were found to be upregulated during the osteogenic differentiation process of the BMSCs. Conclusion. Elastic fixation can promote fracture healing and osteoblast differentiation in callus, and the ability of elastic fixation to promote osteogenic differentiation of BMSCs may be achieved by upregulating genes such as THBS1 and OGN. Cite this article: Bone Joint Res 2024;13(10):559–572

Introduction. In my paediatric Orthopaedic practice I use Kirchner wires for the fixation of the TSF on bone. I noted a significant percentage of wire loosening during the post-operative period. The aim of this project was to establish the effectiveness of the wire clamping mechanism and find ways to reduce the incidence of wire loosening when using the TSF. Materials and Methods. In the first instance wire slippage was measured intra-operatively after the tensioner was removed using an intra-operative professional camera. Following this study mechanical tests were performed in the lab measuring the pull out properties of Kirchner wires using different bolts and different torque levels in order to tighten the wire on the fixator. Results. Our clinical study confirmed wire slippage intra-operatively immediately after the tensioner was removed. Wire slippage after the tensioner was removed was found to vary from 0.01 mm to 0.51 mm (mean 0.19 mm). Our mechanical tests showed that the ideal torque for tightening the wire on the frame using a bolt was around 15 N.m. A comparison between cannulated and slotted bolts suggested that cannulated bolts are more effective as a clamping mechanism. A comparison between aluminium made Taylor Spatial frame rings and stainless steel made Ilizarov rings suggested that the Taylor Spatial frame rings are more effective as part of a clamping mechanism. Conclusions. It is important that clinicians routinely measure the torque they use to clamp wires on circular external fixators. Clinicians and manufacturers are informed that the type of bolt used is important in maintaining wire tension. Manufacturers should design the ideal bolt which effectively grips the wire without the risk of fracture. The Ilizarov frame clamping mechanism can be effectively used with the Taylor Spatial frame

Chronic extensor mechanism insufficiency around TKA is a very challenging pathology to treat. An insufficient extensor mechanism negatively affects implant survival and patient outcomes. There are several risk factors for extensor mechanism disruption and the surgeon should be aware and avoid these problems in the perioperative period. In appropriately selected patients, reconstruction of the extensor mechanism is a valid option. Whole extensor mechanism and Achilles tendon allograft reconstruction of the deficient extensor mechanism have been proposed with good early published results. These reconstructions, however, are expensive and with time may stretch and lead to recurrence of an extensor lag. An alternative to allograft, is the use of Marlex mesh as popularised by Browne and Hanssen. This technique uses a knitted monofilament polypropylene mesh that is secured to the patient's native lateral tissue and covered by an appropriately dissected and distalised vastus medialis muscle. The technique can be used for both patellar and quadriceps tendon deficiencies and can be done with or without implant revision and is currently the treatment of choice at the presenter's institution. The surgeon should be aware of the complexity and limitations of these three reconstructive techniques

Sarcopenia is an age-related geriatric syndrome which is associated with subsequent disability and morbidity. Currently there is no promising therapy approved for the treatment of sarcopenia. The receptor activator of nuclear factor NF-κB ligand (RANKL) and its receptor (RANK) are expressed in bone and skeletal muscle. Activation of the NF-κB pathway mainly inhibits myogenic differentiation, which leads to skeletal muscle dysfunction and loss. LYVE1 and CD206 positive macrophage has been reported to be associated with progressive impairment of skeletal muscle function with aging. The study aims to investigate the effects of an anti-RANKL treatment on sarcopenic skeletal muscle and explore the related mechanisms on muscle inflammation and the polarization status of macrophages. Sarcopenic senescence-accelerated mouse P8 (SAMP8) mice at month 8 were treated intraperitoneally with 5mg/kg anti-RANKL (IK22/5) or isotype control (2A3; Bio X Cell) antibody every 4 weeks and harvested at month 10. Senescence accelerated mouse resistant-1 (SAMR1) were collected at month 10 as the age-matched non-sarcopenic group. Ex-vivo functional assessment, grip strength and immunostaining of C/EBPa, CD206, F4/80, LYVE1 and PAX7 were performed. Data analysis was done with one-way ANOVA, and the significant level was set at p≤0.05. At month 10, tetanic force/specific tetanic force, twitch force/specific twitch force in anti-RANKL group were significantly higher than control group (all p<0.01). The mice in the anti-RANKL treatment group also showed significantly higher grip strength than Con group (p<0.001). The SAMP8 mice at month 10 expressed significantly more C/EBPa, CD206 and LYVE1 positive area than in SAMR1, while anti-RANKL treatment significantly decreased C/EBPa, CD206 and LYVE1 positive area. The anti-RANKL treatment protected against skeletal muscle dysfunctions through suppressing muscle inflammation and modulating M2 macrophages, which may represent a novel therapeutic approach for sarcopenia. Acknowledgment: Collaborative Research Fund (CRF, Ref: C4032-21GF)

Osteoarthritis (OA) is a major global disease with increasing prevalence. It is one of the most significant causes of disability worldwide and represents a major burden in terms of healthcare delivery and impact on the quality of life of patients. It is a cause of severe chronic pain and has given rise to alarming levels of opioid use and addiction. Despite this prevalence, there are no disease-modifying treatments which delay or reverse the degrative changes within joints which are characteristics of the disease. All treatments are symptom-modifying with the exception of joint arthroplasty, which is currently the most common surgical procedure carried out in US hospitals. Several pharmaceutical and biological interventions have been tested in recent years, including metalloproteinase inhibitors, chondrogenic agents such as Kartogenin, IL-1 antagonists and monoclonal antibodies. So far, none of these has provided an effective disease-modifying treatment. Cellular therapies have a great deal of promise because of their anti-inflammatory and regenerative effects. Mesenchymal stromal cells (MSCs) have been widely studied as a treatment for OA in preclinical and clinical assessments with generally positive results. As the clinical testing of these cells proceeds serious questions emerge relating to the quality and consistency of the therapeutic product and the need for better standardisation with regard to, for example, the tissue source and expansion conditions. Of equal importance is the need for deeper insight into the therapeutic mechanism, specifically the activity and phenotype of cells transplanted to the OA environment, their fate and interaction with local cells

Extensor mechanism complications after or during total knee arthroplasty are problematic. The prevalence ranges from 1–12% in TKR patients. Treatment results for these problems are inferior to the results of similar problems in non-TKR patients. Furthermore, the treatment algorithm is fundamentally different from that of non-TKR patients. The surgeon's first question does not focus on primary fixation; rather the surgeon must ask if the patient needs surgery and if so am I prepared to augment the repair? Quadriceps tendon rupture, periprosthetic patellar fracture, and patellar tendon rupture have similar treatment algorithms. Patients who are able to perform a straight leg raise and have less than a 20-degree extensor lag are generally treated non-operatively with extension bracing. The remaining patients will need surgical reconstruction of the extensor mechanism. Loose patellar components are removed. Primary repair alone is associated with poor results. Whole extensor mechanism allograft, Achilles tendon allograft, and synthetic mesh reconstruction are the current techniques for augmentation. In the acute setting if these are not available hamstring tendon harvest and augmentation is an option. Achilles tendons and synthetic mesh are easier to obtain than and entire extensor mechanism but are limited to patients that have an intact patella and the patella that can be mobilised to within 2–3 cm of the joint line. No matter which technique is used the principles are: rigid distal/tubercle fixation, coverage of allograft/mesh with host tissue to decrease infection, tensioning the augment material in extension, no flexion testing of reconstruction and post-operative extension bracing

Extensor mechanism complications after or during total knee arthroplasty (TKA) are problematic. The prevalence ranges from 1%-12% in TKA patients. Treatment results for these problems are inferior to the results of similar problems in non-TKA patients. Furthermore, the treatment algorithm is fundamentally different from that of non-TKA patients. The surgeon's first question does not focus on primary fixation; rather the surgeon must ask if the patient needs surgery and if so am I prepared to augment the repair? Quadriceps tendon rupture, peri-prosthetic patellar fracture, and patellar tendon rupture have similar treatment algorithms. Patients who are able to perform a straight leg raise and have less than a 20-degree extensor lag are generally treated non-operatively with extension bracing. The remaining patients will need surgical reconstruction of the extensor mechanism. Loose patellar components are removed. Primary repair alone is associated with poor results. Whole extensor mechanism allograft, Achilles tendon allograft, and synthetic mesh reconstruction are the current techniques for augmentation. In the acute setting if these are not available, hamstring tendon harvest and augmentation is an option. Achilles tendons and synthetic mesh are easier to obtain than an entire extensor mechanism but are limited to patients that have an intact patella and the patella that can be mobilised to within 2–3 cm of the joint line. No matter which technique is used the principles are: rigid distal/tubercle fixation, coverage of allograft/mesh with host tissue to decrease infection, tensioning the augment material in extension, no flexion testing of reconstruction and post-operative extension bracing

Aims. Kashin-Beck disease (KBD) is a kind of chronic osteochondropathy, thought to be caused by environmental risk factors such as T-2 toxin. However, the exact aetiology of KBD remains unclear. In this study, we explored the functional relevance and biological mechanism of cartilage oligosaccharide matrix protein (COMP) in the articular cartilage damage of KBD. Methods. The articular cartilage specimens were collected from five KBD patients and five control subjects for cell culture. The messenger RNA (mRNA) and protein expression levels were detected by quantitative reverse transcription PCR (qRT-PCR) and western blot. The survival rate of C28/I2 chondrocyte cell line was detected by MTT assay after T-2 toxin intervention. The cell viability and mRNA expression levels of apoptosis related genes between COMP-overexpression groups and control groups were examined after cell transfection. Results. The mRNA and protein expression levels of COMP were significantly lower in KBD chondrocytes than control chondrocytes. After the T-2 toxin intervention, the COMP mRNA expression of C28/I2 chondrocyte reduced and the protein level of COMP in three intervention groups was significantly lower than in the control group. MTT assay showed that the survival rate of COMP overexpression KBD chondrocytes were notably higher than in the blank control group. The mRNA expression levels of Survivin, SOX9, Caspase-3, and type II collagen were also significantly different among COMP overexpression, negative control, and blank control groups. Conclusion. Our study results confirmed the functional relevance of COMP with KBD. COMP may play an important role in the excessive chondrocytes apoptosis of KBD patients. Cite this article: Bone Joint Res 2020;9(9):578–586

Abstract. Objectives. Catastrophic neck injuries in rugby tackling are rare (2 per 100,000 players per year) with 38% of these injuries occurring in the tackle. The aim of this study was to determine the primary mechanism of cervical spine injury during rugby tackling and to highlight the effect of tackling technique on intervertebral joint loads. Methods. In vivo and in vitro experimental data were integrated to generate realistic computer simulations representative of misdirected tackles. MRI images were used to inform the creation of a musculoskeletal model. In vivo kinematics and neck muscle excitations were collected during lab-based staged tackling of the player. Impact forces were collected in vitro using an instrumented anthropometric test device during experimental simulations of rugby collisions. Experimental kinematics and muscle excitations were prescribed to the model and impact forces applied to seven skull locations (three cranial and four lateral). To examine the effects of technique on intervertebral joint loads the model's neck angle was altered in steps of 5° about each rotational axis resulting in a total of 1,623 experimentally informed simulations of misdirected tackles. Results. Neck flexion angles and cranial impact locations had the largest effects on maximal compression, anterior shear and flexion moment loads. During posterior cranial impacts compression forces and flexion moments increased from 1500 to 3200 N and 30 to 60 Nm respectively between neck angles of 30° extension and 30° flexion. This was more evident at the C5-C6 and C6-C7 joints. Anterior shear loads remained stable throughout neck angle ranges however during anterior impacts they were directed posteriorly when the neck was flexed. Conclusions. The combination of estimated joint loads in the lower cervical spine support buckling as the primary injury mechanism of anterior bilateral facet dislocations observed in misdirected rugby tackles and highlights the importance of adopting a correct tackling technique. Declaration of Interest. (b) declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported:I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project

A key component to the success of total knee replacement is the health and integrity of the extensor mechanism. While there are issues related to the patella, such as fracture, dislocation, subluxation, clunk due to peripatellar fibrosis and anterior knee pain, the overall integrity of the extensor mechanism is of tantamount importance in providing an excellent functional outcome. During total knee replacement it is of utmost importance to preserve the anatomic insertion of the patellar tendon on the tibial tubercle. However, after total knee replacement, a fall or extreme osteoporosis of the patella may cause a rupture of the patellar tendon, distally or proximally, and possibly the quadriceps tendon off of the proximal pole of the patella. Simple repairs of the patellar tendon avulsion may involve use of the semitendonosis and gracilis tendons along with primary repair of the tendon. Usually, patella infera develops after such a repair affecting overall strength and function. For severe disruptions of the extensor mechanism that are accompanied by a significant extensor lag, autologous tissue repair may not be possible. Thus, there are three techniques for reconstruction of this difficult problem: Extensor mechanism allograft with bone-patellar tendon-patella-quadriceps tendon, extensor mechanism allograft with os calcis-Achilles tendon construct and Marlex-mesh reconstruction for patellar tendon avulsion. The key to success of extensor mechanism allograft is proper tensioning of the allograft at full extensor and immobilisation for 6 weeks. Rosenberg's early experience showed that the allograft works best placed at maximum tension in extension. Rubash has described the use of the os calcis-Achilles tendon which does not utilise a patellar substitute. Hansen has recently described excellent results with the use of Marlex mesh to act as a structural reinforcement to the patellar tendon when it is avulsed

A key component to the success of total knee replacement is the health and integrity of the extensor mechanism. While there are issues related to the patella, such as fracture, dislocation, subluxation, clunk due to peripatellar fibrosis and anterior knee pain, the overall integrity of the extensor mechanism is of tantamount importance in providing an excellent functional outcome. During total knee replacement it is of utmost importance to preserve the anatomic insertion of the patellar tendon on the tibial tubercle. However, after total knee replacement, a fall or extreme osteoporosis of the patella may cause a rupture of the patellar tendon, distally or proximally, and possibly the quadriceps tendon off of the proximal pole of the patella. Simple repairs of the patellar tendon avulsion may involve use of the semitendonosis and gracilis tendons along with primary repair of the tendon. Usually, patella infera develops after such a repair affecting overall strength and function. For severe disruptions of the extensor mechanism that are accompanied by a significant extensor lag, autologous tissue repair may not be possible. Thus, there are three techniques for reconstruction of this difficult problem: Extensor mechanism allograft with bone-patellar tendon-patella-quadriceps tendon, extensor mechanism allograft with os calcis-Achilles tendon construct and Marlex-mesh reconstruction for patellar tendon avulsion. The key to success of extensor mechanism allograft is proper tensioning of the allograft at full extensor and immobilisation for 6 weeks. Rosenberg's early experience showed that the allograft works best placed at maximum tension in extension. Rubash has described the use of the os calsis-Achilles tendon which does not utilise a patellar substitute. Hansen has recently described excellent results with the use of Marlex mesh to act as a structural reinforcement to the patellar tendon when it is avulsed

General Principles. All repairs should be repaired in full extension. Repairs should be immobilised in full extension for 6–12 weeks. Gradual resumption of motion in a hinged brace over an additional 6–8 weeks almost always yields flexion to at least 90 degrees. Marlex mesh has been shown to be an excellent replacement as well as an augment for deficient soft tissue. Acute tibial tuberosity avulsion. Open repair is best accomplished with a non-absorbable heavy Krackow suture, secured distally around a screw and washer followed by 6 to 8 weeks of immobilization. Augmentation with a semitendinosus graft or Marlex mesh can provide additional support. Acute Patella Tendon Rupture. End-to-end repair is standard, but re-rupture is not uncommon, so supplemental semitendinosus reconstruction is recommended. The tendon is harvested proximally, left attached distally and passed through a transverse hole in the inferior patella. The gracilis tendon can be harvested and sutured to semitendinosus for additional length, if needed. Acute Quadriceps Tendon Rupture. These can be repaired end-to-end with a non-absorbable heavy Krackow suture. A superficial quadriceps fascial turndown or mesh may be a useful adjunct. Patella Fracture. Treatment depends on the status of the patellar component and the loss of active extension. If the component remains well fixed and the patient has less than a 20-degree lag, non-operative treatment in extension. A loose component and/or > 20-degree extensor lag requires ORIF +/− component revision. Chronic Disruptions. While standard repair techniques are possible, tissue retraction usually prevents a “tension-free” repair. If the patella remains viable and has not retracted proximally an Achilles tendon graft is appropriate. In chronic disruptions with loss of the patella, allograft extensor mechanism reconstruction may be considered. Marlex mesh repair has also been shown to be effective in reconstruction of chronic patellar and quadriceps tendon defects

Aims. Methicillin-resistant Staphylococcus aureus (MRSA) can cause wound infections via a ‘Trojan Horse’ mechanism, in which neutrophils engulf intestinal MRSA and travel to the wound, releasing MRSA after apoptosis. The possible role of intestinal MRSA in prosthetic joint infection (PJI) is unknown. Methods. Rats underwent intestinal colonization with green fluorescent protein (GFP)-tagged MRSA by gavage and an intra-articular wire was then surgically implanted. After ten days, the presence of PJI was determined by bacterial cultures of the distal femur, joint capsule, and implant. We excluded several other possibilities for PJI development. Intraoperative contamination was excluded by culturing the specimen obtained from surgical site. Extracellular bacteraemia-associated PJI was excluded by comparing with the infection rate after intravenous injection of MRSA or MRSA-carrying neutrophils. To further support this theory, we tested the efficacy of prophylactic membrane-permeable and non-membrane-permeable antibiotics in this model. Results. After undergoing knee surgery eight or 72 hours after colonization, five out of 20 rats (25.0%) and two out of 20 rats (10.0%) developed PJI, respectively. Strikingly, 11 out of 20 rats (55.0%) developed PJI after intravenous injection of MRSA-carrying neutrophils that were isolated from rats with intestinal MRSA colonization. None of the rats receiving intravenous injections of MRSA developed PJI. These results suggest that intestinal MRSA carried by neutrophils could cause PJI in our rat model. Ten out of 20 (50.0%) rats treated with non-membrane-permeable gentamicin developed PJI, whereas only one out of 20 (5.0%) rats treated with membrane-permeable linezolid developed PJI. Conclusion. Neutrophils as carriers of intestinal MRSA may play an important role in PJI development. Cite this article:Bone Joint Res. 2020;9(4):152–161

Extensor mechanism disruption in total knee arthroplasty (TKA) occurs infrequently but often requires surgical intervention. We compared two cohorts undergoing extensor mechanism allograft reconstruction, one group had an extensor mechanism rupture, and the other had a recurrent ankylosed knee. Thirteen consecutive patients with extensor mechanism disruption or ankylosis after TKA were treated. Two different types of extensor mechanism allografts were used: quadriceps tendon-patella-patella tendon-tibial tubercle, and Achilles tendon allograft(Fig1). Demographic factors, diagnosis at extensor failure, Knee Society clinical rating scores, radiographs, and patient satisfaction were recorded. The average time from extensor mechanism disruption to surgery was 6.6 months (range, 1-24 months). At a mean followup of 24 months (range, 6-46 months), all patients were community ambulators. None of the patients showed a postoperative extensor lag. Average postoperative maximum flexion was 97° (90-115°) for the ruptured group and 80° (75-90) for the ankylosed grup. All patients thought their functional status had improved, and 87% were satisfied with the results of the allograft reconstruction (Fig 2, 3, 4, 5). One patient had allograft failure due to recurrent infection after re-revision for sepsis. The total extensor mechanism allograft and Achilles tendon allograft both were successful in the treatment of the failed extensor mechanism and showed promising results for the treatment of the ankylosed knee

General Principles: All repairs should be repaired in full extension. Repairs should be immobilised in full extension for 6–12 weeks. Gradual resumption of motion in a hinged brace over an additional 6–8 weeks almost always yields flexion to at least 90 degrees. Marlex Mesh has been shown to be an excellent replacement as well as an augment for deficient soft tissue. Acute tibial tuberosity avulsion: Open repair is best accomplished with a non-absorbable heavy Krackow suture, secured distally around a screw and washer followed by 6 to 8 weeks of immobilization. Augmentation with a semitendinosus graft or Marlex can provide additional support. Acute Patella Tendon Rupture: End-to-end repair is standard, but re-rupture is not uncommon, so supplemental semitendinosus reconstruction is recommended. The tendon is harvested proximally, left attached distally and passed through a transverse hole in the inferior patella. The gracilis tendon can be harvested and sutured to semitendinosus for additional length, if needed. Acute Quadriceps Tendon Rupture: These can be repaired end-to-end with a non-absorbable heavy Krackow suture. A superficial quadriceps fascial turndown or mesh may be a useful adjunct. Patella Fracture: Treatment depends on the status of the patellar component and the loss of active extension. If the component remains well fixed and the patient has less than a 20-degree lag, non-operative treatment in extension. A loose component and/or > 20-degree extensor lag requires ORIF +/− component revision. Chronic Disruptions: While standard repair techniques are possible, tissue retraction usually prevents a “tension-free” repair. If the patella remains viable and has not retracted proximally an Achilles tendon graft is appropriate. In chronic disruptions with loss of the patella, allograft extensor mechanism reconstruction may be considered. Marlex mesh repair has also been shown to be effective in reconstruction of chronic patellar and quadriceps tendon defects

Introduction: knee revision in absence of Extensor Mechanism has been always a challenging problem in Orthopaedics. Many authors are in favour to abandone any endoprosthetic substitution in front of such a situation. We think osteotendinous allografts, in this particular case whole Extensor Mechanism allografts, could play an essential role before any Knee Arthrodesis. Material and Method: From 1999 up to 2004 11 patients (4 male, 7 female) (mean age 72, range 68 to 86) underwent to a whole Extensor Mechanism allografting procedure. Mean follow up was 2.7 years (1 to 5 years). In the first four cases a whole Extensor Mechanism allograft was implanted, while the next seven cases the allograft was reinforced by means of a Leeds-Keio Dacron band. Results: There was no infections in this serie. The mean obtained R.O.M. in the first three months was – 5 of active extension (range 0 to −15) and 95 active flexion (range 80 – 110). However 3 from the 4 former operated cases had a progressive loss of active extension up to −25 (range −20 to −35) at 18 months, that did not increase after this period. Ultrasonic exams showed a lengthening of the patellar tendon in these cases. None of these 3 patients wished to undergo to a patellar tendon reinforcement. On the other hand those later cases, where patellar tendon was reinforced did not show any change over the time (at 18 months mean active extension was maintained to −5 (range 0 to 15). Conclusions: Extensor mechanism allografts are very useful in difficult knee revisions with absence of extensor mechanism, so that knee arthrodesis is not the method of choice for these patients. However augmentation of patellar tendon is necessary to maintain with the years an active extension

Supracondylar fractures of the humerus (SCH) are one of the most common orthopaedic injuries in childhood. Numerous studies worldwide demonstrate that play equipment is a common mechanism of injury for SCH. Our study aimed to identify the prevalence of play equipment related SCH in a large population in Western Sydney. We conducted a retrospective analysis of 856 infants who suffered a SCH between 2001–2007 and were treated at The Children's Hospital at Westmead. We obtained data on patient demographics, mechanism of injury, severity of SCH (Gartland classification), and management of SCH (open reduction vs closed reduction vs. non operative management). Of the total 856 patients, 739 provided useful information for analysis. In 696 of these patients the mechanism of injury could be determined according to the patients information provided in the medical record. The mechanisms of injury were as follows: trampoline 72 (10.3%), monkey bars 58 (8.3%), slides 26 (3.7%), other playground equipment 84 (12.0%), home furniture 157 (22.6%), bikes 39 (5.6%), non-equipment related fall 260 (37.3%). Of the patient demographics, there was a significant correlation between the age groups (0–3, 4–7, 8+ years) and severity of SCH (Ï24 = 18.36, p=0.001). Fifty-two percent of Gartland type three fractures occurred in the age group of 4–7 years. The study demonstrates that playground equipment represents a major mechanism of injury of SCH in children. In particular trampoline related SCH and to a lesser degree monkey bar related SCH, represent an area in which primary preventative strategies should be targeted

Purpose. Previous retrieval studies demonstrate increased tibial baseplate roughness leads to higher polyethylene backside wear in total knee arthroplasty (TKA). Micromotion between the polyethylene backside and baseplate is affected by the locking mechanism design and can further increase backside wear. This study's purpose was to examine modern locking mechanisms influence, in the setting of both polished and non-polished tibial baseplates, on backside tibial polyethylene damage and wear. Methods. Five TKA models were selected with different tibial baseplate and/or locking mechanism designs. Six retrieval tibial polyethylenes from each TKA model were matched based on time in vivo (TIV), age at TKA revision, BMI, gender, number of times revised, and revision reason. Two observers visually assessed each polyethylene. Primary outcomes were visual damage scores, individual visual damage modes, and linear wear rates determined on micro-computed tomography (micro-CT) scan in mm/year. Demographics were compared by one-way ANOVA. Damage scores, damage modes, and linear wear were analyzed by the Kruskal-Wallis test and Dunn's multiple comparisons test. Results. There were no differences among the groups based on TIV (p=0.962), age (p=0.609), BMI (p=0.951), gender, revision number, or reason for revision. There was a significant difference across groups for visual total damage score (p=0.031). The polished tibial design with a partial peripheral capture locking mechanism and anterior constraint demonstrated a significantly lower score compared to one of the non-polished tibial designs with a complete peripheral-rim locking mechanism (13.0 vs. 22.0, p=0.019). Otherwise, mean total damage scores were not significant between groups. There were identifiable differences among the groups based on abrasions (p=0.006). The polished design with a tongue-in-groove locking mechanism demonstrated a significantly higher score compared to one of the designs with a non-polished baseplate (5.83 vs. 0.83, p=0.016). Only the two designs with non-polished baseplates demonstrated dimpling (5.67 and 8.67), which was significant when compared against all other groups (p<0.0001), but not against each other (p>0.99). No other significant differences were identified when examining burnishing, cold flow, scratching, or pitting. No polyethylene components exhibited embedded debris or delamination. There was a significant difference among groups for linear wear on micro-CT scanning (p=0.003). Two of the polished baseplate designs, one with the partial peripheral rim capture and one with the tongue-in-groove locking mechanism, demonstrated significantly lower wear rates than the non-polished design with a complete peripheral-rim locking mechanism (p=0.008 and p=0.032, respectively). There were no other differences in wear rates between groups. Conclusions. Total damage scores and wear rates were similar between all groups except when comparing two of the polished TKA designs to one of the non-polished baseplate designs. The other TKA model with a non-polished tibial baseplate had similar damage scores and wear rates to the polished designs, likely due to its updated locking mechanism. Dimpling was specific for non-polished tibial baseplates while abrasions were identified in the design with a tongue-in-groove locking mechanism. Our study showed even in the setting of a non-polished tibial baseplate, modern locking mechanisms can decrease backside damage and wear similar to that of other current generation TKA designs. For any figures or tables, please contact authors directly (see Info & Metrics tab above).