We undertook this study to investigate the outcomes of surgical treatment for acute carpal tunnel syndrome following our protocol for concurrent nerve decompression and skeletal stabilization for bony wrist trauma to be undertaken within 48-hours.

We identified all patients treated at our trauma centre following this protocol between 1 January 2014 and 31 December 2019. All patients were clinically reviewed at least 12 months following surgery and assessed using the Brief Michigan Hand Outcomes Questionnaire (bMHQ), the Boston Carpal Tunnel Questionnaire (BCTQ) and sensory assessment with Semmes-Weinstein monofilament testing.

The study group was made up of 35 patients. Thirty-three patients were treated within 36-hours. Patients treated with our unit protocol for early surgery comprising nerve decompression and bony stabilization within 36-hours, report excellent outcomes at medium term follow up.

We propose that nerve decompression and bony surgical stabilization should be undertaken as soon as practically possible once the diagnosis is made. This is emergent treatment to protect and preserve nerve function. In our experience, the vast majority of patients were treated within 24-hours.

The risk of AVN is high in Unstable Slipped Capital Femoral Epiphysis (SCFE) and the optimal surgical treatment remains controversial. Our AVN rates in severe, unstable SCFE remained unchanged following the introduction of the Modified Dunn Procedure (MDP) and as a result, our practice evolved towards performing an Anterior Open Reduction and Decompression (AOR) in an attempt to potentially reduce the “second hit” phenomenon that may contribute. The aim of this study was to determine the early surgical outcomes in Unstable SCFE following AOR compared to the MDP.

All moderate to severe, Loder unstable SCFEs between 2008 and 2022 undergoing either an AOR or MDP were included. AVN was defined as a non-viable post-operative SPECT-CT scan.

Eighteen patients who underwent AOR and 100 who underwent MPD were included. There was no significant difference in severity (mean PSA 64 vs 66 degrees, p = 0.641), or delay to surgery (p = 0.973) between each group. There was no significant difference in the AVN rate at 27.8% compared to 24% in the AOR and MDP groups respectively (p = 0.732). The mean operative time in the AOR group was 24 minutes less, however this was not statistically significant (p = 0.084). The post-reduction PSA was 26 degrees (range, 13–39) in the AOR group and 9 degrees (range, -7 to 29) in the MDP group (p<0.001). Intra-operative femoral head monitoring had a lower positive predictive value in the AOR group (71% compared to 90%).

Preliminary results suggest the AVN rate is not significantly different following AOR. There is less of an associated learning curve with the AOR, but as anticipated, a less anatomical reduction was achieved in this group. We still feel that there is a role for the MDP in unstable slips with a larger remodelling component.

Aim

Implant-associated infection remains one of the biggest challenges facing orthopaedics and there is an urgent clinical need to develop new prophylactic strategies. We have previously shown that CSA-90, a broad-spectrum antimicrobial, prevented infection in an infected open fracture model. In this study we developed a novel model of implant-associated infection, in which to further test the potential of CSA-90 as a prophylactic agent.

Despite of the high success of TKA, 20% of recipients remain dissatisfied with their surgery. There is an increasing discordance in the literature on what is an optimal goal for component alignment. Furthermore, the unique patient specific anatomical characteristics will also play a role. The dynamic characteristic of a TKR is a product of the complex interaction between a patient's individual anatomical characteristics and the specific alignment of the components in that patient knee joint. These interactions can be better understood with computational models. Our objective was to characterise ligament characteristics by measuring knee joint laxity with functional radiograph and with the aid of a computational model and an optimisation study to estimate the subject specific free length of the ligaments.

Pre-operative CT and functional radiographs, varus and valgus stressed X-rays assessing the collateral ligaments, were captured for 10 patients. CT scan was segmented and 3D–2D pose estimation was performed against the radiographs. Patient specific tibio-femoral joint computational model was created. The model was virtually positioned to the functional radiograph positions to simulate the boundary conditions when the knee is stressed. The model was simulated to achieve static equilibrium. Optimisation was done on ligament free length and a scaling coefficient, flexion factor, to consider the ligaments wrapping behaviour.

Our findings show the generic values for reference strain differ significantly from reference strains calculated from the optimised ligament parameters, up to 35% as percentage strain. There was also a wide variation in the reference strain values between subjects and ligaments, with a range of 37% strain between subjects. Additionally, the knee laxity recorded clinically shows a large variation between patients and it appears to be divorced from coronal alignment measured in CT. This suggests the ligaments characteristics vary widely between subjects and non-functional imaging is insufficient to determine its characteristics. These large variations necessitate a subject-specific approach when creating knee computational models and functional radiographs may be a viable method to characterise patient specific ligaments.

Introduction

Entry into orthopaedic higher surgical training remains extremely competitive, however little evidence exists regarding the validity of short-listing and interviewing for selection. This paper assesses the relative correlations of short-listing and interview scores in predicting subsequent performance as an orthopaedic trainee.

The saphenous nerve is classically described as innervating skin of the medial foot extending to the first MTP joint and thus is at risk in surgery to the medial ankle and forefoot. However, it has previously been demonstrated by the senior author that the dorsomedial branch of the superficial peroneal nerve consistently supplies the dorsomedial forefoot, leading to debate as to whether the saphenous nerve should routinely be included in ankle blocks for forefoot surgery. We undertook a cadaveric study to assess the presence and variability of the saphenous nerve.

29 feet were dissected from a level 10 cm above the medial malleolus, and distally to the termination of the saphenous nerve. In 24 specimens (83%), a saphenous nerve was present at the ankle joint. In 5 specimens the nerve terminated at the level of the ankle joint, and in 19 specimens the nerve extended to supply the skin distal to the ankle. At the ankle, the mean distance of the nerve from the tibialis anterior tendon and saphenous vein was 14mm and 3mm respectively. The mean distance reached in the foot was 5.1cm. 28% of specimens had a saphenous nerve that reached the first metatarsal and no specimens had a nerve that reached the great toe.

The current study shows that the course of the saphenous nerve is highly variable, and when present usually terminates within 5cm of the ankle. The saphenous nerve is at risk in anteromedial arthroscopy portal placement, and should be included in local anaesthetic ankle blocks in forefoot surgery, as a significant proportion of nerves supply the medial forefoot.

Sclerostin is a negative regulator of osteoblast differentiation and bone formation. Expressed by osteocytes, it acts through antagonising the Wnt/â-catenin pathway and/or BMP activity. Distraction osteogenesis, used for limb lengthening and reconstruction, can be complicated by disuse osteopenia and poor healing response, both of which would benefit from pro anabolic therapy.

We examined the effects of Sclerostin Antibody (Scl-AbIII, Amgen Inc.,) in a rat model of distraction osteogenesis. A femoral osteotomy was stabilized with an external fixator in male Sprague Dawley rats. After a week of latency, the gap was distracted twice daily for 14 days to a total of 7 mm. Saline or Scl-Ab was administered twice weekly throughout the distraction period and up to 4, 6 or 8 weeks post commencement of distraction. Three groups were examined: Saline, Continuous Scl-Ab throughout the study (C Scl-Ab), and Delayed Scl-Ab with commencement of Scl-Ab after distraction (D Scl-Ab).

Regenerate bone mineral content (BMC), determined by DEXA, was increased 36% at 4 weeks and 86% at 6 weeks with C Scl-Ab, resulting in a 65% increase in bone mineral density (BMD) at 6 weeks, compared with Saline (p<0.01). D Scl-Ab treatment showed a 41% increase in BMC and a 31% increase in BMD compared with Saline at 6 weeks (p<0.05). At 8 weeks, C Scl-Ab remained significantly increased over Saline (72% in BMC; 60% in BMD).

Micro-CT scans of the regenerate revealed increases in bone volume of 88% with C Scl Ab and 65% with D Scl-Ab compared with Saline at 6 weeks (p<0.05). By 8 weeks, these increases were 36% for C Scl-Ab (p<0.05) and 37% for D Scl-Ab compared with Saline (p<0.01). Importantly, mean moment of inertia was increased over two-fold in both Scl-Ab groups at 6 weeks compared with Saline (p<0.05). Histology at 6 weeks confirmed micro-CT data with 85–88% increases in bone volume/tissue volume (BV/TV) in the regenerate with both C Scl-Ab and D Scl-Ab compared with Saline (p<0.05). Analysis of bone formation at 6 weeks revealed increases in mineral apposition rate of 56% in C Scl-Ab and 52% in D Scl-Ab compared with Saline (p<0.05).

Scl-Ab treatment increased bone formation in this model of distraction osteogenesis, resulting in a larger regenerate callus (increased BMC and BV/TV). We expect further studies to reveal increases in mechanical strength. Scl-Ab may hold promise as a therapeutic to accelerate regenerate formation and consolidation in distraction osteogenesis for limb reconstruction.

Anatomic reduction (subcapital re-alignment osteotomy) via surgical hip dislocation – increasingly popular. While the reported AVN rates are very low, experiences seem to differ greatly between centres. We present our early experience with the first 29 primary cases and a modified fixation technique.

We modified the fixation from threaded Steinman pins to cannulated 6.5mm fully-threaded screws: retrograde guidewire placement before reduction of the head ensured an even spread in the femoral neck and head. The mean PSA (posterior slip angle) at presentation (between 12/2008 and 01/2011) was overall 68° (45–90°). 59% (17/29) were stable slips (mean PSA 68°), and 41% (12/29) were unstable slips unable to mobilise (mean PSA 67°). The vascularity of the femoral head was assessed postoperatively with a bone scan including tomography.

The slip angle was corrected to a mean PSA of 5.8° (7° anteversion to 25° PSA). We encountered no complications related to our modified fixation technique.

All cases with a well vascularised femoral head on the post-operative bone scan (15/17 stable slips and 8/12 unstable slips) healed with excellent short term results.

Both stable slips with decreased vascularity on bone scan (2/17, 12%) had been longstanding severe slips with retrospectively suspected partial closure of the physis, which has been described as a factor for increased risk of avascular necrosis (AVN). One of these cases was complicated by a posterior redislocation due to acetabular deficiency. In the unstable group, 4/12 cases (33%) had avascular heads intra-operatively and cold postoperative bone scans, 3 have progressed to AVN and collapse.

Anatomic reduction while sparing the blood supply of the femoral head is a promising concept with excellent short term results in most stable and many unstable SCFE cases. Extra vigilance for closed/closing physes in longstanding severe cases seems advisable. Regardless of treatment, some unstable cases inevitably go on to AVN.

CPT is a uniquely difficult condition, often associated with Neurofibromatosis (NF1), where bone healing is compromised. Although rare, the severity of this condition and the multiple procedures often entailed in treating it, warrant research attention. As study material is limited, animal models of the disorder are desirable for testing new treatments.

We sought to create a model of CPT where both copies of the NF1 gene were ablated at the fracture site, as has been found in some clinical specimens. NF1 floxed mice had fracture surgery; both closed fracture and open osteotomy were performed. Either a Cre- or control GFP-adenovirus was injected into the fracture site at day zero. Recombination was confirmed in ZAP reporter mice. Additionally, cell culture studies were used to examine the possible responses of NF1+/+ (wild type) NF1+/− or NF1−/− to drugs which may rescue the dysregulated Ras/MAPK pathway in NF1.

In closed fractures, radiographic bridging was 100% in NF1+/+ calluses and <40% in NF1−/− calluses (P<0.05). In open fractures, radiographic bridging was 75% in NF1+/+ calluses and <30% in NF1−/− calluses (P<0.05). In both fracture repair models the NF1−/− state was associated with a significant up to 15-fold increase in fibrotic tissue invading the callus by week 3. In NF1−/− fractures, large numbers of TRAP+ cells were observed histologically in the fibrotic tissue. Closed fractures also showed a significant increase in BRDU labelled proliferating cells in the callus. In cell culture models of NF1 deficient osteogenesis, NF1−/− progenitors were found to be significantly impaired in their capacity to form a calcified matrix as measured by Alizarin Red S staining and osteogenic markers (Runx2, Osteocalcin, Alp expression). However, when differentiated calvarial NF1 floxed osteoblasts were treated with Cre adenovirus, mineralization was not affected, suggesting that NF1 impacts on osteogenic differentiation rather than mature cell function. Treatment with MEK inhibitor PD0325901 was found to rescue the NF1−/− progenitor differentiation phenotype and permit robust mineralization. Treatment with the JNK inhibitor SP600125 was also able to improve ALP activity and mineralization in NF1+/− osteoprogenitors compared to control cells.

This model of NF1 −/− induction at a fracture or osteotomy site closely replicates the clinical condition of CPT, with lack of bone healing and fibrous tissue invasion. Underlying defects in bone cell differentiation in NF1 deficiencies can be at least partially rescued by JNK and MEK inhibitors.

Rapid prototyping (RP), especially useful in surgical specialities involving critical three-dimensional relationships, has recently become cheaper to access both in terms of file processing and commercially available printing resources.

One potential problem has been the accuracy of models generated. We performed computed tomography on a cadaveric human patella followed by data conversion using open source software through to selective-laser-sintering of a polyamide model, to allow comparative morphometric measurements (bone v. model) using vernier calipers. Statistical testing was with Student's t-test.

No significant differences in the dimensional measurements could be demonstrated. These data provide us with optimism as to the accuracy of the technology, and the feasibility of using RP cheaply to generate appropriate models for operative rehearsal of intricate orthopaedic procedures.

A Ruys, School of Aerospace, Mechanical and Mechatronic Engineering, University of Sydney, Sydney

The effects of bone anabolics can be maximised by systemic co-treatment with an anti-catabolic. Local treatment may reduce the total drug required and produce superior outcomes, although high dose local bisphosphonate has been reported to impair bone formation. We have explored local co-delivery of anabolic/anti- catabolic bone drugs at different doses.

We manufactured biodegradable poly-D,L-lactic acid (PDLLA) polymer pellets containing 25g BMP-7 as an anabolic with or without 0.002mg-2mg Pamidronate (PAM) as an anti-catabolic. Polymer pellets were surgically implanted into the hind limb muscle of female C57BL6 mice. Animals were sacrificed at three weeks post- implantation and bone formation was assessed by radiography, microcomputed tomography (microCT) and histology. Histological staining on five Âm paraffin sections included haematoxylin/eosin, alcian blue/picrosirius red, and tartrate- resistant acid phosphatase (TRAP).

Radiographic and microCT data confirmed that 0.02mg and 0.2mg local PAM doses significantly augmented BMP-7 induced bone formation. In contrast, 2mg local PAM dramatically reduced the amount of bone present. This dose was comparable to that used by Choi et al who also reported impaired bone formation in a skull defect model.2 three-dimensional microCT and histological analyses of the ectopic bone and surrounding muscle showed a cortical shell covering the polymer pellet, which had not completely resorbed.

Histological analysis at the pellet/bone interface showed tissue granulation and no inflammation, suggesting a high biocompatibility of the PDLLA polymer. The presence of bisphosphonate also decreased the amount of fatty marrow tissue seen within between the cortical shell and the unresorbed polymer.

For the first time we can demonstrate synergy with local BMP/bisphosphonate. This study confirms that high local PAM doses can have negative effects, indicating a need to avoid overdosing. The lack of implant degradation suggests a need to optimise polymer degradation for bone tissue engineering application.

Developing biomaterials for bone regeneration that are highly bioactive, resorbable and mechanically strong remains a challenge. Zreiqat's lab recently developed novel scaffolds through the controlled substitution of strontium (Sr) and zinc (Zn) into calcium silicate, to form Sr-Hardystonite and Hardystonite, respectively and investigated their in vivo biocompatibility and osteoconductivity

We synthesized 3D scaffolds of Sr-Hardystonite, Hardystonite and compared them to the clinically used tricalcium phosphate (micro-TCP) (6 × 6 × 6 mm) using a polyurethane foam template to produce a porous scaffold. The scaffolds were surgically implanted in the proximal tibial metaphysis of each tibia of Female Wistar rats. Animals were sacrificed at three weeks and six weeks post-implantation and bone formation and scaffold resorption were assessed by microcomputed tomography (micro-CT) histomorphometry and histology. Histological staining on undecalcified sections included Toluidine blue, tartrate-resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP).

The bone formation rate and mineral apposition rate will be determined by analysing the extent and separation of fluorescent markers by fluorescent microscopy micro-CT results revealed higher resorbability of the developed scaffolds (Sr-Hardystonite and Hardystonite) which was more pronounced with the Sr-Hardystonite. Toluidine blue staining revealed that the developed ceramics were well tolerated with no signs of rejection, necrosis, or infection. At three weeks post implantation, apparent bone formation was evident both at the periphery and within the pores of the all the scaffolds tested. Bone filled in the pores of the Sr- Hardystonite and Hardystonite scaffolds and was in close contact with the ceramic. In contrast, the control scaffolds showed more limited bone ingrowth and a cellular layer separating the ceramic scaffolds from the bone. By six weeks the Hardystonite and Sr Hardystonite scaffolds were integrated with the bone with most pores filled with new bone. The control scaffold showed new bone formation in the plane of the cortical bone but little new bone where the scaffold entered the marrow space. Sr Hardystonite showed the greatest resorbability with replacement of the ceramic material by bone.

We have developed novel engineered scaffolds (Sr-Hardystonite) for bone tissue regeneration. The developed scaffolds resorbed faster than the clinically used micro- TCP with greater amount of bone formation replacing the resorbed scaffold.

R Appleyard, Murray Maxwell Biomechanics Lab, Royal North Shore Hospital, Sydney

The fundamental mechanisms that underlie tendon breakdown are ill understood. There is an emerging hypothesis that altered mechanical strain modulates the metabolism and/or phenotype of tenocytes, disrupting the balance of matrix synthesis and degradation, and that rupture then occurs through an abnormal tendon matrix. The critically regulated genes have not yet been determined. We have developed sheep model in sheep where both stress-deprived and over-stressed areas can be examined in the one tendon, to evaluate the pathological and molecular changes over time. We have also used ‘wild type’ and genetically modified mice to determine the role of specific enzymes and proteoglycans in tendon degeneration. Stress-deprived and over-stressed regions showed classical changes of increased cellularity and vascularity, rounded tenocytes and interfascicular matrix infiltration. These structural changes resolved for up to one year after injury. Resolution was more rapid in over-stressed regions. Irrespective of the initiating stress, proteoglycan staining and chondroid metaplasia increased in tendon with time. There were distinct molecular and temporal differences between regions, which are reviewed here. While tendon degeneration has traditionally been regarded as a single field of change, our studies show that at a molecular level, the injured tendon may be regarded as a number of distinct regions—overloaded and underloaded, adjacent to bone or adjacent to muscle. Each region manifests distinct molecular changes, driven by relevant gene expression.

While collagen metabolism in pathological tendon has received much attention, accumulation of proteoglycan is also consistently induced by altered mechanical loading. We suggest that ADAMTS enzymes, which cleave aggrecan, versican and small proteoglycans, may play a significant role in tendon homeostasis and pathology. Regulating proteoglycan turnover may represent a novel target for treating tendon degeneration. We have initiated studies using mesenchymal stem cells (MSC), not to directly augment healing but to modify the molecular pathology in tendon resulting from altered loading. Preliminary data indicates that injection of MSC into an acute tendon defect significantly abrogates the increase in expression of aggrecan and collagen degrading metalloproteinases in the adjacent over-stressed tendon. This may decrease the resultant degeneration. The effects of MSC in treating tendon degeneration are reviewed here, as are the possible benefits of radiofrequency microtenotomy.

Bone morphogenetic proteins (BMPs) are able to induce osteogenic differentiation in many cells, including muscle cells. However, the actual contribution of muscle cells to bone formation and repair is unclear. Our objective was to examine the capacity of myogenic cells to contribute to BMP-induced ectopic bone formation and fracture repair.

Osteogenic gene expression was measured by quantitative PCR in osteoprogenitors, myoblasts, and fibroblasts following BMP-2 treatment. The MyoD-Cre x ROSA26R and MyoD-Cre x Z/AP mouse strains were used to track the fate of MyoD+ cells in vivo. In these double-transgenic mice, MyoD+ progenitors undergo a permanent recombination event to induce reporter gene expression. Ectopic bone was produced by the intramuscular implantation of BMP-7. Closed tibial fractures and open tibial fractures with periosteal stripping were also performed. Cellular contribution was tracked at one, two and three week time points by histological staining.

Osteoprogenitors and myoblasts exhibited comparable expression of early and late bone markers; in contrast bone marker expression was considerably less in fibroblasts. The sensitivity of cells to BMP-2 correlated with the expression of BMP receptor-1a (Bmpr1a). Pilot experiments using the MyoD-Cre x Rosa26R mice identified a contribution by MyoD expressing cells in BMP-induced ectopic bone formation. However, false positive LacZ staining in osteoclasts led us to seek alternative systems such as the MyoD-cre x Z/AP mice that have negligible background staining. Initially, a minor contribution from MyoD expressing cells was noted in the ectopic bones in the MyoD-cre x Z/AP mice, but without false positive osteoclast staining. Soft tissue trauma usually precedes the formation of ectopic bone. Hence, to mimic the clinical condition more precisely, physical injury to the muscle was performed. Traumatising the muscle two days prior to BMP-7 implantation: (1) induced MyoD expression in quiescent satellite cells; (2) increased ectopic bone formation; and (3) greatly enhanced the number of MyoD positive cells in the ectopic bone. In open tibial fractures the majority of the initial callus was MyoD+ indicating a significant contribution by myogenic cells. In contrast, closed fractures with the periosteum intact had a negligible myogenic contribution.

Myoblasts but not fibroblasts were highly responsive to BMP stimulation and this was associated with BMP receptor expression. Our transgenic mouse models demonstrate for the first time that muscle progenitors can significantly contribute to ectopic bone formation and fracture repair. This may have translational applications for clinical orthopaedic therapies.

The aims of this study were (1) to assess whether rotational stability testing in Gartland III supracondylar fractures can be used intra-operatively in order to assess fracture stability following fixation with lateral-entry wires and (2) to quantify the incidence of rotational instability following lateral-entry wire fixation in Gartland type III supracondylar humeral fractures in children.

Twenty-one consecutive patients admitted with Grade III supracondylar fractures at the Children's Hospital at Westmead were surgically treated according to a predetermined protocol. Following closed fracture reduction, 2 lateral-entry wires were inserted under radiographic control. Stability was then assessed by comparing lateral x-ray images in internal and external rotation. If the fracture was found to be rotationally unstable by the operating surgeon, a third lateral-entry wire was inserted and images repeated. A medial wire was used only if instability was demonstrated after the insertion of three lateral wires.

Rotational stability was achieved with two lateral-entry wires in 6 cases, three lateral-entry wires in 10 cases and with an additional medial wire in 5 cases. Our results were compared to a control group of 24 patients treated at our hospital prior to introduction of this protocol. No patients returned to theatre following introduction of our protocol as opposed to 6 patients in the control group. On analysis of radiographs, the protocol resulted in significantly less fracture position loss as evidenced by change in Baumann's angle (p<0.05) and lateral rotational percentage (p<0.05).

We conclude that the introduction of rotational stability testing allows intra-operative assessment of fracture fixation. Supracondylar fractures that are rotationally stable intra-operatively following wire fixation are unlikely to displace post-operatively. Only a small proportion (26%) of these fractures were rotationally stable with 2 lateral-entry wires. This may be a reflection of either the fracture configuration or inability to adequately engage the medial column.

Background

Distraction Osteogenesis can be complicated by regenerate insufficiency resulting in prolonged implant usage or regenerate failure with malalignment or fracture. Experimental evidence has demonstrated that bisphosphonates may mediate improved local limb BMD and regenerate strength.