Background

Calcaneal osteomyelitis remains a difficult condition to treat with high rates of recurrence and below knee amputation; particularly in cases of severe soft tissue destruction.

Background

The treatment of chronic calcaneal osteomyelitis is a challenging and increasing problem because of the high prevalence of diabetes mellitus and operative fixation of heel fractures. In 1931, Gaenslen reported treatment of hematogenous calcaneal osteomyelitis by surgical excision through a midline, sagittal plantar incision. We have refined this approach to allow successful healing and early mobilization in a modern series of complex patients with hematogenous, diabetic, and postsurgical osteomyelitis.

Introduction

Primary ankle arthroplasty (TAR) is increasingly used to treat end-stage ankle arthritis. Reported revision rates of TAR vary from 8.5% to 11.1% at 9 years. Revision surgery remains technically challenging with options ranging from simple joint debridement to tibio-talar-calcaneal fusion. The efficacy of these procedures remains unclear and there is no consensus on optimal revision options.

Tendinopathy can commonly occur around the foot and ankle resulting in isolated rupture, debilitating pain and degenerative foot deformity. The pathophysiology and key cells involved are not fully understood. This is partly because the dense collagen matrix that surrounds relatively few resident cells limits the ability of previous techniques to identify and target those cells of interest. In this study, we apply novel single cell RNA sequencing (CITE-Seq) techniques to healthy and tendinopathic foot/ankle tendons. For the first time we have identified multiple sub-populations of cells in human tendons. These findings challenge the view that there is a single principal tendon cell type and open new avenues for further study. Healthy tendon samples were obtained from patients undergoing tendon transfer procedures; including tibialis posterior and FHL. Diseased tendon samples were obtained during debridement of intractable Achilles and peroneal tendinopathy, and during fusion of degenerative joints. Single cell RNA sequencing with surface proteomic analysis identified 10 sub-populations of human tendon derived cells. These included groups expressing genes associated with fibro-adipogenic progenitors (FAPs) as well as ITGA7+VCAM1- recently described in mouse muscle but, as yet, not human tendon. In addition we have identified previously unrecognised sub-classes of collagen type 1 associated tendon cells. Each sub-class expresses a different set of extra-cellular matrix genes suggesting they each play a unique role in maintaining the structural integrity of normal tendon. Diseased tendon harboured a greater proportion of macrophages and cytotoxic lymphocytes than healthy tendon. This inflammatory response is potentially driven by resident tendon fibroblasts which show increased expression of pro-inflammatory cytokines. Finally, identification of a previously unknown sub-population of cells found predominantly in tendinopathic tissue offers new insight into the underlying pathophysiology. Further work aims to identify novel proteins targets for possible therapeutic pathways.

Introduction

The aim of this study was to identify the effects of first MTPJ arthritis, ankle arthritis and hallux valgus on patient reported outcomes, and to assess the efficacy of surgery.

The diagnosis of Lisfranc ligament disruption is notoriously difficult. Radiographs and MRI scans are often ambiguous therefore a stress-test examination under anaesthesia is commonly required. Two midfoot stress-tests are in current practice, namely the varus first ray stress-test and the pronation abduction test. The optimal type of stress-test is not however evaluated in the literature. We hypothesised that after the loss of the main plantar stabiliser (the Lisfranc ligament) the patient would demonstrate dorsal instability, not the classic 1^st/2^nd metatarsal diastasis commonly described. We therefore devised a push-up test (placement of a force under the 2^nd metatarsal in an attempt to elevate the base away from the middle cuneiform on the lateral radiograph). We aimed to initially test our hypothesis on a cadaveric model.

Twelve fresh frozen cadaveric specimens without previous foot injury were used. The 2^nd tarsometatarsal joint was exposed and the Lisfranc ligament and dorsal capsule were incised. An image intensifier was positioned and standard anteroposterior (AP) and lateral views were obtained. Two previously reported AP stress-tests (varus first ray stress test, pronation abduction test) and the novel test under investigation (‘Lisfranc Push-Up’ test) were duly performed. Images were obtained once the investigator felt the appropriate views were achieved.

All twelve of the Lisfranc Push-Up tests showed dorsal subluxation of the 2^nd metatarsal on the middle cuneiform of greater than 2mm on the lateral radiograph. No diastasis of the 1^st/2^nd metatarsals was seen in any of the specimens on the AP radiograph for either of the other two stress-tests.

The authors have described a novel way of demonstrating the dorsal instability associated with the ligamentous Lisfranc injury. Our results support the Lisfranc Push-Up test as a reproducible and sensitive method for assessing ligamentous Lisfranc injuries. In our cadaveric model the previously described stress-tests do not work.

Operative and non-operative treatment regimens for Achilles tendon ruptures vary greatly but commonly involve rigid casting or functional bracing. The aim of our study was to investigate the extent of tendon apposition following such treatments.

Twelve fresh-frozen, adult below knee lower-extremity cadaveric specimens with intact proximal tibiofibular joints were used. Each was prepared by excising a 10cm × 5cm skin and soft tissue window exposing the Achilles tendon. With the ankle in neutral position, the tendon was transfixed with a 2mm k-wire into the tibia, 8cm from its calcaneal insertion. A typical post-rupture gap was created by excising a 2.5cm portion of tendon between 3.5cm and 6cm from its calcaneal insertion.

The specimens were then placed into a low profile walker boot (SideKICK^TM, Procare) without wedges and a window cut into the back. The distance between the proximal and distal Achilles tendon cut edges was measured and repeated with 1, 2 and 3 (10mm) wedges. Subsequently the specimens were placed into a complete below knee cast in full equinus which was also windowed.

The Achilles tendon gap (mean +/− SD) measured: 2.7cm (0.5) with no wedge, 2.3cm (0.4) with 1, 2.0cm (0.4) with 2, 1.5cm (0.4) with 3 wedges and 0.4cm (0.3) in full equinus cast.

The choice of treatment had a significant effect on tendon gap (p< 0.0001 – repeated measures ANOVA), and all pairwise comparisons were significantly different (Bonferroni), with all p< 0.001, apart from 0 wedge vs. 1 wedge (p< 0.01) and 1 wedge vs. 2 wedges (p< 0.05).

Our results showed that each wedge apposed the tendon edges by approximately 0.5cm with the equinus cast achieving the best apposition. Surgeons should consider this when planning appropriate immobilisation regimes for Achilles tendon ruptures.

During surgical reduction of ankle injuries with syndesmotic instability surgeons often use the anteroposterior (AP) and mortise radiographs to assess reduction. Current literature predicts 50% are malreduced mainly in the sagittal plane. Our aim was to develop a radiographic measure based on the lateral view to assess both the normal and abnormal fibula/tibia relationship after simulated syndesmotic malreduction and to evaluate the effect on commonly used AP and mortise measurements.

Nine fresh-frozen cadaveric specimens were dissected to the level of the syndesmosis. AP, mortise and talar dome lateral radiographs were obtained before and following syndesmosis division and posterior fibula displacement. On the lateral radiograph a line was drawn (Orthoview) from the anterior border of the fibula bisecting a line drawn from the anterior to posterior lips of the distal tibia. The ratio of the anterior-posterior segments was calculated. Also a line was drawn from the posterior border of the fibula and the distance was measured to the posterior lip of the tibia.

At 0, 2, 4 and 6mm of displacement the ratio measured 1.3±0.2, 1.1±0.2, 0.9±0.2 and 0.7±0.2 respectively with all pairwise comparisons being significantly different. Inter- and intra-observer variability varied from substantial to perfect. The only significant medial clear space (MCS) difference was on the mortise view between 0mm (2.0±0.3mm) and 6mm (2.4±0.4mm) displacement.

Our new measure of syndesmotic reduction is reproducible and can detect from 2mm of saggital fibular displacement. At maximum fibular displacement the increase in MCS was less than 1mm. This demonstrates standard mortise radiographs are poor at detecting syndesmotic reduction. An interesting observation was in all specimens prior to any displacement, the posterior fibular line always bisected the posterior lip of the tibia or lay just anterior to it, never posterior. This could serve as a useful adjunct for surgeons when assessing syndesmotic reduction intra-operatively.