Aims

Machine learning (ML), a branch of artificial intelligence that uses algorithms to learn from data and make predictions, offers a pathway towards more personalized and tailored surgical treatments. This approach is particularly relevant to prevalent joint diseases such as osteoarthritis (OA). In contrast to end-stage disease, where joint arthroplasty provides excellent results, early stages of OA currently lack effective therapies to halt or reverse progression. Accurate prediction of OA progression is crucial if timely interventions are to be developed, to enhance patient care and optimize the design of clinical trials.

Aims

To explore key stakeholder views around feasibility and acceptability of trials seeking to prevent post-traumatic osteoarthritis (PTOA) following knee injury, and provide guidance for next steps in PTOA trial design.

Abstract

Aims

Accumulated evidence indicates that local cell origins may ingrain differences in the phenotypic activity of human osteoblasts. We hypothesized that these differences may also exist in osteoblasts harvested from the same bone type at periarticular sites, including those adjacent to the fixation sites for total joint implant components.

Aims

To investigate factors that contribute to patient decisions regarding attendance for arthroplasty during the COVID-19 pandemic.

Charcot neuroarthropathy is a rare but serious complication of diabetes, causing progressive destruction of the bones and joints of the foot leading to deformity, altered biomechanics and an increased risk of ulceration.

Management is complicated by a lack of consensus on diagnostic criteria and an incomplete understanding of the pathogenesis. In this review, we consider recent insights into the development of Charcot neuroarthropathy.

It is likely to be dependent on several interrelated factors which may include a genetic pre-disposition in combination with diabetic neuropathy. This leads to decreased neuropeptides (nitric oxide and calcitonin gene-related peptide), which may affect the normal coupling of bone formation and resorption, and increased levels of Receptor activator of nuclear factor kappa-B ligand, potentiating osteoclastogenesis.

Repetitive unrecognized trauma due to neuropathy increases levels of pro-inflammatory cytokines (interleukin-1β, interleukin-6, tumour necrosis factor α) which could also contribute to increased bone resorption, in combination with a pre-inflammatory state, with increased autoimmune reactivity and a profile of monocytes primed to transform into osteoclasts - cluster of differentiation 14 (CD14).

Increased blood glucose and loss of circulating Receptor for Advanced Glycation End-Products (AGLEPs), leading to increased non-enzymatic glycation of collagen and accumulation of AGLEPs in the tissues of the foot, may also contribute to the pathological process.

An understanding of the relative contributions of each of these mechanisms and a final common pathway for the development of Charcot neuroarthropathy are still lacking.

Cite this article: S. E. Johnson-Lynn, A. W. McCaskie, A. P. Coll, A. H. N. Robinson. Neuroarthropathy in diabetes: pathogenesis of Charcot arthropathy. Bone Joint Res 2018;7:373–378. DOI: 10.1302/2046-3758.75.BJR-2017-0334.R1.

Controlled differentiation of Human mesenchymal stem cells (hMSCs) is required for timely induction of bone growth in implantable biomaterials. Differentiation of hMSCs towards a particular lineage depends upon their microenvironment, which is a complex mixture of various physical, chemical and biological parameters. The role of Bone morphogenic protein (BMP2) in early induction of bone formation is well established. Clinical experience and in vitro study has shown that presentation of this protein in small quantities by surface immobilisation significantly induces osteogenic differentiation compared to large quantities provided in solution. This project focuses on developing and understanding responsive micro/nano porous interfaces which deliver BMP2 in a dose dependent fashion to control osteogenic diffentiation of hMSCs. We hypothesise that use of porous membranes primed with LbL deposition of biomacromolecules such as COL and HA will help in induction of cell attachment and growth whilst controlled and localised delivery of BMP2 released from the layers of these porous constructs will induce sustained differentiation of hMSCs. By controlling pore size of membranes, rate of release of BMP2 can be controlled. We use fluorescently labelled Dextran (Flu-DEX) as model protein to study control release mechanism, which is of similar size to BMP2. Polycarbonate (PC) track etched membranes with various pore sizes were used for LbL assembly of COL/HA/Flu-DEX along with hydrolytically degradable polymer Poly-Beta amino ester (Poly2). Six bilayers were constructed into porous membranes with (COL-Flu-DEX)6 and (Poly2-Flu-DEX)6. Use of hydrolytically degradable polymer significantly enhances release of Flu-DEX compared to control (COL-Flu-DEX)6 assembly. Compared to flat (non porous) surface, release from porous samples maintained a relatively slow and steady release. We are currently investigating release of BMP2 using this approach and their influence on the differentiation of hMSCs in vitro

Background A biomaterial serves to support, organize and directly influence the behaviour of growing cells. Chitosan has the capability to be a very useful biomaterial in the speciality of orthopaedics, due to its excellent biocompatibility, and physical properties that allow topographical modification. Chitosan films have potential to be used to coat implant surfaces, regulating bone cells at the implant interface. Enhanced integration may therefore help towards solving problems such as aseptic loosening.

Method 85% deacylated chitosan (Sigma) was dissolved in 2% acetic overnight. The viscous chitosan was then sterilized by autoclaving for 10 minutes. PDMS patterned stamps produced from a silicon mould were added to the viscous chitosan and as the chitosan film forms the topographic impression is left on the surface. The gel was then dried for 36 hours in a sterile system. The pH is neutralized with NaOH1M for 24 hours. The gel was washed in sterile hanks balanced salt solution until the pH was 7.4. Osteoblasts were then grown on these surfaces in a cell culture system and analysed by light microscopy and image analysis.

Results We have successfully designed a protocol for the production of sterile topographically modified chitosan, with surface features that can be produced in the range of 1–100um. We have shown that cells on un-modified chitosan differentiate and form bone at a much slower rate than on chitosan with a modified surface. Findings supported by in-situ alkaline phosphatase levels. Control can be exerted on cell shape and inter-cellular interactions based upon shape and surface area between shapes; with a smaller surface area making adhesion more difficult.

Conclusion. Our data shows that osteoblasts can be controlled by altering chitosans surface topography. Being able to influence biology by changing biomaterial surface features will enhance interaction at the bone implant interface, allowing greater implant integration.

Statement of purpose: To evaluate survivorship and knee function in patients who have undergone Kinematic Condylar Total Knee Replacement at a minimum of 15 years.

Methods: We evaluated all patients undergoing primary cemented TKR with the Kinematic Condylar implant (Howmedica), between January 1981 and December 1988. All operations were performed by a single surgeon through a medial parapatellar approach, with sparing of the PCL, all cemented and no patellae resurfaced.

Operation notes were analysed to confirm the type of procedure, underlying diagnosis, and thickness of tibial insert. Information was derived from patient records and postal questionnaire to all surviving patients, which included: WOMAC, SF-36, satisfaction scale and history of revision surgery.

Results: We have identified a total of 804 consecutive cases, 185 of these were bilateral giving a total of 619 patients. Mean age at implantation was 66 (range 17 to 83), with female:male ratio of 3:1. The underlying diagnosis was Osteoarthritis in 49%, and Rheumatoid Arthritis in 51% of patients.

As at September 2003 there were 153 patients (25%) still alive, using revision as an endpoint survivorship was 59.3% at a mean time since implantation of 17 years 8 months. Pain and function portions of the WOMAC questionnaire revealed mean scores of 37 and 47 out of 100.

Conclusion: This cohort has been shown to have 92% implant survivorship at ten years. We have shown that the survivorship deteriorates significantly between 10 and 17 years. Functional and pain scores after 17 years for patients with surviving implants were poor.

Survival was significantly better in females, no effect from pre-operative diagnosis was seen. 73% of these patients had 6mm tibial inserts, we postulate that the deterioration in survival is related to accelerated poly-ethylene wear beyond 10 years.