Aims

The aim of this study was to estimate the 90-day periprosthetic joint infection (PJI) rates following total knee arthroplasty (TKA) and total hip arthroplasty (THA) for osteoarthritis (OA).

Aims

National joint registries under-report revisions for periprosthetic joint infection (PJI). We aimed to validate PJI reporting to the Australian Orthopaedic Association National Joint Arthroplasty Registry (AOANJRR) and the factors associated with its accuracy. We then applied these data to refine estimates of the total national burden of PJI.

Aims

This study aimed to describe the use of revision knee arthroplasty in Australia and examine changes in lifetime risk over a decade.

Aims

This study aims to describe the pre- and postoperative self-reported health and quality of life from a national cohort of patients undergoing elective total conventional hip arthroplasty (THA) and total knee arthroplasty (TKA) in Australia. For context, these data will be compared with patient-reported outcome measures (PROMs) data from other international nation-wide registries.

Aims

Displaced femoral neck fractures (FNF) may be treated with partial (hemiarthroplasty, HA) or total hip arthroplasty (THA), with recent recommendations advising that THA be used in community-ambulant patients. This study aims to determine the association between the proportion of FNF treated with THA and year of surgery, day of the week, surgeon practice, and private versus public hospitals, adjusting for known confounders.

Aims

Femoral stems with exchangeable (modular) necks were introduced to offer surgeons an increased choice when determining the version, offset and length of the femoral neck during total hip arthroplasty (THA). It was hoped that this would improve outcomes and reduce complications, particularly dislocation. In 2010, the Australian Orthopaedic Association National Joint Replacement Registry (AOANJRR) first reported an increased rate of revision after primary THA using femoral stems with an exchangeable neck. The aim of this study was to provide a more comprehensive up-to-date analysis of primary THA using femoral stems with exchangeable and fixed necks.

We assessed the outcome of patients who were lost to follow-up after arthroplasty by a single surgeon. The aim was to validate the surgeon’s data set with the Australian Orthopaedic Association National Joint Replacement Registry and determine the outcome of those patients lost to follow-up.

Prospective data on patient demographics, operative details and outcomes of the surgeon’s 1192 primary unicompartmental knee arthroplasty (UKA) procedures were analysed. There were 69 knees in patients who were lost to follow-up, among whom the Registry identified 31 deaths and eight revisions.

The cumulative percentage revision (CPR) at seven years using the additional Registry data was 8.8% (95% confidence interval (CI) 7 to 11). Using the surgeon’s data, the CPR at seven years was 8% (95% CI 6.3 to 10.1) for the best-case scenario where loss to follow-up was excluded, and 16% (95% CI 13.8 to 19.4) for the worst-case scenario, where all patients lost to follow-up were deemed to have been revised. There was a significantly higher mortality rate in those patients lost to follow-up.

This study demonstrates that a national joint registry can be used by individual surgeons to establish more accurate revision rates in their arthroplasty patients. This is expected to facilitate a more rigorous audit of surgical outcomes by surgeons and lead to more accurate and uniform reporting of the results of arthroplasty in general.

Mononuclear osteoclast precursors are present in the wear-particle-associated macrophage infiltrate found in the membrane surrounding loose implants. These cells are capable of differentiating into osteoclastic bone-resorbing cells when co-cultured with the rat osteoblast-like cell line, UMR 106, in the presence of 1,25(OH)₂ vitamin D₃. In order to develop an in vitro model of osteoclast differentiation which more closely parallels the cellular microenvironment at the bone-implant interface in situ, we determined whether osteoblast-like human bone-derived cells were capable of supporting the differentiation of osteoclasts from arthroplasty-derived cells and analysed the humoral conditions required for this to occur.

Long-term co-culture of arthroplasty-derived cells and human trabecular-bone-derived cells (HBDCs) resulted in the formation of numerous tartrate-resistant-acid-phosphatase (TRAP) and vitronectin-receptor (VNR)-positive multinucleated cells capable of extensive resorption of lacunar bone. The addition of 1,25(OH)₂ vitamin D₃ was not required for the formation of osteoclasts and bone resorption. During the formation there was release of substantial levels of M-CSF and PGE₂. Exogenous PGE₂ (10⁻⁸ to 10⁻⁶M) was found to stimulate strongly the resorption of osteoclastic bone. Our study has shown that HBDCs are capable of supporting the formation of osteoclasts from mononuclear phagocyte precursors present in the periprosthetic tissues surrounding a loose implant. The release of M-CSF and PGE₂ by activated cells at the bone-implant interface may be important for the formation of osteoclasts at sites of pathological bone resorption associated with aseptic loosening.

Bone loss around replacement prostheses may be related to the activation of mononuclear phagocytes (MNP) by prosthetic wear particles. We investigated how osteoblast-like cells were regulated by human MNP stimulated by particles of prosthetic material.

Particles of titanium-6-aluminium-4-vanadium (TiAlV) stimulated MNP to release interleukin (IL)-1β, tumour necrosis factor (TNF)α, IL-6 and prostaglandin E₂ (PGE₂). All these mediators are implicated in regulating bone metabolism. Particle-activated MNP inhibited bone cell proliferation and stimulated release of IL-6 and PGE₂. The number of cells expressing alkaline phosphatase, a marker associated with mature osteo-blastic cells, was reduced. Experiments with blocking antibodies showed that TNFα was responsible for the reduction in proliferation and the numbers of cells expressing alkaline phosphatase. By contrast, IL-1β stimulated cell proliferation and differentiation. Both IL-1β and TNFα stimulated IL-6 and PGE₂release from the osteoblast-like cells.

Our results suggest that particle-activated mono-nuclear phagocytes can induce a change in the balance between bone formation and resorption by a number of mechanisms.

Our aim was to determine whether in vitro studies would detect differences in the cellular response to wear particles of two titanium alloys commonly used in the manufacture of joint replacement prostheses. Particles were of the order of 1 μm in diameter representative of those found adjacent to failed prostheses.

Exposure of human monocytes to titanium 6-aluminium 4- vanadium (TiAlV) at concentrations of 4 x 10⁷ particles/ml produced a mean prostaglandin E₂ release of 2627.6 pM; this was significantly higher than the 317.4 pM induced by titanium 6-aluminium 7-niobium alloy (TiAlNb) particles (p = 0.006). Commercially-pure titanium particles induced a release of 347.8 pM. In addition, TiAlV stimulated significantly more release of the other cell mediators, interleukin-1, tumour necrosis factor and interleukin-6. At lower concentrations of particles there was less mediator release and less obvious differences between materials. None of the materials caused significant toxicity.

The levels of inflammatory mediators released by phagocytic cells in response to wear particles may influence the amount of periprosthetic bone loss. Our findings have shown that in vitro studies can detect differences in cellular response induced by particles of similar titanium alloys in common clinical use, although in vivo studies have shown little difference. While in vitro studies should not be used as the only form of assessment, they must be considered when assessing the relative biocompatibility of different implant materials.