Consumer Prices for Surgical Management of Ankle Arthritis: Limited Availability and Wide Variability.

Background: Healthcare costs for the surgical management of ankle arthritis continue to rise. Patients are generally unaware of the prices of the services they use. Understanding the costs associated with surgical management of ankle arthritis is an important facet of patient care. The purposes of this study were to (1) determine the access to the surgical cost of total ankle arthroplasty (TAAs) and ankle arthrodesis and (2) the variability of the price between the two procedures. Methods: Fifty foot and ankle centers (25 academic, 25 private) that perform TAAs and ankle arthrodeses were contacted using a standardized patient script. The described patient was a 63-year-old man who had failed conservative treatment of ankle arthritis. Each institution was contacted up to three times in an attempt to obtain a full-bundled surgical quote for a TAA and an ankle arthrodesis. Results: Twenty-one centers (42%, 14 academic, 7 private) were able to provide a quote for a TAA and an ankle arthrodesis. The mean bundled price for a TAA was $50,332 (SD ±$25,744), with the mean academic and private center quote being $56,529 and$37,937, respectively. The mean bundled price for an ankle arthrodesis was $41,756 (SD ±$26,033), with the mean academic and private center quote being $48,116 and$29,037, respectively. No statistically significant difference was found between the bundled prices for TAA and ankle arthrodesis. Discussion: This study demonstrated limited availability of consumer prices for TAA and ankle arthrodesis. When comparing different institutions for surgical management of ankle arthritis, there was a wide range of quotes for both TAA and ankle arthrodesis. When comparing the choice of surgical management for ankle arthritis, no statistically significant difference was observed in price between TAA and ankle arthrodesis

Expression of the chemokine receptor CCR5 in psoriasis and results of a randomized placebo controlled trial with a CCR5 inhibitor

Several reports have indicated that the chemokine receptor CCR5 and its ligands, especially CCL5 (formerly known as RANTES), may play a role in the pathogenesis of psoriasis. The purpose of this investigation was to examine the expression of CCR5 and its ligands in chronic plaque psoriasis and to evaluate the clinical and immunohistochemical effect of a CCR5 receptor inhibitor. Immunohistochemical analysis showed low but significant increased total numbers of CCR5 positive cells in epidermis and dermis of lesional skin in comparison to non-lesional skin. However, relative expression of CCR5 proportional to the cells observed revealed that the difference between lesional and non-lesional skin was only statistically significant in the epidermis for CD3 positive cells and in the dermis for CD68 positive cells. Quantification of mRNA by reverse transcriptase-polymerase chain reaction only showed an increased expression of CCL5 (RANTES) in lesional skin. A randomized placebo-controlled clinical trial in 32 psoriasis patients revealed no significant clinical effect and no changes at the immunohistochemical level comparing patients treated with placebo or a CCR5 inhibitor SCH351125. We conclude that although CCR5 expression is increased in psoriatic lesions, this receptor does not play a crucial role in the pathogenesis of psoriasis

The role of dendritic cells in the immunopathogenesis of psoriasis

Psoriasis vulgaris is a chronic inflammatory skin disease that is marked by a complex interplay of dendritic cells (DCs), T-cells, cytokines, and downstream transcription factors as part of a self-sustaining type 1 cytokine network. As integral players of the immune system, DCs represent antigen-presenting cells that are crucial for efficient activation of T-cells and B-cells. DCs have also been linked to distinct chronic inflammatory conditions, including psoriasis. In the setting of psoriasis therapy, DC/T cell interactions serve as a potential target for biologic response modifiers. Here we describe the major DC subsets as well as the immunologic involvement of DCs within the context of psoriatic lesions

Osteochondral lesions of the talus: Current treatment modalities and future possibilities

Purpose of review: Symptomatic osteochondral lesions of the talus are a common clinical finding for orthopaedic surgeons that treat disorders of the ankle. Multiple treatment options exist for this entity. We will review recent advances in the understanding of osteochondral defects, their diagnosis and classification, treatment options, and the future direction that the field will take. Recent findings: In the last decade, major clinical progress has been made in the areas of mosaicplasty/osteochondral autograft transplantation, allograft transplantation, and autologous chondrocyte implantation. From the basic science aspect, biologic scaffold and mesenchymal stem cell research are poised to revolutionize the treatment possibilities. Summary: In short, we are on the cusp of a new era in orthopaedic surgery that will bring tissue engineering to the forefront of medicine. In no clinical disorder is this potential more exciting than for the treatment of osteochondral lesions. © 2006 Lippincott Williams & Wilkins

Risk factors for periprosthetic joint infection following total ankle replacement

•A total of 8 studies met the inclusion criteria, all were determined to be of low quality.•A limited strength of recommendation can be made that certain patient characteristics are associated with an increased risk of PJI.•Inflammatory arthritis, prior ankle surgery, age <65 years, BMI <19, PVD, chronic lung disease, hypothyroidism, and low preoperative AOFAS scores.•There is conflicting evidence in the literature regarding the effect of obesity, tobacco use, diabetes, and duration of surgery.•High quality evidence is needed to further determine the risk factors associated with a PJI following TAR. Identifying preoperative patient characteristics that correlate with an increased risk of periprosthetic joint infection (PJI) following total ankle replacement (TAR) is of great interest to orthopaedic surgeons, as this may assist with appropriate patient selection. The purpose of this study is to systematically review the literature to identify risk factors that are associated with PJI following TAR. Utilizing the terms “(risk factor OR risk OR risks) AND (infection OR infected) AND (ankle replacement OR ankle arthroplasty)” we searched the PubMed/MEDLINE electronic databases. The quality of the included studies was then assessed using the AAOS Clinical Practice Guideline and Systematic Review Methodology. Recommendations were made using the overall strength of evidence. Eight studies met the inclusion criteria. A limited strength of recommendation can be made that the following preoperative patient characteristics correlate with an increased risk of PJI following TAR: inflammatory arthritis, prior ankle surgery, age less than 65 years, body mass index less than 19, peripheral vascular disease, chronic lung disease, hypothyroidism, and low preoperative AOFAS hindfoot scores. There is conflicting evidence in the literature regarding the effect of obesity, tobacco use, diabetes, and duration of surgery. Several risk factors were identified as having an association with PJI following TAR. These factors may alert surgeons that a higher rate of PJI is possible. However, because of the low level of evidence of reported studies, only a limited strength of recommendation can be ascribed to regard these as risk factors for PJI at this time

Distribution of Neuropeptides in the Synovium of Charcot Neuroarthropathy

Category: Basic Sciences/Biologics Introduction/Purpose: The pathology of Charcot neuroarthropathy (CNA) presents inflammation, and bone and cartilage destruction. It is still unclear how the neuropathic signals lead to joint inflammation and destruction. Neuropeptides are secreted by neurons and involve in the regulation of inflammation. Synovium is richly innervated and known to play a critical role in the pathology of inflammatory arthritis. This study is designed to investigate the distribution of several neuropeptides, such as vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP), in CNA synovium, in comparison with non-CNA synovium, with immunohistochemistry. Methods: Synovial samples were collected from CNA patients (n=3) and patients with osteoarthritis and intraarticular fracture (non-CNA; n=3), during foot and ankle surgery (approved by IRB). The tissue samples were fixed with 4% paraformaldehyde, embedded in O.T.C media and sectioned with a cryostat. From each patient, 6-9 sections were randomly selected for immunohistochemistry. After blocking the tissue sections with normal serum, primary antibody of SP, VIP and CGRP was separately applied and incubated at 4ºC overnight. The biotinylated secondary antibody and ABC kit (Victor Laboratories) were applied subsequently. DAB (3,3’-diaminobenzidine) was used for colorimetric detection (brown) of immunohistochemical reactions. The cell nuclei were stained with hematoxylin. The staining was viewed under a microscope and images were taken with a digital camera. Results: In the non-CNA synovium, SP was stained around neuro-vascular bundles and intensely stained on the surface of the synovium, i.e. the intimal layer. In the CNA synovium, SP staining was increased and more diffuse into the subintimal layer of the synovium (Fig 1). In non-CNA synovium, VIP was detected along the surface area of the synovium but not limited in the intimal layer. In CNA synovium, VIP was a similar staining pattern with a reduced staining intensity. The CGRP staining was primarily limited in the intimal layer in the non-CNA synovium. In CNA synovium, CGRP was stained in the intimal layer with an increased intensity. Conclusion: SP, VIP and CGRP are well-studied neuropeptides and have broad biological and pathological functions. All of them were detected in the intimal layer, where fibroblast-like synoviocytes are located. Fibroblast-like synoviocytes are fundamental elements of joint inflammation and are capable of degradation of bone and cartilage directly and indirectly. The changed patterns of SP, VIP and CGRP distributions in CNA synovium revealed by immunohistochemistry indicate a possible pathological pathway in CNA development: the unbalanced neuropathic signals direct fibroblast-like synoviocytes to an inflammatory state, which trigger the cascade of bone and cartilage destruction in CNA