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      Gene Expression in Osteolysis: Review on the Identification of Altered Molecular Pathways in Preclinical and Clinical Studies

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          Abstract

          Aseptic loosening (AL) due to osteolysis is the primary cause of joint prosthesis failure. Currently, a second surgery is still the only available treatment for AL, with its associated drawbacks. The present review aims at identifying genes whose expression is altered in osteolysis, and that could be the target of new pharmacological treatments, with the goal of replacing surgery. This review also aims at identifying the molecular pathways altered by different wear particles. We reviewed preclinical and clinical studies from 2010 to 2016, analyzing gene expression of tissues or cells affected by osteolysis. A total of 32 in vitro, 16 in vivo and six clinical studies were included. These studies revealed that genes belonging to both inflammation and osteoclastogenesis pathways are mainly involved in osteolysis. More precisely, an increase in genes encoding for the following factors were observed: Interleukins 6 and 1β (IL16 and β), Tumor Necrosis Factor α (TNFα), nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), Nuclear factor of activated T-cells, cytoplasmic 1 (NFATC1), Cathepsin K (CATK) and Tartrate-resistant acid phosphatase (TRAP). Titanium (Ti) and Polyethylene (PE) were the most studied particles, showing that Ti up-regulated inflammation and osteoclastogenesis related genes, while PE up-regulated primarily osteoclastogenesis related genes.

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          Aseptic loosening, not only a question of wear: a review of different theories.

          Today, aseptic loosening is the most common cause of revision of major arthroplasties. Aseptic loosening accounts for more than two-thirds of hip revisions and almost one-half of knee revisions in Sweden. Several theories on the cause of aseptic loosening have been proposed. Most of these theories, however, are based on empiric observations, experimental animal models or anecdotal cases. In this review, we discuss the most common theories concerning aseptic loosening. It emerges from this review that aseptic loosening has a multifactorial etiology and cannot be explained by a single theory.
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            Total hip arthroplasties: what are the reasons for revision?

            Primary total hip arthroplasties have reported success rates of greater than 95% in many series with a longer than 10-year follow-up. Revision total hip arthroplasty due to such factors as increased high-activity levels, younger patients undergoing the procedure and increasing life expectancy has become more prevalent. An understanding of the mechanisms and timing of total hip arthroplasty failure can direct efforts aimed at reducing revision rates. This study was conducted to evaluate the indications for revision hip arthroplasty and relate these to the time after the index primary hip arthroplasty. A review of all revision hip arthroplasties at two centres over a 6-year time period identified 225 patients who underwent 237 revisions. The overall mean time to revision was 83 months (range: 0-360 months). The cause of failure was aseptic loosening in 123 hips (51.9%), instability in 40 hips (16.9%) and infection in 37 hips (5.5%). When stratified into two groups (less than 5 years, more than 5 years after the index primary hip arthroplasty), 118 of 237 (50%) revisions occurred in less than 5 years, with 33% due to instability and 24% resulting from infection. The majority of the causes of failure within 5 years in these early revisions were instability and deep infection. The success of hip arthroplasty is likely to be compromized if technical aspects of the surgery for appropriate component positioning and critical protocols to minimise complications such as infection are not given the proper attention.
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              Macrophages-Key cells in the response to wear debris from joint replacements.

              The generation of wear debris is an inevitable result of normal usage of joint replacements. Wear debris particles stimulate local and systemic biological reactions resulting in chronic inflammation, periprosthetic bone destruction, and eventually, implant loosening, and revision surgery. The latter may be indicated in up to 15% patients in the decade following the arthroplasty using conventional polyethylene. Macrophages play multiple roles in both inflammation and in maintaining tissue homeostasis. As sentinels of the innate immune system, they are central to the initiation of this inflammatory cascade, characterized by the release of proinflammatory and pro-osteoclastic factors. Similar to the response to pathogens, wear particles elicit a macrophage response, based on the unique properties of the cells belonging to this lineage, including sensing, chemotaxis, phagocytosis, and adaptive stimulation. The biological processes involved are complex, redundant, both local and systemic, and highly adaptive. Cells of the monocyte/macrophage lineage are implicated in this phenomenon, ultimately resulting in differentiation and activation of bone resorbing osteoclasts. Simultaneously, other distinct macrophage populations inhibit inflammation and protect the bone-implant interface from osteolysis. Here, the current knowledge about the physiology of monocyte/macrophage lineage cells is reviewed. In addition, the pattern and consequences of their interaction with wear debris and the recent developments in this field are presented.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                25 February 2017
                March 2017
                : 18
                : 3
                : 499
                Affiliations
                Laboratory of Preclinical and Surgical Studies, Rizzoli Orthopedic Institute, via di Barbiano 1/10, 40136 Bologna, Italy; francesca.veronesi@ 123456ior.it (F.V.); milena.fini@ 123456ior.it (M.F.)
                Author notes
                [* ]Correspondence: matilde.tschon@ 123456ior.it ; Tel.: +39-051-636-6558
                Article
                ijms-18-00499
                10.3390/ijms18030499
                5372515
                28245614
                5d8febcb-5a58-4da1-9da7-04a7650c101b
                © 2017 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 19 January 2017
                : 21 February 2017
                Categories
                Review

                Molecular biology
                osteolysis,aseptic loosening,genomics,gene expression,inflammation,osteoclastogenesis

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