We provide characterization data of hydroxyapatite (nHAp) and titanium dioxide (nTiO2) nanoparticles as potential materials for ion sorption, e.g. in targeted therapy, barrier materials for waste repositories or photovoltaics. The study is focused on the determination of the values of protonation and ion exchange constants and site densities (∑SOH, ∑X; [mol kg-1]) of nTiO2 and nHAp for further Ra kinetics and sorption experiments. These data are very important for further investigation of the materials, which can be used e.g. as drug delivery systems or in engineered barriers of deep geological repositories. The characterization was based on the evaluation of the dependence of titrating agent consumption on pH. Titration results were evaluated on the basis of several model combinations, however the combination of the Chemical Equilibrium Model (CEM) and Ion Exchange Model (IExM) fits best to the experimental titration curves. However, the differences between the two sorbents were relatively large. Due to stability in a broad pH range and available surface sites, nTiO2 seems to have a wide application range. The applicability of nHAp is not so wide because of its dissolution under pH 5. Both sorbents are virtually able to sorb cationic species on deprotonated edge and layer sites with different capacities, which can be important for sorption and decontaminating applications.

• Publication type
• Journal Article MeSH

Millions of total joint replacements are performed annually worldwide, and the number is increasing every year. The overall proportion of patients achieving a successful outcome is about 80-90% in a 10-20-years time horizon postoperatively, periprosthetic osteolysis (PPOL) and aseptic loosening (AL) being the most frequent reasons for knee and hip implant failure and reoperations. The chemokine system (chemokine receptors and chemokines) is crucially involved in the inflammatory and osteolytic processes leading to PPOL/AL. Thus, the modulation of the interactions within the chemokine system may influence the extent of PPOL. Indeed, recent studies in murine models reported that (i) blocking the CCR2-CCL2 or CXCR2-CXCL2 axis or (ii) activation of the CXCR4-CXCL12 axis attenuate the osteolysis of artificial joints. Importantly, chemokines, inhibitory mutant chemokines, antagonists of chemokine receptors, or neutralizing antibodies to the chemokine system attached to or incorporated into the implant surface may influence the tissue responses and mitigate PPOL, thus increasing prosthesis longevity. This review summarizes the current state of the art of the knowledge of the chemokine system in human PPOL/AL. Furthermore, the potential for attenuating cell trafficking to the bone-implant interface and influencing tissue responses through modulation of the chemokine system is delineated. Additionally, the prospects of using immunoregenerative biomaterials (including chemokines) for the prevention of failed implants are discussed. Finally, this review highlights the need for a more sophisticated understanding of implant debris-induced changes in the chemokine system to mitigate this response effectively.

• Keywords
• aseptic loosening, chemokine receptors, immunoregenerative implant, osteolysis, therapeutics, tissue homeostasis, wear particles,
• Publication type
• Journal Article MeSH
• Review MeSH

The innate immune system consists of functionally specialized "modules" that are activated in response to a particular set of stimuli via sensors located on the surface or inside the tissue cells. These cells screen tissues for a wide range of exogenous and endogenous danger/damage-induced signals with the aim to reject or tolerate them and maintain tissue integrity. In this line of thinking, inflammation evolved as an adaptive tool for restoring tissue homeostasis. A number of diseases are mediated by a maladaptation of the innate immune response, perpetuating chronic inflammation and tissue damage. Here, we review recent evidence on the cross talk between innate immune sensors and development of rheumatoid arthritis, osteoarthritis, and aseptic loosening of total joint replacements. In relation to the latter topic, there is a growing body of evidence that aseptic loosening and periprosthetic osteolysis results from long-term maladaptation of periprosthetic tissues to the presence of by-products continuously released from an artificial joint.

• MeSH
• Lectins, C-Type metabolism   MeSH
• Humans MeSH
• Osteoarthritis immunology   physiopathology   MeSH
• Osteolysis physiopathology   MeSH
• Immunity, Innate physiology   MeSH
• Joint Prosthesis adverse effects   MeSH
• Receptor for Advanced Glycation End Products MeSH
• Receptors, Cytoplasmic and Nuclear metabolism   MeSH
• Receptors, Immunologic metabolism   MeSH
• Arthritis, Rheumatoid immunology   physiopathology   MeSH
• Nod Signaling Adaptor Proteins metabolism   MeSH
• Toll-Like Receptors metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Lectins, C-Type MeSH
• Receptor for Advanced Glycation End Products MeSH
• Receptors, Cytoplasmic and Nuclear MeSH
• Receptors, Immunologic MeSH
• Nod Signaling Adaptor Proteins MeSH
• Toll-Like Receptors MeSH

Numerous studies provide detailed insight into the triggering and amplification mechanisms of the inflammatory response associated with prosthetic wear particles, promoting final dominance of bone resorption over bone formation in multiple bone multicellular units around an implant. In fact, inflammation is a highly regulated process tightly linked to simultaneous stimulation of tissue protective and regenerative mechanisms in order to prevent collateral damage of periprosthetic tissues. A variety of cytokines, chemokines, hormones and specific cell populations, including macrophages, dendritic and stem cells, attempt to balance tissue architecture and minimize inflammation. Based on this fact, we postulate that the local tissue homeostatic mechanisms more effectively regulate the pro-inflammatory/pro-osteolytic cells/pathways in patients with none/mild periprosthetic osteolysis (PPOL) than in patients with severe PPOL. In this line of thinking, 'particle disease theory' can be understood, at least partially, in terms of the failure of local tissue homeostatic mechanisms. As a result, we envision focusing current research on homeostatic mechanisms in addition to traditional efforts to elucidate details of pro-inflammatory/pro-osteolytic pathways. We believe this approach could open new avenues for research and potential therapeutic strategies.

• MeSH
• Cellular Microenvironment immunology   MeSH
• Hajdu-Cheney Syndrome etiology   immunology   prevention & control   MeSH
• Humans MeSH
• Inflammation Mediators immunology   MeSH
• Arthroplasty, Replacement, Hip * MeSH
• Osteogenesis MeSH
• Joint Prosthesis MeSH
• Prosthesis Failure etiology   MeSH
• Inflammation etiology   prevention & control   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Inflammation Mediators MeSH