Innate Immunity Sensors Participating in Pathophysiology of Joint Diseases: A Brief Overview

Gallo, Jiří; Raška, Milan; Konttinen, Yrjö T.; Nich, Christophe; Goodman, Stuart B.

doi:10.1615/jlongtermeffmedimplants.2014010825

Cited by 8 publications

(5 citation statements)

References 178 publications

(138 reference statements)

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“…However, treatment of aseptic and septic loosening of orthopaedic and dental implants may benefit from considering the role of the immune system [166–168]. For example, blockade of pro-inflammatory mediators such as PGE2 [169], pro-inflammatory cytokines [170], or recruitment of monocyte/macrophage cells by interfering with CCL2/CCR2 axis [171, 172], or inactivation of the pro-inflammatory transcription factor NF-κB [173, 174] has been investigated.…”

Section: Opportunities For Enhancing Bone Repair By Modulating Infmentioning

confidence: 99%

Inflammation, fracture and bone repair

Loi

Córdova

Pajarinen

et al. 2016

Bone

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The reconstitution of lost bone is a subject that is germane to many orthopaedic conditions including fractures and non-unions, infection, inflammatory arthritis, osteoporosis, osteonecrosis, metabolic bone disease, tumors, and periprosthetic particle-associated osteolysis. In this regard, the processes of acute and chronic inflammation play an integral role. Acute inflammation is initiated by endogenous or exogenous adverse stimuli, and can become chronic in nature if not resolved by normal homeostatic mechanisms. Dysregulated inflammation leads to increased bone resorption and suppressed bone formation. Crosstalk amongst inflammatory cells (polymorphonuclear leukocytes and cells of the monocyte-macrophage-osteoclast lineage) and cells related to bone healing (cells of the mesenchymal stem cell-osteoblast lineage and vascular lineage) is essential to the formation, repair and remodeling of bone. In this review, the authors provide a comprehensive summary of the literature related to inflammation and bone repair. Special emphasis is placed on the underlying cellular and molecular mechanisms, and potential interventions that can favorably modulate the outcome of clinical conditions that involve bone repair.

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Section: Opportunities For Enhancing Bone Repair By Modulating Infmentioning

confidence: 99%

Inflammation, fracture and bone repair

Loi

Córdova

Pajarinen

et al. 2016

Bone

Self Cite

973

883

View full text Add to dashboard Cite

show abstract

“…The intensity of the response could be linked, in part, to similarities between prosthetic particles (especially polyethylene) and bacteria in terms of size and chemical composition [54]. Prosthetic and bacterial byproducts come in contact with a set of innate immunity receptors located on the surface of immune cells and/or intracellularly [55]. The innate immune receptors trigger an acute inflammatory response, resulting in the upregulation and release of inflammatory cytokines, chemokines and reactive oxygen species (ROS).…”

Section: From Stimulation Of Receptors Of Innate Immunity To Fueling mentioning

confidence: 99%

Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

Goodman

Gallo

2019

JCM

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177

163

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Clinical studies, as well as in vitro and in vivo experiments have demonstrated that byproducts from joint replacements induce an inflammatory reaction that can result in periprosthetic osteolysis (PPOL) and aseptic loosening (AL). Particle-stimulated macrophages and other cells release cytokines, chemokines, and other pro-inflammatory substances that perpetuate chronic inflammation, induce osteoclastic bone resorption and suppress bone formation. Differentiation, maturation, activation, and survival of osteoclasts at the bone–implant interface are under the control of the receptor activator of nuclear factor kappa-Β ligand (RANKL)-dependent pathways, and the transcription factors like nuclear factor κB (NF-κB) and activator protein-1 (AP-1). Mechanical factors such as prosthetic micromotion and oscillations in fluid pressures also contribute to PPOL. The treatment for progressive PPOL is only surgical. In order to mitigate ongoing loss of host bone, a number of non-operative approaches have been proposed. However, except for the use of bisphosphonates in selected cases, none are evidence based. To date, the most successful and effective approach to preventing PPOL is usage of wear-resistant bearing couples in combination with advanced implant designs, reducing the load of metallic and polymer particles. These innovations have significantly decreased the revision rate due to AL and PPOL in the last decade.

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“…Figure 2 shows a scheme of the three main actions of clinical, Celsus-defined inflammation. The presence of particulate matter (i.e., biological agents, infective cells, spores, protein aggregates, small-size debris, and products of biological strife, damage to cells and tissues), even inert components, and/or biologically active materials/agents are detected by tissue physical or biochemical integrity status sensors [377][378][379]. Their stimulation elicits the local (and/or systemic) release of mediators of inflammation, i.e., by mast cells [380][381][382].…”

Section: Tissue-related Inflammation Mechanisms: CI Clinical Inflamma...mentioning

confidence: 99%

The Metabolic Syndrome, a Human Disease

Alemany

2024

IJMS

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This review focuses on the question of metabolic syndrome (MS) being a complex, but essentially monophyletic, galaxy of associated diseases/disorders, or just a syndrome of related but rather independent pathologies. The human nature of MS (its exceptionality in Nature and its close interdependence with human action and evolution) is presented and discussed. The text also describes the close interdependence of its components, with special emphasis on the description of their interrelations (including their syndromic development and recruitment), as well as their consequences upon energy handling and partition. The main theories on MS’s origin and development are presented in relation to hepatic steatosis, type 2 diabetes, and obesity, but encompass most of the MS components described so far. The differential effects of sex and its biological consequences are considered under the light of human social needs and evolution, which are also directly related to MS epidemiology, severity, and relations with senescence. The triggering and maintenance factors of MS are discussed, with especial emphasis on inflammation, a complex process affecting different levels of organization and which is a critical element for MS development. Inflammation is also related to the operation of connective tissue (including the adipose organ) and the widely studied and acknowledged influence of diet. The role of diet composition, including the transcendence of the anaplerotic maintenance of the Krebs cycle from dietary amino acid supply (and its timing), is developed in the context of testosterone and β-estradiol control of the insulin-glycaemia hepatic core system of carbohydrate-triacylglycerol energy handling. The high probability of MS acting as a unique complex biological control system (essentially monophyletic) is presented, together with additional perspectives/considerations on the treatment of this ‘very’ human disease.

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Innate Immunity Sensors Participating in Pathophysiology of Joint Diseases: A Brief Overview

Cited by 8 publications

References 178 publications

Inflammation, fracture and bone repair

Inflammation, fracture and bone repair

Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

The Metabolic Syndrome, a Human Disease

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