Literature DB >> 31313107

Influence of single nucleotide polymorphisms (SNPs) in genetic susceptibility towards periprosthetic osteolysis.

Supriya Jagga1, Ashish Ranjan Sharma1, Manojit Bhattacharya1, Chiranjib Chakraborty2,3, Sang-Soo Lee4.   

Abstract

Wear debris-induced inflammatory osteolysis remains a significant limiting factor for implant replacement surgeries. Hence, a comprehensive understanding of the complex network of cellular and molecular signals leading to these inflammatory responses is required. Both macrophages and monocytes have a critical role in the instigation of the inflammatory reaction to wear debris but differ in the extent to which they induce cytokine expression in patients. Lately, single nucleotide polymorphisms (SNPs) have been associated with genetic susceptibility among individual patients with implant failure. Studies have shown that SNPs in key pro-inflammatory cytokines and their receptors are associated with osteolytic susceptibility. Likewise, SNPs within several genes involved in the regulation of bone turnover have also been found to be associated with wear debris induced osteolysis. It is presumed that SNP variance might play a decisive role in the activation and signaling of macrophages, osteoblasts, chondrocytes, fibroblasts and other cells involved in inflammatory bone loss. Understanding the extent to which SNPs exist among genes that are responsible for inflammatory bone loss may provide potential targets for developing future therapeutic interventions. Herein, we attempt to summarize the various susceptible genes with possible SNP variance that could contribute to the severity of periprosthetic osteolysis in patients with implants.

Entities:  

Keywords:  Inflammation; Periprosthetic osteolysis; Single nucleotide polymorphism; Wear debris

Mesh:

Substances:

Year:  2019        PMID: 31313107     DOI: 10.1007/s13258-019-00845-3

Source DB:  PubMed          Journal:  Genes Genomics        ISSN: 1976-9571            Impact factor:   1.839


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2.  Sclerostin-Mediated Impaired Osteogenesis by Fibroblast-Like Synoviocytes in the Particle-Induced Osteolysis Model.

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