ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2018
Genomewide Association Study Identifies Cxcl Family Members as Partial Mediators of LPS-Induced Periodontitis.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- New insights into nanotherapeutics for periodontitis: a triple concerto of antimicrobial activity, immunomodulation and periodontium regeneration.Journal of nanobiotechnology · 2024Review
- Local delivery of a CXCR3 antagonist decreases the progression of bone resorption induced by LPS injection in a murine model.Clinical oral investigations · 2022Article
- mRNA Transcriptome Analysis of Bone in a Mouse Model of Implant-Associated Staphylococcus aureus Osteomyelitis.Infection and immunity · 2021Article
- Inhibition of the CXCL9-CXCR3 axis suppresses the progression of experimental apical periodontitis by blocking macrophage migration and activation.Scientific reports · 2021Article
- Intermediate monocytes correlate with CXCR3+ Th17 cells but not with bone characteristics in untreated early rheumatoid arthritis.PloS one · 2021Article
- The Complex Molecular Picture of Gut and Oral Microbiota-Brain-Depression System: What We Know and What We Need to Know.Frontiers in psychiatry · 2021Review
- Cxcl9l and Cxcr3.2 regulate recruitment of osteoclast progenitors to bone matrix in a medaka osteoporosis model.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- An Evidence-Based Update on the Molecular Mechanisms Underlying Periodontal Diseases.International journal of molecular sciences · 2020Review
- Genomics of periodontal disease and tooth morbidity.Periodontology 2000 · 2020Review
- Evaluating the Role of CXCR3 in Pain Modulation: A Literature Review.Journal of pain research · 2020Review
- A GWAS approach identifies Dapp1 as a determinant of air pollution-induced airway hyperreactivity.PLoS genetics · 2019Article
- RNA sequencing for ligature induced periodontitis in mice revealed important role of S100A8 and S100A9 for periodontal destruction.Scientific reports · 2019Article
- The Osteocyte as a Novel Key Player in Understanding Periodontitis Through its Expression of RANKL and Sclerostin: a Review.Current osteoporosis reports · 2019Review
- Evaluation of chemokine CXCL10 in human gingival crevicular fluid, saliva, and serum as periodontitis biomarker.Journal of inflammation research · 2018Article
- Identification of Common miRNAs Differentially Expressed in Periodontitis and Pancreatic Cancer.In vivo (Athens, Greece)Article
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10 authors at 1 institution in 1 country.
Funding
Abstract
Periodontitis (PD) is characterized by bacterial infection and inflammation of tooth-supporting structures and can lead to tooth loss. PD affects ∼47% of the US population over age 30 years and has a heritability of about 50%. Although the host immunoinflammatory response and genetic background play a role, little is known of the underlying genetic factors. We examined natural genetic variation in lipopolysaccharide (LPS)-induced PD across a panel of inbred mouse strains, the hybrid mouse diversity panel (HMDP). We observed a strain-dependent sixfold difference in LPS-induced bone loss across the HMDP with a heritability of 53%. We performed a genomewide association study (GWAS) using FAST-LMM, which corrects for population structure, and identified loci significantly associated with PD. We examined candidate genes at a locus on chromosome 5, which suggested a relationship between LPS-induced bone loss and, together with expression data, identified Cxcl family members as associated with PD. We observed an increase in Cxcl10 protein, as well as immune cells and pro-inflammatory cytokines in C57BL/6J (high bone loss strain) but not in A/J (low bone loss strain) after LPS injections. Genetic deletion of CXCR3 (Cxcl9 and10 receptor) demonstrated a ∼50% reduction in bone loss and reduced osteoclasts after LPS injections. Furthermore, WT mice treated with AMG-487 (a CXCR3 antagonist) showed a ∼45% reduction in bone loss and decreased osteoclasts after LPS injections. We conclude that CXCR3 is a strong candidate for modulating the host response in individuals susceptible to PD. © 2018 American Society for Bone and Mineral Research.
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