Periodontitis, the bone loss disease of the bones that surround our teeth, is initiated by a bacterial infection of the gums. Since the etiology in humans is not fully understood, one can make use of mouse models, such as genetically modified mice. Obvious benefits of such approaches, is the comparison with susceptibility of mice that have the exact genetic background apart from this one gene. A shortcoming is, of course, that humans are genetically very diverse, where two non-related individuals may differ every 250 base pairs of the DNA. In an attempt to account for genetic diversity, an admirable approach to hunt for periodontitis susceptibility genes, was presented in the August issue of the JBMR [link: Genomewide Association Study Identifies Cxcl Family Members as Partial Mediators of LPS-Induced Periodontitis.
Hiyari S, Green E, Pan C, Lari S, Davar M, Davis R, Camargo PM, Tetradis S, Lusis AJ, Pirih FQ.
J Bone Miner Res. 2018 Aug;33(8):1450-1463. doi: 10.1002/jbmr.3440. Epub 2018 May 22]. Gums from no less than 104 genetically different mouse strains were injected with LPS from a periodontopathogen, a bacterial product that is known to contribute to periodontitis progression. These mouse strains were ranked on the severity of periodontitis they developed, by simply measuring bone height of the bone that surrounded the teeth. With Genome wide analysis (GWAS), hotspots of suspect genes of the cxcl family were found on chromosome 5. Studies using a CXCR3 knock-out mouse, and studies using a CXCR3 agonist confirmed periodontitis susceptibility.
Use of such rigorous approaches may map genes associated with inflammation related bone loss.