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. Author manuscript; available in PMC: 2019 May 18.
Published in final edited form as: Innate Immun. 2016 Sep 22;22(8):598–611. doi: 10.1177/1753425916666652

Figure 1.

Figure 1.

Role of NOD2 and RIP2 on inflammatory bone resorption and osteoclastogenesis in vivo. Alveolar bone resorption induced in the experimental periodontitis model assessed by μCT is significantly attenuated in Nod2KO mice. (A) Representative images of tridimensional reconstructions of hemi-maxillae segments in the of mice from each genotype and experimental condition (Aa- or PBS-injected) scanned by μCT. Threshold was set to allow visualization of mineralized tissues only. The graph represents the average and SD of the relative reduction in mineralized tissue content [bone volume (BV) fraction] in the standardized ROI assessed in comparison with the BV fraction of the ROI in WT control samples (set to 100%). Samples from at least three different animals were analyzed for each group. (B) Representative images of eosin-stained sections (40× magnification) representative of each genotype and experimental condition, depicting the area in which osteoclasts were counted: from the apex of the palatal root to the area subjacent to the major palatine artery and nerve. Representative images (100× magnification) of the immunohistochemical staining for TRAP. The graph presents average and SDs of the numbers of osteoclasts in the area of interest, according to the genetic background and presence or absence of disease induction. Asterisk (*) indicates significant difference between the indicated pair of bars (Student’s t-test with Welch’s correction for unequal variances).