Design of the tooth extraction procedure and CT measurement.

<p>(a) This CT image details the condition of third molar teeth covered with cortical bone. The regions of interest in CT image analysis were (I) the buccal cortical bone area, which was taken for biopsy during surgery; and (II) the region under the cortical bone, which indicates cancellous bone near the third molar tooth. (b) Removal of the third molar tooth. The envelope flap is raised, revealing the cortical bone. The line indicates the biopsy area. (c) Orthopantomographs showing impacted third molar teeth.</p

Correlation between histological features and age in cortical bone.

<p>(a) There is a statistically significant negative correlation between age and osteocytic density (cells/mm²) (n = 56, r = −0.51, <i>P = </i>0.0001). (b) Density of bone lacunae (lacunae/mm²) does not correlate significantly with age (n = 56, r = −0.257, <i>P = </i>0.0555). (c) Density of empty lacunae (empty lacunae/mm²) does not correlate significantly with age (n = 56, r = 0.059, <i>P = </i>0.6678).</p

Three age categories of histological features of cortical bone.

<p>(a) Three age categories of osteocytic density (cells/mm²). There are statistically significant differences (ANOVA and Bonferroni correction, *<i>P</i><0.05, **<i>P</i><0.01). (b) Three age categories of bone lacunae density (lacunae/mm²). There are no statistically significant differences (ANOVA and Bonferroni correction, <i>P</i> = 0.139). (c) Three age categories of empty bone lacunae density (empty lacunae/mm²). There are no statistically significant differences (ANOVA and Bonferroni correction, <i>P</i> = 0.470).</p

Schematic illustration of the formation mechanisms of the chronic focal bone consolidation.

<p>Schematic illustration of the formation mechanisms of the chronic focal osteomyelitis. The chronic bacterial infection around tooth would induce tissue damage and it resulted in osteocytes death and resulted in micropetrosis. These accumulation of micropetrosis might induce bone sclerosis. Red arrow head shows cancellous bone consolidation.</p

Pathological features.

<p>(a) A representative image of viable bone (x100). Normal-appearing bone that is remodeling, with osteoblasts, and osteocytes present. Occasional empty osteocytic lacunae (<10–20% of lacunae per high magnification) may be present in the absence of an inflammatory reaction. (b) High magnification of viable bone (x200). There are osteoblasts at the border of bone marrow. Arrow head shows osteoblasts. (c) Non-viable bone (×100). Empty osteocytic lacunae and absence of osteoblasts. Empty lacunae are representative of osteocytic death. Arrow head shows empty lacunae. (d) High magnification of non-viable bone (×200). Osteoclasts are present; however, the inflammatory reaction is minimal. (e) Osteomyelitis: prominent inflammatory cell infiltration in fibrous marrow, with osteoblastic activity creating irregular bony trabeculae (×200). (f) High magnification of osteomyelitis (×200). Necrotic bone (sequestrum), abundant bacterial colonies are shown.</p

Three age categories of cortical and cancellous bone radiodensity.

<p>(a) Three age categories of cortical bone radiodensity are not significantly differences (ANOVA and Bonferroni correction, <i>P</i> = 0.180; <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073897#pone-0073897-g003" target="_blank">Figure 3c</a>). (b) Three age categories of cancellous bone radiodensity are significant differences (ANOVA and Bonferroni correction, *<i>P</i><0.05, **<i>P</i><0.01; <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073897#pone-0073897-g003" target="_blank">Figure 3d</a>).</p

Inter- and intraobserver reliability of the HU measurement.

<p>Inter- and intraobserver reliability of the HU measurement.</p

The distribution of three age categories of pathological features.

<p>The distribution of three age categories of pathological features. Old generation shows 100% focal sclerotic osteomyelitis histopathologically, whereas young generation shows relatively few osteomyelitis.</p

Supplementary_file_AJHPM-2017-12-241_(Kanno_Y)_(1) - Validity and Reliability of the Dying Care Process and Outcome Scales Before and After Death From the Bereaved Family Members’ Perspective

<p>Supplementary_file_AJHPM-2017-12-241_(Kanno_Y)_(1) for Validity and Reliability of the Dying Care Process and Outcome Scales Before and After Death From the Bereaved Family Members’ Perspective by Yusuke Kanno, Kazuki Sato, Megumi Shimizu, Yuko Funamizu, Hideaki Andoh, Megumi Kishino, Tomomi Senaga, Tetsu Takahashi, and Mitsunori Miyashita in American Journal of Hospice and Palliative Medicine®</p

NKG2D⁺ IFN-γ⁺ CD8⁺ T Cells Are Responsible for Palladium Allergy

<div><p>Nickel, cobalt, and chromium are well known to be causal agents of allergic contact dermatitis. Palladium (Pd) can also cause allergic disease and exposure results from wide use of this metal in dental restorations and jewelry. Metal allergy is categorized as a delayed-type hypersensitivity, and metal-responsive T cell clones have been isolated from allergic patients. However, compared to nickel, little is known about the pathology of allergic disease mediated by Pd, and pathogenic T cells are poorly understood. To identify the pathogenic T cells that are responsible for onset of Pd allergy, we enriched metal-responsive lymphocytes by sequential adoptive transfer of involved lymph node cells. Here we show that sequential adoptive transfer gradually increased the incidence and the intensity of Pd allergy, and CD8⁺ T cells are responsible for the disease as CD8⁺ T cell-depleted mice and β2-microglobulin-deficient mice did not develop Pd allergy. In addition, we found that draining lymph node cells skewed toward CD8⁺ T cells in response to Pd challenge in 8th adoptive transferred recipient mice. The CD8⁺ T cells expressed NKG2D, a costimulatory molecule involved in the production of IFN-γ. NKG2D ligand was also induced in Pd-injected tissues. Furthermore, both NKG2D ligand-transgenic mice, where NKG2D is downmodulated, and IFN-γ-deficient mice showed impaired Pd allergy. Taken together, these results indicate that IFN-γ-producing NKG2D⁺ CD8⁺ T cells are responsible for Pd allergy and suggest that NKG2D is a potential therapeutic target for treatment of metal allergy.</p></div