ABSTRACT
Objective To investigate the influences of loading time and loading angle on the stress, displacement of human periodontal ligament in dynamic jaw. Methods The three-dimensional assembly model of the mandible front teeth, periodontal ligament and alveolar bone was reconstructed by using the reverse engineering technology. The thickness of periodontal membranes was 0.2 mm. The stress, displacement at different positions of the periodontal ligaments during different jaw cycles were analyzed under dynamic load in the direction from bucca to tongue side with 0°, 15°, 30°, 45°, 60°, 75°, 90° angle to the long axis of the tooth. Results During one jaw cycle, the ratio of the maximum to minimum value of the maximum residual stress due to different loading angles was 5.5, and the ratio of the maximum to minimum value of the maximum displacement was 8.1. The ratio of the maximum to minimum value of the maximum displacement which was caused by five jaw cycles was increased in the range from 1.02 to 1.35 with the increase of loading angles. The ratio of the maximum to minimum value of the maximum residual stress which was caused by different loading angles was increased in the range from 1.86 to 3.00 with the increase of jaw cycles. The location of the maximum stress was at the tongue side of the cervical margin at different loading angles, and the location of the maximum residual stress was distributed at different positions of the cervical margin. Most stress was accumulated at the root of the periodontal ligament under the 0° dynamic load. Conclusions The situation of the accumulated residual stresses and the uncertainties in the distribution of the maximum residual stresses should be observed in the clinical choice of mandible incisors fixed by bridge abutments; large angle force applied to the tooth was harmful to the periodontal ligament and rapid succession of chewing hard food should be avoided as much as possible during the clinical treatment.
ABSTRACT
<p><b>BACKGROUND</b>Previous discovery that long-term administration of pentoxifylline (PTX) to mice chronically exposed to smoke led to the development of pulmonary fibrosis rather than emphysema initiated our curiosity on whether the Wnt/β-catenin pathway, a set of signaling proteins essential to organ development and lung morphogenesis in particular were activated in the pathogenesis of pulmonary fibrosis.</p><p><b>METHODS</b>Male BALB/c mice were randomized into four study groups: Group Sm, smoke exposure and taken regular forage; Group PTX, no smoke but taken PTX-rich forage; Group Sm + PTX, smoke exposure and taken PTX-rich forage; Group control: shamed smoke exposure and taken regular forage. Animals were sacrificed at day 120. Morphometry of the lung sections and the expressions of TGF-β(1), hydroxyproline, β-catenin, cyclin D1, T cell factor 1 (Tcf-1) and lymphoid enhancer factor 1 (Lef-1) mRNA, etc, in the lung homogenate or in situ were qualitatively or quantitatively analyzed.</p><p><b>RESULTS</b>As expected, smoke exposure along with PTX administration for 120 days, lungs of the mice progressed to be a fibrosis-like phenotype, with elevated fibrosis score (3.9 ± 1.1 vs. 1.7 ± 0.6 in Group Sm, P < 0.05). TGF-β(1) (pg/g) (1452.4 ± 465.7 vs. 818.9 ± 202.8 in Group Sm, P < 0.05) and hydroxyproline (mg/g) (5.6 ± 0.6, vs. 2.4 ± 0.1 in Group Sm, P < 0.05) were also consistently increased. The upregulation of β-catenin measured either by counting the cell with positive staining in microscopic field (17.4 ± 7.9 vs. 9.9 ± 2.9 in Group Sm, P < 0.05) or by estimation of the proportion of blue-stained area by Masson's trichrome (11.8 ± 5.6 vs. 4.7 ± 2.4 in Group Sm) in Group SM + PTX was much more noticeable as than those in Group Sm. The expression of β-catenin measured by positive cell counts was correlated to TGF-β(1) concentration in lung tissue (r = 0.758, P < 0.001). PTX per se caused neither fibrosis nor emphysema though expression of β-catenin and downstream gene cyclin D(1) may also be altered by this medication.</p><p><b>CONCLUSIONS</b>PTX mediated transformation of pulmonary emphysema into pulmonary fibrosis under chronic cigarette smoke exposure is associated with upregulation of β-catenin and elevation of TGF-β(1), implying that activation of Wnt/β-catenin signaling may be involved in the pathogenesis of pulmonary fibrosis.</p>