Craig W. Dreyer

Evidence for endothelial junctions acting as a fluid flux pathway in tensioned periodontal ligament

A continuous tension load of 1.0 N applied to the rat maxillary first molar for 30 min led to a significant increase (p < 0.05) in the mean number of junctions/microns of endothelial perimeter. The mean number of junctions/microns was compared with the mean number of tissue channels/microns 2 as previously reported by fitting linear and quadratic equations. An increase in the mean number of junctions/microns was associated with an increase in mean number of tissue channels/microns 2 (p < 0.01) in control and experimental periodontal ligament. Significant increases in the mean number of junctions/microns occurred in the middle-third zone for venous capillaries (p < 0.01) and in the tooth-third zone for postcapillary-sized venules (p < 0.001). It is concluded that the endothelial junctions of venous capillaries and postcapillary-sized venules provide significant pathways for fluid transport across the tensioned walls of the microvascular bed of the periodontal ligament.

Immunohistochemical detection of nerve growth factor and its receptors in the rat periodontal ligament during tooth movement

OBJECTIVES Nerve growth factor (NGF) and its receptors, p75 and tyrosine receptor kinase A (Trk A), have been shown to increase following trauma. The aims of this study were to examine changes in the detection of NGF and its receptors during orthodontic tooth movement in the rat, and the effects of anti-NGF on these changes. DESIGN Orthodontic separators were placed between the right maxillary first and second molars of Sprague-Dawley rats which were equally divided into two groups. Animals from the second group were injected with anti-NGF. The left sides served as controls, and animals were sacrificed at 0, 3, 7 and 14 days. RESULTS Results of immunohistochemical localisation for p75, Trk A, calcitonin gene-related peptide (CGRP) and NGF showed staining intensity increased at day 3, with a peak at day 7 and decreasing intensity at day 14. Anti-NGF injected animals showed reduced staining at all observation periods. CONCLUSION Data suggest that orthodontic injury induces NGF production, leading to sprouting and invasion by CGRP-positive nerve fibers and that injection of anti-NGF reduces NGF tissue levels and prevents innervation by CGRP-positive fibers.

Microvascular Luminal Volume Changes in Aged Mouse Periodontal Ligament

Data for the microvascular bed in the aged periodontal ligament have not been established. This investigation tested the hypothesis that the luminal microvascular volume decreased in the aged ligament. Mice 35 days old and one year old were vascular-perfused and the mandibular first molar periodontal ligament processed for electron microscopy. Tissue quadrats from each circumferential third ligament region were recorded at 150-μm intervals from the alveolar crest to the apex for randomized sampling of blood vessel lumina. The data were analyzed with a generalized linear model at the p < 0.01 level for the interaction of the aging effect with differences across regions. Stereological parameters were established for vessel lumen volume, and for surface and length densities. Mean ligament width decreased from 119.9 ± 16.94 (μm ± SE) in young mice to 60.0 ± 10.58 (μm ± SE) in aged mice. The luminal volume of 8.63 ± 1.37 (% ± SE) in young ligament increased to 9.83 ± 2.14 (% ± SE) in aged ligament. Collecting venules and the combined group of arterio-venous anastomoses with terminal arterioles showed a two-fold increase in luminal volume density (p < 0.01). In aged ligament, regional shifts affected the microvascular bed distribution, but these changes were not consistent across regions, or with depth. The average cross-sectional tissue area served per capillary decreased from 2117 μm2 to 1451 μm 2 for young and old. Average ligament thickness served per capillary dropped from 52.5 μm to 27.5 μm. These reductions in average diffusion distances indicated a change in the quality of the diffusion barrier with age.

A scanning electron microscope study of microcorrosion casts of the microvasculature of the marmoset palate, gingiva and periodontal ligament

In the hard palate, sagittally oriented capillary loops, 8-10 microns in diameter and 70-250 microns high, extended perpendicularly from a subcapillary plexus to the connective tissue papillae. These loops formed a well-delineated vascular spine beneath the rugal crests. Capillary loop density was estimated to be 200-270/mm2 on the rugal crest, 75-160/mm2 on the rugal slopes and 70-140/mm2 in the trough. In the gingiva, the crevicular loop system was separated by a gap from the vestibular, palatal and col loop systems. Anastomoses occurred between these systems at a deeper level. The crevicular circular plexus varied from 1 to 4 vessels. Apical to the gingival margin the buccal vasculature was composed of occluso-apically orientated loops draining towards the vestibular sulcus. The capillary loops were 60-120 microns high near the gingival margin, compared with 40-60 microns near the mucogingival junction. The mucogingival margin was demarcated by a change in capillary orientation. The periodontal ligament contained mainly postcapillary-sized venules, 10-25 microns in diameter, orientated occluso-apically. Capillary loops, 50-100 microns long and directed at right angles to the root surface, occurred in the cervical third. These microvascular patterns of the marmoset are different from those of the mouse and rat.

A morphometric, electron microscopic analysis of tissue channels shown by ionic tracer in normal and tensioned rat molar apical periodontal ligament

A 1.0 newton continuous, extrusive load was applied to the right maxillary molar for 30 min to determine the presence of channels as shown by the distribution of tracer across the interstitial compartment of normal and tensioned PDL. Sodium ferrocyanide (1% w/v), perfused via the common carotid arteries, was the tracer probe and tris(ethylenediamine) cobalt III chloride (1% w/v) the precipitating ion. Left molar control PDL had an overall mean of 0.43 +/- 0.05/microns2 tissue channels at 0.2 microns from the vascular endothelium, and 0.15 +/- 0.04/microns2 at 7-8 microns. On the experimental side, the overall mean number of tissue channels was 0.65 +/- 0.13/microns2 at 0-2 microns and 0.19 +/- 0.07/microns2 at 7-8 microns. A significant depth effect (P less than 0.01) was present in the control and experimental interstitial tissues for tissue channels adjacent to the endothelium of different categories of vessel. Extrusion increased the tissue channel density adjacent to arterial capillaries (P less than 0.01), venous capillaries (P less than 0.01) and postcapillary-sized venules (P less than 0.01). These findings implicate these three types of vessel as being functionally important in fluid exchange across endothelial boundaries in the PDL.

Ultrasound Measurements of the Masseter Muscle as Predictors of Cephalometric Indices in Orthodontics: A Pilot Study

This study investigated the potential of ultrasound measurements of the masseter muscle to accurately predict indices normally derived from cephalograms. Masseter muscle measurements on 11 adults (22 to 30 y) were made using lateral cephalometrics and extended field-of-view ultrasound. The ultrasound technique was validated in a simulation pilot study using 12 dry skulls and raw chicken breasts. Twenty cephalometric variables were analyzed against four ultrasound measurements of the masseter muscle. Highly significant correlations (r = 0.81-0.85, p = 0.001-0.002) between ultrasound measurements of the masseter muscle and cephalometric measurements representing the length of the superficial masseter muscle, the length and shape of the mandible and vertical facial proportions were demonstrated. Predictive equations from regression analyses were constructed to deduce ramus length and shape from the ultrasound measurements. The results provide pilot data suggesting that ultrasound is a potential clinical tool for sequential evaluation of masseter muscle length in orthodontics and facial muscle growth studies.

The influence of miniscrew insertion torque

Objective The aim of this in vitro study was to evaluate the progressive development of surface microdamage produced following the insertion of orthodontic miniscrews (OMs) into 1.5 mm thick porcine tibia bone using maximum insertion torque values of 12 Ncm, 18 Ncm, and 24 Ncm. Methods Aarhus OMs (diameter 1.5 mm; length 6 mm) were inserted into 1.5 mm porcine bone using a torque limiting hand screwdriver set at 12 Ncm, 18 Ncm, and 24 Ncm. A custom rig equipped with a compression load cell was used to record the compression force exerted during manual insertion. A sequential staining technique was used to identify microdamage viewed under laser confocal microscopy. Virtual slices were created and stitched together to form a compressed two-dimensional composition of the microdamage. Histomorphometric parameters, including total damage area, diffuse damage area, maximum crack length, maximum damage radius, and maximum diffuse damage radius, were measured. Kruskal-Wallis Tests and Wilcoxon Rank-Sum Tests were used to analyse the generated data. Results All OMs inserted using 12 Ncm failed to insert completely, while partial insertion was observed for two OMs inserted at 18 Ncm. Complete insertion was achieved for all OMs inserted at 24 Ncm. Histomorphometrically, OMs inserted using 24 Ncm produced a significantly larger diffuse damage area (P < 0.05; P < 0.05) and maximum diffuse damage radius (P < 0.05; P < 0.05), for both the entry and exit surfaces, respectively, compared with the 12 Ncm and 18 Ncm groups. Conclusions Insertion torque can influence the degree of OM insertion and, subsequently, the amount of microdamage formed following insertion into 1.5 mm thick porcine tibia bone. An increase in insertion torque corresponds with greater insertion depth and larger amounts of microdamage.

Influence of cortical bone thickness on miniscrew microcrack formation

Introduction The aim of this in‐vitro study was to investigate the influence of cortical bone thickness on the amount of surface microdamage produced after insertion of orthodontic miniscrews (OM) in porcine tibia bone. Methods Aarhus OMs (Medicon, Tuttlingen, Germany; diameter, 1.5 mm; length, 6 mm) were inserted into 1.0 mm (group A; n = 10), 1.5 mm (group B; n = 10), and 2.0 mm (group C; n = 10) of porcine cortical bone using a torque‐limiting hand screwdriver set at 18 Ncm. A sequential staining technique was used to identify microdamage under laser confocal microscopy. Virtual slices were stitched together using ImageJ software (National Institutes of Health, Bethesda, Md) to form a compressed 2‐dimensional composition of the microdamage. The ImageJ software was used to quantify the total damage area, diffuse damage area, maximum crack length, maximum damage radius, and maximum diffuse damage radius. Kruskal‐Wallis tests and Wilcoxon rank sum tests were used to analyze the data. Results All OMs in group A (1.0 mm) were inserted completely; however, 2 OMs from group B (1.5 mm) and all OMs in group C (2.0 mm) failed to insert completely. The entry surface of group C (2.0 mm) exhibited significantly higher amounts of total damage, diffuse damage area, maximum crack length, and maximum crack damage radius compared with groups A (1.0 mm) and B (1.5 mm). The maximum crack length observed on the entry and exit surfaces ranged from 1.03 to 3.06 mm. Conclusions In this study, we demonstrated a higher level of microdamage after the insertion of OMs into 2.0‐mm thick cortical bone compared with 1.0‐mm thick cortical bone. Therefore, clinicians need to consider the thickness of the cortical bone at the insertion site, because mechanisms to reduce cortical bone thickness would likely reduce the amount of microdamage formed. A safety zone of 3.5 mm from the OM is also recommended for OMs inserted into 1.0‐ and 1.5‐mm cortical bone thicknesses to minimize any detrimental effects after targeted remodeling. HighlightsCortical bone thickness affects the amount of microdamage after miniscrew insertion.Significant microdamage was seen when miniscrews were placed in 2‐mm thick bone.Less microdamage occurred when bone was 1 or 1.5 mm thick.Clinicians should consider cortical bone thickness at the insertion site.A 3.5‐mm safety zone should be used for miniscrews in 1‐ to 1.5‐mm thick bone.