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Purpose: The aim of this study was to evaluate polyetheretherketone (PEEK) as a patient-specific implant (PSI) material in maxillofacial reconstructive surgery. Materials and methods: The retrospective study included a cohort of 24 patients who underwent maxillofacial surgery using PEEK PSIs. Each patient underwent preoperative multislice computed tomography (CT) with 0 degrees tilt of gantry. Based on the CT scan, the PEEK PSIs were planned and manufactured using three-dimensional (3D) modeling and computer-aided design/computer-aided manufacturing (CAD/CAM) techniques. All procedures were performed under general anesthesia. Implants were placed intraorally, extraorally or through subciliary, transconjuctival or coronal incisions. Results: In 22 of 24 cases, the PEEK PSI fit well without adjustments. Although the fit to the surrounding bone was perfect in almost all of the cases, the outer contour of the PSI was modified in nine cases before fixation. However, intraoperative implant modification did not affect the infection rate. In two cases, postoperative wound dehiscence and infection needed additional treatment and healed without removal of the implants. Conclusion: The follow-up data in this study showed good outcomes with reliable results for PSI made of PEEK in the maxillofacial region. (C) 2019 European Association for Cranio-Maxillo-Facial Surgery. Published by Elsevier Ltd.

Background: Up to 90% of strokes could be prevented by effective treatment of the risk factors. However, there are major problems with the implementation of prevention. For example, only 40% of patients taking medication have blood pressure (BP) at treatment goals and 60% of patients with atrial fibrillation (AF) use anti-coagulant medication. Hypothesis: Remote home monitoring of risk factors after minor stroke or TIA may lead to better control of risk factors by increasing measurements and patient awareness and uncovering undetected risk factors. This pilot study investigates the feasibility of home monitoring of risk factors after minor stroke or TIA. Methods and Patients: Patients (n=30, mean age 57 yrs, range 34-79, 37% females) with recent minor stroke or TIA were supplied with a remote home monitoring system at discharge. The system comprised of a cloud backend for data storage and processing, patient user interface (UI), and wireless BP meter and light-weight EKG device with secured connection to clinician UI, through which BP and EKG could be followed real-time and individualized alarm limits could be set. EKG was automatically analyzed in the cloud backend to detect AF. The patients were contacted by phone at two weeks by stroke nurse and they returned the remote home monitoring system at final visit at three months. Additionally they were contacted if AF was detected or their BP required medication adjustment. Results: Twenty-nine (97%) patients completed the study. One patient discontinued due to unrelated serious illness. One patient did not follow the monitoring program. Of the remaining 28 patients (93%) with complete monitoring data, BP medication needed adjustment in 11 patients (39%) and new AF was detected in 3 patients (11%). Patients appraised that the home monitoring system was easy to use (score 8.6/10) and most would recommend it to peers (score 8.9/10). Conclusions: Remote home monitoring of risk factors after minor stroke or TIA is feasible and may be an efficient way to improve secondary prevention.

Clinical studies suggest that maternal smoking during pregnancy can reduce the crown size of the child's teeth. Delayed dental age compared with chronological age has also been reported in children whose parents smoke. Among the main components of tobacco smoke are nonhalogenated polycyclic aromatic hydrocarbons (PAHs), many of which are highly toxic. Humans are exposed to PAH compounds mainly via tobacco smoke and diet. The aim of our study was to investigate the effect of PAHs on tooth formation and the function of tooth-forming cells. We exposed mouse (NMRI) E18 mandibular first and second molar explants to 7,12-dimethylbenz[a]anthracene (DMBA), a toxic PAH compound, in organ culture for 7 or 12 days. DMBA concentrations used were 0.1, 0.5, 1, and 2 microM. The mesiodistal width of each first molar (12-day culture) was measured in stereomicroscopic images, and the teeth were analysed histologically. DMBA exposure significantly reduced the mesiodistal width of the first molars. DMBA impaired or delayed amelogenesis and dentinogenesis in both molars at the lowest concentration of 0.1 microM. DMBA affected enamel formation more severely than dentin formation and occasionally prevented amelogenesis completely. Elongation and polarization of ameloblasts were impaired, and blood vessel architecture of the dental papilla (future pulp) was altered. Cusps were thin and sharp. In line with the finding that maternal smoking during pregnancy has an adverse effect on child's tooth development, this study shows the toxic influence of PAHs on tooth development in vitro.

Exposure to environmental dioxins via mother’s milk may be one causative factor of mineralization defects in children’s teeth. A prerequisite for the completion of enamel mineralization is the removal of enamel matrix. To test the hypothesis that dioxins interfere with enamel maturation, we administered lactating Han/Wistar rats a single dose of 2,3,7,8-tetrachlorodibenzo -p-dioxin (TCDD; 50 or 1000 μg/kg) on the day after delivery and analyzed tissue sections of the pup heads at post-natal days (Pn) 9 and 22. By Pn22, the first and second molars of the exposed pups, but not controls, showed retention of enamel matrix. Predentin was thicker than normal. Immunostaining for the aryl hydrocarbon/dioxin receptor (AhR) and cytochrome P4501A1 (CYP1A1) in ameloblasts and odontoblasts was reduced, suggesting that TCDD interferes with tooth mineralization via AhR. Extinction of AhR may lead to abolition of CYP1A1 expression as a sign of impaired dental cell function.

Previous studies have shown that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can arrest molar tooth development in rats after in utero and lactational exposure, and that the sensitive stage is temporally restricted. To define the stage in which TCDD is able to arrest tooth development and the cellular background of the effect, mouse embryonic molar tooth explants including various early developmental stages from initiation to late cap stage were exposed to TCDD in organ culture. TCDD did not inhibit morphogenesis of the first molar teeth including the early bud-staged E12 first molars, but the teeth were smaller than in control cultures. Accordingly, the second molars underwent morphogenesis in the presence of TCDD when explanted at E15 when they were at the bud stage. TCDD arrested their development when explanted at E14 when they had not yet reached the early bud stage. Immunohistochemical localization of incorporated bromodeoxyuridine in cultured E14 teeth showed that TCDD did not affect cell proliferation. Localization of apoptosis by terminal deoxynucleotidyl transferase (TdT)-mediated nick end labeling (TUNEL) method revealed that TCDD enhanced apoptosis of dental epithelial cells, especially in the dental lamina of both the first and second molars, and in the inner dental epithelium at the cusp tips of the first molars. Thus, TCDD can arrest tooth development in vitro if the exposure starts at the initiation stage, whereas exposure at later stages leads to smaller tooth size and deformation of cuspal morphology. TCDD interferes with tooth development by stimulating apoptosis in those cells of the dental epithelium, which are predetermined to undergo apoptosis during normal development.

Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to mouse embryonic teeth, sharing features of early development with salivary glands in common, involves enhanced apoptosis and depends on the expression of epidermal growth factor (EGF) receptor. EGF receptor signaling, on the other hand, is essential for salivary gland branching morphogenesis. To see if TCDD impairs salivary gland morphogenesis and if the impairment is associated with EGF receptor signaling, we cultured mouse (NMRI) E13 submandibular glands with TCDD or TCDD in combination with EGF or fibronectin (FN), both previously found to enhance branching morphogenesis. Explants were examined stereo-microscopically and processed to paraffin sections. TCDD exposure impaired epithelial branching and cleft formation, resulting in enlarged buds. The glands were smaller than normal. EGF and FN alone concentration-dependently stimulated or inhibited branching morphogenesis but when co-administered with TCDD, failed to compensate for its effect. TCDD induced cytochrome P4501A1 expression in the glandular epithelium, indicating activation of the aryl hydrocarbon receptor. TCDD somewhat increased epithelial apoptosis as observed by terminal deoxynucleotidyl transferase (TdT)-mediated nick end-labeling method but the increase could not be correlated with morphological changes. The frequency of proliferating cells was not altered. Corresponding to the reduced cleft sites in TCDD-exposed explants, FN immunoreactivity in the epithelium was reduced. The results show that TCDD, comparably with EGF and FN at morphogenesis-inhibiting concentrations, impaired salivary gland branching morphogenesis in vitro. Together with the failure of EGF and FN at morphogenesis-stimulating concentrations to compensate for the effect of TCDD this implies that TCDD toxicity to developing salivary gland involves reduced EGF receptor signaling.

Dioxins are ubiquitous environmental pollutants that afflict developing teeth. To find out if the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the continuously erupting rat incisor is associated with the sensitivity to TCDD acute lethality and to see the histological basis for any macroscopic findings, we exposed 25 resistant Han/Wistar (Kuopio; H/W) and 20 sensitive Long-Evans (Turku/AB; L-E) female rats to total doses of 0.17, 1.7, 17, and 170 (only H/W rats) micro g/kg TCDD. Each dose group comprised five animals. The treatment was started when the rats were 10 weeks old and continued for 20 weeks. The exposure time covered two life cycles of the incisor. Stereomicroscopic examination of the dissected mandibles showed color defects and pulpal perforation of the lower incisors at 17 and 170 micro g/kg TCDD. Tissue sections revealed odontoblastic and pulpal cell death and the consequent arrest of dentin formation at the incisal tooth end at the same doses. H/W rat incisors were affected closer to the germinative tooth end at 170 than at 17 micro g/kg TCDD, resulting in a larger perforation. In accordance with the enamel discoloration, the postsecretory enamel organ underwent, albeit inconsistently, precocious squamous metaplasia with pronounced proliferation. Thus, both the mesenchymal and, to a lesser extent, epithelial elements of the forming tooth were affected dose-dependently at relatively high doses of TCDD. Similar responses in both strains implied that the impaired formation of the incisor tooth, at least of its mesenchymal elements, is not associated with the differential resistance of H/W and L-E rats to TCDD acute lethality.