Skeletal stability after mandible bilateral sagittal split osteotomy - comparison of patient-specific implant and mini-plate fixation: A retrospective study.

The aim of the study was to compare the stability of the virtual surgical planning (VSP) and computer-aided design accompanied by patient-specific implants (PSIs) and conventional mini-plates in mandible advancement with bilateral sagittal split osteotomy (BSSO). This retrospective study evaluates the clinical and cephalometric records of 53 patients (12 male, 41 female) treated with BSSO in Helsinki University Hospital. Subjects were divided into two groups: VSP-PSI (21 patients: 4 male and 17 female; mean age 38 years, range 25-53 years); and conventional wafer-based repositioning with mini-plate fixation (32 patients: 8 male and 24 female; mean age 39 years, range 21-56 years). The effect of the amount and direction of the advancement on the stability was also analysed individually. The standardized lateral cephalometric radiographs in three time points were analysed to compare the groups. After surgery (T2), there were no differences between groups in cephalometric variables. During follow-up (T2-T3), the cephalometric variables in both Groups A and B were stable, so there was no difference in stability between the VSP-PSI and the conventional mini-plate groups. During follow-up, the mandibles rotated clockwise or counterclockwise, relapsed towards their original direction, and the changes were statistically significant (jaw relationship; p = 0.018, soft tissue profile; p = 0.025); when the advancement of mandible was >6 mm, the increase in gonial angle compared to mandibles advanced ≤6 mm was statistically significant (p = 0.03). VSP-PSI and conventional mini-plate fixation can be considered equally stable. Large advancements with counterclockwise rotation regardless of fixation method are more susceptible to relapse. VSP-PSI alone cannot solve the relapse-related concerns in mandible osteotomy.

Non-progressive mandibular changes in children with Type I and II craniofacial microsomia.

OBJECTIVE: To describe the mandibular growth of craniofacial microsomia (CFM) patients during early childhood to adolescence with attention to symmetry. MATERIALS AND METHODS: Altogether 61 CFM patients were studied at the Cleft Palate and Craniofacial Center, Helsinki University Hospital between 1986 and 2006. In this cohort study, we measured and analysed 293 radiographs (posteroanterior, panoramic and lateral); 165 radiographs of 40 patients met the final inclusion criteria. The vertical height of the ramus in anteroposterior and panoramic radiographs, the length of the mandible in anteroposterior radiographs and the maxillary protrusion and mandibular retrognathia in lateral cephalograms were measured in four different age groups. RESULTS: A statistical difference existed between the groups in the vertical height of the ramus and in the mandibular length. The vertical height of the ramus measured from the panoramic radiograph grew on both sides, and the ratios remained unchanged. In the sagittal dimension, the maxilla and mandible grew forward, but no significant differences emerged between the groups. CONCLUSIONS: Results suggest that mild-type CFM is not progressive in nature. During growth, mandibular asymmetry measured in the horizontal, vertical and sagittal planes did not increase.

Craniofacial structures, occlusal features, and TMD symptoms in juvenile idiopathic arthritis patients: a retrospective study.

BACKGROUND: Juvenile idiopathic arthritis (JIA) is a chronic inflammatory disease in which temporomandibular joint (TMJ) arthritis commonly occurs. It may be asymptomatic and could cause problems in the growing joints. Our aim was to evaluate the craniofacial structures, occlusal features and temporomandibular dysfunction (TMD) symptoms of patients with JIA. METHODS: The study consisted of 195 JIA patients treated at the Department of Oral and Maxillofacial Diseases, Helsinki University Hospital (HUH), Finland between 2015 and 2019. We retrospectively screened their medical and dental records and classified them according to age at JIA diagnosis (<7 and ≥7 years). RESULTS: Most of the patients had Angle Class I occlusion in both sides. Among all the patients, the mean overjet, and overbite were 3.3 mm and 2.4 mm, respectively. There were more open bite patients in the ≥7 years old group than in the <7 years old group (P = 0.010). Of all patients, 47% reported at least one TMD symptom. The TMD symptoms were more common in participants ≥7 years old than those <7 years old (P = 0.005). CONCLUSION: Occlusal features and the incidence of malocclusions seem to have similar tendency among the JIA patients with systematic visits in rheumatologist and orthodontist as in the healthy population, except for open bite that is more common with JIA patients. While treating JIA patients, a well-functioning collaboration between paediatric rheumatologists and orthodontists is essential, as well as a clear screening protocol to detect potentially asymptomatic TMJ arthritis. Particular attention should be paid to children with JIA under school age.

Facial asymmetry in children with either unilateral lambdoid craniosynostosis or positional posterior plagiocephaly.

BACKGROUND: In unilateral lambdoid craniosynostosis (ULC), the posteriorly situated lambdoid suture of the cranial vault fuses prematurely. Positional posterior plagiocephaly (PPP) causes flattening of the posterior side of the head, either through external forces or through underlying differences in brain development. Both conditions cause occipital flattening of the head, but the aetiology is different. MATERIALS AND METHODS: Eight ULC children were compared with 16 sex- and age-matched PPP children. 3D computer tomography scans of all 24 children were analysed with Dolphin imaging software. The location and symmetry of the temporomandibular joint (Co), and the symmetry of the maxillary anterior nasal spine (ANS) and the mandibular symphysis (Pgn) were analysed. Furthermore, the mandibular bone (Co-Pgn) length, corpus length, ramus height, positional changes in the external acoustic meatus (PoL) and the distance from the orbital margin to the articular fossa were measured. RESULTS: In all eight ULC children, the Co was anteriorly displaced on the affected side compared with the unaffected side. In all ULC and PPP children, the ANS, which is considered the bony maxillary midpoint, was shifted towards the affected side. In all ULC children, the mandibular bone (Co-Pgn) was shorter on the affected side. The PoL was antero-inferiorly positioned in all ULC children on the affected side compared with the unaffected side. CONCLUSIONS: Our results show that both types of posterior plagiocephaly are associated with an asymmetric position of the Co and asymmetry of the mandible and maxilla. Facial asymmetry was more frequently seen in ULC than PPP children.

Treatment compliance of adolescent orthodontic patients with headgear activator and twin-block appliance assessed prospectively using microelectronic wear-time documentation.

BACKGROUND: Success of orthodontic removable appliance treatment relies on patient compliance. The aim of this quantitative and qualitative study was to explore the compliance and self-reported experience of adolescents in orthodontic treatment with headgear activator (HGA) or twin-block (TB) appliance. MATERIALS/METHODS: The study group comprised 52 adolescents with a mean age of 12.6 (±1.3) years at the start of the treatment. The patients were treated at a free-of-charge public dental clinic. Participants were randomly allocated to two equal groups to be treated with either HGA or TB. Patient compliance was evaluated as appliance wear time and subjective experience. Appliance wear time was recorded with Theramon® microchip, and the self-reported subjective experience using a questionnaire. RESULTS: In total, 30 patients completed the treatment during the follow-up period. HGA was worn on average 7 hours per day and TB 9 hours per day by those patients, who successfully completed the treatment. During a mean observation period of 13 months (range 7-23 months), the mean actual wear time was 43 per cent less than the advised 12 or 18 hours per day in the whole patient group, and 55 per cent in those patients, who completed the treatment. Compliance level was unrelated to the appliance type. LIMITATIONS: Study assessed a relatively small number of patients. CONCLUSIONS/IMPLICATIONS: Adolescent patients wear HGA and TB less than advised. Individual variation in treatment adherence is considerable. Thereby, microelectronic wear-time documentation can be a cost-effective mean of identifying non-compliance.

Blepharocheilodontic (BCD) syndrome: New insights on craniofacial and dental features.

Blepharocheilodontic (BCD) syndrome is a rare condition characterized by bilateral cleft lip and palate (BCLP), eyelid abnormalities, and oligodontia. Despite orofacial clefting and oligodontia being central features of the condition, detailed reports of dental and craniofacial characteristics are scarce. The aim of this study was to analyze the dental and craniofacial features in a group of patients with BCD syndrome (three of which were related). Cephalometric radiographic analyses were performed on BCD syndrome patients (all radiographs taken at age 8 years) and compared to 40 randomly selected age-matched controls (20 non-syndromic BCLP, 20 non-cleft). Also, we assessed clinical records, photographs, dental study casts, and dental radiographs to determine the extent and pattern of tooth agenesis, dental morphology and malocclusion. BCD syndrome patients showed a very severe skeletal III malocclusion (maxillary-mandibular sagittal discrepancy) and reduced anterior lower face measurement compared to non-syndromic BCLP and non-cleft controls (P = 0.001, P = 0.027). All patients exhibited oligodontia (mean number of missing permanent teeth 13.7, range 7-17). All patients exhibited missing upper central and lateral incisor, upper canine and premolar teeth. Variations in dental morphology included taurodontism, conical-shaped teeth, and notching of the incisal edges. All patients had a short and narrow maxilla which translated into anterior and posterior cross bites. We conclude that, in our BCD syndrome group, the craniofacial skeletal defects are more severe than patients with BCLP. The pattern of tooth agenesis is unusual as it included teeth that are normally highly resistant to agenesis, namely upper central incisor and canine teeth. © 2017 Wiley Periodicals, Inc.

Lambdoid Synostosis Versus Positional Posterior Plagiocephaly, a Comparison of Skull Base and Shape of Calvarium Using Computed Tomography Imaging.

The differential diagnostics between the common positional posterior plagiocephaly and relatively rare lambdoid synostosis is important due to the differences in their treatment plan and clinical management. However, the clinical criteria for the diagnosis of lambdoid synostosis are not clear since there is a considerable overlap in the features of positional posterior plagiocephaly and unilateral lambdoid synostosis. To systematically evaluate the clinical findings in these 2 patient groups, we quantitatively compared the characteristics of endocranial skull base and ectocranial calvarium in 3D computed tomography, in 9 children (mean age 2.9 years) with unilateral lambdoid synostosis and 9 children with positional posterior plagiocephaly. The groups were sex and age matched. Our results show that the skull bases in the lambdoid synostosis are posteriorly shorter and more twisted than in positional posterior plagiocephaly. Anterior twisting was mild in both skull types. Our study confirmed earlier suggested diagnostic feature: prominent ipsilateral mastoidal bossing downward and laterally in all lambdoid skulls. In positional posterior plagiocephaly the bossing was typically not detected. Interestingly, there was a great variation in the position of the ipsilateral ear and external auditory meatus in both patient groups. Thus, neither antero-posterior nor vertical position of ear is a reliable differential diagnostic feature between lambdoid synostosis or positional posterior plagiocephaly.

Severely hypoplastic amelogenesis imperfecta with taurodontism.

BACKGROUND: The prominent dental feature of a boy was severely hypoplastic enamel in both primary and permanent teeth. CASE REPORT: Many permanent teeth were already infected while emerging in the oral cavity. Panoramic radiograph showed enlarged and elongated pulp chambers (taurodontism) in the permanent first molars. The clinical and radiological diagnosis was either hypomaturation-hypoplastic amelogenesis imperfecta with taurodontism (AIHHT) or tricho-dento-osseous syndrome (TDO). Histological examination of the upper right permanent first molar revealed thin lamellar or somewhat thicker amorphous enamel on approximal surface only with no rods or incremental lines visible. Histologically, the Witkop type AIG designated 'enamel agenesis' cannot be excluded. The medical and dental history of the family members, as well as the boy's medical examination, was noncontributing. He had thick, blond, curly hair. The bone structure of the jaws and skull was normal. For genetic analysis, DLX3 gene was sequenced but no mutation was found. CONCLUSIONS: Since the gene defect of TDO has been localized only in the DLX3 gene, the more probable diagnosis was AI.

2,3,7,8-tetrachlorodibenzo-p-dioxin specifically reduces mRNA for the mineralization-related dentin sialophosphoprotein in cultured mouse embryonic molar teeth.

Previous studies show that the most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), interferes with mineralization of the dental matrices in developing mouse and rat teeth. Culture of mouse embryonic molar teeth with TCDD leads to the failure of enamel to be deposited and dentin to undergo mineralization. Lactationally exposed rats show defectively matured enamel and retardation of dentin mineralization. To see if the impaired mineralization is associated with changes in the expression of dentin sialophosphoprotein (Dspp), Bono1 and/or matrix metalloproteinase-20 (MMP-20), thought to be involved in mineralization of the dental hard tissues, we cultured mouse (NMRI) E18 mandibular molars for 3, 5 or 7 days and exposed them to 1 microM TCDD after 2 days of culture. As detected by in situ hybridization of tissue sections, localization and intensity of Bono1 and MMP-20 expression showed no definite difference between the control and exposed tooth explants, suggesting that TCDD does not affect their expression. On the contrary, TCDD reduced or prevented the expression of Dspp in secretory odontoblasts and decreased it in presecretory ameloblasts. The results suggest that the retardation of dentin mineralization by TCDD in mouse molar teeth involves specific interference with Dspp expression.

7,12-dimethylbenz[a]anthracene interferes with the development of cultured mouse mandibular molars.

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.

Interference by 2,3,7,8-tetrachlorodibenzo-p-dioxin with cultured mouse submandibular gland branching morphogenesis involves reduced epidermal growth factor receptor signaling.

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.

Developmental toxicity of dioxin to mouse embryonic teeth in vitro: arrest of tooth morphogenesis involves stimulation of apoptotic program in the dental epithelium.

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.

Response of the incisor tooth to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a dioxin-resistant and a dioxin-sensitive rat strain.

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.