Calcification of the interclinoid ligament (ICL) of the sella turcica, or sella turcica bridging, has been associated with severe craniofacial deviations. Despite no comprehensive study on the sella turcica bridge, a relationship with tooth and eruption disturbances has been reported. In order to investigate whether congenital absence of the second mandibular premolar, or the presence of a palatally displaced canine (PDC), is associated with sella bridging, a retrospective study was performed. Lateral cephalometric radiographs from 20 males and 14 females, aged between 8 and 16 years, with a PDC and second mandibular premolar aplasia were reviewed and compared with a control group. A standardized scoring scale was established to quantify the extent of a sella turcica bridge from each radiograph (no calcification, partially calcified, and completely calcified). The prevalence of complete calcification of the ICL in adolescents with dental anomalies was equal to 17.6 per cent, while an incidence 9.9 per cent was found in the control group. A partially calcified sella turcica was observed in 58.8 per cent of adolescents with dental anomalies compared with 33.7 per cent in the control group. The association between the degree of calcification of the ICL and the presence of dental anomalies in the studied adolescents was statistically significant according to chi-square statistics (P = 0.004). This was confirmed by Fisher's exact test (P = 0.003). According to these findings, the prevalence of a sella turcica bridge in adolescents with dental anomalies is increased, while age and gender do not greatly influence ossification of the ICL. The very early appearance during development of a sella turcica bridge should alert clinicians to possible tooth anomalies in life later.

Vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), is a multifunctional cytokine. It is overexpressed in several conditions, which are characterized by vascular hyperpermeability and angiogenesis. In this investigation, we have evaluated the possibility that VEGF/VPF could be expressed in periapical lesions. We studied 17 periapical granulomas and 6 periapical cysts by immunohistochemistry. An immunopositive reaction for VEGF/VPF was observed in all 23 periapical lesions; however, the intensity of immunostaining by anti-VEGF antibody varied according to histopathological findings. In periapical granulomas without epithelium, almost all of the inflammatory cells were immunoreactive to anti-VEGF/VIP antibody. In periapical granulomas, which had rests of Malassez in them, some inflammatory cells were stained. On the other hand, epithelial cells always were stained by VEGF/VPF antibody, both in periapical lesions with epithelium and in radicular cysts. This study demonstrated that periapical lesions express VEGF/VPF, although with some differences in cell immunolabeling, which correlated to the lesions' stages of development. Initially, VEGF/VPF would assure angiogenesis and vascular hyperpermeability, resulting in accumulation of inflammatory cells, later it could be involved in cyst fluid accumulation. We hypothesize, therefore, that VEGF/VPF expression plays an important role in the pathogenesis of periapical granulomas and enlargement of radicular cysts by several mechanisms.

The acrofacial dysostoses (AFDs) are a heterogeneous group of disorders combining defects of craniofacial and limb development. The predominantly preaxial form is called Nager AFD, the predominantly postaxial form of AFD (POADS) is also known as the Genée-Wiedemann or Miller syndrome. The former appears to be about twice as common as the latter with well-documented autosomal dominant and recessive occurrences in both conditions. Only 1 AD occurrence of POADS is known, but 5 sets of sibs are suggestive of AR inheritance. Heterogeneity of apparently nonsyndromal AFD of both types is powerful support for the hypothesis that the AFDs are polytopic field defects arising during blastogenesis. Six other previously described forms of AFD include the AFD syndrome of Kelly et al. (AR), the Rodríguez or Madrid form of AFD (AR or XLR), the Reynolds or Idaho form of AFD (AD), the Arens or Tel Aviv type of AFD (AF?), the presumed AR AFD syndrome of Richieri-Costa et al., and the AD Patterson-Stevenson-Fontaine syndrome. Here we review the AFDs and report on a previously apparently undescribed autosomal or X-linked dominant form of AFD with mental retardation in a Sicilian mother and her 4 sons.

Objective: To investigate condylar symmetry and condyle fossa relationships in subjects with functional posterior crossbite comparing findings before and after rapid maxillary expansion (RME) treatment through low-dose computed tomography (CT). Materials and Methods: Twenty-six patients (14 girls and 12 boys, mean age 9.6 6 1.4 years) with functional posterior crossbite (FPXB) diagnosis underwent rapid palatal expansion with a Hyrax appliance. Patients' temporomandibular joints (TMJ) underwent multislice CT scans before rapid palatal expansion (T0) and after (T1). Joint spaces were compared with those of a control sample of 13 subjects (7 girls and 5 boys, mean age 11 6 0.6 years). Results: Anterior space (AS), superior space (SS), and posterior space (PS) joint space measurements at T0 between the FPXB side and contralateral side demonstrated no statistically significant differences. After RME treatment (T1), all three joint spaces increased on both the FPXB side and the non-crossbite side. However, differences were statistically significant only for the SS when comparing the two sides at T1. SS increased more than AS and PS in the non-crossbite condyle (0.28 mm) and FPXB condyle (0.37 mm), and PS increased only on the FPXB side (0.34 mm). Conclusions: There were no statistically significant differences in condyle position within the glenoid fossa between the FPXB and non-crossbite side before treatment. Increases in joint spaces were observed after treatment with RME on both sides. These changes were, however, of small amounts.