IL-33 and ST2 are expressed in periapical granulomas and radicular cysts. Increased numbers of IL-33- and ST2-positive fibroblasts in periapical lesions when compared to healthy periapical tissues suggest that IL-33/ST2 signaling may be involved in periapical inflammation and tissue fibrosis.

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Segmental neurofibromatosis is a rare clinical finding generally with no family history and facial involvement. There are four subtypes of segmental neurofibromatosis: true segmental, localized cases with deep involvement, hereditary segmental and bilateral segmental neurofibromatosis. Here we report three patients from the same family (father, son and granddaughter) with segmental bilateral neurofibromatosis on the face. This form hasn't noticed in the literature.

A periapical lesion occurs as periapical tissue reacts to a dental pulp anaerobic infection. Th is phenomenon may result from carious lesions, tooth fractures, or iatrogenic and other circumstances that allow for bacteria to penetrate into the pulpal tissues. Objectives: Th is study histologically evaluated experimentally induced periapical lesions using the Autodesk Au-toCAD 2010 software. Additionally, based on the amounts of alveolar bone destruction sizes in the mouse model regions, a proposed experimental periapical lesion gradation criterion was created. Methods: Twelve BALB/c mice were utilizised in a periapical model, whereby their mandibular right fi rst molars were coronally opened, allowing for pulp exposure to host oral bacterial fl ora. Th ese mice were sacrifi ced two and four weeks following pulp exposure. Following each sacrifi ce, hemi-mandibles were fi xed in 4% paraformaldehyde, decalcifi ed in 3% formic acid, embedded in paraffi n and cut into 4-μm-thick sections. Th e sections were stained with haematoxylin-eosin and examined with light microscopy (40x). Section images that included the mandibular fi rst molar distal roots and passed through the apical foramens were selected for analysis. Th e periodontal ligament sizes were measured using the Autodesk AutoCAD 2010 software. Results: Th ere was a highly signifi cant lesgion size difference at the two diff erent time points following the lesion induction (p=0.002). Th e periapical lesions were classifi ed according to periapical bone resorption sizes. We determined the values of quartiles (25% and 75%) and median areas (50%) of the mean lesion values at both experimental periods. Th ese data enabled for scoring of the lesions with grades from 1 to 4. Th e area of the normal periodontal ligament space was assigned with a grade of 0. Conclusion: Th is newly designed gradation criteria represent a signifi cant advantage compared with the previous descriptive methods used for determining periapical tissue bone destruction levels. It Th e criteria achieves this advantage by excluding subjectivity, facilitating a numerical presentation of the data and reducing the possibility of making errors by using the highly availably Autodesk AutoCAD 2010 software.