This study evaluated structural and molecular issues of dentin caries-like lesions produced by different artificial models (ACL) compared with natural caries lesions (NCL). One hundred twenty-four sound occlusal dentin blocks and 47 carious blocks were obtained and surface hardness was analyzed (SH1). They were assigned to groups according to ACL: GB: Biological; GC: Chemical; GIS: In situ; GNC: natural caries (control). Blocks from groups 1, 2 and 3 were submitted to caries lesion induction. NCL and ACL blocks were submitted to surface hardness (SH 2), FT-Raman and µEDXRF analysis. All blocks were longitudinally sectioned and one of the halves was submitted to cross-sectional hardness (CSH) and the other to SEM analysis. SH1and SH2 data were submitted to t test (unpaired and paired, respectively), CSH and SEM data to two-way and one-way ANOVA respectively, and Tukey and t tests, respectively (p<0.05). Data from FT-Raman/µEDXRF were submitted to one-way ANOVA and Dunnett multiple-comparisons test (a=0.05). GB and GNC showed lowest SH2 values that were significantly different from GC and GIS. Regarding CSH, GB and GNC showed no significant difference between them. SEM showed similar caries lesion depth for GB and GNC, being significantly higher than for GC and GIS. µEDXRF showed similar values of calcium and phosphate for GB and GNC; GNC values were significantly different from GIS. No significant difference was found among the groups concerning phosphate, carbonate and CH bonds values. For collagen type I, GC values were significantly different compared to other groups. It may be concluded that caries-like lesions produced by GB were the closest model to NCL.

This research evaluated the bone repair process after implantation of homogenous demineralized dentin matrix (HDDM) in surgical defects in the parietal bone of rabbits with alloxan-induced diabetes, using a polytetrafluorethylene (PTFe) barrier for guided bone regeneration. Thirty-six rabbits were used and divided into four groups: control (C, n = 12), diabetic (D, n = 12, left parietal bone), diabetic with PTFe (DPTFe, same 12 rabbits, right parietal bone), and diabetic with PTFe associated to HDDM (D-PTFe+HDDM, n = 12). Bone defects were created in the parietal bone of the rabbits and the experimental treatments were performed, where applicable. The rabbits were sacrificed after 15, 30, 60 and 90 days. The bone defects were examined radiographically and by optical density (ANOVA and Tukey test, p < .05). The radiographic findings showed that the D-PTFe+HDDM group presented greater radiopacity and better trabecular bone arrangement when compared to that of the C, D and D-PTFe groups. The statistical analysis showed significant differences in the optical density of the newly formed bone among the studied groups. It was possible to conclude that HDDM was biocompatible in diabetic rabbits.

This paper reports on a 4-year-old male who had dyskeratosis congenita and who acquired severe aplastic anemia. The patient developed hyperpigmentation of the face, neck and chest region, arms, shoulders and legs. In addition, he had dry skin, deformed fingernails and toenails, sparse hair and eyebrows and hyperkeratosis of the dorsum of the hands and feet. Laboratory and histological analysis revealed severe pancytopenia and dyserythropoiesis of red blood cells, hypocellularity of white blood cells and decreased megakaryocytes with dysplasia. The intraoral examination identified bleeding gums; petechiae of the palate, tongue and cheek mucosa; and an atrophic, smooth and shining dorsal surface of the tongue. There were deep carious lesions in the deciduous mandibular molars and maxillary anterior teeth; as well as mobility of mandibular left canine, which had bone loss. The treatment for oral lesions included diet changes, improved oral hygiene, and extraction of the deciduous teeth destroyed by caries.

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