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Odontogenic tumors that produce abnormal tooth-like structures are repeatedly observed in mandibles of mice that carry both albumin-myc and albumin-ras transgenes. The earliest lesions appear among the periodontal ligament mesenchymal cells, but later lesions include an epithelial component. Subsequent tumor development recapitulates the process of normal tooth formation, which requires multiple sequential cell signals, and results in cell differentiation, matrix secretion, and mineralization. Tumor cells with epithelial morphology produce ras oncoprotein, consistent with an epithelial origin of these tumors. As albumin regulatory sequences direct oncogene expression in these mice, our findings also suggest that some of the albumin present in normal teeth may be locally produced and have a role in tooth mineral formation. The reproducibility of this phenotype makes these mice an excellent model for studies of both normal and neoplastic odontogenesis. [ABSTRACT FROM AUTHOR]

The hard covering tissues, enamel or enameloid, of representative vertebrate teeth were immunohistochemically stained using specific monoclonal antibodies against bovine amelogenins and bovine enamelins in order to determine the phylogenetic distribution of enamelin and amelogenin proteins. Immunohistochemically, only enamelin proteins were present in lower vertebrate (shark, bony fish, and larval amphibian) teeth and dermal denticles. Both enamelin and amelogenin proteins were present in higher vertebrate (mammal, reptile, and adult amphibian) teeth. Large hydroxyapatite crystal size and high levels of mineralization, characteristics common to both enamel and enameloid, are probably due to the presence of the common protein enamelin. The evolution of enamel from enameloid in the tetrapods seems to have involved the development of the gene for amelogenin. [ABSTRACT FROM AUTHOR]

Developing enamel matrix contains a complex mixture of proteins whose characterization is essential to an understanding of amelogenesis. It is not known whether each component is the product of an individual gene, or whether they are interrelated by physiologic or artifactual breakdown. To define these relationships, monoclonal antibodies were prepared to enamel proteins and we have previously reported the characterization of six antibodies to amelogenins which did not react with enamelins (Christner et al. (1985) Arch. Oral Biol. 30:849-854). We now report the isolation of antibody to enamelins which stains the enamel matrix but does not cross-react with amelogenins. These results suggest that amelogenins and enamelins are distinct classes of proteins. [ABSTRACT FROM AUTHOR]

The organic matrix of osteodentine forms in two stages. Coarse fibril bundles (α matrix) (fibril diameter 1,000-2,000 Å) oriented parallel to long axis of the tooth are formed first by scleroblasts of types 1 and 2. Type 1 is a stellate pulp cell with sparse RER; type 2 a rounded cell containing packed arrays of RER develops from type 1. When bundles of coarse fibrils reach a diameter of 20-30 μ, a second type of matrix with fine β fibrils (fibril diameter about 500 Å) forms circumferentially around the coarse fibril bundles. Associated scleroblasts of type 3 contain arrays of RER and have numerous short blunt processes at the cell-matrix interface. Matrix deposition forces type 3 scleroblasts into canals surrounding blood vessels (dental osteons or denteons). After organic matrix deposition is completed, calcification occurs throughout the coarse and fine matrix. Coarse fibril matrix is less heavily calcified than fine fibril matrix. The fibrils in coarse (α) matrix are less heavily calcified than the surrounding interfibrillar matrix. Calcification is not an incremental process. In mature osteodentine, associated cells, scleroblasts of type 4, have only small amounts of RER and show no cytoplasmic processes. Osteodentine is compared to vasodentine, orthodentine and bone. [ABSTRACT FROM AUTHOR]

Introduction: Minor physical anomalies (MPAs) are insignificant errors of morphogenesis, which may reflect basic neurobiological features underlying the disease. Despite several studies about the presence of MPAs in bipolar disorders, the evidence in favor of a neurodevelopmental basis for the disease is still controversial. Objectives: The aim of this meta-analysis was to assess the standardized weighted mean effect sizes of MPAs in bipolar disorders, and to investigate if MPAs may be found predominantly in the head and facial regions in patients with bipolar affective disorder compared to healthy controls (HC). Methods: Four studies, involving 155 patients with bipolar disorders (BPD), as well as 187 HC, were involved in the analysis after literature search. For the investigation of MPAs in the periferial (MPA-P) and in the head and facial regions (MPA-FC) two studies involving 121 BPD patients, as well as 133 HC passed the inclusion criteria. Results: The MPAs of BPD were significantly higher compared to HC (SMD = 0.62, p = 0.003). Another important finding of the present study is that BPD patients' MPA-P scores do not significantly differ from those of healthy controls. In contrast, BPD patients' MPA-CF scores were found to be significantly higher compared to HC subjects (SMD = 0.84, p < 0.001). Conclusions: The findings of the present study suggest an early insult during the development of the brain in bipolar affective disorder. [ABSTRACT FROM AUTHOR]

Introduction: Suicide is the most severe consequence of major depressive disorder (MDD). The most novel researches assume the role of immunological dysregulation in the background – several studies have reported alterations of inflammatory cells related to both MDD and suicidal behaviour (SB). Objectives: Changes in the number of certain immune cells and their ratios have been proposed as potential biomarkers of suicide risk (SR). The aim of our research was to investigate alterations of these values related not only to MDD as an assumed inflammatory state, but also to an increased risk of SB. Methods: In our restrospective cohort study carried out between January 2015 and January 2020, we investigated laboratory parameters of psychiatric patients diagnosed with MDD (n =101). Individuals with recent (≤48 hours prior) suicide attempt (SA) (n =22) and with past SA (>48 hours prior) (n =19) represented the high SR group. MDD patients with no history of SA (n =60) composed the intermediate SR group. We compared the number of neutrophil granulocytes, monocytes, lymphocytes, platelets, leukocytes, neutrophil-to-lymphocyte (NLR), monocyte-to-lymphocyte (MLR), platelet-to-lymphocyte ratio (PLR), red blood cell distribution width (RDW) and erythrocyte sedimentation rate (ESR). Furthermore, we evaluated alterations of these parameters related to antidepressant (AD) treatment, which has been proved to have anti-inflammatory effects. Statistical analyses were carried out using GraphPad 9.5.0 and MedCalc 16.8 programmes. Results: We found a significant increase in neutrophil granulocyte count (p =0.016), NLR (p =0.031, Fig. 1), monocyte count (p ≤0.0001), MLR (p =0.005, Fig. 2), leukocyte count (p =0.048) and ESR (p =0.037) in patients with recent SA compared to patients with no history of SA. Moreover, there was a significant elevation in monocyte count (p ≤0.0001), MLR (p =0.020, Fig. 3), ESR (p =0.041) and RDW (p =0.037) in patients with high SR compared to patients with intermediate SR. AD treatment resulted in a significant decrease in neutrophil granulocyte count (p =0.0163) and NLR (p =0.016), however, it did not affect the rest of the parameters. Image: Image 2: Image 3: Conclusions: Assuming immunological mechanisms in the background of MDD and SB, our findings support the role of NLR as a biomarker of acute SR, though its alterations may be masked by AD therapy in the long term. However, MLR – remaining unaffected by AD treatment – may be a possible indicator of both acute and long term suicidal vulnerability. In order to further specify the diagnostic value of these parameters, future prospective research is needed. The study was supported by the FIKP-IV and the TNIL projects. Disclosure of Interest: None Declared [ABSTRACT FROM AUTHOR]