Nonsurgical endodontic management using MTA for perforative defect of internal root resorption: report of a long term follow-up

Internal root resorption is an uncommon lesion following a dental injury. The use of mineral trioxide aggregate (MTA) is a conservative approach to repair lesions with periodontal communication. This case report presents a long-term follow-up of a nonsurgical endodontic management using MTA for perforative defect of internal root resorption. During the endodontic treatment, the granulation tissue was removed and the root canal prepared. Calcium hydroxide was placed as a temporary dressing for 30 days. After this period, the root canal space and the perforation defect were filled with MTA. The clinical findings and periapical radiographs indicated success of treatment until 2 years of follow-up. However, the radiograph after 8 years showed an extensive radiolucent area in the middle third of the root with separation of the apical and coronal root segments. These findings were observed more accurately by using cone-beam computerized tomography.     

Chlorhexidine induces DNA damage in rat peripheral leukocytes and oral mucosal cells

OBJECTIVE: Chlorhexidine digluconate is widely used in dental practice for decreasing plaque control, controlling gingivitis and disinfecting root canals. However, the undesirable effects of chlorhexidine digluconate regarding its genotoxicity are conflicting in the literature. Thus, the aim of this study was to investigate the genotoxicity of chlorhexidine digluconate in rat peripheral blood and oral mucosal cells by the single cell gel (comet) assay and micronucleus assay. METHODS: Thirty male Wistar rats were distributed into three groups: negative control; experimental group orally treated with 0.5 ml of 0.12% chlorhexidine digluconate, twice daily, during 8 days; and positive control, which received 4-nitroquinoline 1-oxide at 0.5 g/l by drinking water. RESULTS: A statistically significant increase of DNA damage was observed in leukocytes and oral mucosal cells of the chlorhexidine digluconate treated group, as assessed by the comet assay. However, no increase of micronucleated cells was detected in reticulocytes from peripheral blood cells. CONCLUSIONS: Taken together, the data indicate that chlorhexidine digluconate is able to induce primary DNA damage in leukocytes and in oral mucosal cells, but no chromosome breakage or loss in erythrocytes.     

Influence of leucite content on slow crack growth of dental porcelains.

OBJECTIVES: To determine the stress corrosion susceptibility coefficient, n, of seven dental porcelains (A: Ceramco I; B: Ceramco-II; C: Ceramco-III; D: d.Sign; E: Cerabien; F: Vitadur-Alpha; and G: Ultropaline) after aging in air or artificial saliva, and correlate results with leucite content (LC). METHODS: Bars were fired according to manufacturers' instructions and polished before induction of cracks by a Vickers indenter (19.6N, 20s). Four specimens were stored in air/room temperature, and three in saliva/37 degrees C. Five indentations were made per specimen and crack lengths measured at the following times: approximately 0; 1; 3; 10; 30; 100; 300; 1000 and 3000 h. The stress corrosion coefficient n was calculated by linear regression analysis after plotting crack length as a function of time, considering that the slope of the curve was [2/(3n+2)]. Microstructural analysis was performed to determine LC. RESULTS: LC of the porcelains were 22% (A and B); 6% (C); 15% (D); 0% (E and F); and 13% (G). Except for porcelains A and D, all materials showed a decrease in their n values when stored in artificial saliva. However, the decrease was more pronounced for porcelains B, F, and G. Ranking of materials varied according to storage media (in air, porcelain G showed higher n compared to A, while in saliva both showed similar coefficients). No correlation was found between n values and LC in air or saliva. SIGNIFICANCE: Storage media influenced the n value obtained for most of the materials. LC did not affect resistance to slow crack growth regardless of the test environment.     

Clonality analysis of giant cell lesions of the jaws

Despite the importance of clonality to understand the pathogenesis and progression of tumors, it has not been investigated yet in giant cell lesions of the jaws. The aim of this study was to analyze the clonality of peripheral giant cell lesions (PGCL) and central giant cell lesions (CGCL) of the jaws. Six samples of PGCL and 5 samples of CGCL were analyzed in this study using the polymorphic human androgen receptor locus (HUMARA) assay. Three out of the 5 samples of the CGCL and 3 out of 6 samples of PGCL exhibited a monoclonal pattern. Our findings demonstrate that some giant cell lesions of the jaws are clonal, which indicate that these lesions may have a common genetic mechanism of development. Further studies are necessary to better elucidate the molecular mechanisms involved in the pathogenesis of such lesions.     

Myeloid sarcoma occurring concurrently with drug-induced gingival enlargement

BACKGROUND: Myeloid sarcoma is an extramedullary malignancy of myeloblasts. An unusual case of myeloid sarcoma presenting in the gingiva and affected by drug-induced gingival enlargement is presented. METHODS: A 63-year-old male taking amlodipine for his hypertension presented with a 3-week gingival enlargement. Although the obvious clinical impression was that of drug-induced gingival enlargement, an incisional biopsy was performed to corroborate chemical enlargement while ruling out diseases such as lymphoma and leukemia. RESULTS: Microscopic examination of the thickened gingiva revealed surface stratified squamous epithelium having needle-like rete pegs characteristic of drug-induced gingival enlargement. Beneath the surface epithelium, the fibrous tissue was virtually replaced by a dense infiltrate of malignant cells. Immunohistochemical studies were performed with CD117 and myeloperoxidase identifying the malignant cell population as myeloblasts, leading to a diagnosis of myeloid sarcoma. CONCLUSION: Myeloid sarcoma and hematopoietic malignancies must be included in a differential diagnosis of gingival enlargement until the definitive diagnosis is reached by histologic/laboratory examination.     

Topical 5‐azacytidine accelerates skin wound healing in rats

The development of new methods to improve skin wound healing may affect the outcomes of a number of medical conditions. Here, we evaluate the molecular and clinical effects of topical 5‐azacytidine on wound healing in rats. 5‐Azacytidine decreases the expression of follistatin‐1, which negatively regulates activins. Activins, in turn, promote cell growth in different tissues, including the skin. Eight‐week‐old male Wistar rats were submitted to 8.0‐mm punch‐wounding in the dorsal region. After 3 days, rats were randomly assigned to receive either a control treatment or the topical application of a solution containing 5‐azacytidine (10 mM) once per day. Photo documentation and sample collection were performed on days 5, 9, and 15. Overall, 5‐azacytidine promoted a significant acceleration of complete wound healing (99.7% ± 0.7.0 vs. 71.2% ± 2.8 on day 15; n = 10; p < 0.01), accompanied by up to threefold reduction in follistatin expression. Histological examination of the skin revealed efficient reepithelization and cell proliferation, as evaluated by the BrdU incorporation method. 5‐Azacytidine treatment also resulted in increased gene expression of transforming growth factor‐beta and the keratinocyte markers involucrin and cytokeratin, as well as decreased expression of cytokines such as tumor necrosis factor‐alpha and interleukin‐10. Lastly, when recombinant follistatin was applied to the skin in parallel with topical 5‐azacytidine, most of the beneficial effects of the drug were lost. Thus, 5‐azacytidine acts, at least in part through the follistatin/activin pathway, to improve skin wound healing in rodents.     

Genetic Epilepsy Syndromes Without Structural Brain Abnormalities: Clinical Features and Experimental Models

Research in genetics of epilepsy represents an area of great interest both for clinical purposes and for understanding the basic mechanisms of epilepsy. Most mutations in epilepsies without structural brain abnormalities have been identified in ion channel genes, but an increasing number of genes involved in a diversity of functional and developmental processes are being recognized through whole exome or genome sequencing. Targeted molecular diagnosis is now available for different forms of epilepsy. The identification of epileptogenic mutations in patients before epilepsy onset and the possibility of developing therapeutic strategies tested in experimental models may facilitate experimental approaches that prevent epilepsy or decrease its severity. Functional analysis is essential for better understanding pathogenic mechanisms and gene interactions. In vitro experimental systems are either cells that usually do not express the protein of interest or neurons in primary cultures. In vivo/ex vivo systems are organisms or preparations obtained from them (e.g., brain slices), which should better model the complexity of brain circuits and actual pathophysiological conditions. Neurons differentiated from induced pluripotent stem cells generated from the skin fibroblasts of patients have recently allowed the study of mutations in human neurons having the genetic background of a given patient. However, there is remarkable complexity underlying epileptogenesis in the clinical dimension, as reflected by the fact that experimental models have not provided yet results having clinical translation and that, with a few exceptions concerning rare conditions, no new curative treatment has emerged from any genetic finding in epilepsy.