Managing a bleeding patient can be a challenge during dental surgery. Profuse hemorrhage due to platelet defects, coagulation disorders, vascular anomalies, medication-induced patients, as well as inherited bleeding ailments result in soft tissue hematoma, septic shock, compromised airway, and in some severe cases, death could occur. A vast array of surgical hemostatic agents are available to stop bleeding, including chitosan-based hemostatic agents. Chitosan has an advantage over other topical hemostatic materials for its ability to promote shorter bleeding times and assist in healing. Massive behind-the-scene research and development efforts are ongoing to increase the performance of chitosan as a hemostatic agent. Numerous studies on chitosan use in dental hemostasis have registered it as being safe, biodegradable, biocompatible, promoting healing, antimicrobial and bioactive. This article reviews the application of chitosan in managing hemostasis in dental patients.
Epithelial-mesenchymal transition (EMT) is a critical process that occurs during the embryonic development, wound healing, organ fibrosis and the onset of malignancy. Emerging evidence suggests that the EMT is involved in the invasion and metastasis of cancers. The inflammatory reaction antecedent to fibrosis in the onset of oral submucous fibrosis (OSF) and the role of EMT in its malignant transformation indicates a hitherto unexplored involvement of EMT. This review focuses on the role of EMT markers which are regulators of the EMT mediated complex network of molecular mechanisms involved in the pathogenesis of OSF and OSCC. Further the gene enrichment analysis and pathway analysis supports the association of the upregulated and downregulated genes in various EMT regulating pathways.
The aim of direct pulp capping (DPC) is to promote pulp healing and mineralized tissue barrier formation by placing a dental biomaterial directly over the exposed pulp. Successful application of this approach avoids the need for further and more extensive treatment. In order to ensure a complete pulp healing with the placement of restorative materials, a mineralized tissue barrier must form to protect the pulp from microbial invasion. The formation of mineralized tissue barrier can only be induced when there is a significant reduction in pulp inflammation and infection. Consequently, promoting the healing of pulp inflammation may provide a favorable therapeutic opportunity to maintain the sustainability of DPC treatment. Mineralized tissue formation was observed as the favorable reaction of exposed pulp tissue against a variety of dental biomaterials utilized for DPC. This observation reveals an intrinsic capacity of pulp tissue for healing. Therefore, this review focuses on the DPC and its healing procedure as well as the materials used for DPC treatment and their mechanisms of action to promote pulpal healing. In addition, the factors that can affect the healing process of DPC, clinical considerations and future perspective has been described.
Tooth agenesis in the reduction of tooth number which includes hypodontia, oligodontia and anodontia is caused by disturbances and gene mutations that occur during odontogenesis. To date, several genetic mutations that unlock the causes of non-syndromic tooth agenesis are being discovered; these have been associated with certain illnesses because tooth development involves the interaction of several genes for tooth epithelium and mesenchyme odontogenesis. Mutation of candidate genes PAX9 and MSX1 have been identified as the main causes of hypodontia and oligodontia; meanwhile, AXIN2 mutation is associated with anodontia. Previous study using animal models reported that PAX9-deficient knockout mice exhibit missing molars due to an arrest of tooth development at the bud stage. PAX9 frameshift, missense and nonsense mutations are reported to be responsible; however, the most severe condition showed by the phenotype is caused by haploinsufficiency. This suggests that PAX9 is dosage-sensitive. Understanding the mechanism of genetic mutations will benefit clinicians and human geneticists in future alternative treatment investigations.