Preprosthetic Management of “Flabby Ridge” on Edentulous Patient

For edentulous patients, the integrity of the osteomucosal-bearing surface is a significant factor for the balance of the future removable prosthesis. The supporting tissues are influenced by several factors. Physiological bone resorption, senescence, and changes caused by systemic diseases and polypharmacy lead to modifications in these tissues. Similarly, trauma caused by an ill-fitted prosthesis influences the degree of bone resorption and the development of hyperplastic tissue. The etiology of bone resorption is multifactorial and complex, with continuous individual variations that are often unexplained. Although, no study has been able to establish the importance of the different factors in relation to each other, it is often reported that chronic excessive mechanical pressure in relation to occlusal constraints is responsible for the appearance of local resorption’s areas. The aim of this work is to present, through three clinical cases, the various factors involved in the alteration of the osteomucous-bearing surface and eventually, possible therapeutic attitude to deal with

Prosthetic Rehabilitation on Edentulous Patients with Microstomia: About Three Cases

Limited oral opening is an acquired or congenital abnormal condition that compromises patient esthetics, nutrition, and quality of life. In addition, it may hinder conventional prosthetic procedures of edentulous patients, make it challenging, and present difficulties at all its stages. This clinical report presents different clinical treatment options suitable to be chosen by the prosthodontic carer in the case of reduced oral aperture

Identifying novel mechanisms of biallelic TP53 loss refines poor outcome for patients with multiple myeloma

Abstract Biallelic TP53 inactivation is the most important high-risk factor associated with poor survival in multiple myeloma. Classical biallelic TP53 inactivation has been defined as simultaneous mutation and copy number loss in most studies; however, numerous studies have demonstrated that other factors could lead to the inactivation of TP53. Here, we hypothesized that novel biallelic TP53 inactivated samples existed in the multiple myeloma population. A random forest regression model that exploited an expression signature of 16 differentially expressed genes between classical biallelic TP53 and TP53 wild-type samples was subsequently established and used to identify novel biallelic TP53 samples from monoallelic TP53 groups. The model reflected high accuracy and robust performance in newly diagnosed relapsed and refractory populations. Patient survival of classical and novel biallelic TP53 samples was consistently much worse than those with mono-allelic or wild-type TP53 status. We also demonstrated that some predicted biallelic TP53 samples simultaneously had copy number loss and aberrant splicing, resulting in overexpression of high-risk transcript variants, leading to biallelic inactivation. We discovered that splice site mutation and overexpression of the splicing factor MED18 were reasons for aberrant splicing. Taken together, our study unveiled the complex transcriptome of TP53, some of which might benefit future studies targeting abnormal TP53