Types and tissue sources of bone grafts in dental implants

Using bone grafts has been described in the literature for multiple decades and has been applied within the different medical fields. Furthermore, in the field of dentistry, evidence shows that these approaches have been widely used for different purposes, including the management of craniofacial defects and dental implantology. However, it should be noted that many disadvantages have been reported for the different tissue sources of bone grafting in dental implants despite the wide acceptance of the outcomes and favorable prognosis with these materials. Therefore, many efforts were conducted to innovate further approaches with reduced disadvantages and favorable outcomes. Our present study discusses the types and tissue sources of bone grafts in the settings of dental implants. This can provide dentists with better information and enhanced knowledge levels about the tissue sources of dental implants, which should help them decide the most appropriate source with the least adverse events. Different tissue sources were reported in the literature, including materials that are no longer used for their disadvantages and associated complications. Among the proposed materials, biomimetics has been reported with favorable outcomes and reduced adverse events, and using combinations of these materials can furtherly enhance the prognosis. Further research is needed to innovate additional modalities that can overcome the currently reported limitations.

Riboceine Rescues Auranofin-Induced Craniofacial Defects in Zebrafish

Craniofacial abnormalities are a common group of congenital developmental disorders that can require intensive oral surgery as part of their treatment. Neural crest cells (NCCs) contribute to the facial structures; however, they are extremely sensitive to high levels of oxidative stress, which result in craniofacial abnormalities under perturbed developmental environments. The oxidative stress-inducing compound auranofin (AFN) disrupts craniofacial development in wildtype zebrafish embryos. Here, we tested whether the antioxidant Riboceine (RBC) rescues craniofacial defects arising from exposure to AFN. RBC rescued AFN-induced cellular apoptosis and distinct defects of the cranial cartilage in zebrafish larvae. Zebrafish embryos exposed to AFN have higher expression of antioxidant genes gstp1 and prxd1, with RBC treatment partially rescuing these gene expression profiles. Our data suggest that antioxidants may have utility in preventing defects in the craniofacial cartilage owing to environmental or genetic risk, perhaps by enhancing cell survival.

Ciliary Hedgehog signaling regulates cell survival to build the facial midline

Craniofacial defects are among the most common phenotypes caused by ciliopathies, yet the developmental and molecular etiology of these defects is poorly understood. We investigated multiple mouse models of human ciliopathies (including Tctn2, Cc2d2a and Tmem231 mutants) and discovered that each displays hypotelorism, a narrowing of the midface. As early in development as the end of gastrulation, Tctn2 mutants displayed reduced activation of the Hedgehog (HH) pathway in the prechordal plate, the head organizer. This prechordal plate defect preceded a reduction of HH pathway activation and Shh expression in the adjacent neurectoderm. Concomitant with the reduction of HH pathway activity, Tctn2 mutants exhibited increased cell death in the neurectoderm and facial ectoderm, culminating in a collapse of the facial midline. Enhancing HH signaling by decreasing the gene dosage of a negative regulator of the pathway, Ptch1, decreased cell death and rescued the midface defect in both Tctn2 and Cc2d2a mutants. These results reveal that ciliary HH signaling mediates communication between the prechordal plate and the neurectoderm to provide cellular survival cues essential for development of the facial midline.

Acquired Facial, Maxillofacial, and Oral Asymmetries—A Review Highlighting Diagnosis and Management

Facial asymmetry refers to the absence of, or the deviation from the regular mirror image of facial structures, relative to a referenced midline axis. It can be attributed to a wide spectrum of deformities, including congenital, developmental, or acquired conditions, which can originate either prenatally or postnatally. Though highly prevalent, asymmetry commonly goes undiagnosed due to its subtle or relative nature. Among the spectrum of conditions, acquired cases are triggered postnatally, in previously normal individuals, thus subjecting them to sudden, eventful psychological and psychosocial disharmony. When detected early, timely management may help intervene progressive growth of these conditions. This, therefore, emphasizes the need for a thorough diagnostic workup including medical/dental history, clinical examinations, study models, photographic and radiographic records for a case-by-case basis to prevent severe functional and aesthetic complications. Recently, advanced diagnostic procedures, such as stereophotogrammetry, 3D stereolithographic models, skeletal scintigraphy (radionucleotide scans), 3D computed tomographic scans, cone-beam computed tomography, and magnetic resonance imaging, have provided innovative diagnostic instruments for numerous craniofacial defects. This descriptive review aims at focusing on the factors leading to frequently encountered conditions of acquired facial asymmetry and highlights their clinical evaluation, conservative and surgical interventions by a multi-disciplinary team of clinicians.

STUDY OF INCIDENCE OF THE CORONAL APPROACH IN CRANIOFACIAL TRAUMA AND ADVANTAGEOUS OF TITANIUM MESH IN RECONSTRUCTION OF CRANIOFACIAL DEFECTS.

INTRODUCTION: The coronal approach gives a broad exposure to the frontal bone, the calvaria, the nasal bones, the orbits, the subcondylar region, the zygoma and the zygomatic arch and gives ideal aesthetic results with less complication. The common craniofacial fractures are Nasal bones (45%), cranial bones (24%), Mandible (13%), Zygoma (13%), Orbital blowout (3%), Maxilla (2%). Common causes of fractures are Road trafc accident, Assault, Industrial accidents, Recreational accidents, Frontal bone fracture. METHOD: The study was carried out for a period of one year from March 2020 to March 2021. The study conducted in St Joseph dental college ELURU in the department of Oral and Maxillofacial Surgery. The age limit for this study was below 30 years. The number of subjects involved in this study was 5. Number of females was 3 and males were 2 in this study. RESULT: Number of female participants in this study was 3 and number of male participants was 2.Number of male participants with coronal incision were 1 and number of participants with pretrichial incision were 2.Out of 2 one for male participant and one for female participant. CONCLUSION: The coronal ap has recently become a preferred approach for access to the craniofacial skeleton and orbit. This method of exposure has become particularly useful with increased indications for rigid internal xation and primary bone grafting in the management of complex facial fractures.

Tessier Number 3 and 4 Clefts: Clinical Presentation and Associated Clefts in a South African Population

Introduction The defects found in Tessier clefts number 3 and number 4 come in various forms in different patients. These variations have to a great extent affected not only documentation of these craniofacial defects but invariably their treatment and communication amongst craniofacial researchers. This study has not only documented the clinical presentation of these clefts in a South African population but has also incorporated the clinical presentation of Tessier clefts number 3 and 4 from different regions of the world. Methods The records of 8 patients, who had been treated for either Tessier clefts number 3 or 4, were reviewed and compared with 16 studies pulled from the literature systematically. The defects recorded as well as associated clefts and other congenital malformations were documented, and findings were compared. Results The anatomical and clinical presentation of the patients was compared to the reviewed literature and the different parameters were documented. In addition, associated clefts were also recorded in the study—it was noted that the association pattern recorded in Tessier cleft number 4 in this study did not conform to its traditional counterpart. Conclusion This study concluded that the clinical presentations of these clefts, however variable, seem to have a similar presentation worldwide. Additionally, associated clefts do not conform to the original Tessier classification system and therefore it is imperative for these patterns to be clearly mapped out.

Depression and Antidepressants During Pregnancy: Craniofacial Defects Due to Stem/Progenitor Cell Deregulation Mediated by Serotonin

Depression is a common and debilitating mood disorder that increases in prevalence during pregnancy. Worldwide, 7 to 12% of pregnant women experience depression, in which the associated risk factors include socio-demographic, psychological, and socioeconomic variables. Maternal depression could have psychological, anatomical, and physiological consequences in the newborn. Depression has been related to a downregulation in serotonin levels in the brain. Accordingly, the most commonly prescribed pharmacotherapy is based on selective serotonin reuptake inhibitors (SSRIs), which increase local serotonin concentration. Even though the use of SSRIs has few adverse effects compared with other antidepressants, altering serotonin levels has been associated with the advent of anatomical and physiological changes in utero, leading to defects in craniofacial development, including craniosynostosis, cleft palate, and dental defects. Migration and proliferation of neural crest cells, which contribute to the formation of bone, cartilage, palate, teeth, and salivary glands in the craniofacial region, are regulated by serotonin. Specifically, craniofacial progenitor cells are affected by serotonin levels, producing a misbalance between their proliferation and differentiation. Thus, it is possible to hypothesize that craniofacial development will be affected by the changes in serotonin levels, happening during maternal depression or after the use of SSRIs, which cross the placental barrier, increasing the risk of craniofacial defects. In this review, we provide a synthesis of the current research on depression and the use of SSRI during pregnancy, and how this could be related to craniofacial defects using an interdisciplinary perspective integrating psychological, clinical, and developmental biology perspectives. We discuss the mechanisms by which serotonin could influence craniofacial development and stem/progenitor cells, proposing some transcription factors as mediators of serotonin signaling, and craniofacial stem/progenitor cell biology. We finally highlight the importance of non-pharmacological therapies for depression on fertile and pregnant women, and provide an individual analysis of the risk–benefit balance for the use of antidepressants during pregnancy

A importância da Odontologia na assistência a indivíduos com defeitos congênitos

Introduction: Birth defects are structural or functional changes that occur during intrauterine life. The dentist must recognize the craniofacial defects, complement the phenotypic characterization and manage them within a multidisciplinary team. The present review aims to assist the dentist to diagnose these findings and present syndromic conditions typically associated with craniofacial malformations Literature Review: Craniofacial manifestations of birth defects are conditions that must be recognized by dentists, as they are frequently present in their daily practices, and this professional may be the first to identify such findings. The main syndromic clinical pictures typically associated with micrognathia, oral clefts and skeletal dysplasias with craniofacial manifestation are presented, pointing out their clinical and genetic features. Discussion: The dentist must perform a detailed anamnesis including family history, as well as should recognize both clinical and radiographically the dysmorphisms, observing the patient systemically. Conclusion: Dentistry professionals should receive theoretical-practical training for the diagnosis, treatment and surveillance of individuals with congenital defects, either in individual assessment or as part of a multiprofessional team.

Null cyp1b1 Activity in Zebrafish Leads to Variable Craniofacial Defects Associated with Altered Expression of Extracellular Matrix and Lipid Metabolism Genes

CYP1B1 loss of function (LoF) is the main known genetic alteration present in recessive primary congenital glaucoma (PCG), an infrequent disease characterized by delayed embryonic development of the ocular iridocorneal angle; however, the underlying molecular mechanisms are poorly understood. To model CYP1B1 LoF underlying PCG, we developed a cyp1b1 knockout (KO) zebrafish line using CRISPR/Cas9 genome editing. This line carries the c.535_667del frameshift mutation that results in the 72% mRNA reduction with the residual mRNA predicted to produce an inactive truncated protein (p.(His179Glyfs*6)). Microphthalmia and jaw maldevelopment were observed in 23% of F0 somatic mosaic mutant larvae (144 hpf). These early phenotypes were not detected in cyp1b1-KO F3 larvae (144 hpf), but 27% of adult (four months) zebrafish exhibited uni- or bilateral craniofacial alterations, indicating the existence of incomplete penetrance and variable expressivity. These phenotypes increased to 86% in the adult offspring of inbred progenitors with craniofacial defects. No glaucoma-related phenotypes were observed in cyp1b1 mutants. Transcriptomic analyses of the offspring (seven dpf) of cyp1b1-KO progenitors with adult-onset craniofacial defects revealed functionally enriched differentially expressed genes related to extracellular matrix and cell adhesion, cell growth and proliferation, lipid metabolism (retinoids, steroids and fatty acids and oxidation–reduction processes that include several cytochrome P450 genes) and inflammation. In summary, this study shows the complexity of the phenotypes and molecular pathways associated with cyp1b1 LoF, with species dependency, and provides evidence for the dysregulation of extracellular matrix gene expression as one of the mechanisms underlying the pathogenicity associated with cyp1b1 disruption.