The temporomandibular joint (TMJ) is a complex structure that joins the temporal bone to the mandible in order to facilitate mastication and speech. All the components of the TMJ must work in tandem with the contralateral side to produce the dynamic movements required for speech and mastication. Any dysfunction between the two TMJs or within one TMJ itself may lead to painful or non-painful temporomandibular disorders (TMDs). There is a wide range of causes for TMDs, including biomechanical, biological, and bio-psychosocial factors, but there are limited treatment options available due to a lack of understanding of the etiology and pathogenesis of TMDs. In order to provide improved interventions and treatment, there needs to be a better understanding of the etiopathogenesis of TMDs at the tissue, cellular, and molecular level. One specific area of interest is the mandibular condylar cartilage (MCC), which has been shown to undergo cellular changes in response to altered occlusion in mice. The aim of this study was to examine how the TMJ responds to altered occlusion (unilateral maxillary molar tooth extractions) in skeletally and dentally mature mice to better understand the adaptive potential of the TMJ and progression of occlusal-related TMDs. The results showed that there were no changes in morphology of the condyle or cellular organization of the MCC in adult mice after extraction of the 3 maxillary right molars, and thus, no adaptive changes occur in response to altered occlusion in skeletally mature mice with stable occlusion.

Blood glucose homeostasis is the maintenance of blood glucose levels within a narrow range. The tight regulation of blood glucose levels is critical, as hypoglycemia can be acutely fatal and hyperglycemia leads to diabetes and its associated complications. Pancreatic islets play an essential role in maintaining normoglycemia. They are composed of insulin-secreting beta cells, glucagon-secreting alpha cells, and somatostatin-secreting delta cells, which coordinate to regulate blood glucose levels through paracrine interactions. Breakdown of these interactions contributes to the development of diabetes.This dissertation focuses on how beta, alpha, and delta cells are affected by changes in paracrine interactions and disease, with a focus on how delta cells contribute to the regulation of beta cells as well as alpha cells. Chapter 1 provides an overview of the beta, alpha and delta cells within the pancreatic islet and how their interactions shape glucose homeostasis, as well as a section on other known somatostatin-secreting cells. Chapter 2 focuses on UCN3 and its role as a marker but not a driver of beta cell maturity. Chapter 3 investigates how SST signaling affects gene expression in beta and alpha cells. Chapter 4 presents work on the contribution of delta cells and SST signaling to the glycemic set point and how this occurs through paracrine interaction with beta cells. Chapter 5 further discusses the role of delta cells in the control of blood glucose levels. Chapter 6 returns to the topic of beta cell and alpha cell gene expression and what changes occur in a model of obesity. Chapter 7 provides a summary of the work and potential future directions.