• Effects of Glycemic Control on Soft Tissue Wound Healing around Dental Implants for Patients with Type 2 Diabetes

      Hurwitz, Morgan Barker; Oates, Thomas W. (2019)
      This study evaluated the effects of glycemic status on soft tissue wound healing following dental implant placement. A total of 164 edentulous patients with HbA1c levels up to 11.5% received two mandibular transmucosal dental implants. Patients’ self-reported pain (VAS and # days with pain) and soft tissue healing (edema, erythema, exudate, oral pain, flap closure, infection, and hematoma) were evaluated one week after placement. HbA1c and diabetes status were not significantly associated with any soft tissue healing complications. Pain_VAS was significantly correlated with Edema, Infection, Days in Pain and Oral Pain. Flap Closure was correlated with Oral Pain. Infection was correlated with Oral Pain and Days_Pain. Stepwise regression also identified HbA1c as significantly contributing to the VAS pain score. The findings of this study clarify the low risk for post-surgical healing complications independent of poor glycemic control, extending the opportunities for dental implant therapy for patients with diabetes.
    • Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection

      Venkataraman, Thiagarajan; Frieman, Matthew B.; 0000-0003-0921-6345 (2017)
      SARS coronavirus (SARS-CoV) is a pathogenic respiratory virus that causes acute lung injury in humans. In turn, the host mounts a wound healing response to repair the injury. One of the major sequelae caused by SARS-CoV is pulmonary fibrosis (PF), which occurs more frequently in older patients. Fibrosis is caused by a dysregulated wound healing response and the molecular pathways underlying the development of fibrosis are not completely understood. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound healing pathway, controlled by the epidermal growth factor receptor (EGFR) is critical to recovery from SARS-CoV induced tissue damage. In mice with constitutively active EGFR, [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection the EGFR ligands amphiregulin and HB-EGF are upregulated and exogenous addition of these ligands during infection of wildtype mice leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses.