Hatice HASTÜRK

Dr. Hatice Hasturk is an Associate Professor and the Director of Center for Clinical and Translational Research Center at the Forsyth Institute.  She is also serves as faculty member at the Harvard University and Boston University Dental Medicine. Dr. Hasturk received her dental degree in 1988 and her PhD in periodontology in 1995 from Hacettepe University, Ankara, Turkey.  She received certificate of advanced graduate sciences (CAGS) in periodontology from Boston University in 2004.  She is a board-certified periodontist practicing part time along with her research activities.  Dr. Hasturk’s research has focused on the mechanisms between periodontitis and systemic inflammatory diseases including diabetes, cardiovascular disease, rheumatoid arthritis, cancer and treatment of periodontal diseases by regulation of inflammatory response. She has received numerous NIH and Industry grants studying inflammation and novel therapeutics in resolution of inflammation.  She has authored/coauthored more than 80 scientific publications and numerous abstracts and book chapters in peer-reviewed dental and medical journals. She is a member of Massachusetts Dental Society, American Dental Association, American/International Association of Dental Research, American Academy of Periodontology, International Academy of Periodontology, IADR Periodontal Research Group, American Diabetes Association and New York Medical Sciences.

 

Biological Concepts in Periodontal Regeneration: Role of Inflammation and Therapeutic Approaches


Periodontal disease is a bacterial biofilm-induced chronic inflammatory disease resulting in loss of connective tissue attachment to the teeth and osteoclast-mediated alveolar bone resorption.  Leukocytes play multiple roles in the progression of periodontal disease, including phagocytosis and killing of bacteria, secretion of inflammatory cytokines, mounting of specific immune response and activation of osteoclasts. As in other osteolytic inflammatory diseases such as arthritis, current tissue engineering procedures remain limited.  There is a critical need for new therapeutics in regeneration. The classic triad of regenerative medicine (scaffold, cells and soluble mediators) is insufficient due to our inability to control inflammation during regeneration. Recent results from our laboratory reveal that endogenous control of inflammation directly impacts bone healing and regeneration. Mediators of resolution of inflammation also have actions beyond control of leukocytes including receptor mediated control of osteoclast and osteoblast function in wound healing and bone regeneration. This lecture will review current and novel biological concepts in tissue regeneration and the paradigm shift in understanding the role of resolution of inflammation and novel therapeutics in regenerative periodontal approaches.

 

Peri-Implant Tissue Response in Diabetic Patients

 

Diabetes Mellitus is a complex metabolic disorder characterized by chronic hyperglycemia. Diminished insulin production, impaired insulin action, or a combination of both result in the inability of glucose to be transported from the blood stream into the tissues, which in turn results in high glucose levels and excretion of sugar in the urine. In addition, lipid and protein metabolism are altered in diabetes. Uncontrolled diabetes (chronic hyperglycemia) is associated with several long-term complications, including microvascular diseases (retinopathy, nephropathy and neuropathy) and macrovascular diseases (cardiovascular and cerebrovascular conditions), increases susceptibility to infections, and poor wound healing. Uncontrolled or poorly controlled diabetes is associated with an increased susceptibility to and severity of infections, including periodontitis. Older adults (>45 years old) with poorly controlled diabetes have been found to be 2.9 times more likely to have severe periodontal disease than those without diabetes. Evidence indicates that diabetes alters the response of the periodontal tissues to local factors, thereby hastening bone loss and delaying postsurgical healing. It has been reported that wound healing in diabetes is impaired with altered fibroblast collagen metabolism. In this lecture, the tissue and metabolic processes affected by diabetes and the impact on the peri-implant wound healing will be discussed.