McCauley Lab's research interests:
William K. and Mary Anne Najjar Professor
Dean, U-M School of Dentistry
Laurie K. McCauley is the William K. and Mary Anne Najjar Professor and Dean of the School of Dentistry, and Professor in the Department of Pathology at the Medical School at the University of Michigan. Dr. McCauley earned her B.S., D.D.S., M.S. and Ph.D. (Veterinary Pathobiology) all from The Ohio State University. She has had several visiting scientist/professor appointments including the Institut de Genetique et de Biologie Moleculaire et Cellulaire, the École Normale Supérieure de Lyon, and the Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women’s Hospital, Harvard Medical School.
Dr. McCauley is a diplomate of the American Board of Periodontology, a fellow in the American Association for the Advancement of Science, a former council member of the American Society for Bone and Mineral Research (ASBMR), former Associate Editor of the Journal of Bone and Mineral Research (JBMR), a Fellow in the American College of Dentists and the International College of Dentists, and also served on the National Institutes of Health, National Advisory Dental & Craniofacial Research Council. For more than twenty years, Dr. McCauley has led an active research program in hormonal controls of bone remodeling, parathyroid hormone anabolic actions in bone, and prostate cancer skeletal metastasis. Among her many recognitions are the inaugural Paula Stern Achievement award from the ASBMR, a distinguished scientist award from the International Association for Dental Research, The Ohio State College of Dentistry Distinguished Alumnus award, and membership in the National Academy of Medicine.
Laurie K. McCauley (Editor), Martha J. Somerman (Editor)
June 2012, Wiley-Blackwell
The most recent publications are reported below via PubMed search.
To see all PubMed results go to this complete listing of publications by Dr. McCauley.
Macrophages and skeletal health.
Pharmacol Ther. 2017 Feb 07;:
Authors: Michalski MN, McCauley LK
Bone is in a constant state of remodeling, a process which was once attributed solely to osteoblasts and osteoclasts. Decades of research has identified many other populations of cells in the bone that participate and mediate skeletal homeostasis. Recently, osteal macrophages emerged as vital participants in skeletal remodeling and osseous repair. The exact mechanistic roles of these tissue-resident macrophages are currently under investigation. Macrophages are highly plastic in response to their micro-environment and are typically classified as being pro- or anti-inflammatory (pro-resolving) in nature. Given that inflammatory states result in decreased bone mass, proinflammatory macrophages may be negative regulators of bone turnover. Pro-resolving macrophages have been shown to release anabolic factors and may present a target for therapeutic intervention in inflammation-induced bone loss and fracture healing. The process of apoptotic cell clearance, termed efferocytosis, is mediated by pro-resolving macrophages and may contribute to steady-state bone turnover as well as fracture healing and anabolic effects of osteoporosis therapies. Parathyroid hormone is an anabolic agent in bone that is more effective in the presence of mature phagocytic macrophages, further supporting the hypothesis that efferocytic macrophages are positive contributors to bone turnover. Therapies which alter macrophage plasticity in tissues other than bone should be explored for their potential to treat bone loss either alone or in conjunction with current bone therapeutics. A better understanding of the exact mechanisms by which macrophages mediate bone homeostasis will lead to an expansion of pharmacologic targets for the treatment of osteoporosis and inflammation-induced bone loss.
PMID: 28185913 [PubMed - as supplied by publisher]
Case-Based Review of Osteonecrosis of the Jaw (ONJ) and Application of the International Recommendations for Management From the International Task Force on ONJ.
J Clin Densitom. 2016 Dec 09;:
Authors: Khan AA, Morrison A, Kendler DL, Rizzoli R, Hanley DA, Felsenberg D, McCauley LK, O'Ryan F, Reid IR, Ruggiero SL, Taguchi A, Tetradis S, Watts NB, Brandi ML, Peters E, Guise T, Eastell R, Cheung AM, Morin SN, Masri B, Cooper C, Morgan SL, Obermayer-Pietsch B, Langdahl BL, Dabagh RA, Davison KS, Sándor GK, Josse RG, Bhandari M, El Rabbany M, Pierroz DD, Sulimani R, Saunders DP, Brown JP, Compston J, International Task Force on Osteonecrosis of the Jaw
Osteonecrosis of the jaw (ONJ) has been associated with antiresorptive therapy in both oncology and osteoporosis patients. This debilitating condition is very rare and advances in diagnosis and management may now effectively reduce the risk of its development and offer valuable treatment options for affected patients. This paper provides a case-based review of ONJ and application of the International Task Force on ONJ (referred to as the "Task Force") recommendations for the diagnosis and management of ONJ. The Task Force was supported by 14 international societies and achieved consensus from representatives of these multidisciplinary societies on key issues pertaining to the diagnosis and management of ONJ. The frequency of ONJ in oncology patients receiving oncology doses of bisphosphonate (BP) or denosumab is estimated at 1%-15%, and the frequency in the osteoporosis patient population receiving much lower doses of BP or denosumab is estimated at 0.001%-0.01%. Although the diagnosis of ONJ is primarily clinical, imaging may be helpful in confirming the diagnosis and staging. In those with multiple risk factors for ONJ for whom major invasive oral surgery is being planned, interruption of BP or denosumab therapy (in cancer patients) is advised, if possible, before surgery, until the surgical site heals. Major oral surgery in this context could include multiple extractions if surgical extractions are required, not simple forceps extractions. ONJ development may be reduced by optimizing oral hygiene and postoperatively using topical and systemic antibiotics as appropriate. Periodontal disease should be managed before starting oncology doses of BP or denosumab. Local debridement may be successful in disease unresponsive to conservative therapy. Successful surgical intervention has been reported in those with stage 3 disease; less severe disease is best managed conservatively. Teriparatide may be helpful in healing ONJ lesions and may be considered in osteoporosis patients at a high fracture risk in the absence of contraindications. Resumption of BP or denosumab therapy following healing of ONJ lesions is recommended, and there have not been reports of subsequent local recurrence.
PMID: 27956123 [PubMed - as supplied by publisher]
Preprogrammed Long-Term Systemic Pulsatile Delivery of Parathyroid Hormone to Strengthen Bone.
Adv Healthc Mater. 2017 Feb;6(3):
Authors: Dang M, Koh AJ, Danciu T, McCauley LK, Ma PX
Parathyroid hormone (PTH) is the only US Food and Drug Administration (FDA)-approved anabolic agent for the treatment of osteoporosis. The anabolic action of PTH depends on the mode of PTH administration. Pulsatile administration promotes bone formation, however continuous PTH exposure results in bone resorption. In addition, the therapeutic effect of PTH is optimal when the dose and duration fit the therapeutic window. Current PTH treatment requires daily injection, which is neither a convenient nor a favorable choice of patients. Here, an implantable and biodegradable device capable of long-term pulsatile delivery of PTH is developed as a patient-friendly alternative. The advanced materials and fabrication techniques developed in this work enable us to preprogram a pulsatile delivery device to systemically deliver 21 daily pulses of PTH that build bone in vivo. In addition, the device is biodegradable and absorbable in vivo so that no retraction procedure is needed. Therefore, this implantable and biodegradable pulsatile device holds promise to promote bone growth and treat various conditions of bone loss without the burden of daily injections or secondary surgeries.
PMID: 27930873 [PubMed - in process]
Local pulsatile PTH delivery regenerates bone defects via enhanced bone remodeling in a cell-free scaffold.
Biomaterials. 2017 Jan;114:1-9
Authors: Dang M, Koh AJ, Jin X, McCauley LK, Ma PX
Parathyroid hormone (PTH) is currently the only FDA-approved anabolic drug to treat osteoporosis, and is systemically administered through daily injections. A new local pulsatile PTH delivery device was developed from biodegradable polymers to expand the application of PTH from systemic treatment to spatially controlled local bone defect regeneration in this work. This is the first time that local pulsatile PTH delivery has been demonstrated to promote bone regeneration via enhanced bone remodeling. The biodegradable delivery device was designed to locally deliver PTH in a preprogrammed pulsatile manner. The PTH delivery was utilized to facilitate the regeneration of a bone defect spatially defined with a cell-free biomimetic nanofibrous (NF) scaffold. The local pulsatile PTH delivery (daily pulse for 21 days) not only promoted the regeneration of a critical-sized bone defect with negligible systemic side effects in a mouse model, but also advantageously achieved higher quality regenerated bone than the standard systemic PTH injection. These results demonstrate a promising and novel pulsatile PTH delivery device for spatially defined local bone regeneration.
PMID: 27835763 [PubMed - in process]
Osteoporosis and Periodontitis.
Curr Osteoporos Rep. 2016 Dec;14(6):284-291
Authors: Wang CJ, McCauley LK
Osteoporosis and periodontitis are both diseases characterized by bone resorption. Osteoporosis features systemic degenerative bone loss that leads to loss of skeletal cancellous microstructure and subsequent fracture, whereas periodontitis involves local inflammatory bone loss, following an infectious breach of the alveolar cortical bone, and it may result in tooth loss. Most cross-sectional studies have confirmed the association of osteoporosis and periodontitis primarily on radiographic measurements and to a lesser degree on clinical parameters. Multiple shared risk factors include age, genetics, hormonal change, smoking, as well as calcium and vitamin D deficiency. Both diseases could also be risk factors for each other and have a mutual impact that requires concomitant management. Suggested mechanisms underlying the linkage are disruption of the homeostasis concerning bone remodeling, hormonal balance, and inflammation resolution. A mutual interventional approach is emerging with complex treatment interactions. Prevention and management of both diseases require interdisciplinary approaches and warrants future well-controlled longitudinal and interventional studies for evidence-based clinical guidelines.
PMID: 27696284 [PubMed - in process]
Cover Image, Volume 117, Number 7, July 2016.
J Cell Biochem. 2016 Jul;117(7):i
Authors: Al-Dujaili SA, Koh AJ, Dang M, Mi X, Chang W, Ma PX, McCauley LK
Cover: The cover image, by Laurie K. McCauley et al., is based on the Article Calcium Sensing Receptor Function Supports Osteoblast Survival and Acts as a Co-Factor in PTH Anabolic Actions in Bone, DOI: 10.1002/jcb.25447.
PMID: 27145428 [PubMed - in process]
Modulation of Osteoblastic Cell Efferocytosis by Bone Marrow Macrophages.
J Cell Biochem. 2016 Dec;117(12):2697-2706
Authors: Michalski MN, Koh AJ, Weidner S, Roca H, McCauley LK
Apoptosis occurs at an extraordinary rate in the human body and the effective clearance of dead cells (efferocytosis) is necessary to maintain homeostasis and promote healing, yet the contribution and impact of this process in bone is unclear. Bone formation requires that bone marrow stromal cells (BMSCs) differentiate into osteoblasts which direct matrix formation and either become osteocytes, bone lining cells, or undergo apoptosis. A series of experiments were performed to identify the regulators and consequences of macrophage efferocytosis of apoptotic BMSCs (apBMSCs). Bone marrow derived macrophages treated with the anti-inflammatory cytokine interleukin-10 (IL-10) exhibited increased efferocytosis of apBMSCs compared to vehicle treated macrophages. Additionally, IL-10 increased anti-inflammatory M2-like macrophages (CD206(+) ), and further enhanced efferocytosis within the CD206(+) population. Stattic, an inhibitor of STAT3 phosphorylation, reduced the IL-10-mediated shift in M2 macrophage polarization and diminished IL-10-directed efferocytosis of apBMSCs by macrophages implicating the STAT3 signaling pathway. Cell culture supernatants and RNA from macrophages co-cultured with apoptotic bone cells showed increased secretion of monocyte chemotactic protein 1/chemokine (C-C motif) ligand 2 (MCP-1/CCL2) and transforming growth factor beta 1 (TGF-β1) and increased ccl2 gene expression. In conclusion, IL-10 increases M2 macrophage polarization and enhances macrophage-mediated engulfment of apBMSCs in a STAT3 phosphorylation-dependent manner. After engulfment of apoptotic bone cells, macrophages secrete TGF-β1 and MCP-1/CCL2, factors which fuel the remodeling process. A better understanding of the role of macrophage efferocytosis as it relates to normal and abnormal bone turnover will provide vital information for future therapeutic approaches to treat bone related diseases. J. Cell. Biochem. 117: 2697-2706, 2016. © 2016 Wiley Periodicals, Inc.
PMID: 27061191 [PubMed - in process]
Calcium Sensing Receptor Function Supports Osteoblast Survival and Acts as a Co-Factor in PTH Anabolic Actions in Bone.
J Cell Biochem. 2016 Jul;117(7):1556-67
Authors: Al-Dujaili SA, Koh AJ, Dang M, Mi X, Chang W, Ma PX, McCauley LK
Anabolic actions of PTH in bone involve increased deposition of mineralizing matrix. Regulatory feedback of the process may be important to maintain calcium homeostasis and, in turn, calcium may inform the process. This investigation clarified the role of calcium availability and the calcium sensing receptor (CaSR) in the anabolic actions of PTH. CaSR function promoted osteoblastic cell numbers, with lower cell numbers in post-confluent cultures of primary calvarial cells from Col1-CaSR knock-out (KO) mice, and for calvarial cells from wild-type (WT) mice treated with a calcilytic. Increased apoptosis of calvarial cells with calcilytic treatment suggested CaSR is critical for protection against stage-dependent cell death. Whole and cortical, but not trabecular, bone parameters were significantly lower in Col1-CaSR KO mice versus WT littermates. Intact Col1-CaSR KO mice had lower serum P1NP levels relative to WT. PTH treatment displayed anabolic actions in WT and, to a lesser degree, KO mice, and rescued the lower P1NP levels in KO mice. Furthermore, PTH effects on whole tibiae were inhibited by osteoblast-specific CaSR ablation. Vertebral body implants (vossicles) from untreated Col1-CaSR KO and WT mice had similar bone volumes after 4 weeks of implantation in athymic mice. These findings suggest that trabecular bone formation can occur independently of the CaSR, and that the CaSR plays a collaborative role in the PTH anabolic effects on bone. J. Cell. Biochem. 117: 1556-1567, 2016. © 2015 Wiley Periodicals, Inc.
PMID: 26579618 [PubMed - in process]
Juxtacrine interaction of macrophages and bone marrow stromal cells induce interleukin-6 signals and promote cell migration.
Bone Res. 2015;3:15014
Authors: Chang J, Koh AJ, Roca H, McCauley LK
The bone marrow contains a heterogeneous milieu of cells, including macrophages, which are key cellular mediators for resolving infection and inflammation. Macrophages are most well known for their ability to phagocytose foreign bodies or apoptotic cells to maintain homeostasis; however, little is known about their function in the bone microenvironment. In the current study, we investigated the in vitro interaction of murine macrophages and bone marrow stromal cells (BMSCs), with focus on the juxtacrine induction of IL-6 signaling and the resultant effect on BMSC migration and growth. The juxtacrine interaction of primary mouse macrophages and BMSCs activated IL-6 signaling in the co-cultures, which subsequently enhanced BMSC migration and increased BMSC numbers. BMSCs and macrophages harvested from IL-6 knockout mice revealed that IL-6 signaling was essential for enhancement of BMSC migration and increased BMSC numbers via juxtacrine interactions. BMSCs were the main contributor of IL-6 signaling, and hence activation of the IL-6/gp130/STAT3 pathway. Meanwhile, macrophage derived IL-6 remained important for the overall production of IL-6 protein in the co-cultures. Taken together, these findings show the function of macrophages as co-inducers of migration and growth of BMSCs, which could directly influence bone formation and turnover.
PMID: 26558138 [PubMed]
Macrophages: Their Emerging Roles in Bone.
J Bone Miner Res. 2015 Dec;30(12):2140-9
Authors: Sinder BP, Pettit AR, McCauley LK
Macrophages are present in nearly all tissues and are critical for development, homeostasis, and regeneration. Resident tissue macrophages of bone, termed osteal macrophages, are recently classified myeloid cells that are distinct from osteoclasts. Osteal macrophages are located immediately adjacent to osteoblasts, regulate bone formation, and play diverse roles in skeletal homeostasis. Genetic or pharmacological modulation of macrophages in vivo results in significant bone phenotypes, and these phenotypes depend on which macrophage subsets are altered. Macrophages are also key mediators of osseous wound healing and fracture repair, with distinct roles at various stages of the repair process. A central function of macrophages is their phagocytic ability. Each day, billions of cells die in the body and efferocytosis (phagocytosis of apoptotic cells) is a critical process in both clearing dead cells and recruitment of replacement progenitor cells to maintain homeostasis. Recent data suggest a role for efferocytosis in bone biology and these new mechanisms are outlined. Finally, although macrophages have an established role in primary tumors, emerging evidence suggests that macrophages in bone support cancers which preferentially metastasize to the skeleton. Collectively, this developing area of osteoimmunology raises new questions and promises to provide novel insights into pathophysiologic conditions as well as therapeutic and regenerative approaches vital for skeletal health.
PMID: 26531055 [PubMed - indexed for MEDLINE]
Bone marrow macrophages support prostate cancer growth in bone.
Oncotarget. 2015 Nov 03;6(34):35782-96
Authors: Soki FN, Cho SW, Kim YW, Jones JD, Park SI, Koh AJ, Entezami P, Daignault-Newton S, Pienta KJ, Roca H, McCauley LK
Resident macrophages in bone play important roles in bone remodeling, repair, and hematopoietic stem cell maintenance, yet their role in skeletal metastasis remains under investigated. The purpose of this study was to determine the role of macrophages in prostate cancer skeletal metastasis, using two in vivo mouse models of conditional macrophage depletion. RM-1 syngeneic tumor growth was analyzed in an inducible macrophage (CSF-1 receptor positive cells) ablation model (MAFIA mice). There was a significant reduction in tumor growth in the tibiae of macrophage-ablated mice, compared with control non-ablated mice. Similar results were observed when macrophage ablation was performed using liposome-encapsulated clodronate and human PC-3 prostate cancer cells where tumor-bearing long bones had increased numbers of tumor associated-macrophages. Although tumors were consistently smaller in macrophage-depleted mice, paradoxical results of macrophage depletion on bone were observed. Histomorphometric and micro-CT analyses demonstrated that clodronate-treated mice had increased bone volume, while MAFIA mice had reduced bone volume. These results suggest that the effect of macrophage depletion on tumor growth was independent of its effect on bone responses and that macrophages in bone may be more important to tumor growth than the bone itself. In conclusion, resident macrophages play a pivotal role in prostate cancer growth in bone.
PMID: 26459393 [PubMed - indexed for MEDLINE]
PTH and Vitamin D Repress DMP1 in Cementoblasts.
J Dent Res. 2015 Oct;94(10):1408-16
Authors: Wang L, Tran AB, Nociti FH, Thumbigere-Math V, Foster BL, Krieger CC, Kantovitz KR, Novince CM, Koh AJ, McCauley LK, Somerman MJ
A complex feedback mechanism between parathyroid hormone (PTH), 1,25(OH)2D3 (1,25D), and fibroblast growth factor 23 (FGF-23) maintains mineral homeostasis, in part by regulating calcium and phosphate absorption/reabsorption. Previously, we showed that 1,25D regulates mineral homeostasis by repressing dentin matrix protein 1 (DMP1) via the vitamin D receptor pathway. Similar to 1,25D, PTH may modulate DMP1, but the underlying mechanism remains unknown. Immortalized murine cementoblasts (OCCM.30), similar to osteoblasts and known to express DMP1, were treated with PTH (1-34). Real-time quantitative polymerase chain reaction (PCR) and Western blot revealed that PTH decreased DMP1 gene transcription (85%) and protein expression (30%), respectively. PTH mediated the downregulation of DMP1 via the cAMP/protein kinase A (PKA) pathway. Immunohistochemistry confirmed the decreased localization of DMP1 in vivo in cellular cementum and alveolar bone of mice treated with a single dose (50 µg/kg) of PTH (1-34). RNA-seq was employed to further identify patterns of gene expression shared by PTH and 1,25D in regulating DMP1, as well as other factors involved in mineral homeostasis. PTH and 1,25D mutually upregulated 36 genes and mutually downregulated 27 genes by ≥2-fold expression (P ≤ 0.05). Many identified genes were linked with the regulation of bone/tooth homeostasis, cell growth and differentiation, calcium signaling, and DMP1 transcription. Validation of RNA-seq results via PCR array confirmed a similar gene expression pattern in response to PTH and 1,25D treatment. Collectively, these results suggest that PTH and 1,25D share complementary effects in maintaining mineral homeostasis by mutual regulation of genes/proteins associated with calcium and phosphate metabolism while also exerting distinct roles on factors modulating mineral metabolism. Furthermore, PTH may modulate phosphate homeostasis by downregulating DMP1 expression via the cAMP/PKA pathway. Targeting genes/proteins mutually governed by PTH and 1,25D may be a viable approach for designing new therapies for preserving mineralized tissue health.
PMID: 26276370 [PubMed - indexed for MEDLINE]
Inflammation and skeletal metastasis.
Bonekey Rep. 2015;4:706
Authors: Roca H, McCauley LK
On the road to metastasis a cancer cell has to overcome two major obstacles: the physical escape from the primary tumor to a distant tissue and the adaptation to the new microenvironment via colonization and the formation of a secondary tumor. Accumulated scientific findings support the hypothesis that inflammation is a critical component of the tumor microenvironment and develops as a result of tumor-induced recruitment of inflammatory cells and their reciprocal interaction with other cells from the tumor network. These interactions modulate immune responses to suppress antitumor immunity and activate feedback amplification signaling loops that link nearly all the cells in the cancer inflammatory milieu. The coordinated regulation of cytokines/chemokines, receptors and other inflammatory mediators enables the different steps of the metastatic cascade. As a target organ for colonization, the bone is rich in inflammatory mediators that are critical for successful cancer growth. In this review, we focus on the inflammatory cells, molecules and mechanisms that facilitate the expansion of cancer cells from the primary tumor to their new 'home' in the skeleton.
PMID: 26131358 [PubMed]
Diagnosis and management of osteonecrosis of the jaw: a systematic review and international consensus.
J Bone Miner Res. 2015 Jan;30(1):3-23
Authors: Khan AA, Morrison A, Hanley DA, Felsenberg D, McCauley LK, O'Ryan F, Reid IR, Ruggiero SL, Taguchi A, Tetradis S, Watts NB, Brandi ML, Peters E, Guise T, Eastell R, Cheung AM, Morin SN, Masri B, Cooper C, Morgan SL, Obermayer-Pietsch B, Langdahl BL, Al Dabagh R, Davison KS, Kendler DL, Sándor GK, Josse RG, Bhandari M, El Rabbany M, Pierroz DD, Sulimani R, Saunders DP, Brown JP, Compston J, International Task Force on Osteonecrosis of the Jaw
This work provides a systematic review of the literature from January 2003 to April 2014 pertaining to the incidence, pathophysiology, diagnosis, and treatment of osteonecrosis of the jaw (ONJ), and offers recommendations for its management based on multidisciplinary international consensus. ONJ is associated with oncology-dose parenteral antiresorptive therapy of bisphosphonates (BP) and denosumab (Dmab). The incidence of ONJ is greatest in the oncology patient population (1% to 15%), where high doses of these medications are used at frequent intervals. In the osteoporosis patient population, the incidence of ONJ is estimated at 0.001% to 0.01%, marginally higher than the incidence in the general population (<0.001%). New insights into the pathophysiology of ONJ include antiresorptive effects of BPs and Dmab, effects of BPs on gamma delta T-cells and on monocyte and macrophage function, as well as the role of local bacterial infection, inflammation, and necrosis. Advances in imaging include the use of cone beam computerized tomography assessing cortical and cancellous architecture with lower radiation exposure, magnetic resonance imaging, bone scanning, and positron emission tomography, although plain films often suffice. Other risk factors for ONJ include glucocorticoid use, maxillary or mandibular bone surgery, poor oral hygiene, chronic inflammation, diabetes mellitus, ill-fitting dentures, as well as other drugs, including antiangiogenic agents. Prevention strategies for ONJ include elimination or stabilization of oral disease prior to initiation of antiresorptive agents, as well as maintenance of good oral hygiene. In those patients at high risk for the development of ONJ, including cancer patients receiving high-dose BP or Dmab therapy, consideration should be given to withholding antiresorptive therapy following extensive oral surgery until the surgical site heals with mature mucosal coverage. Management of ONJ is based on the stage of the disease, size of the lesions, and the presence of contributing drug therapy and comorbidity. Conservative therapy includes topical antibiotic oral rinses and systemic antibiotic therapy. Localized surgical debridement is indicated in advanced nonresponsive disease and has been successful. Early data have suggested enhanced osseous wound healing with teriparatide in those without contraindications for its use. Experimental therapy includes bone marrow stem cell intralesional transplantation, low-level laser therapy, local platelet-derived growth factor application, hyperbaric oxygen, and tissue grafting.
PMID: 25414052 [PubMed - indexed for MEDLINE]
Alumni PhD Students
Hen-Li Chen – Associate Professor, National Yang-Ming University, Institute of Oral Biology, Taipei, Taiwan
Burak Demiralp – Associate Professor, Dept. of Periodontology, Hacettepe University, Ankara, Turkey
Tolga Tozum – Associate Professor, Dept. of Periodontology, Hacettepe University, Ankara, Turkey
Abraham Schnieder – Associate Professor, University of Maryland, NIH
Glenda Pettway – Scientist at Kimberly Clark Corporation, Atlanta, GA
Chad Novince – Post-Doc, Department of Oral Health Sciences, Medical University of South Carolina
Fabiana Soki - Radiology Resident, University of Maryland
Kristiann Dougherty - Professor of Psychology-Science, Valencia College, Orlando, FL
Junro Yamashita – Assistant Professor & Assistant Research Scientist, Dept. of Biologic and Materials Sciences, University of Michigan
Jinhui Liao – Post-Doc
Flavia Pirih – Assistant Professor, Director of the Pre-doctoral Program in the Section of Periodontics, Associated Clinical Specialties, School of Dentistry, UCLA
Xin Li – Assistant Professor, Basic Science and Craniofacial Biology, NYU
Sun Wook Cho – Assistant professor, Department of Endocrinology, Seoul National University Hospital, Seoul, Korea
Serkin Park – Assistant Professor, Vanderbilt University
Saja Al-Dujaili - Research Fellow, Pediatric Surgery, University of Michigan Medical School, Ann Arbor, Mi
Jacqueline Jones-Triche - Assistant Professor, University of Alabama at Birmingham and Troy University
Dr. Dale Sweeney – Periodontist, Port Huron, MI
Dr. Alan Padbury – Periodontist, Padbury & Padbury Periodontics, Jackson, MI
Dr. Jill Bashutski - Clinical Assistant Professor, POM, U of M, School of Dentistry, Ann Arbor, MI
Dr. Flavia Pirih – Assistant Professor, Director of the Pre-doctoral Program in the Section of Periodontics, Associated Clinical Specialties, School of Dentistry, UCLA
Dr. Jia Chang - Assistant Professor, Department of Periodontology, University of Florida College of Dentistry
Rahime Nohutcu – Faculty of Dentistry, Dept. of Periodontology, Hacettepe University, Ankara, Turkey
Janice Berry – Retired, University of Michigan Office of Research