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Amjad Javed, M.Sc., Ph.D.

Associate Dean of Research
SDB 714
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(205) 996-5124

Kelsey Hoggatt

Business Officer II
SDB 715
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(205) 996-7998

Chris Washington

Program Coordinator II
SDB 704
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Research Seminars

 

Amm Lab

Two researchers in a lab working with equipment.

PI Name: Hope M. Amm, Ph.D.
SOD Research Themes: Oral Cancer and Bone Marrow Microenvironment; Craniofacial Development and Genetics
Research Focus: Dr. Amm’s research focuses on oral tumors, including odontogenic tumors and squamous cell carcinomas. Her long term research goal is to conduct translational research to elucidate cellular signaling within human tumors and cancers for the development of better diagnostics and treatments.

  • Project Summary

    We work with patient samples, benign and malignant, to conduct translational and basic science research. Studies include biomarker-based imaging for defining surgical margins for patients with ameloblastoma and other tumors/cancers. We also focusing on targeting of known tumor-driving pathways and proteins (PTCH1, BRAF) for the development of small molecule therapies for the treatment of oral tumors. We also examine the roles of tumor signaling and interactions with the oral microenvironment, particularly the oral microbiome, and molecular abnormalities to understand tumorigenesis.

  • Lab Members
    • Revati Suryawanshi (Researcher III)
    • Sree Bhamidipaati (Masters’ student)
  • Publications
    • HM Amm, AB Morlandt. 2019. “Genetic factors affecting outcomes in oral cancer.” Improving Outcomes in Oral Cancer – A Clinical and Translational Update. Ed: D Kademani. Springer Nature.
    • HM Amm, M MacDougall. Molecular signaling in benign odontogenic neoplasia pathogenesis. Curr Oral Health Rep. 2016. 3: 82-92.
    • AD Steg, MR Burke, HM Amm, AA Katre, ZC Dobbins, DH Jeong, CN Landen. Proteasome inhibition reverses hedgehog inhibitor and taxane resistance in ovarian cancer. Oncotarget. 2014. 5: 7065-80. PMCID: PMC4196184.
    • HM Amm, MD Casimir, DB Clark, P Sohn, M MacDougall. Matrix metalloproteinases in keratocystic odontogenic tumors and cells. 2014. Connect Tissue Res. 55: 97-101.
    • HM Amm, DL Rollins, C Ren, J Dong, P DeVilliers, H Rivera, M MacDougall. Establishment and characterization of a primary calcifying epithelial odontogenic tumor cell population. J Oral Pathol Med. 2014. 43: 183-190. PMCID: PMC4128328.
    • HM Amm, C Ren, P DeVilliers, Y Wu, J Deatherage, Z Liu, M MacDougall. Targeting the sonic hedgehog pathway in keratocystic odontogenic tumor. Journal of Biologic Chemistry. 2012. 287: 27117-25. PMCID: PMC3411054.
    • LD Stone, AVF Massicano, JM Warram, AB Morlandt, SE Lapi, HM Amm. 89Zr-panitumumab PET Imaging for Preoperative Assessment of Ameloblastoma in a PDX model. Scientific Reports. 2022. 12:19187
  • Resources & Support

    Resources

    Ameloblastoma animal models, tumor and cancer cell models

    Support

    NIDCR, Oral and Maxillofacial Surgery Foundation

  • Contact

    Hope M. Amm, Ph.D.
    This email address is being protected from spambots. You need JavaScript enabled to view it.
    (205) 934-5405

Biomaterials Research Lab

Dentist examining patient's mouth.

PI Name: Nathaniel Lawson
SOD Research Theme: Biomaterials
Research Focus: We perform mechanical, optical, and some biologic property testing for dental materials. We perform mostly contracted research for dental manufacturers to help in the development process of new products, optimize the performance of dental materials, assist with the creation of instructions for use, and compare new products to existing products.

  • Project Summary

    Our lab is devoted to performing mechanical, adhesive, optical, and some biologic property testing for dental materials. We perform mostly contracted research for dental manufacturers to help in the development process of new products, optimize the performance of dental materials, assist with the creation of instructions for use, and compare new products to existing products. Our lab focuses on dental composites, ceramics, adhesives and cements. We can perform a wide variety of tests, some of which are described here:

    Mechanical property testing

    1. Wear (opposing ceramics or enamel)
    2. Flexural strength (biaxial and 3-point) and fracture toughness
    3. Crown strength testing
    4. Depth of cure
    5. Shrinkage stress
    6. Hardness

    Adhesive property testing

    1. Shear bond strength
    2. Crown retention strength

    Optical property testing

    1. Gloss
    2. Translucency
    3. Staining / Color stability

    Biologic property testing

    1. Artificial caries model / inhibition of demineralization
    2. Calcium /fluoride release and recharge
    3. Hydroxyapetite formation
  • Lab Members
    • Nathaniel Lawson, D.M.D., Ph.D. (Associate Professor)
    • Thomas Lawson, M.S. (Volunteer Assistant Professor)
    • John Burgess, D.D.S., M.S. (Adjunct Professor)
    • Chan-Te Huang (Chief Resident)
    • Shantanu Mankar (Resident)
    • Faimeena Farheen (Volunteer researcher)
  • Publications
    • Lawson NC, Jurado CA, Huang CT, Morris GP, Burgess JO, Liu PR, Kinderknecht KE, Lin CP, Givan DA. Effect of Surface Treatment and Cement on Fracture Load of Traditional Zirconia (3Y), Translucent Zirconia (5Y), and Lithium Disilicate Crowns. J Prosthodont. 2019 Jul;28(6):659-665.
    • Kwon SJ, Lawson NC, McLaren EE, Nejat AH, Burgess JO. Comparison of the mechanical properties of translucent zirconia and lithium disilicate. J Prosthet Dent. 2018 Jul;120(1):132-137.
    • Lawson NC, Bansal R, Burgess JO. Wear, strength, modulus and hardness of CAD/CAM restorative materials. Dent Mater. 2016 Nov;32(11):e275-e283.
  • Support

    Industry Funded Support

  • Contact

    Nathaniel Lawson, D.M.D., Ph.D.
    Associate Professor
    SDB 602
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    (205) 975-8302

Learn more

Cheon Lab

Dr. Cheon.

PI Name: Kyounga Cheon D.M.D, M.S.
SOD Research Theme: Biomaterial Science, Biomimetic Tissue Regeneration, and Oral Microbiology
Research Focus: The Cheon Lab focuses on regenerative dental research - to develop a highly innovative injectable nitric oxide releasing biomimetic nanomatrix gel targeting pulp-dentin complex regeneration with an interdisciplinary team collaboration (School of Dentistry, School of Engineering, and industry partners).

Cunha-Cruz Lab

Joana Cuhna-Cruz

PI Name: Joana Cunha-Cruz, M.P.H., D.D.S., Ph.D.
SOD Research Themes: Clinical Outcomes and Implementation Science, Oral Health Inequities
Research Focus: Dr. Cunha-Cruz research focuses on epidemiological and clinical studies on etiology and management of oral conditions and the development, implementation, and dissemination of strategies to improve dental care delivery systems to reduce disparities.

Hassan Lab

Dr. Hassan and a researcher in a lab discussing information displayed on a computer.

PI Name: Quamarul Hassan
SOD Research Theme: Craniofacial Development/Genetics
Research Focus: We are seeking to understand genetic changes that occur during the maturation of the bone building cells, osteoblasts. Specifically, we study the epigenetic controls that drive osteoblast differentiation from their parent stem cell population. We perform these studies in mouse models to identify how epigenetic modulators affect bone density, physiology, and structure.

  • Project Summary

    Our lab is devoted to making novel biomedical discoveries that will help to lay the foundation for the next generation of therapeutics to prevent bone loss disorders. We are furthering this goal by seeking to understand genetic changes that occur during the maturation of the bone building cells, osteoblasts. Specifically, we study the epigenetic controls that drive osteoblast differentiation from their parent stem cell population. We perform these studies in mouse models to identify how epigenetic modulators affect bone density, physiology, and structure. Our lab is making these scientific strides along three major projects:

    1. miR-23a cluster regulation of an epigenetic axis controlling osteoblast differentiation
    2. The role of BAF45a in BAF chromatin remodeling to epigenetically promote osteogenesis
    3. Long non-coding RNA Dio3os regulation of thyroid hormone signaling
  • Lab Members
    • Quamarul Hassan, D.V.M., Ph.D. (Associate Professor)
    • Delores Stacks, Ph.D. (Post Doctoral /Dental Academic Research Trainee - DART)
    • Tanner Godfrey (D.M.D./Ph.D. Dual Degree Student/DART Alumni)
    • Theodore Busby (Graduate Student/DART Scholar)
    • Benjamin Wildman (Graduate Student/DART Alumni)
    • Yuechuan Chen, D.D.S. (Visiting Scientist)
  • Publications
    • Wildman BJ, Godfrey TC, Rehan M, Chen Y, Afreen L, Hassan MQ. MICROmanagement of Runx2 Function in Skeletal Cells. Current Molecular Biology Reports. 2019; 5(1): 55-64.
    • Godfrey TC, Wildman BJ, Beloti MM, Kemper AG, Ferraz EP, Roy B, Rehan M, Afreen LH, Kim E, Lengner CJ, Hassan MQ. MiR-23a cluster regulates HoxA cluster function during osteoblast differentiation. Journal of Biological Chemistry. 2018; 293(45):17646-17660, PMID: 30242124.
    • Godfrey T, Wildman BJ, Javed A, Lengner CJ, Hassan MQ. (2017) Epigenetic remodeling and modification to preserve skeletogenesis in vivo, Connective Tissue Research. 2017; 59(sup1): 52-54. PMID: 29745807.
  • Resources
    • miR-23a cluster zip inducible knockdown mouse model
    • Baf45a deletion mouse model
    • EZH2 deletion mouse model
  • Support

    Grant Number: 1R01AR069578 (2017-2021)
    Funding Source: NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
    Dr. Quamarul Hassan: Principal Investigator
    Project Title: An Epigenetic Axis in Bone Formation

    Award Number: T90DE022736 (Training Grant)
    Funding Source: National Institute of Dental and Craniofacial Research/NIH/DHHS
    Project Title: Dental Academic Research Training Program (DART)
    Project Period: (2017-2022)
    Dr. Quamarul Hassan: Co-Director

    Grant Number: 1 F30 DE027280-01A1
    Principal Investigator: Godfrey, Tanner Cole
    Project Title: The Role of Baf45a in Bone Formation
    Funding Source: National Institute of Dental and Craniofacial Research/NIH/DHHS
    Award Issue Date: 04/30/2018
    Dr. Quamarul Hassan: Mentor and Sponsor

    Award Number: AR072615-01A1
    Funding source: NIH/NIAID
    Title: MicroRNA-based therapy for rheumatoid arthritis
    This project is to translate the potential of miR-17 as therapeutic RNA for Rheumatoid Arthritis.
    Project Period: 09/15/2018 – 08/31/2023
    Dr. Quamarul Hassan: Co-investigator

  • Contact

    Quamarul Hassan, Ph.D.
    Professor
    SDB 707
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    (205) 975-3020

Javed Lab

Model of mice skeletons.

PI Name: Amjad Javed
SOD Research Theme: Craniofacial Genetics and development, Biomaterial and Biomimetic
Research Focus: The central focus of our laboratory is to understand the molecular mechanisms that govern the formation and remodeling of skeletal tissues such as Cartilage, Bone, Teeth, and Tendon. Skeletal cell differentiation involves the stepwise establishment of specific genetic programs in mesenchymal stem cells. We are exploring the signaling role of runt related transcription factor (Runx), and Specificity protein 7 (Sp7) in the coordinated regulation of various mesenchymal cell types such as Chondrocyte, Osteoblast, Osteocyte, Odontoblast, and Adipocytes.

  • Research Focus Continued

    Throughout our life, bone is constantly renewed via a two-part process called remodeling. This process consists of bone resorption and bone formation. During resorption, old bone tissue is broken down and removed by special cells called osteoclasts. During bone formation, new bone tissue is laid down to replace the old. This task is performed by special cells called osteoblasts. Osteoclast and osteoblast function is regulated by several genes, growth factors and cytokines and hormones such as calcitonin, parathyroid hormone, vitamin D, estrogen and testosterone. Runx2 protein is required for normal differentiation and hormonal responsiveness of the osteoblasts. Our lab utilizes biochemical, cellular, genetic and molecular approaches to identify molecular pathways that convey the osteogenic signal to nuclear transcription factors for the formation and activity of bone cells.

    Global deletion of Runx2 and Sp7 gene results in a complete absence of bone formation and null mice die either in utero or shortly after birth. To circumvent early lethality, we have developed mouse models where these genes can be inactivated in a spatiotemporal fashion. Our efforts are directed to understand the cell-specific roles of these genes during postnatal bone formation and remodeling, fracture healing, osteoporosis, and aging. We are also investigating the molecular and cellular basis of skeletal abnormalities in human Cleidocranial dysplasia, lipodystrophy and mineral homeostasis.

  • Project Summary

    Runx2 Regulated Osteoblast Signaling for Marrow Adipogenesis and Energy Homeostasis: Patients with metabolic diseases, such as obesity, diabetes, and lipodystrophy exhibits altered bone and fat mass, fat distribution and energy homeostasis. The underlying mechanisms involved in these dysregulations are poorly understood. We aim to identify molecular mechanisms underlying the metabolic diseases with comorbidity of the bone and fat, especially novel factors secreted by the bone synthesizing osteoblast that can regulate bone marrow adipogenesis, peripheral fat distribution, and energy homeostasis.

    Craniofacial Development and Dysmorphogenesis: Tooth development in mammals requires a series of complex interactions between odontogenic epithelium and mesenchyme of the early jaw primordia. The molecular interactions required to generate teeth are mediated by signaling molecules, and transcription factors to specify gene expression. Runx2 is an essential transcription factor for lineage commitment and differentiation of skeletal and dental cells. In humans, mutations in the Runx2 and Sp7 gene are associated with Cleidocranial dysplasia (CCD), and Osteogenesis Imperfecta (OI), respectively. We utilize the conditional gene knock-out mouse model to study regulatory control for initiation and developmental progression of tooth organ and unique gene circuitry supporting the development and formation of supernumerary teeth.

    Molecular Regulation of Synthesis and Degeneration of Cartilage: Multiple skeletal disorders in humans result from the perturbation of the balance between proliferation and hypertrophic maturation of chondrocytes within the growth plate. These include chondrodysplasias, Beckwith-Wiedemann syndrome, dwarfisms, and neoplasms affecting cartilage and bone. Impairments in musculoskeletal joint function are among the most prevalent degenerative disease and the leading causes of morbidity and significant disability worldwide. However, the mechanisms leading to an imbalance between chondrocyte proliferation and hypertrophic maturation remain unknown. We are utilizing cartilage-specific models to uncover molecular signals regulating the fate of hypertrophic chondrocyte in postnatal cartilage synthesis during normal development and how it is deregulated in disease.

  • Lab Members
    • Harunur Rashid, Ph.D. (Postdoctoral Fellow)
    • Deepa Gadde (Undergraduate Research Student)
    • Nimra Khan (Undergraduate Research Student)
    • Saisha Awasthi (Undergraduate Research Student)
    • Vashti Convers (Undergraduate Research Student)
    • Zahab Aleezada (Undergraduate Research Student)
  • Publications
    • Khass M, Rashid H, Burrows PD, Bridges SL Jr, Javed A, Schroeder HW Jr. “Disruption of the preB cell receptor complex leads to decreased bone mass”. Front Immunol. 2019. PMCID: PMC6736987
    • Chen J, Deng L, Porter C, Alexander G, Patel D, Vines J, Zhang X, Chasteen-Boyd D, Sung HJ, Li YP, Javed A, Gilbert S, Cheon K, Jun HW. “Angiogenic and osteogenic synergy of human mesenchymal stem cells and human umbilical vein endothelial cells co-cultured on a nanomatrix”. Sci Rep. 2018. PMCID: PMC6200728
    • Bae JM, Clarke JC, Rashid H, Adhami MD, McCullough K, Scott JS, Chen H, Sinha KM, de Crombrugghe B, Javed A. “Specificity protein 7 is required for proliferation and differentiation of ameloblasts and odontoblasts”. J Bone Miner Res. 2018. PMCID: PMC6002875
    • Rashid H, Chen H, Hassan Q, Javed A. “Dwarfism in homozygous Agc1CreERT mice is associated with decreased expression of aggrecan”. Genesis. 2017. PMCID: PMC5648336
    • Trotter TN, Li M, Pan Q, Peker D, Rowan PD, Li J, Zhan F, Suva LJ, Javed A, Yang Y. “Myeloma cell-derived Runx2 promotes myeloma progression in bone”. Blood. 2015. PMCID: PMC4458799
    • Adhami MD, Rashid H, Chen H, Javed A. “Runx2 activity in committed osteoblasts is not essential for embryonic skeletogenesis”. Connect Tissue Res. 2014. PMCID: PMC4269215
    • Clarke JC, Bae JM, Adhami M, Rashid H, Chen H, Napierala D, Gutierrez SE, Sinha K, de Crombrugghe B, Javed A. “Specificity protein 7 is not essential for tooth morphogenesis”. Connect Tissue Res. 2014. PMCID: PMC4269224
    • Rashid H, Ma C, Chen H, Wang H, Hassan MQ, Sinha K, de Crombrugghe B, Javed A. “Sp7 and Runx2 molecular complex synergistically regulate expression of target genes”. Connect Tissue Res. 2014. PMCID: PMC4269247
    • Adhami MD, Rashid H, Chen H, Clarke JC, Yang Y, Javed A. “Loss of Runx2 in committed osteoblasts impairs postnatal skeletogenesis”. J Bone Miner Res. 2015. PMCID: PMC4280286
    • Chen H, Ghori-Javed FY, Rashid H, Adhami MD, Serra R, Gutierrez SE, Javed A. “Runx2 regulates endochondral ossification through control of chondrocyte proliferation and differentiation”. J Bone Miner Res. 2014. PMCID: PMC4535340
  • Support
    • National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
    • National Institute of Dental and Craniofacial Research (NIDCR)
    • National Institute on Aging (NIA)
  • Contact

    Amjad Javed, M.Sc., Ph.D.
    Professor and Director Postgraduate Education
    Associate Dean for Research
    SDB 714
    This email address is being protected from spambots. You need JavaScript enabled to view it.
    (205) 996-5124

Lamani Lab

Researcher using a pipette in the lab.

PI Name: Ejvis Lamani
SOD Research Theme: Craniofacial Development/Genetics
Research Focus: Dr. Lamani is a clinician scientist with advance training in Orthodontics specializing in craniofacial growth and development. Her interest lies on craniofacial biology and genetics with emphasis on dental development and related human genetic disorders. Her research aim is to translate the molecular biology and genetics of human growth and development to the treatment and future prevention of craniofacial and dental anomalies.

  • Project Summary

    Dr. Lamani’s team is working on understanding the pathology and clinical management of disorders such as Short Root Anomaly, External Apical Root Resorption, and Hypodontia. She is also involved in studies of TMJ function and disorders.

  • Lab Members
    • Ejvis Lamani, D.M.D., Ph.D. (Assistant Professor)
    • Frank Litchfield, D.M.D. (Graduate Student)
    • Giana Lupinetti, D.M.D. (Graduate Student)
    • Najd Aswad, B.D.S. (Graduate Student)
    • Balraj Bains, B.D.S. (Graduate Student)
    • Nellie Bahaei (Undergraduate Student)
    • Kayla Holcombe (Undergraduate Student)
  • Contact

    Ejvis Lamani, D.M.D., Ph.D.
    Assistant Professor
    SDB 313
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    (205) 934-3251

Taichman Lab

Close up of gloved hands using a pipette in a lab.

PI Name: Russell S. Taichman, D.M.D., D.M.Sc.
SOD Research Theme: Oral Cancer/Bone Marrow Microenvironment
Research Focus: Our laboratory works at the intersection of how hematopoietic stem cells (HSCs), mesenchymal stem cells (MSCs) and disseminated tumor cells (DTCs) home, localize and engage the bone marrow microenvironment or niche for survival, function and protection from injury. We explore the paracrine, autocrine, intracrine and cell-matrix and adhesive interactions which regulate stem cell function. We have taken a broad systems approach to understanding the normal physiology of the marrow in terms of cytokine and hormonal regulation of stem cell function including the identification of unique stem cell properties of normal resident stem cells and DTCs.

  • Areas of focus

    HSC Niche Investigations

    Hematopoietic stem cell differentiation occurs in proximity to osteoblasts with in the bone marrow cavity. In 1992, we were the first to hypothesize that this intimate physical association established early in life is to facilitate interactions between bone and hematopoietic cells. To test this hypothesis we explored the ability of human osteoblasts to serve as a source of essential hematopoietic growth factors and adhesion molecules to serve as a ‘niche’ for the localization and support hematopoietic stem cells. In 2003, this field exploded starting with several reports suggesting that indeed osteoblasts were critical niche contributors to HSC maintenance. Shortly thereafter and continuing to this day are reports that suggest that other members of the bone marrow niche either contribute or take priority to osteoblasts in terms of HSC support. The majority of the newer work has been contributed using genetic and animal models. Our work continues to remain the foundation of this often-debated area, and continues to among the only data in the human system.

    Metastatic Tumor Cells Parasitize the HSC Niche

    The dissemination of prostate cancer (PCa) cells by a primary tumor into the circulation occurs early in the disease process. In fact, disseminated tumor cells (DTCs) are found in the bone marrow of majority of PCa patients at the time of primary diagnosis. While most DTCs do not develop into metastases, many do leading to morbidity and death. Predicting whether an individual will suffer a clinical recurrence following primary treatment remains a substantial challenge and relies purely on broad clinical and pathological criteria. Understanding how DTCs function will transform our ability treat metastases. In 2002 we were only the second team to publish that SDF-1/CXCL12 pathway regulates metastasis, and from there we have gone on to demonstrate that circulating PCa cells target the ‘niche,’ in marrow that houses HSCs. We demonstrated that (i) DTCs co-localize with HSCs in marrow, (ii) DTCs use the same receptors as HSCs to localize to the niche, and, critically, (iii) in competition studies DTCs compete for occupancy of the niche with HSCs. In ongoing investigations, we explore the niche mechanisms used to regulate quiescence of DTCs and how “niche-engaged” DTCs acquire a cancer stem cell phenotype.

    Tissue Regeneration Investigations Using Marrow Derived Stem-Like Cells

    Our group is interested in developing therapies for the regeneration of craniofacial injuries or conditions which will require the development of multiple tissue components. Previously, we demonstrated that a significant proportion of the osseous regenerative capacity resides in a low density cellular fraction which is resistant to agents that induce apoptosis of cells actively undergoing DNA synthesis. FACS analysis further identified very small cells which do not express CD45 or other hematopoietic lineage markers (Lin-), and in mouse marrow expresses the Sca-1 antigen. These small, CXCL12-responsive, Lin-Sca-1+CD45- cells had previously been described as having embryonic-like features. Therefore, the cells were described as very small embryonic-like (VSEL) cells representing less than 0.02% of nucleated cells in marrow. VSEL cells express genes that are expressed by embryonic stem cells (Oct4, nanog, SSEA-1). Our work has been aimed at characterizing these unique cells to lay the foundation for future therapeutic investigator initiated trials.

    Hormonal regulation of tissue interfaces

    The effect of erythropoietin (Epo) on non-hematopoietic tissues remains controversial. Recent studies have demonstrated that Epo has extensive non-hematopoietic biological functions. We have explored the role of Epo in bone physiology and have noted that high levels of Epo and locally delivered Epo activates (i) HSCs to secrete BMPs that activate MSCs to produce bone and (i) Epo inhibits osteoclastic bone formation. Our studies suggest that Epo or Epo-like agents may represent a therapeutic strategy for tissue regeneration and continue to explore these possibilities with knowledge the anabolic activity of Epo is likely to be context and tissue dependent.

    Academic Leadership

    Dramatic changes in the scope and mode of delivering health care are on the horizon. Therefore, a strategic approach to address the emerging opportunities and challenges is required. This will necessitate new and sustained leadership initiatives to position the profession with the skills, knowledge and passion guide oral health care into the future.

  • Contact

    Russell Taichman, D.M.D., D.M.Sc.
    Professor
    SDB 406
    This email address is being protected from spambots. You need JavaScript enabled to view it.
    205-934-4720

Zhang Lab

Dr. Ping Zhang posing for a photo in the lab.

PI Name: Ping Zhang
SOD Research Theme: Oral Microbiology, Infection/Host Response
Research Focus: The Zhang Lab focuses on studying the host-microbial interactions in the pathogenesis of oral infectious diseases, with a specific interest in understanding the signaling mechanisms involved in the regulation of inflammation and bone loss in the context of infection with periodontal pathogens.

  • Project Summary

    Our primary research interests are to understand the host-microbial interactions in the pathogenesis of periodontitis. We are particularly interested in understanding how the innate signaling pathways regulate inflammation and bone loss, and the complex signaling crosstalk between inflammation and osteoclastogeneiss. We are also interested in understanding the regulation of osteoclast precursors during chronic infection, and the role of osteoclast precursors in regulating host immune response and bone loss.

    Increasing evidence suggests that periodontitis contributes to the development of Alzheimer’s disease. Our group is also interested in understanding if there is a cause-effect relationship between periodontal infection and the development of AD-associated neuropathology, and if so, what are the underlying mechanisms.

    In addition, with a team of collaborators, we have been working on the development and characterization of various adjuvants and antigen delivery systems in potentiating immune responses to microbial antigens. Studies also involve identification of immunologic molecules and downstream signaling pathways in regulating the host immune responses to subunit mucosal vaccines against oral microbial pathogens.

  • Lab Members
    • Greg Harber, M.S. (Lab manager)
    • Zhaofei Li, D.D.S., Ph.D. (Postdoc /Dental Academic Research Trainee - DART)
    • Yanfang Zhao, D.D.S., Ph.D. (Postdoc)
    • Xiaoxiao Hao, M.D., Ph.D. (Postdoc)
  • Publications
    • Chen Z, Su L, Xu Q, Katz J, Michalek M, Fan M, Feng X, and Zhang P. IL-1R/TLR through MyD88 divergently modulates osteoclastogenesis through regulation of nuclear factor T cells C1 (NFATc1) and B lymphocyte-induced maturation protein-1 (Blimp1). J Biol Chem. 2015;290:30163-30174
    • Yang Y, Li Y, Lin Y, Du M, Zhang P, and Fan M. Comparison of immunological and microbiological characteristics in children and the elderly with or without dental caries. Eur J Oral Sci. 2015;123:80-87. PMID:25702606
    • Chen L, Qin B, Du M, Zhong H, Xu Q, Li Y, Zhang P, and Fan M. Extensive description and comparison of human supra-gingival microbiome in root caries and health. PLOS One.2015;10:e0117064.PMID: 25658087
    • Xu Q, Li ZF, Zhang P, Cao LH, and Fan MW. Effects of 1,25-dihydroxyvitamin D3 on Macrophage cytokine secretion stimulated by Porphyromonas gingivalis. Jpn J Infec Dis. 2016;69:482-487. PMID: 27000452
    • Wang P, Devalankar DA, Dai Q, Zhang P and Michalek SM. Synthesis and evaluation of QS-21-based immunoadjuvants with a terminal-functionalized side chain incorporated in the west wing Trisaccharide. J Org Chem. 2016;81:9560-9566. PMID: 27709937
    • Su L, Xu Q, Zhang P, Michalek SM, Katz J. The phenotype and function of myeloid-derived suppressor cells induced by Prophyromonas gingivalis infection. Infection and Immunity. 2017;85:e00213-17. PMID: 28533469
    • Liang S, Ren H, Guo H, Xing W, Liu C, Ji Y, Jiang H, Zhang P, and Du M. Periodontal infection with Prophyromonas gingivalis induces preterm birth and lower birth weight in rats. Mol Oral Microbiol. 2018;33:312-321. PMID: 29754448
    • Guo H, Ren H, Liang S, Ji Y, Jiang H, Zhang P, and Du M. Phosphatidylinositol 3-kinase/Akt signal pathway resists the apoptosis and inflammation in human extravillous trophoblasts induced by Porphyromonas gingivalis. Mol Immunol. 2018;104:100-107. PMID: 30448607
    • Wang P, Skalamera D, Sui X, Zhang P, and Michalek SM. Synthesis and evaluation of a QS-17/18-based vaccine adjuvant. J Med Chem. 2019;62:1669-1676. PMID:30656932
    • Wang P, Skalamera D, Sui X, Zhang P, and Michalek SM. Synthesis and evaluation of QS-7-based vaccine adjuvants. ACS Infec Dis. 2019;5:974-981. PMID:30920199
    • Li Y, Shi Z, Jules J, Chen S, Kesterson RA, Zhao D, Zhang P, and Feng X. Specific RANK cytoplasmic motifs drive osteoclastogenesis. J Bone Miner Res. 2019;34:1938-1951. PMID 31173390
    • Wang P, Ding X, Kim H, Skalamera D, Michalek SM, and Zhang P. Vaccine adjuvants derivatized from Momordica saponins I and II. J Med Chem. 2019; Epub ahead of print. PMID: 31657920
  • Support

    National Institute of Dental and Craniofacial Research: R01DE026465

    National Institute of General Medical Sciences: R01GM120159

    National Institute of Dental and Craniofacial Research: R90DE022736

  • Contact

    Ping Zhang, D.D.S., Ph.D.
    Professor
    SDB 804
    This email address is being protected from spambots. You need JavaScript enabled to view it.
    (205) 996-9803

Contact Us

Amjad Javed, M.Sc., Ph.D.

Associate Dean of Research
SDB 714
This email address is being protected from spambots. You need JavaScript enabled to view it.
(205) 996-5124

Kelsey Hoggatt

Business Officer II
SDB 715
This email address is being protected from spambots. You need JavaScript enabled to view it.
(205) 996-7998

Chris Washington

Program Coordinator II
SDB 704
This email address is being protected from spambots. You need JavaScript enabled to view it.

Research Seminars