Marcelo Mattos, DDS, MSc, PhD, DMD
Marcelo Mattos, DDS, MSc, PhD, DMD

Marcelo Mattos, DDS, MSc, PhD, DMD

Assistant Professor
School of Dentistry

Expertise/Specializations

  • Periodontics
  • Oral Medicine
  • Oral Biology
  • Oral Microbiology/Immunology

Academic Appointments

Department

  • Periodontics

Position

  • Assistant Professor

Teaching Activity

  • Clinical and didactic teaching.

Biography

Dr. Marcelo Mattos is an Assistant Professor and the Junior year course director of the Department of Periodontics at Creighton University School of Dentistry. He received his education at Fluminense Federal University (Brazilian dental degree), Federal University of Rio de Janeiro (Masters), State University of Rio de Janeiro (Ph.D.) and The University of Pennsylvania (U.S. Dental Degree), where he was a faculty from 2014 to 2017 and pre-doctoral Periodontics director from 2015-2017. He has wide experience in Periodontics, with more than twenty years of clinical practice and research on epidemiology, oral microbiology and oral biology topics related to periodontology. He has several peer-reviewed publications in leading scientific journals and conducts research projects in this institution.

Publications and Presentations

Articles

  • Osteocytes Play an Important Role in Experimental Periodontitis in Healthy and Diabetic Mice Through Expression of RANKL.
    publication dateDec 8, 2017  publication descriptionJournal of Clinical Periodontology
    publication descriptionAIM:
    Periodontitis results from bacteria induced inflammation. A key cytokine, RANKL is produced by a number of cell types. The cellular source of RANKL critical for periodontitis has not been established.
    METHODS:
    We induced periodontal bone loss by oral inoculation of Porphyromonas gingivalis and Fusobacterium nucleatum in both normoglycemic and streptozotocin induced type 1 diabetic mice. Experimental transgenic mice had osteocyte specific deletion of floxed RANKL mediated by DMP-1 driven Cre recombinase. Outcomes were assessed by micro-CT, histomorphometric analysis, immunofluorescent analysis of RANKL and TRAP staining for osteoclasts and osteoclast activity.
    RESULTS:
    Oral infection stimulated RANKL expression in osteocytes of wild type mice, which was increased by diabetes and blocked in transgenic mice. Infected wild type mice had significant bone loss and increased osteoclast numbers and activity, which were further enhanced by diabetes. No bone loss or increase in osteoclastogenesis or activity was detected in experimental transgenic mice that were normoglycemic or diabetic.
    CONCLUSIONS:
    This study demonstrates for the first time the essential role of osteocytes in bacteria induced periodontal bone loss and in diabetes-enhanced periodontitis., Journal of Clinical Periodontology, 45, March, 285 - 292, 2017
  • Diabetes Enhances IL-17 Expression and Alters the Oral Microbiome to Increase Its Pathogenicity.
    publication dateJun 14, 2017  publication descriptionCell Host Microbe.
    publication descriptionDiabetes is a risk factor for periodontitis, an inflammatory bone disorder and the greatest cause of tooth loss in adults. Diabetes has a significant impact on the gut microbiota; however, studies in the oral cavity have been inconclusive. By 16S rRNA sequencing, we show here that diabetes causes a shift in oral bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mice is more pathogenic. Furthermore, treatment with IL-17 antibody decreases the pathogenicity of the oral microbiota in diabetic mice; when transferred to recipient germ-free mice, oral microbiota from IL-17-treated donors induced reduced neutrophil recruitment, reduced IL-6 and RANKL, and less bone resorption. Thus, diabetes-enhanced IL-17 alters the oral microbiota and renders it more pathogenic. Our findings provide a mechanistic basis to better understand how diabetes can increase the risk and severity of tooth loss., Cell host microbe, 22, 1, 120 - 128 e4, 2017
  • TNFα contributes to diabetes impaired angiogenesis in fracture healing.
    publication dateFeb 14, 2017  publication descriptionBone
    publication description“Diabetes increases the likelihood of fracture, interferes with fracture healing and impairs angiogenesis. The latter may be significant due to the critical nature of angiogenesis in fracture healing. Although it is known that diabetes interferes with angiogenesis the mechanisms remain poorly defined. We examined fracture healing in normoglycemic and streptozotocin-induced diabetic mice and quantified the degree of angiogenesis with antibodies to three different vascular markers, CD34, CD31 and Factor VIII. The role of diabetes-enhanced inflammation was investigated by treatment of the TNFα-specific inhibitor, pegsunercept starting 10 days after induction of fractures. Diabetes decreased both angiogenesis and VEGFA expression. The reduced angiogenesis and VEGFA expression in diabetic fractures was rescued by specific inhibition of TNF in vivo. In addition, the TNF inhibitor rescued the negative effect of diabetes on endothelial cell proliferation and endothelial cell apoptosis. The effect of TNFα in vitro was enhanced by high glucose and an advanced glycation endproduct to impair microvascular cell proliferation and stimulate apoptosis. The effect of TNF, high glucose and an AGE was mediated by the transcription factor FOXO1, which increased expression of p21 and caspase-3. These studies indicate that inflammation plays a major role in diabetes-impaired angiogenesis in endochondral bone formation through its effect on microvascular endothelial cells and FOXO1”., Bone, 99, 26 - 38, 2017

  • NF-κB Has a Direct Role in Inhibiting Bmp- and Wnt-Induced Matrix Protein Expression.


    The host response to pathogens through nuclear factor κB (NF-κB) is an essential defense mechanism for eukaryotic organisms. NF-κB-mediated host responses inhibit bone and other connective tissue synthesis and are thought to affect the transcription of matrix proteins through multiple indirect pathways. We demonstrate that inhibiting NF-κB in osteoblasts increases osteocalcin expression in vivo in mice with periodontal disease. Mutating NF-κB binding sites on osteocalcin (OC) or bone sialoprotein (Bsp) promoters rescues the negative impact of NF-κB on their transcription and that NF-κB can inhibit Wnt- and Bmp-induced OC and Bsp transcription, even when protein synthesis is inhibited, indicating a direct effect of NF-κB. This inhibition depends on p65-p50 NF-κB heterodimer formation and deacetylation by HDAC1 but is not affected by the noncanonical NF-κB pathway. Moreover, NF-κB reduces Runx2 and β-catenin binding to OC/Bsp promoters independently of their nuclear localization. Thus, inflammatory signals stimulate the direct interaction of NF-κB with response elements to inhibit binding of β-catenin and Runx2 binding to nearby consensus sites and reduce expression of matrix proteins. This direct mechanism provides a new explanation for the rapid decrease in new bone formation after inflammation-related NF-κB activation., Journal Bone Mineral Research, Issue 1, 52 - 64, 2016
  • Sustained, localized salicylic acid delivery enhances diabetic bone regeneration via prolonged mitigation of inflammation.
    publication date2016  publication descriptionJournal of biomedical materials research.
    publication description“Diabetes is a metabolic disorder caused by insulin resistance and/or deficiency and impairs bone quality and bone healing due to altered gene expression, reduced vascularization, and prolonged inflammation. No effective treatments for diabetic bone healing are currently available, and most existing treatments do not directly address the diabetic complications that impair bone healing. We recently demonstrated that sustained and localized delivery of salicylic acid (SA) via an SA-based polymer provides a low-cost approach to enhance diabetic bone regeneration. Herein, we report mechanistic studies that delve into the biological action and local pharmacokinetics of SA-releasing polymers shown to enhance diabetic bone regeneration. The results suggest that low SA concentrations were locally maintained at the bone defect site for more than 1 month. As a result of the sustained SA release, a significantly reduced inflammation was observed in diabetic animals, which in turn, yielded reduced osteoclast density and activity, as well as increased osteoblastogenesis. Based upon these results, localized and sustained SA delivery from the SA-based polymer effectively improved bone regeneration in diabetic animals by affecting both osteoclasts and osteoblasts, thereby providing a positive basis for clinical treatments. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 2595-2603, 2016”., Journal Biomedical Material Research, 104; 10, 2595-2603, 2016
  • Osteoblast Lineage Cells Play an Essential Role in Periodontal Bone Loss Through Activation of Nuclear Factor-Kappa B.


    Bacterial pathogens stimulate periodontitis, the most common osteolytic disease in humans and the most common cause of tooth loss in adults. Previous studies identified leukocytes and their products as key factors in this process. We demonstrate for the first time that osteoblast lineage cells play a critical role in periodontal disease. Oral infection stimulated nuclear localization of NF-κB in osteoblasts and osteocytes in the periodontium of wild type but not transgenic mice that expressed a lineage specific dominant negative mutant of IKK (IKK-DN) in osteoblast lineage cells. Wild-type mice were also susceptible to bacteria induced periodontal bone loss but transgenic mice were not. The lack of bone loss in the experimental group was linked to reduced RANKL expression by osteoblast lineage cells that led to diminished osteoclast mediated bone resorption and greater coupled new bone formation. The results demonstrate that osteoblast lineage cells are key contributors to periodontal bone loss through an NF-κB mediated mechanism., Scientific Reports, 15, 5, 2015

  • Prevalence of potential bacterial respiratory pathogens in the oral cavity of hospitalized individuals.

    OBJECTIVE:
    To assess the prevalence of oral colonization by bacterial respiratory pathogens in hospitalized patients.
    METHODS:
    Thirty patients undergoing myocardium revascularisation surgery were evaluated. At baseline (pre-operative phase), full-mouth clinical periodontal assessment was performed. Saliva and biofilm samples were obtained from subjects at baseline and in the post-operative phase, after orotracheal extubation. DNA was extracted from samples and species of Acinetobacter, Pseudomonas, Staphylococcus aureus and Dialister pneumosintes were detected by PCR or culture (for staphylococci isolates).
    RESULTS:
    Most of the subjects were males, with a history of hypertension and smoking. Thirteen were edentulous (ED) and 17 were dentate (DE), with moderate chronic periodontitis. The most prevalent bacteria in saliva were Staphylococcus spp. (85.7%), Pseudomonas spp. (83.8%), and Acinetobacter spp. (53.3%). There was a trend for D. pneumosintes to be more frequently detected in DE (43.7%) than ED (11.5%) patients. In plaque samples, DE with >14 teeth showed a higher prevalence of Pseudomonas spp. (100%) than individuals with < or =14 teeth (69.1%; p=0.048). Conversely, P. aeruginosa was more prevalent in subjects with fewer teeth (35.5%) than with >14 teeth (5.7%; p=0.037). All staphylococci isolates were coagulase-negative, and about 11% were positive for the mecA gene. These mecA-positive isolates showed a tendency to increase in all samples, whereas P. aeruginosa reduced after surgery. A strong correlation between the presence of Acinetobacter spp. and Pseudomonas spp. was observed (rho=0.886, p<0.05).
    CONCLUSIONS:
    The oral cavity of hospitalized patients harbors high frequencies of bacterial respiratory pathogens, supporting its potential role as a reservoir for these species., Archives of Oral Biology, 55; 1, 21 - 28, 2010

Research and Scholarship

Research and Scholarship Interests


  • ·      Periodontal pathogenesis.
    ·      Oral microbiome and host microbiome interplay.
    ·      Bacterial invasion strategies.
    ·      Viral participation in periodontal diseases.
    ·      Periodontal-systemic interactions.