Peer-Reviewed Validation of a Systems-Level Periodontitis Architecture with Boston University Henry M Goldman School of Dental Medicine host–microbiome interactions research

Partner Description

Boston University Henry M. Goldman School of Dental Medicine
The Henry M. Goldman School of Dental Medicine at Boston University is an internationally respected center for oral health research and education. Its faculty are leaders in periodontal biology, immunology, and translational dental science, with long-standing contributions to understanding host–microbiome interactions driving periodontal disease.

Challenge

Periodontitis is a chronic, multifactorial inflammatory disease driven by dynamic interactions between the oral microbiome and host immune, epithelial, connective tissue, vascular, and bone cells. Although extensive research has identified numerous molecular pathways involved in disease initiation and progression, this knowledge was dispersed across hundreds of independent studies. The field lacked a unified, systems-level molecular framework capable of integrating these interactions across cell types and biological scales. Importantly, no comprehensive molecular architecture of periodontitis had been rigorously validated through peer review.

How CytoSolve® Helped

CytoSolve® collaborated with investigators affiliated with Boston University’s Henry M. Goldman School of Dental Medicine to develop and validate a molecular systems architecture describing host–microbiome interactions in periodontitis. Using CytoSolve’s supervised bioinformatics workflow, the team conducted a systematic literature review spanning publications from 1980 through 2022 across PubMed, MEDLINE, and Google Scholar.

From an initial set of 977 articles, 209 peer-reviewed studies met strict inclusion criteria and were curated to extract experimentally supported molecular interactions. These interactions were organized across eight critical cell types within the periodontal microenvironment—gingival epithelial cells, fibroblasts, periodontal ligament cells, endothelial cells, keratinocytes, immune cells, microbial cells, and bone cells—and consolidated into fourteen interconnected molecular systems.

The resulting architecture linked molecular pathways to higher-order biological processes, including immune modulation, soft-tissue degradation, and alveolar bone loss. All interactions were explicitly traceable to primary literature sources, ensuring transparency, reproducibility, and auditability. The complete framework and methodology underwent independent peer review and were published in JADA Foundational Science, providing external validation of both the systems architecture and CytoSolve’s approach.

Key Benefits Realized

  • First peer-reviewed molecular systems architecture integrating host–microbiome interactions in periodontitis.
  • Unification of fragmented periodontal biology into a coherent, multi-cellular systems framework.
  • Explicit definition of fourteen molecular systems governing immune modulation, soft-tissue loss, and bone loss.
  • Evidence-traceable interaction network enabling reproducibility and rigorous scientific scrutiny.
  • Identification of potential therapeutic targets across epithelial, immune, connective tissue, and bone compartments.
  • Foundational platform for future in silico modeling and mechanism-based combination therapy discovery.

Outcome

This collaboration with Boston University’s Henry M. Goldman School of Dental Medicine resulted in the first peer-reviewed validation of a comprehensive molecular systems architecture of periodontitis, published in JADA Foundational Science. The validated framework provides the periodontal research community with an integrative, mechanistic view of disease pathogenesis, linking microbial dysbiosis to host immune responses and tissue destruction. It establishes a robust systems biology foundation for future computational modeling, therapeutic target prioritization, and the development of more effective, mechanism-driven interventions for periodontal disease.