Dental Disease related Glycan Introduction

Introduction Published Data What We Can Offer? Why Choose Us? FAQs Related Products and Services

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Introduction

Periodontitis, often referred to as periodontal disease, constitutes a widespread oral disorder marked by inflammatory destruction of periodontal structures. During its initial stage (gingivitis), this disorder manifests as marked by gum inflammation, redness, and potential bleeding. When progressing to advanced periodontitis, tissue detachment from teeth occurs, accompanied by bone degradation and potential tooth loss. The pathology primarily stems from bacterial colonization in oral tissues, infiltrating periodontal structures. Contributing factors encompass tobacco use, diabetes mellitus, immunodeficiency conditions, genetic predisposition, and specific pharmacological treatments. Diagnosis typically involves clinical evaluation of gingival status using visual inspection, periodontal probing, and radiographic assessment of alveolar bone levels. Therapeutic approaches integrate intensified home hygiene protocols with periodontal debridement. Epidemiologically, around 50% of Americans aged 30+ experience some disease manifestation, escalating to 70% in those over 65, with higher prevalence observed in males versus females.

Fig.1 N-glycosylation linked to dyslipidemia risk factors. (OA Literature) Fig.1 N-glycosylation associated with risk factors for dyslipidemia.^1,3

The Role of Glycans in Dental Disease

The human oral cavity harbors a complex microbial ecosystem, housing approximately 700 bacterial species spanning diverse taxonomic groups. Within this community, specific gram-negative anaerobic species forming subgingival biofilm matrices induce periodontitis – a prevalent inflammatory disorder. Notably, the bacterial consortium termed the "red complex" (Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia) are primary contributors to periodontal pathogenesis. Emerging evidence demonstrates that T. forsythia and P. gingivalis employ protein glycosylation mechanisms to subvert host immune defenses, facilitating persistent colonization and subsequent tissue degradation.

Fig 2. Schematic of O-glycan core structure attached to a peptide motif in Tannerella S-layer proteins and signaling interplay between a CLR and TLR2 triggered by O-glycans and TLR2 ligands correspondingly. (OA Literature) Fig.2 Schematic diagram of the O-glycan core structure linked to a peptide motif in Tannerella surface-layer proteins and signaling crosstalk between a C-type lectin-like receptor (CLR) and TLR2 activated by O-glycans and TLR2 ligands, respectively.^1,3

Protein modification with complex glycans is increasingly identified across numerous pathogenic and commensal bacteria, proving critical for their successful adaptation within hosts. Specifically, viridans group streptococci implicated in caries and gingivitis produce serine-rich proteins requiring O-glycosylation stability. These microbes also possess binding domains recognizing O-linked sialoglycans or oral mucins to facilitate mucosal cell adherence. If introduced into circulation during dental interventions, identical binding proteins identify platelet glycoproteins like GPIb-α, transporting bacteria to damaged cardiac valves and causing severe bacterial endocarditis. Further studies revealed that surface glycans of periodontal pathogens coordinate dendritic cell cytokine profiles to direct T cell responses, enabling microbial persistence and inducing periodontal inflammation. Additionally, surface carbohydrates may shield certain periodontal bacteria from serum complement or aid immune evasion through molecular mimicry. Consequently, pathogen glycans represent promising targets for treating oral diseases.

Published Data

Fig 3. Principal component analysis of serum (a) and salivary (b) IgA N-glycosylation datasets in controls and at four different stages of APSC. (OA Literature) Fig.3 Principal component analysis of serum (a) and salivary (b) IgA N-glycosylation profiles from controls and four APSC stages.^2,3

The study investigated the total N-glycans of serum and salivary IgA from patients undergoing autologous peripheral stem-cell transplantation (APSCT) at four distinct stages, comparing them to healthy controls. Capillary electrophoresis detected 31 serum and 38 salivary N-glycan structures. A key finding was that 14 of the serum glycan structures and 6 of the salivary glycan structures exhibited significant changes when compared to the control group, indicating a systemic and local immune response to transplantation. Specifically, the sialoform to neutral (SF/NF) carbohydrate ratio in serum was significantly elevated across all examined APSCT stages compared to controls. This suggests an increase in sialylated glycans, often associated with inflammatory processes or immune modulation. The salivary IgA N-glycome profile was also found to reflect the impact of APSCT on local oral immunity. Furthermore, the study noted that the highly variable cariological and periodontal status, along with person-specific oral flora, could further influence the glycosylation patterns of secreted salivary IgA. This corroborates prior findings of serum and gingival crevicular fluid (GCF) IgG hypogalactosylation during periodontitis progression, highlighting glycans' significant relationship with oral health.

What We Can Offer?

Creative Biolabs leverages its extensive experience and cutting-edge technology to provide a comprehensive suite of services focused on Glycan in Dental Disease, designed to meet the diverse needs of our clients.

Oral Sample Glycan Profiling
Bacterial Glycosylation Analysis
Anti-Glycan Antibody Development
Glyco-Biomarker Discovery & Validation
Host-Pathogen Glycan Interaction Studies
Custom Glycosylation Studies

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Why Choose Us?

Choosing Creative Biolabs for your Glycan in Dental Disease research means partnering with a leader in glycobiology, committed to delivering exceptional results and unparalleled scientific support.

Unrivaled Expertise: Over years of specialized experience in glycobiology and dental research.
Cutting-Edge Technology: Access to state-of-the-art glycomics platforms for high-resolution analysis.
Comprehensive Solutions: From sample preparation to advanced data interpretation and strategic recommendations.
Customized Approach: Tailored services to meet the unique requirements of each research project.
Actionable Insights: Delivering meaningful data that translates directly into diagnostic and therapeutic advancements.

FAQs

Here are some common scientific questions about glycan analysis in dental disease research.

Q: What are the primary applications of glycan analysis in understanding oral infectious diseases?

A: Glycan analysis is crucial for understanding how pathogens adhere to host cells and evade the immune system. It helps identify specific glycan targets for anti-adhesion therapies, unravel mechanisms of biofilm formation, and discover novel biomarkers for disease progression and diagnosis in conditions like periodontitis and dental caries.

Q: How does the analysis of bacterial glycans contribute to the development of new dental therapeutics?

A: By characterizing bacterial surface glycans, researchers can identify critical virulence factors and immune modulators. This knowledge is instrumental in designing targeted therapeutics, such as specific inhibitors of glycan-mediated interactions, or in developing vaccines that disrupt bacterial colonization and pathogenicity in the oral cavity.

Q: What level of detail can glycan analysis provide regarding the structure and function of glycans in oral samples?

A: Advanced glycan analysis, particularly using high-resolution mass spectrometry, can provide extremely detailed information about glycan structures, including their composition, branching patterns, and linkages. This depth of information is essential for correlating specific glycan motifs with biological functions or disease states.