Periodontal Disease Pathogenesis

• Provides a continuation of periodontal disease pathogenesis.

Learning Outcomes

• Recap gingival histology, immunology, and pathogenesis knowledge.
• Review chemical mediators relevant to periodontal disease and their role in the host response.
• Identify bacterial, cellular, tissue, and clinical features of disease and host response in the four stages of gingivitis to periodontitis.
• Explain contributing factors that impact disease progression.

GDC Learning Outcomes

• Describe oral diseases, their prevention, diagnosis, and treatment relevance.
• Explain the etiology and pathogenesis of oral disease
• Describe relevant physiology for patient management.
• Assess and manage periodontal and soft tissues, accounting for risk and lifestyle factors
• Explain the impact of periodontal and general health on treatment plans and outcomes.

Recall of knowledge

• Gingival histology
• Immunology
• Biofilm
• Virulence factors
• Gingivitis & Periodontitis
• Pathogenesis of periodontal disease

The role of the Host Immune System

• The environmental, acquired, and genetic risk factors are all factors that contribute to periodontal disease. These factors include specific pathogenic bacteria, antibodies, PMNs, antigens, LPS, other virulence factors.

Histological Stages of Periodontitis

• The host response, tissue level features, clinical features, bacterial and cellular features all impact periodontal disease.
• The four stages include Initial, Early, Established and Advanced lesions.

Initial Lesion

• This stage commences 2-4 days after plaque accumulation.
• Bacterial Features: Presence of LPS and bacterial virulence factors.
• Cellular Features: Characterized by the presence of PMNs (Polymorphonuclear Neutrophils)
• Tissue Level Features: Highlighted in the image, showing the junctional epithelium.
• Host Response: Release of IL-1α, PGE2, MMP, and TNFα.

Early Lesion

• This stage commences 4-7 days after plaque accumulation.
• Bacterial Features: Presence of LPS and bacterial virulence factors.
• Cellular Features: IL-8
• Tissue Level Features: Formation of epithelial ridges, as shown in the image.
• Host Response: Release of IL-8, IL-1α, PGE2, MMP, TNFα, IL-1B, and IL-6.

Established Lesion

• This stage occurs 21 days after plaque biofilm accumulation.
• LPS and bacterial virulence factors contribute as bacterial features.
• IL-8 MMP, LT, IL-1B, IL-6 are cellular features.
• Tissue level features include Epithelial ridges, MMP, IL-8 and IL-1α.
• CD4, IL-1α, β, TNFα,IL-8, IgG IL-6, TNFα, IL-1β PGE2, IL-1ra IL-10, IL-6 IL-12, TIMP, and TNF MMP contribute to the host response.

Advanced Lesion

• LPs and bacterial virulence contribute to the bacterial features
• There are various cellular features including IL-1α, IL-8 IL-1B, IL-1ra PGE2, IL-6 MMP, IL-10 TNF and IL-12 Collagen.
• Epithelial ridges, Collagen MMP, IL-1B TIMP,IL-6 contribute to the tissue level response
• CD4, IL-1α, β, TNFα,IL-8, IgG IL-6, TNFα, IL-1β PGE2, IL-1ra IL-10, IL-6 IL-12, TIMP, and TNF MMP contribute to the host response.

Pathogenesis model

• The Pathogenesis model of Periodontal Disease, as detailed by Page and Korman in 1997, highlights the interplay of risk factors (genetics, smoking, systemic health), various immune cells (PMNs/T cells), and bacterial factors (LPS, virulence factors, antigens), alongside the release of cytokines, leading to connective tissue and bone destruction, with MMPS, PGE2, and TNFa playing pivotal roles.

Periodontitis Pathogenesis

• The Meyle & Chapple adapted model of periodontitis pathogenesis identifies a transition from clinical health to gingivitis and then to periodontitis based on several factors. In clinical health, there is health-promoting biofilm and a proportionate host response. Gingivitis is marked by incipient dysbiosis and proportionate PMNs, while periodontitis involves frank dysbiosis, a disproportionate host response, and subsequent connective tissue and bone damage. These states are influenced by behavioral and environmental risk factors, as well as genetic and epigenetic effects.