Periodontal Disease development

• Pathogenesis is the development of disease, including the chain of events leading to it.

Etiology of Periodontal Disease

• Periodontal disease results from a complex interaction between bacteria in dental plaque and the host's tissues.
• Bacterial plaque induces a host inflammatory response, making plaque the primary initiating factor in periodontal disease.
• The immunity in the presence of plaque causes periodontal destruction.

Bacterial Plaque

• A diverse microbial community on the tooth surface is embedded in a matrix of bacterial and salivary polymers (Marsh and Martin 1992).
• Exists as a biofilm.
• Saliva and GCF are the main sources of nutrients.

Calculus

• Calculus covered by plaque, which induces an inflammatory response in periodontal tissues.
• Calculus is a predisposing risk factor for periodontal disease because of its hard and rough texture.

Plaque Biofilm Composition

• Includes water (80-90%).
• Includes microorganisms (70% of dry weight), considered the main component when water is removed.
• Includes an intercellular matrix (20-30% of plaque mass), composed of organic (polysaccharides, proteins, glycoproteins, lipids) and inorganic materials (phosphorus and calcium) from saliva, GCF, and bacterial products.
• Includes open fluid-filled channels.

Specificity of the Dentition

• Bacteria accumulates on tooth surfaces, causing disease due to teeth being the only exposed hard organ, penetrating epithelium, and not shedding surfaces.

Plaque Formation Phases

• Acquired pellicle formation.
• Initial attachment.
• Maturation.
• Dispersion.

Mechanism of Plaque Formation Phases

• Formation of a conditioning film (acquired pellicle) on the tooth surface.
• A reversible phase involving physicochemical interactions between salivary bacteria and the acquired pellicle.
• Short-range specific stereo-chemical molecular interactions between primary bacterial colonizers and host receptor molecules in the acquired pellicle.
• Attachment of secondary colonizers to already attached primary colonizers (co-aggregation).
• Growth and the formation of a climax community.

Formation of Acquired Pellicle

• Both host and bacteria adsorb on to the enamel forming a biofilm.
• The thin film usually takes 90-120 min for the adsorption of molecules to reach a plateau.
• Conditioning film contains proteins, glycoproteins, lipids, glycolipids from saliva, and extracellular molecules from bacteria.
• Adsorbed molecules act as receptors or adhesins for oral bacteria.
• Bacteria in the phase is planktonic.

Non-Specific Reversible Chemical Interactions

• Few oral bacteria are motile and transported passively by saliva flow.
• The process stars with cocci then rods
• Referred to as primary colonizers, predominately gram-positive facultative species.
• Cells approach pellicle coated enamel, long range physico- chemical forces combine to provide a weak, non-specific area of attraction.
• Reversible phase

Attachment of Secondary Colonisers

• Enhanced plaque accumulation due to intra- and inter-genetic co-aggregation between primary and secondary colonizers.
• Fusobacteria co-aggregates with a wide range of bacteria, serving as an example.
• Secondary colonizers are gram-negative anaerobic species.

Growth and Formation of a Climax Community (Maturation)

• Bacteria are in near proximity within dental biofilm and will interact.
• Some interactions could be beneficial which then facilitate development of food chains.

Periodontitis Pathogenesis

• Other interactions may lead to the complex host molecules degrading. As plaque mass increases, the buffering and antimicrobial properties are lesser and less penetrable and protect enamel.
• Antibiotics cannot enter the biofilm due to the channels (Filtration mechanism).

Definition of Periodontitis (Tonetti et al 2018)

• It is a chronic inflammatory disease associated with dysbiotic plaque biofilm that results in progressive periodontal attachment loss and bone destruction.
• It result from complex interactions of biofilm and the inflammatory immune system.
• The inflammatory immune response accounts for 80% risk of periodontal tissue damage.
• Immune response is proportionate in gingivitis but here there is dysbiosis.
• In periodontitis, frank dysbiosis leads to a disproportionate inflammatory response (hyper inflammatory response).

Stages of Pathogenesis of Biofilm Induced Gingivitis and Periodontitis

• Stage 1 appears within 2-4 days; permeability of vascular bed; PMNs cells; gingival fluid flow
• Stage 2 appears within 4-7 days; Vascular proliferation; lymphocytes cells; Erythema
• Stage 3 Appears within 14-21 days; Stage II + blood stasis; Plasma cells & B lymphocyte
• Stage 4 Appears after a month; Degeneration; Plasma cells; Loss of connective tissue attachment and alveolar bone

Pristine Gingiva vs Clinically Healthy Gingiva

• Pristine gingivae, free from any histological inflammation, are extremely difficult to achieve without extreme measures of fastidious plaque control.
• 'Clinically healthy gingiva' is a term used to describe the level of gingival health attained by patients practising a meticulous standard of oral hygiene. Nevertheless, an initial inflammatory lesion can form at a histological level following plaque biofilm formation even in such motivated patients.

Initial Lesion (Stage 1)

• Inflammation begins within 24 hours of plaque accumulation.
• Cellular response develops in 2–4 days.
• Gingiva appear clinically healthy

Early Lesion (Stage 2)

• Seen after about 4-7 days of biofilm formation
• Mild redness of the gingiva and clinical signs of inflammation.
• Increases in lymphocytes and neutrophils and lymphocytes predominates.
• Early damage of the cells and collagen.
• Rete pegs proliferation in junctional epithelium maintain the epithelial barrier function.
• Can persist without shifting to established gingivitis.

Established Lesion (Stage 3)

• The 2–3 week stage involves plasma cells and B lymphocytes predominating.
• The junctional epithelium transforms into pocket epithelium which then allows subgingival plaque to extend apically.
• Obvious clinical features of gingivitis.
• The stage may remain stable or become active and progress to periodontitis.

Advanced Lesion (Stage 4)

• Plasma cells are present and constitute greater than 50% of the cell types.
• Loss of periodontal connective tissue attachment.
• Apical migration of the junctional epithelium and the formation of a true periodontal pocket.
• Alveolar bone loss.

Periodontal Health Recap

• No inflammation or bleeding
• No recession
• No deep pockets (1-3 mm sulcus)
• Distance between bone and CEJ = 2 mm

False Pocket (Psuedo Pocket)

• Pocket greater than 3 mm
• No CAL
• No bone loss.
• Caused by gingival enlargement
• Is NOT periodontitis

Periodontitis Scenario 1

• Clinical attachment loss (CAL)
• Deep pocket >3 mm
• Bone loss
• No recession.

Periodontitis Scenario 2

• Clinical attachment loss (CAL)
• No deep pocket (2mm here)
• Recession (2mm for example)
• Bone loss.

Periodontitis Scenario 3

• No recession (Gingival margin is 1 mm above CEJ)
• No deep pocket (the depth of the sulcus is 3 mm)
• Yet 2 mm CAL
• There is bone loss.
• Happens when the base of the sulcus is below the CEJ

Summary

• CAL can manifest in three patterns
• Deep periodontal pockets.
• Recession.
• Combination (Pocket + recession, happens in advanced cases).
• Mild CAL of 1-2mm may at times occur without deep pockets or recession.