Pathogenesis of Periodontal Disease - Part 2

Pathogenesis of Periodontal Disease - Part 2

• Learning Outcomes: Students should be able to recap gingival histology, immunology, and pathogenesis; revise chemical mediators relevant to periodontal disease and their role in the host response; describe bacterial, cellular, tissue level and clinical features of gingivitis to periodontitis (initial, early, established, and advanced lesions); and explain factors affecting disease progression.

• GDC Learning Outcomes: Describe oral diseases; explain the aetiology and pathogenesis of oral disease; describe relevant physiology and its application to patient management; assess and manage health of periodontal and soft tissues, considering risk and lifestyle factors; explain patient's periodontal and general health impact on overall treatment plans and outcomes.

Recall of Knowledge

• Key Concepts: Gingival histology, immunology, biofilm, virulence factors, gingivitis & periodontitis, and pathogenesis of periodontal diseases.

Initial, Early, Established, and Advanced Lesions

• Initial Lesion: Occurs 2-4 days after plaque accumulation; bacterial features include Porphyromonas gingivalis, treponema denticola, aggregatibacter actinomycetemcomitans, tannerella forsythia; cellular features include neutrophils; tissue features include tiny blood vessels in the junctional epithelium becoming inflamed and leaking; no visible symptoms.

• Early Lesion: Occurs 4-7 days after plaque accumulation; bacterial features are similar to the initial lesion; cellular features include cytopathic changes in gingival fibroblasts, and an increase of inflammatory infiltrate; tissue features include increase in inflammatory infiltrate and increase in the number of junctional epithelial cells to wall off the lesion; red inflamed gingiva, early pocketing, plaque presence as clinical features.

• Established Lesion: Occurs 21 days after biofilm accumulation; bacterial features include Porphyromonas gingivalis, treponema denticola, aggregatibacter actinomycetemcomitans, tannerella forsythia; cellular features include plasma cells, b-cells and t-cells; tissue features include noticeable proliferation of junctional epithelium and migration apically, loss of collagen; clinical features include inflammation, bleeding, pocket formation and no bone loss.

• Advanced Lesion: Bacterial features include similar bacteria; cellular features are primarily plasma cells; tissue features include apical migration of the junctional epithelium and alveolar bone loss; clinical features include true pocketing, bone loss, mobile teeth, and loss of gingival fibers and connective tissue attachment; damage is irreversible.

Model of Periodontal Disease

• Factors: Environmental, acquired, and genetic risk factors, including antibodies, PMNs, cytokines, prostaglandins, specific pathogenic bacteria, antigens, LPS, and other virulence factors influence connective tissue and bone metabolism. Host inflammatory responses, along with clinical expression of the disease stage, initiation, and progression, play a role.

Pathogenesis Model of Periodontal Disease (Korman 1997)

• Factors: Risk factors (genetics, smoking, systemic), antibodies, PMNs/T-cells, LPS, virulence factors, antigens, MMPs, PGE2, and TNFα play a role in damaging connective tissue and bone.