Pathogenesis of Periodontal Disease Part 2 PDF

Pathogenesis of Periodontal Disease – Part 2 Intended Learning Outcomes By the end of this session students should be able to:  Recap previous knowledge of gingival histology, immunology and pathogenesis.  Revise the di:erent types of chemical mediators relevant to periodontal disease and...

Pathogenesis of Periodontal Disease – Part 2 Intended Learning Outcomes By the end of this session students should be able to:  Recap previous knowledge of gingival histology, immunology and pathogenesis.  Revise the di:erent types of chemical mediators relevant to periodontal disease and their role in the host response.  Describe bacterial, cellular, =ssue level & clinical features of disease and host response in the four stages of gingivi=s to periodon==s; 1. Ini=al lesion 2. Early lesion 3. Established lesion 4. Advanced lesion  Explain what contribu=ng factors impact the progression of disease 2 GDC Learning Outcomes  1.1.2 Describe oral diseases and their relevance to preven=on, diagnosis and treatment  1.1.4 Explain the ae=ology and pathogenesis of oral disease  1.1.6 Describe relevant and appropriate physiology and explain its applica=on to pa=ent management  1.11.1 Assess and manage the health of periodontal and soI =ssues taking into account risk and lifestyle factors  1.11.2 Explain and take account of the impact of the pa=ent’s periodontal and general health on the overall treatment plans and outcomes 3 Recall of knowledge Gingival histology Immunology BioMlm Virulence factors Gingivi=s & Periodon==s Pathogenesis of periodontal disease 4  d v m T-cells type of wbc that fight i i j P g e p m n l r m u infection and disease by e u m n recognising and destroying r c a l p infected cells. By activating b y t s c cells to produce antibodies and i t i e t macrophages to destroys MOs. Interlucins , chemical o o o n i medication d r k c o a i n e g signalling for o n c n neutrophils. Part of n l e a Neutrophils type of white initial response. f t n f k s l blood cells. i s i r l l c e e t a g l a r p h i c u c r o u l m a s s m e z y Macrophages specialist cell that’s involved in e n the detection, phagocytosis and distruction of mos. Cytokines activate immune cells which can lead to tissue damage. Interlucims , T cells , 6 What is the role of host immune system? 7 Histological Stages of PeriodonFFs 8 We need to consider Bacteri Cellular al features feature s ImpacFng Clinical Tissue features level factors features Host response 9 4 stages/lesions Establishe IniFal Early Advanced d 10  INITIAL LESION – commences 2-4 days aPer plaque accumulaFon Bacterial features Porphyromonas gingivalis , treponmema denticola , aggregatibacter actinomycetemcomitans, tannerella forsythia. Cellular features Collagen fibres begin to breakdown increasing space for infiltrates. Tissue level features Tiny blood vessels near junctional epithelium become inflamed and leak cgf into the surrounding tissues. Clinical features Polymorphonuclear neutrophils are attracted to the area No observable symptoms present. and migrate throughout the junctional epithelium. A number of cells,mediators are released. This includes t- Host response lymphocytes , PMNs T-lymphocytes alter fibroblast in the affected. PMNS / neutrophils are a type of white blood cell and respond as part of the body’s innate immune system function. They release anti-inflammatory molecules called cytokines. 11 12  EARLY LESION – commences 4-7days aPer plaque accumulaFon Bacterial features Porphyromonas gingivalis , treponmema denticola , aggregatibacter actinomycetemcomitans, tannerella forsythia. Cellular features Cytophatic changes seen in the gingival fibroblast. Tissue level features Inflammatory infiltrate increases and will take up 10-15% of the gingival connective tissue beneath JE Junctional epithelium cells. proliferate in numbers to try and wall off the growing lesion. Clinical features Red inflamed gingiva , early pocketing , plaque presence. Host response Immune response will intensify. PMNs are still present. Lymphocytes such as t-cells begin to increase in number as an immune 13 response. The t-cells increase the ability of macrophages to phagocytosis. 14  ESTABLISHED LESION – 21 days aPer plaque bioUlm accumulaFon Bacterial features Porphyromonas gingivalis , treponmema denticola , aggregatibacter actinomycetemcomitans, tannerella forsythia. Cellular features Plasma cells makeup 10-30% of the cellular infiltrate- they are produced from b-cells and are responsible for the humoral immunity. Tissue level features Junctional epithelium proliferates and migrates apically, revealing more tooth structure. Junctional epithelium is nearly destroyed leading to loss of collagen. Clinical features Inflammation , bleeding, pocket formation, loss of collagen. No bone loss present at this stage. Host response Increased number of plasma cells, B-cells , lymphocytes, macrophages and t-cells. 16  Irreversible damage ADVANCED LESION Bacterial features Porphyromonas gingivalis , treponmema denticola , aggregatibacter actinomycetemcomitans, tannerella forsythia. Cellular features Plasma cells are predominant in the inflammatory infiltrate. Tissue level features Apical migration of the junctional epithelium and alveolar bone loss Clinical features True Pocketing, bone loss, mobile teeth, loss of gingival fibres, loss of connective tissue attachment. Host response Haemostats has failed and damage occurred is irreversible. 18  Pathogenesis model of Periodontal Risk factors, geneFcs, Disease – Page and smoking, systemic Korman 1997 health AnFbodies Cytokines PMN’s / Tcells ConnecFve Fssue / bone destrucFon LPS Virulence factors AnFgens MMPS, PGE2, TNFa 19 A model of periodonFFs pathogenesis (adapted from Meyle & Chapple)