Aetiology and Pathology of Periodontal Disease. Dr. Wendy Turner

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1 Aetiology and Pathology of Periodontal Disease Dr. Wendy Turner

2 Lecture Outline Periodontal structures and the inflammatory response Periodontal disease progression stages Pathogenesis and the host response

3 TOPIC 1: Periodontal structures and the inflammatory response

4 Gingival crevice Knife edge papillae Free gingiva Mucogingival junction Attached gingiva

5 Unique features of Periodontal Features in common with other infections, but. Infections It is a unique tissue that has a challenging function at the border between the mouth, colonized by bacteria, and the tooth with it s underlying tissues

6

7 The inflammatory reaction in Gingivitis Inflammatory and immune reactions to plaque bacteria are the predominant feature of gingivitis and periodontitis. Gingivitis is a plaque induced inflammation of the gingiva and clinical signs are present 4-5 days after undisturbed plaque accumulation and maturation

8 The inflammatory reaction in Gingivitis

9 The Process of Periodontal Disease Local infection from plaque bacteria Time dependent immune response responses Disease

10 QUESTIONS Use this page to make your own notes

11 TOPIC 2: Periodontal disease progression stages

12 Gingivitis: microbiology Approx. 400 species can live in the mouth Approx 10 8 bacteria in deep periodontal pockets (100,000,000)

13 Role of Plaque Inflammation develops as soon as plaque forms on the tooth surface around the gums

14 Within 24 hours, changes are evident in the gums, with increased blood flow in the area The bacterial mix becomes more complex and within two days Gram -ve bacteria also appear in the biofilm

15 Stages in Disease Progression Health Pristine condition Initial Lesion clinically healthy Early lesion Early gingivitis Established lesion Chronic gingivitis Advanced Lesion Chronic periodontitis Kinane D (2001) Periodontology 2000; 25:8-20

16 Initial stage Gingivitis The initial stage of an acute inflammatory response begins within 4 or 5 days of plaque accumulation. Increased migration of neutrophils into sulcus Localised to gingival crevice Tissue swelling and bleeding

17 Early Lesion of Gingivitis (7-14 days) At approximately 1 week, a change to a predominately lymphocytes and neutrophils Increased vascularity Collagen destruction to create space for infiltrate

18 Established Gingivitis (2-3 weeks of plaque accumulation) Plasma cells dominate and loss of collagen continues Inflammatory infiltrate of leucocytes and plasma cells Clinically gums bleed on probing This lesion may remain stable without progressing for months or years, or may become more active and progress to a destructive advanced lesion

19 Established lesion (Gingivitis) Gums bleed on probing into crevice

20 Advanced Lesion (Periodontitis) As chronic local inflammation progresses, pockets develop where the gingiva comes away from the tooth. Damage to collagen fibres is extensive The junctional epithelium grows apically in response to the destructive episodes, in an attempt to maintain epithelial barrier, thereby creating the periodontal pocket Collagen breakdown of PDL fibres continues Osteoclasts are stimulated to resorb alveolar bone Junctional epithelium continues to migrate apically down the root surface- pocket gets deeper and harder to clean

21 Advanced lesion (Periodontitis)

22 QUESTIONS Use this page to make your own notes

23 TOPIC 3: Pathogenesis and the host response

24 How does this destruction to periodontitis occur? Substances produced by the biofilm which can : Directly injure host cells and tissues Activate an inflammatory response Activate a cellular or humoral immune response resulting in injury to the periodontal tissues

25 Host-microbial balance Why does gingivitis then develop? Gingivitis may persist for many years without progression to periodontitis with bone loss But why does this happen in some individuals but not others?

26 Bacteria Colonisation Invasion Destruction Environmental Smoking Host Susceptibility Genetic Acquired Periodontal Diseases

27 From: Mapping the Pathogenesis of Periodontitis: A New Look Kenneth S. Kornman Journal of Periodontology 2 Jul 2008:

28 Pathogenesis Initially classic human and animal studies demonstrated the critical role of bacteria in the initiation of periodontal disease (A in previous slide) In the 1980 s it was shown that specific bacteria could initiate disease by activating host responses which were both protective and destructive. Tissue destruction resulted primarily from mediators such as MMP s, IL-1 and prostaglandins. This was the shift in understanding that whilst bacteria initiate gum disease, the immunologic response was a key mechanism in the pathogenesis (B in previous slide) More recently the role of various risk factors that modify the host response was accepted. This leads and explains the changes in disease presentation (C in previous slide)

29 Host Responses are essential to prevent serious infection may inadvertently result in local tissue damage (= "bystander damage") also stimulate attempts at tissue repair

30 The host-microbial balance Healthy gingiva consistently feature inflammatory cells in both the epithelial and superficial connective tissues This is in response to the continuous presence of bacteria (and their products) in the crevice around the teeth In spite of this constant bacterial challenge, several defence mechanisms may deal with this challenge to stop progression to periodontitis

31 Pathogenesis Plaque bacteria and their products cause an inflammatory response in the soft tissues PMNs, macrophages and lymphocytes migrate into the tissues to combat the bacterial challenge PMNs phagocytose (ingest) bacteria and kill them PMNs accumulate in the periodontal tissues

32 Pathogenesis Plaque bacteria and their products cause an inflammatory response in the soft tissues: Inflammatory mediators (chemokines, cytokines) are released Defence cells migrate into the area The tissues become red and swollen (i.e. gingivitis) as fluid accumulates in tissues

33 Inflammatory Cells Neutrophils (PMNs): Present in tissues and in large numbers within the pocket Kill bacteria by phagocytosis and extra-cellular mechanisms Macrophages: Phagocytosis and removal of damaged tissue Modulation of inflammation by cytokine production Antigen presentation and control of immune mechanisms

34

35 Inflammatory mediators- PMNs PMN is the predominant defence cell in the crevice Migrate from the vessels into the gingival tissues in response to stimuli from plaque bacteria (chemotaxis) First line of defence

36 Inflammatory mediators- Cytokines Cytokines are proteins secreted by cells that transmit signals to other cells (act as messengers) Secreted by PMNs and macrophages Cause increased inflammation, stimulate bone resorption by osteoclasts, stimulate collagen breakdown by fibroblasts

37 Inflammatory mediators- Prostaglandins Produced by macrophages Includes prostaglandin E 2 - PGE 2 Cause vasodilatation and stimulate secretion of other inflammatory mediators PGE2 stimulates fibroblasts to produce MMPs (which break down collagen) PGE2 stimulates osteoclasts to resorb bone

38 Inflammatory mediators- MMPs Matrix metalloproteinases are a family of enzymes that break down proteins COLLAGENASE is a MMP MMPs are produced by PMNs and fibroblasts, and they break down collagen in the tissues In periodontal disease, levels of MMPs are increased as tissue destruction occurs

39 Bone resorption in Periodontitis Bone loss is a hallmark of periodontitis Many of these secreted factors are involved in bone regulation and maintenance, and their imbalance leads to altered bone remodeling. Thus, enhanced osteoclast activity without increase in bone formation occurs and drives the alveolar bone loss.

40 RANK/OPG Normally, alveolar bone is constantly remodelled but the amount of bone formation is = to amount of bone loss During the inflammatory response to plaque in periodontitis, cytokines can induce bone resorption by increasing the expression of RANKL while decreasing OPG production in osteoblasts with net bone loss RANKL= receptor activator of nuclear factor-kappa B ligand OPG= osteoprotegerin

41 Bone resorption Bone resorption is mediated by osteoclasts Osteoclasts are induced by the expression of RANKL on connective tissue cells and T- lymphocytes RANKL is inhibited by an additional molecule, OPG Bacterial factors and host mediators such as IL-1 induce RANKL expression Without RANKL osteoclasts cannot form

42 Bone loss in Periodontitis

43 QUESTIONS Use this page to make your own notes

44 Summary Plaque bacteria are necessary to initiate periodontal inflammation In response to the presence of bacteria, the host mounts an inflammatory response The majority of the tissue destruction is caused by the inflammatory host response to the plaque bacteria The clinical progress of the disease is influenced by the precise nature of the host response (which varies from person to person), and is influenced by environmental factors like smoking or diabetes

45 SUMMARY NOTES Use this page to make your own notes

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