PAP 7 - Pathogenesis of periodontal disease 2 Flashcards Preview

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Flashcards in PAP 7 - Pathogenesis of periodontal disease 2 Deck (18)
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1
Q

what is page and Schroeder?

A

Classified progression of gingival and periodontal inflammation on the basis of then available clinical & histological evidence

2
Q

what are the 4 phases the progressing lesion is divided into?

A
  • inital lesion
  • early lesion
  • established lesion
  • advanced lesion
3
Q

what are initial and easy lesion thought to reflect?

A

the histopathology of clinically early stages of gingivitis

4
Q

what does the established lesion reflect?

A

histopathology of gingivitis

5
Q

what does the advanced lesion reflect?

A

the histopathology of the progression of gingivitis to periodontitis

6
Q

Describe what happens in the initial lesion.

A
  • Occurs within 24-48 hours of plaque accumulation.
  • Plaque mainly Gram +ve, aerobic & saccharolytic.
  • Vasodilation, increased neutrophils (PMNs) & GCF production
  • Tissue damage minimal.
  • Infiltrate confined to small area of connective tissue below the Junctional Epithelium (JE).
  • Bacterial factors are antigenic thus immune response provoked.
7
Q

Describe what happens in an early lesion.

A
  • Occurs after approximately 1 week.
  • Immunoglobulin (Ig) production & cytokine release.
  • Increase in size (< 15% of connective tissue volume) of inflammatory infiltrate – mainly PMNs & lymphocytes.
  • Loss of fibroblasts & collagen in infiltrated area.
  • Proliferation & rete peg formation in JE.
  • Increased GCF.
  • PMNs accumulate in gingival crevice.
  • Gingival swelling resulting in a deeper gingival crevice.
  • Favours growth of Gram –ve micro-organisms with the associated release of endotoxins & enzymes which cause more tissue damage
8
Q

what stage corresponds to the diagnosis of gingivitis?

A

established lesion

9
Q

Describe the established lesion.

A

•Gingival connective tissue largely replaced by inflammatory infiltrate.
•Dominant cell type? Differences found in humans & animals studies:
-in human plasma cells appear to be dominant in older subjects and lymphocytes in younger subjects
•JE replaced by pocket epithelium which shows rete peg growth & ulceration (leaky): pocket epithelium is not attached to the tooth allowing apical migration of the crevice /pocket and the plaque biofilm (no loss of attachment)
•Large numbers of PMNs especially in the pocket epithelium & in the crevice/pocket.
•Increased complement & immunoglobulins
•Bacterial products cause damage:
•Directly by enzymes (epithelium not effective barrier)
•Indirectly by triggering host response - cytokines, complement, enzymes
•Continued loss of collagen in the gingival connective tissue.

10
Q

What stage does periodontitis correspond with?

A

advanced lesion

11
Q

Describe an advanced lesion.

A

•Inflammatory infiltrate extends apically & laterally comprises >50% plasma cells.
•Continued loss of collagen.
•Ulceration & migration of JE apically onto the root surface i.e apically to the ACJ=loss of attachment
•There is an advancing inflammatory front where the host attempts to prevent the spread of the invading bacteria. Apical to this there is:
breakdown of PDL fibres and bone loss seen with osteoclasts on periosteal and end-steal surfaces of crystal bone
•The apically advancing periodontal pocket creates the ideal environment for the growth of the Periodontal Pathogens (Gram Negative Anaerobes = GNABs).

12
Q

Describe the apical migration of the junctional epithelium.

A
  • Damage to PDL fibres below JE causes epithelium to migrate into space.
  • Regulation by underlying connective tissue prevents apical migration – connective tissue damage removes this.
  • Keratinocyte proliferation stimulated – lateral rete peg growth. Results in apical downgrowth?
13
Q

Describe the breakdown of the periodontal ligament (PDL).

A
  • Loss of collagen fibres inserting into bone and cementum.
  • Loss of extracellular matrix (ground substance).
  • Fibroblast damage.
  • Increased host factors in PDL resulting in connective tissue damage?
  • Increased penetration of bacterial factors into PDL causing tissue damage?
14
Q

During the breakdown of the PDL, what occurs?

A
  • loss of surface cementoblast layer
  • destruction of PDL fibres inserted in to cementum
  • formation of isolated resorption lacunae
15
Q

what is resorption of the alveolar bone mediated by?

A

osteoclastic activity

16
Q

whats involved in resorption of the alveolar bone?

A
  • Host-derived & bacterial factors involved.
  • Main host-derived resorption factors are Cytokines, Prostaglandins & Leukotrienes.
  • Secreted by many cells (PMNs, macrophages, fibroblasts, endothelial cells & osteoblasts) during inflammatory & immune reactions.
17
Q

what is the summary of the mechanisms of bone resorption?

A
  • Good evidence that potent bone-resorbing factors such as Prostaglandin E2 (PGE2) & Interleukin-1 (IL-1) are produced in gingival tissues in periodontitis.
  • Some bacterial factors stimulate bone resorption in vitro but in vivo?
  • Host-derived factors constantly present yet resorption apparently intermittent.
  • Related to distance of bone from crevice, extent of inflammatory lesion & effectiveness of host defences in eliminating bacterial factors?
  • Dependent on balance of level of host response & destructive bacterial factors?
18
Q

Give the pathogenesis summary.

A
  • Bacterial products can enter the tissues & cause direct damage but their effects are limited by effectiveness of host response.
  • Without host responses, bacteria would invade tissues resulting in more extensive damage & likely spread to deeper tissues.
  • Some damage seen in tissues probably due to host responses to plaque.
  • Inflammation disturbs normal homeostasis which controls tissue turnover in health.
  • At many sites, periodontal disease is stable with damage balanced by host defences & repair.
  • Progression probably occurs when balance is altered by changes in bacterial/host factors.
  • Relevant bacterial factors include increase in numbers, presence or overgrowth of specific pathogens & direct bacterial tissue invasion.
  • Relevant host factors include reduced effectiveness of host defences or increased tissue damage in response to microbial changes.