PAP 7 - Pathogenesis of periodontal disease 2

Question 1

what is page and Schroeder?

Answer 1

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

Question 2

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

Answer 2

• inital lesion
• early lesion
• established lesion
• advanced lesion

Question 3

what are initial and easy lesion thought to reflect?

Answer 3

the histopathology of clinically early stages of gingivitis

Question 4

what does the established lesion reflect?

Answer 4

histopathology of gingivitis

Question 5

what does the advanced lesion reflect?

Answer 5

the histopathology of the progression of gingivitis to periodontitis

Question 6

Describe what happens in the initial lesion.

Answer 6

• 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.

Question 7

Describe what happens in an early lesion.

Answer 7

• 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

Question 8

what stage corresponds to the diagnosis of gingivitis?

Answer 8

established lesion

Question 9

Describe the established lesion.

Answer 9

•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.

Question 10

What stage does periodontitis correspond with?

Answer 10

advanced lesion

Question 11

Describe an advanced lesion.

Answer 11

•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).

Question 12

Describe the apical migration of the junctional epithelium.

Answer 12

• 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?

Question 13

Describe the breakdown of the periodontal ligament (PDL).

Answer 13

• 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?

Question 14

During the breakdown of the PDL, what occurs?

Answer 14

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

Question 15

what is resorption of the alveolar bone mediated by?

Answer 15

osteoclastic activity

Question 16

whats involved in resorption of the alveolar bone?

Answer 16

• 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.

Question 17

what is the summary of the mechanisms of bone resorption?

Answer 17

• 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?

Question 18

Give the pathogenesis summary.

Answer 18

• 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.