L6 Histopathology and Pathogenesis of Periodontal Disease Flashcards

1
Q

Describe the gingiva in health.

A
  • Thin sulcular and junctional epithelium

- Gingival CT is relatively acellular and fibrous in nature

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2
Q

Describe the gingiva in the early stages of gingivitis.

A
  • Hyperplasia of the junctional epithelium (thickening)
  • Gingival CT has collections of inflammatory cells
  • Deep Rete ridges
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3
Q

Describe the gingiva in periodontitis.

A
  • Deep periodontal pocket
  • Bone loss
  • Plaque and calculus on tooth surface in pocket
  • Loss of PDL
  • Loss of alveolar bone
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4
Q

What are the major histological features of periodontitis?

A
  • Accumulation of inflammatory cells in tissue adjacent to perio pocket
  • Breakdown of PDL
  • Resorption of alveolar bone
  • Apical migration of the epithelial attachment or junctional epithelium
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5
Q

How did Page and Schroeder (1976) classify the stages of periodontal disease?

A
  1. Initial lesion, clinically healthy gingiva
  2. Early lesion, clinical signs of early gingivitis
  3. Established lesion, clinical signs of chronic marginal gingivitis
  4. Advanced lesion, clinical signs of chronic periodontitis
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6
Q

Describe the initial gingival lesion.

A
  • 2-4 days after plaque begins to accumulate
  • No clinical changes, but histological changes are present
  • Neutrophils present
  • Acute inflammatory response: neutrophils present in junctional epithelium and gingival crevice, dilation and increased vascular permeability of gingival vessels, loss of collagen in some areas, inflammatory exudate may be present clinically as increased GCF
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7
Q

Describe the early gingival lesion.

A
  • 4-7 days after plaque accumulation
  • Bacterial plaque in the gingival sulcus
  • Early chronic gingivitis
  • Inflammatory infiltrate now dominated by lymphocytes and marophages
  • Thickened junctional epithelium with elongated Rete ridges
  • Marked collagen loss in inflammed gingival CT
  • Superficial dilated capillaries = bleeding on probing
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8
Q

Describe the established gingival lesion.

A
  • 2-3 weeks ater plaque accumulation
  • Chronic gingivitis
  • Clinical signs of oedema and erythema of gingival margin
  • Further migration of polymorphic neutrophils, lymphocytes and macrophages into the sulcus
  • Plasma cells predominate the infiltrate
  • Further disruption of the JE making it more permeable to plaque products
  • Long rete ridges
  • Loss of JE attachment to enamel
  • Deepening of sulcus allowing subgingival plaque to develop
  • Increased loss of gingival collagen
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9
Q

Describe the advanced gingival lesion.

A
  • Chronic periodontitis
  • Destruction of PDL, loss of alveolar bone and pocket formation
  • Presumed to be caused by changes in plaque microflora, unstable interactions between plaque microorganisms and host defence reactions
  • Death of cementoblasts
  • Apical migration of JE to cover denuded root surface (aka true pocket formation)
  • Extensive chronic inflammatory cell infiltrate, plasma cells dominate
  • Plaque on root surface
  • Hyperplasia of epithelium
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10
Q

Outline the pathogenesis of periodontal disease.

A

1) Plaque attracts neutrophils
2) Neutrophils phagocytose some bacteria, and release lysozyme which is capable of further tissue damage
3) Products of bacterial metabolism can damage junctinal and sulcular epithelial cells
4) Increases permeability, allows more bacterial products through crevicular and junctional epithelium and into the gingival CT
5) Products of bacterial metabolism eg protease,
hyaluronidase, collagenase, damage crevicular and
junctional epithelium and gingival connective tissue

• Inflammatory and immune reactions in the gingival and periodontal tissues are usually protective and restrict bacterial penetration of gingiva. Tissue damage remains localised and minor.
• When balance is altered, either by alterations in
amount or character of plaque flora, or alterations in
host response to plaque products, tissue damage may
occur producing a burst of tissue destruction

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11
Q

Summarise the 2 mechansims of chronic periodontal disease.

A
  • Products of plaque bacterial metabolism damage periodontal tissues
  • The inflmmatory and immunological reactions to the plaque bacteria damage periodontal tissues
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12
Q

Summarise the cause and progression of gingivitis.

A
  • Can be induced within 7-14 days through poor/no oral hygiene
  • Caused by plaque accumulation at the gingiva; margins
  • Reversible
  • Only proceeds to periodontitis in 15% of individuals
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13
Q

Summarise the cause and progression of periodontitis.

A
  • A disease of host susceptibility, probably initiated and/or
    maintained by certain subgingival plaque bacteria
  • Maintaining excellent oral hygiene usually keeps disease in remission
  • Mechanical disruption of the biofilm is an effective treatment
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14
Q

What are the main concepts regarding periodontal disease?

A
  • Specific innate, acquired and environmental risk factors contribute to disease susceptibility
  • Specific bacterial types may cause periodontitis
  • The host immuno-inflammatory response, although ultimately
    protective, is responsible for the tissue destruction of
    periodontitis
  • Periodontitis is associated with coronary heart disease and
    low-birth-weight infants
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