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Periodontics > Gingivitis: Clinical signs, microbiology and pathogenesis > Flashcards

Gingivitis: Clinical signs, microbiology and pathogenesis Flashcards

1
Q

What are the periodontal structures?

A

Gingiva, PDL, cementum and alveolar bone

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2
Q

What are the different structures of the gingiva?

A
  • Gingival margin
  • Gingival sulcus
  • Free gingiva
  • Gingival/ marginal groove
  • The attached gingiva
  • Mucogingival junction
  • Alveolar/ oral mucosa
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3
Q

What are the 5 signs of inflammation?

A
  • Calor – heat
  • Dolor – pain
  • Rubor – redness
  • Tumor – swelling
  • Functio laesa – loss of function
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4
Q

What are the inflammation types of gingiva?

A

Acute:
• Acute Necrotising Ulcerative Gingivitis (ANUG)
• Primary Herpetic Gingivostomatitis

Chronic: Most other types of gingivitis tend to be chronic

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5
Q

What does the inflamed gingiva appear as?

A
  • Red (erythema)
  • Swollen (oedema)
  • Shiny
  • Soft
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6
Q

What are the clinical signs of gingivitis?

A
  • Inflamed gingiva
  • Bleeding on probing after 30 secs
  • No bone destruction
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7
Q

Why is there bleeding on probing with gingivitis?

A
  • Sulcus depths are increased
  • Increased GCF flow
  • Clinical signs are present within about 4-5 days of undisturbed plaque accumulation and maturation
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8
Q

Why is there no bone destruction with gingivitis?

A
  • No breakdown of PDL fibres or bone destruction as part of the disease process
  • Gingivitis is reversible with optimal oral hygiene and removal of any calcified plaque deposits
  • No long term harm
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9
Q

What is the disease process of gingivitis?

A

Exaggerated host response to plaque

Interaction between microorganisms found in dental plaque biofilm and the tissues/ inflammatory cells of the host.

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10
Q

How does gingivitis all happen?

A

• Bacterial products from plaque stimulate epithelial cells to produce inflammatory mediators
→ Inflammatory response
→ Interleukins, prostaglandins, and destructive enzymes e.g. collagenases
• Fluid accumulates in tissues (clinical picture - red and swollen)
• PMNs infiltrate gingival tissues (also lymphocytes and macrophages)
• Neutrophils release destructive enzymes (collagenases) and other inflammatory mediators → positive feedback cycles

  • If plaque is left on the teeth, the host continues its frustrated response to bacterial products
  • Inflammation and destruction spreads to all the periodontal structures
  • Ultimately, if unchecked, the inflammation would spread to the bone, which is resorbed by osteoclasts to make more room for the defence cells – i.e. periodontal disease
  • This pathogenic process differs in extent and severity between individuals and the reasons are multifactorial, but there is clearly a strong genetic component to disease susceptibility
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11
Q

What resorbs bone to cause PD?

A

Osteoclasts resorb the bone – periodontal disease

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12
Q

What is a biofilm?

A

Biofilm - collection of organisms, held together with a matrix structure, on a surface or interface.

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13
Q

What is EM?

A

Extracellular matrix – dense mass of structure

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14
Q

Why are biofilms a problem? (7)

A
  • Microorganisms are more resistant to attack
  • Strength in greater no.’s
  • Phenotype can change in biofilms
  • Slow growth (lack of nutrients) means that antimicrobials (AM) targeting growth are ineffective
  • Re-dox potential of biofilm deactivates AM
  • Anaerobic bacteria predominate in the deeper layers (as oxygen is used by superficial bacteria)
  • Bacteria in biofilm formation can be up to 1000 times more resistant to AM than planktonic form
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15
Q

Why must biofilms be disrupted mechanically?

A

Biofilms protect bacteria and therefore biofilm MUST be disrupted mechanically

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16
Q

What is the ecological/environmental plaque hypothesis?

A
  • Not one specific pathogenic bacteria that causes disease

- The whole ‘biofilms’ virulence and the host response will dictate the progression to periodontitis

17
Q

What the the 3 key factors of the oral microbiology with plaque related gingivitis?

A
  1. Gingivitis and subsequently periodontitis are not caused by one single bacterial species
  2. Initiation of disease results from an interplay between the bacteria present, the local environment and the host response
  3. Biofilms must be mechanically disrupted
18
Q

What is the clinical presentation of ANUG?

A
  • Painful, sloughing of gingival margin
  • Ulceration
  • Poor plaque control
19
Q

What is the aetiology of ANUG?

A
  • Fusospirochaetal complex
  • Often immunocompromised, poor diet and general health
  • Smokers
20
Q

What is a Fusospirochaetal complex?

A

Trench mouth, a progressive painful infection with ulceration, swelling and sloughing off of dead tissue from the mouth and throat due to the spread of infection from the gums

21
Q

What is the treatment of ANUG?

A
  • Improvements in OH
  • Scaling and debridement of teeth
  • Antibiotics: Metronidazole 400mg TDS 3 days supply
  • Hydrogen peroxide mouthwash 1.5 % w/v (peroxyl)
  • CHX m/w 0.2% w/v
22
Q

What is the function of the junctional epithelium?

A

Gives barrier and dense body of collagen fibres resist mastication

23
Q

How is the junctional epithelium kept healthy?

A
  • Intact epithelial barrier
  • Shedding of epithelial cells
  • Outflow of GCF
  • Antimicrobial effects of antibodies
  • Phagocytic function of neutrophils and macrophages
  • Complement activity (attracting macrophages and neutrophils, cell lysis)
  • Neutrophils and macrophages migrate through the JE into the sulcus
  • GCF flows out through the gingival sulcus
  • Collagen fibres maintain the form of the tissues and aid in attachment to the tooth
24
Q

What is the junctional epithelium attached to?

A

Tooth surface

25
Q

What are the stages of gingivitis lesion to PD?

A

Stage I- The initial lesion (first few days)
• Vasodilation and increased vascular permeability
• Increased GCF flow
• Migration of leukocytes from capillaries into dentogingival tissues in response to chemotactic stimuli
• Neutrophils enter the sulcus

Stage II- The early lesion (7 days)
• Increasing vascularity with time
• Lymphocytes and neutrophils are the predominant infiltrating cells
• Fibroblasts degenerate (permitting more leukocyte infiltration)
• Collagen destruction to create space for the infiltrating cells
• Proliferation of basal cells of junctional and sulcular epithelium

Stage III- The established lesion (21 days)
• Further leukocyte migration into the tissues, now including plasma cells
• Collagen destruction apically and laterally, resulting in collagen-depleted spaces extending deeper into the tissues, which are available for leukocyte infiltration
• Engorgement of blood vessels, impaired venous return, sluggish blood flow. Localised anoxemia can lead to blue colour
• Haemoglobin breakdown can deepen colour – red clinically
• Further proliferation of dento-gingival epithelium in an attempt to maintain an intact epithelial barrier

Stage IV- The advanced lesion (Periodontitis)
• Phase of periodontal breakdown
• Only in susceptible patients

26
Q

What % of people have bleeding on probing ?

A

54%

27
Q

What % of people have gingivitis around more than 6 teeth?

A

50%

28
Q

What does BPE code 0 mean?

A

No bleeding
No pocketing over 3mm
No treatment

29
Q

What does BPE code 1 mean?

A

Bleeding on probing

Hygiene instruction

30
Q

What does BPE code 2 mean?

A

Plaque retentive factors present
No pocking over 3.5mm
Hygiene instruction and scale

31
Q

What does BPE code 3 mean?

A

Pocketing between 3.5mm and 5.5mm

Hygiene instruction and supra and sub gingival scale

32
Q

What does BPE code 4 mean?

A

Pockets more than 5.5mm

Full periodontal assessment

33
Q

What does BPE code * mean?

A

Furcation

Full periodontal assessment

34
Q

What is the treatment of plaque related gingivitis?

A
  • OHI
  • Mechanical biofilm disruption
  • Professional prophy
  • Removal of plaque retentive features e.g. poorly fitting dentures, overhanging restorations, crowding – orthodontics

Periodontics (2 decks)

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