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CSP3 YR5- Restorative RESET > The Oral Microbiome, Biofilms, Gingivitis and Periodontitis > Flashcards

The Oral Microbiome, Biofilms, Gingivitis and Periodontitis Flashcards

1
Q

Explain the symbiosis of man and microbes?

A 
Healthy digestive tract
Resistance to colonisation of pathogens
Regulates CVS
Support host defence
Anti-inflamm properties
Additional metabolic potential
Antioxidant activity
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2
Q

Name and explain different types of respiration?

A 
Aerobic: in oxygen
Obligate aerobes: require oxygen
Obligate anaerobes: killed by oxygen
- o2 final electron acceptor 
- fermentation
Facultatice anaerobes: tolerate oxygen and switch to co2
Capnophilic: preferes co2
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3
Q

Saliva functions?

A

ADD

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4
Q

Biofilm definition?

A

Community of microbes characterised by cells that are attached to a surface or to each other and embedded in a matrix of extracellular polymeric substances

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5
Q

Process of biofilm formation - bacterial formation and development?

A 
Bacteria approach surface
Contact and attachment
Adherence and change in cell surface
Metabolic activity changes environment
Quorum sensing and development
Mature biofilm can seed new cells into environment
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6
Q

Number of bacterial species? Genus examples?

A 
770
Streptococcus
Staphylococcus
Bacillus
Aspergillus
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7
Q

Number of fungal species? Genus examples?

A

9-23
Candida
Saccharomycrs
Aspergillus

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8
Q

Viruses? Oral examples?

A

Herpes 90%

HPV 25%

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9
Q

Priming of microbiome may originate in-uterine?

Process of priming?

A

Loosen of epithelial cells due to preg hormone (bacterial penetration)
Bacteria reach lamina propria and vasc tissue
Transfer bac to placenta via bloodstream
Oral bac trapped in placenta tissue
PACs acquire the allergenic info in placenta
APCs return to feral peripheral lymphoid organ
Fetal T regs recognised maternal microbiome as safe and generated in fetal lymphoid tissue

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10
Q

Bacteria in buccal mucosa?

A

Streptococcus

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11
Q

Bacteria in hard palate?

A

Streptococcus

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12
Q

Bacteria in keratinsied gingiva?

A

Streptococcus

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13
Q

Bacteria in saliva?

A

Streptococcus

Porphyromonas

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14
Q

Bacteria in sibgingival plaque?

A

Strep
Fusobacterium
Prevotella

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15
Q

Bacteria in supragingival plaque

A

Strep
Fuse
Coryne

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16
Q

Bacteria in throat?

A

Strep

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17
Q

Bacteria on tongue?

A

Strep

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18
Q

Species of streptococcus?

A

Mutans: Alpha haemolysis, mutans, sobrinus, cricetus, dental caries
Salivarius: alpha, salivarius, vestibularius, keratibised surfaces and vestibule mucosa
Oralis: alpha, borealis, sanguis, mitis, gordonii and cristacus, early colonisers produces glucans, non-kerat, dental plaque
Anginosus: beta, anginosus, intermedius and constellatus, purulent infections (abscesses)

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19
Q

Factors which cause the shift from symbiosis and dysbiosis?

A

Major ecological pressures
Inflammation
Increased temperature or pH
Diet and reduces pH

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20
Q

Carbohydrate sources?

A 
Glucose
Fructose
Sucrose
Lactose
Galactose
Mannose
Celliobiose 
B-glucosides
Trehalose 
Maltose
Raffinose 
Ribulose
Starch
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21
Q

Pellicle? Description? Characterisitics?

A

The layer of material acquired by a cleaned tooth
- mucin, proline rich proteins, statherin and amylase (lysozyme, albumin, Ig, glucans)
Prerequisite for bacterial attachment

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22
Q

Structure of pellicle?

A

90% salivary glycoproteins

- d domain, cys rich, O-glucans (VNTR) and cys rich

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23
Q

Proline rich proteins? Characterisitics?

A

Acidic 16kD: saliva, affin for hydroxyapatite, Ca and PO4 levels and antibacterial activity
Basic 6-9kD: saliva and nasal secretions, complex with tannin
Glycosylated 36kD: newly formed pellicle

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24
Q

Alpha amylase?

A 
Alpha 1-4 glycosidic bonds
Digestive function of starch and amylase
Essential component of salivary pellicle
Bacterial receptor
Forms heterotypic mixed micelle like structure
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25
Q

Bacterial adhesion?

A

Pellicle at the enamel allows adhesion to a bacteria, that can form a chain of bacteria

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26
Q

Stages of development in plaque biofilm?

A 
Start: Clean enamel surface
2s: Pellicle formation
1m: Pioneer bacteria (strep sangius)
2h: icrocolones and extracellular polysaccaride
> 2h: biofilm
48h: mature plaque
2-7d: microbial succession and diversification
> 7d: climax community
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27
Q

Dysbiosis? Definition?

A

A condition in which the normal microbiome pop structure is disturbed often through external burdens such as disease states or medications

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28
Q

Holobiont? Defintion?

A

Host organism and all its symbiotic microbial resident

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29
Q

Microbiome? Defintion?

A

Sum of microbes and their genetic information and the environment in which they interact

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30
Q

Symbiosis? Defintion?

A

Two or more species living closely together in a long term relationship

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31
Q

Biofilm related diseases?

A

Periodontal disease

Dental caries

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32
Q

Assessing a person’s health?

A

By frailty

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33
Q

What does the oral healthcare team gave to consider?

A

Weight loss, smoking cessation, exercise and controlling disease and glycaemia

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34
Q

Educational programmes? Professional targets?

A

Mothers to be
New mothers
Care home workers
People whom have dependable people

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35
Q

Dental check ups? Key touch points?

A

2, 5, 12, 26, 40 and 70

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36
Q

Toothbrush storage? Location and why?

A

Separately in bathroom to avoid horizontal transmission

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37
Q

Saliva levels? Why?

A

Oral microbiome

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38
Q

Bacteria colonisation? Location?

A

Teeth, gingival crevice and hard palate

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39
Q

Dental biofilm? Defintion?

A

Masses of microorganisms that bind to and multiply on a solid surface, typically with a fluid bathing thr microbes

Free flowing microorganisms are called planktonic cells

These communities form microcolonies and interact with each other (quorum sensing)

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40
Q

Acquired salivary pellicle? Characterisitics?

A 
Thin layer
Forms on teeth within seconds
Smooth, colourless and translucent
Bacteria free
Derived from salivary glycoportrind
Affinity for hydroxyapatite
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41
Q

Initial stage of biofilm formation?

A

Attachment of acquired pellicle, which is a thin coat of salivary glycoprots, to a clean tooth surface

Bind to buccal, but list due to desquamantion

Non-shedding surfaces permit extensive development (plaque at retention sites)
- susceptibility for disease

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42
Q

Acquired pellicle formation? Host and bacterial origin?

A

Host: - glycoprot, phosphoprot, statherin, amylase, protein rich peps, and host defence components
Bac: - glucotransferase and glucan

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43
Q

Oral habitats? Location and characterisitics?

A

Buccal mucosa: - sparse, desquamates and masticatory friction
Dorsum tongue: - highly, rough papillary surface, refuge, reservoir for -ve, low redux potential (anaerobic)
Crevicular epith: - pioneer bacteria for initiation, and development of gingival and periodontal disease
Dentures, restorations and orthodontic
Tooth surfaces: supra and subgingival (non-shed)

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44
Q

Teeth as a habitat? Characteristics?

A

Only non-shed area of the oral cavity
Masses of bacteria constantly accumulate at surface to produce biofilm
Biofilm is the initatiting factor in caries and periodontal disease
Shoft from symbiotic to dysbiotic

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45
Q

Areas of tooth decay?

A

Smooth surface cavity
Pit and fissure cavity
Root cavity

46
Q

Factors modulating microbial growth - anatomical characteristics?

A

Anatomical: - shape and topography of teeth, misalignment, poor restorations, and non keratinised sulcular epith

47
Q

Factors modulating microbial growth? Saliva characterisitics?

A

Saliva: - mix of inorganic ions Ca, Na, K, bicarbonate, PO4, Cl and proteins/glycoprots

  • forms salivary pellicle (adhesion site)
  • food source
  • aggregation of bac
  • growth inhib (lysozymes and histatins)
  • pH maintenance (buffering)
48
Q

Factors modulating microbial growth? Gingival crevicular fluid characterisitics?

A

Healthy continuous slow flow, and increases with inflammation

  • similar to serum
  • flushes bac out of sulcus
  • source of nutrients
  • maintain pH
  • defence (IgG/M/A)
  • phago
49
Q

Factors modulating microbial growth? Microbial factors characterisitics?

A

Interaction in promoting and suppressing other bacteria

  • competition; prevent latecomer attachment
  • produce toxins; bacteriocins, kill
  • metabolic end prods; antagonistic agents lower pH/nutrition
  • coagg with bac
  • quorum sensing
  • colonisation resistance; commenasl bac inhibit other bacteria
50
Q

Factors modulating microbial growth?

A

pH: microbes need neutral pH (6.7), pH can fall and acidophilic will flourish
Oxidation: fluctuations favour growth
Antimicrobial therapy: remove commensal bac and allow colonisation of fungus
Diet: fermentable carbs allow acidogenic bacteria to produce extracellular polysacc allow adherence

51
Q

Progression of the oral biofilm? Characterisitics?

A

Remnants from the host diet always present (sucrose and starch)
Constituents if saliva (glycoprot and mineral)
Crevicular exudate (proteins)
Low level oxygen
Extracellular microbial by products
Intaceluular food sources
And back to top

52
Q

Pioneer bacteria?

A 
Streptococci
Staphylcocci
Neiserria
Lactobacillus
Anaerobes: veillonella and fusobac

Oral microbiome changes at the eruption of teeth

53
Q

Plaque biofilm? Defintion?

A

Tenacious microbial community embedded in an inter microbial matrix attached to either soft or hard tissue

Dead and living bacteria and their extracellular products together with compounds from the host (salivary derived)

54
Q

Dental plaque? Distribution?

A

Found on all dental surfaces and applicants
(Abscence if hygiene and protected areas)

Interproximal.areas (contact between 2 teeth)
- occlusal fissures, smooth surfaces buccal and palatal

Supra and subgingival: above and below gingival margin

55
Q

Comparison of supra and subgingival plaque?

A 
Matrix: 30-50 vs 0
Flora: +ve vs -ve
Motile bacteria: few.vs common
Respiration: aerobic (unless thick) vs anaerobic
Meta: carbs vs prots
Species diverse: little vs lots
56
Q

Subgingival plaque? Characterisitics?

A 
Hardest to investigate 
As the gingival crevice depends a new environment is created (pocket - BPE)
- protected from friction
- attachment and adherence less important
- different nutrients
- low o2
- alkaline pH 
- different host defence mech
Established 4 weeks after gingivitis
-ve, cocci and spirochetes 
Over time plaque more complex and becomes obligate or facultative anaerobes 
No matrix prod
50% of bac motile
57
Q

Composition of matrix?

A

Organisms embedded in matrix
Derived from his factor and biofilm
- variety
- different/same sites on same/diff teeth

58
Q

Plaque matrix? Characterisitics?

A

Derived from salivary glycoprots, dead cells and serum prots and polysacc
30-50% of supragingival plaque
None found in deep subgingival plaque

59
Q

Plaque matrix? Functions?

A

Nutrients
Chemical scaffold for shape and structural integrity
Tolerance for environmental factors
Bio active and retains water, nutrients and enzymes
Restrict or exclude penetration of other molecules (antimicrobials)

60
Q

Host factors that prevent colonisation?

A 
Desquamantion
Salivary flow
Mastication
Immunoglobulins in slaiva
Commensal bacteria
61
Q

Mechanisms in which bacteria adhere and attach?

A

Electrostatic
Hydrophinuc
Receptors
Fimbriae

62
Q

Process of biofilm formation?

A
  1. Film formation adsorption of acquired pellicle
  2. Transport microbes
  3. Reversible phase - long range physio chem forces
  4. Irreversible- adhesion receptor
  5. Secondary colonisation
  6. Biofilm maturation
  7. Detachment, colonise other sites
63
Q

Pioneer bacterial species?

A 
S. Sanguinis 
S. Oralis
S. Mitis bioval 1
Actinomyces
Haemophilus
Neiserria
64
Q

Plaque biofilm timeline?

A

2s - acquired pellicle and bacterial adhesion
2 hrs - initial plaque formation (irreversible colonsiation)
6 hrs - supragingival plaque
2 days - plaque mass doubles
5-7 days - plaque mayriatuon by filamentous bacteria
21 days - bacterial rep slows that plaque accumulation becomes relatively stable
12 weeks - well differentiated subgingival plaque formed, -ve

65
Q

How do bacteria cause disease?

A

Quantity and quality of colonies in sulcus and pockets contribute to disease
Local inflammation in gibgival tissue
Production of virulence factors such as enzymes and toxins which stimulate an immune response

66
Q

Gingivitis? Characterisitics?

A

Plaque induced gingivitis is a non specific reversible inflammatory response to an increased accumulation to biofilm around the gingival area due to poor oral hygiene

No specific pathogen associated

Many possess inflammatory modules

Not all gingivitis cases progress to periodontitis

67
Q

Periodontitis? Characterisitics?

A

Localised or generalised
Different stages and grades and associated risk factors
Studies show a high diversity of colonies with increased proteolytic and obligate anaerobe bacteria present

68
Q

Role of oral flora in systemic infection?

A

Evidence linking oral.microbiome to systemic infection

CVD: infective endocarditis, CHD, stroke, atherosclerosis and myocardial infection

Hospital acquired bacteria pneumonia
Diabetes
Adverse preg outcomes

69
Q

Oral microbiome’s effect on the systemic health?

A

Metastatic infection: - microbes entry to circulation, placenta barrier

Metastatic injury: - exo/endo toxins across CV susten in individual with periodontitis

Metastatic inflammation: - locally protected inflammatory products reach and contribute to atherosclerosis or intra uterine inflammation

70
Q

Periodontal diseases? Affect tissues? Most common diseases?

A

Tissues:

  • Alveolar bone
  • Periodontal ligament
  • Cementum
  • Gingivae

Diseases:

  • Plaque induced gingivitis
  • Periodontitis
71
Q

Clinical gingival health? Anatomy and characterisation/

A

Anatomy:
- shallow gingival sulcus (3mm deep)

Characterisation: absence

  • bleeding on probing
  • erythema and oedema
  • attachment and bone loss

Intact periodontium:

  • pale pink gingiva
  • stippled and firm
  • knife edge dental papillae
  • low level plaque and calculus
  • no bleeding
  • full bone support
  • JE attached at CEJ
72
Q

Stable reduced periodontium - to ensure stability it must have an absence of?

A

Absence of:

  • bleeding
  • erythema and oedema
  • symptoms
  • no increased loss of attachment and bone loss

(stop progression of periodontitis)

Must remain on maintenance

73
Q

Dental plaque biofilm-induced gingivitis? Definition?

A
  • An inflammatory lesion resulting from interactions between the dental plaque biofilm and the host’s immune‐inflammatory response, which remains contained within the gingiva and does not extend to the periodontal attachment (cementum, periodontal ligament and alveolar bone)

Such inflammation remains confined to the gingiva and does not extend beyond the mucogingival junction and is reversible by reducing levels of dental plaque at and apical to the gingival margin

74
Q

Further classifications of gingivitis? Types?

A
  • Gingivitis on an intact periodontium
  • Gingivitis on a reduced periodontium in a non-periodontitis patient (e.g., recession, crown lengthening)
  • Gingival inflammation on a reduced periodontium in a successfully treated periodontitis patient
75
Q

Gingivitis - clinical signs? visual signs?

A

Clinical signs:

  • Erythema
  • Oedema
  • Pain
  • Heat
  • Loss of function
  • Halitosis
  • Accumulation of plaque and calculus
  • Red and swollen gingiva
  • increased gingival crevicular flow

Visual signs:

  • swelling (loss of knife-edged papillae)
  • bleeding on probing (discomfort)
  • redness
76
Q

Plaque induced gingivitis? Definition?

A
  • Inflammation of the gingival tissues caused by the presence of the oral biofilm (dental plaque)

Varies with: Oral Hygiene, Age, Gender, Race, Systemic Factors, Certain Drug Therapies, Local Risk Factors

77
Q

How is inflammation determined clinically? Tests and instruments?

A

Tests: UNC15

  • Plaque index (location and distribution of plaque deposits)
  • Gingival index (gingival bleeding)
78
Q

Defining the difference between an intact periodontium and a reduced periodontium?

A
  • Attachment loss: No for both
  • Pocket depths: less than 3mm for both
  • Bleeding on probing: Health less than 10% and Gingivitis greater than 10%
79
Q

Healthy periodontium? Classifications?

A

Sulcus: 1-3mm
Attachment: No loss
PDL: No loss
Alveolar bone: No loss

80
Q

Gingivitis? Classifications?

A

Sulcus: 1-3mm with plaque
Attachment: No loss
PDL: No loss
Alveolar bone: No loss

81
Q

Mild periodontitis? Classifications?

A

Sulcus: 4-5mm
Attachment: 1-2mm loss
PDL: loss
Alveolar bone: No loss

82
Q

Severe periodontitis - sulcus? attachment? PDL? bone?

A

Sulcus: >6mm
Attachment: 3-4mm loss
PDL: loss
Alveolar bone: loss

83
Q

Loe et al. 1965? Experimental Gingivitis?

A
  • All patients developed gingivitis
  • 3 within 10 days
  • 9 between 15 and 21 days
    Shift in microbial composition:
  • pre: +ve cocci and short rods
  • gingivitis: +ve cocci and short rods fell and remainder -ve cocci and short rods, +ve filments, fusobac, vibrios and spirochaetes

Results:

  • patients return to clinical gingival health
  • plaque causes gingival inflammation
  • plaque removal leads to resolution
84
Q

Plaque induced gingivitis? Microflora changes?

A

Increase in plaque mass (10-20 fold) and a shift from Gram+ve streptococci-dominated plaque seen in health to:

  • Actinomyces spp
  • Capnophilic (esp. capnocytophaga spp.)
  • Obligately anaerobic G-ve bacteria

As the lesion progresses and bleeding is seen Bacteroides - Porphyromonas gingivalis Prevotella intermedia together with Spirochaetes increase (believed to be involved with Periodontitis)

85
Q

Local risk factors of gingivitis? Definition? Examples?

A

Those that encourage plaque accumulation at a specific site by either inhibiting its removal during daily oral hygiene practices, and/or creating a biological niche

  • Dental plaque biofilm retention factors
  • Oral dryness
86
Q

Characteristics which -ve impact the immune-inflammatory response - systemic health factors?

A

Characteristics present in an individual, which negatively influence the immune-inflammatory response to a given dental plaque biofilm burden, resulting in exaggerated or “hyper” inflammation.

  • Smoking
  • Metabolic factors – hyperglycemia in people with or without diabetes.
  • Nutritional factors – Severe Vitamin C deficiency, or scurvy
  • Pharmacological agents
  • Elevations in sex steroid hormones – at puberty, during pregnancy,
  • Haematological conditions
    associated with signs of excess gingival inflammation in the absence of excessive plaque biofilm accumulation.
87
Q

Bacteria present during periodontitis that cause damage - How?

A

Porphyromonas, Prevotella, Tannerella - Black pigmented bacteroides species, often isolated from periodontal pockets in large numbers intimately involved with all forms

Periodontitis can impair host defences and damage components of the periodontium by production of collagenases, proteases, hyaluronidase and cytotoxins

88
Q

Periodontal health - What is clinical gingival health? Definition?

A
  • Absence of clinically detectable inflammation
  • Biological level of immune surveillance

‘State free from inflammatory periodontal disease that allows an individual to function normally and avoid consequences due to current or past disease’

89
Q

Periodontium pristine health - Definition? Clinical gingival health?

A

Absence of histological evidence of inflammation and no anatomical change of the periodontal structures

Absence of inflammation on an intact or reduced periodontium (<10% BOP)

90
Q

Gingivitis - Clinical signs? Maintenance?

A

A non-specific inflammatory response to indigenous bacteria

Resultant inflammation and periodontal breakdown (shift in microbial composition occurs several pathogens appears leading to a host driven tissue damage)

Maintenance:
- composition of subgingival plaque needs to be redirected towards one compatible with gingival health

91
Q

Periodontitis - Clinical signs? Management?

A

Plaque-induced inflammation of periodontal tissues:
- loss of CT attachment and alveolar bone

Preceded by plaque biofilm induced gingivitis
Slow to moderate or rapid rate of progression
Life-long disease and requires supportive care
No cure

92
Q

Does plaque cause periodontitis - Factors? Interplay?

A

Complex disease of a multifactorial nature involving interplay between subgingival microbiota, the host immune and inflammatory responses and environmental modifying factors

93
Q

Subgingival biofilm - Definition? Formation? Progression? Combat?

A

Definition:
- The microbial composition is a collection of commensal organisms that coexist in relative harmony
Formation:
- The bacterial biofilm formation initiates gingival inflammation
Progression:
- periodontitis initiation and progression depend on dysbiotic ecological changes in the microbiome in response to nutrients from gingival inflammatory and tissue breakdown products that enrich some species
Combat:
- anti‐bacterial mechanisms that attempt to contain the microbial challenge within the gingival sulcus area once inflammation has initiated

94
Q

Microflora - Definition? Change? Sigmund Socransky’s pyramid of bacteria?

A

Definition:
- the composition of bacteria present in the oral cavity that may or may not contribute to disease
Change:
- progressive change in microflora between health, to gingivitis to periodontitis
Pyramid: involvement in the periodontal disease progression, and categories based on their pathogenicity and role in plaque development
- Aa; A.actinomycetemcomitans
- Green; Capnocytophaga (gingivalis, ochracea, sputigena)
- Orange assoc; C. rectus, E. nodatum
- Orange; P. intermedia/micra and F. nucleatum
- Red; P. gingivalis, T. forsythia/denticola

95
Q

Pyramid of bacteria - Orange assoc? Green?

A

Adhere to pellicle by fimbriae and so avoid flushing by GCF (early colonisers in the sulcus)

96
Q

Pyramid of bacteria - Orange?

A

Bridge species, that form a link between colonisers and highly pathogenic bacteria

Responsible for attachment loss and increased pocket depth

97
Q

Pyramid of bacteria - Red?

A

Previous bacteria form ideal living conditions for strictly anaerobic bacteria (red) and allow their colonisation

Significantly involved in destruction of the periodontium (destruction of soft tissues and bone)

Treponema, Porphyromonas and Tannerella (black-pigmented anaerobes)

98
Q

Periodontitis pathogens - Description? Role? Growth? Secretions?

A

Description:
- non motile, pleomorphic, spindle shaped -ve rod
Role:
- induce apoptosis, invades epithelial cells and endotoxin (high virulence)
Growth:
- anaerobically aggressive periodontal pathogens fimbriae mediate adhesion and the capsule defends against phagocytosis
Secretions:
- collagenase, endotoxin fibrinolysis, phospholipase (destroys Ig)

99
Q

Specific plaque hypothesis?

A

Only a few species out of the collection comprising the resident oral microflora are involved in the disease process

100
Q

Non-specific plaque hypothesis?

A

Disease is considered to be the outcome of the overall activity of the total plaque microflora

101
Q

Ecological plaque hypothesis?

A

Organisms associated with disease may also be present at sound sites, but at levels too low to be clinically relevant. Disease is a result of the shift in the balance of the resident microflora due to the response in a change in local environmental conditions e.g. nutrients available, pH

102
Q

Risk factors for periodontal disease - Description? Factors?

A 
Description:
- multifactorial influences and on multiple immunoinflammaotry responses that make the dysbiotic microbiome changes
Factors:
- Smoking
- Alcohol
- Diabetes
103
Q

Periodontitis - Clinical definition? Detection? Clinical features?

A 
Definition:
- characterised by microbially-associated, host-mediated inflammation that results in loss of periodontal attachment
Detection:
- circumferential assessment of the erupted dentition with a standardised periodontal probe with reference t the CEJ
Clinical features:
- gingival swelling
- blood on brushing
- blood on probing
- loss of stippling
- loss of knife edge margins
- plaque and calculus deposits
- subgingival calculus
- pocketing (apical migration)
- bone loss
- mobility
- furcation
- suppuration
104
Q

Periodontitis Stage I - Description? Clinical signs? Susceptibility?

A

Description:
- borderland between gingivitis and periodontitis and represents early stages of attachment loss
- periodontitis response to persistence of gingival inflammation
Clinical signs:
- interproximal bone loss
- <2mm attachment loss from CEJ
Susceptibility:
- show a degree of clinical attachment loss, heightened susceptibility for progression

105
Q

Periodontitis Stage II - Description? Clinical signs? Management?

A 
Description:
- established periodontitis in which a carefully performed clinical periodontal exam identifies the characteristic damage
Clinical signs:
- interproximal bone loss
- moderate coronal third of tooth
Management:
- application of standard treatment
- professional bacterial removal 
- monitoring for arrest of disease progression
106
Q

Periodontitis Stage III - Description? Clinical signs? Management?

A

Description:
- significant damage to attachment and without advanced treatment, tooth loss may occur
Clinical signs:
- interproximal bone loss
- deep periodontal lesions that extend the middle portion of the root
Management:
- complicated due to intrabony defects, furcation and history of tooth loss (periodontally)

107
Q

Periodontitis Stage IV - Description? Clinical signs? Management?

A

Description:
- considerable damage to periodontal support and significant tooth loss, translating to loss of masticatory function
- without proper control and rehab, the dentition is at risk of being lost
Clinical signs:
- apical third of root
- deep periodontal lesions extending to the apical portion of the root
- hypermobility (from biting)

108
Q

Grades of periodontitis - Description? A? B? C?

A

Progression may differ depending on the rate and may respond differently to treatment

Rate of progression: % bone loss/ patients age (using worst bone loss site)

A - slow, max % bone loss is < half the age
B - medium, all other situations
C - rapid, max % bone loss is > patients age

109
Q

Periodontal health- 4 levels - Pristine health? Clinical health? Periodontal stability? Periodontal control?

A 
Pristine health:
- total absence of inflamm and physiological immune
Clinical health:
- absence of inflammation
- normal support
Periodontal stability:
- in reduced perio (control of factors)
Periodontal remission:
- reduce progression
110
Q

Gingival health following successful treatment of periodontitis - clinical features? modifying factors?

A 
Clinical features: absence
- BOP
- erythema, oedema, suppuration
- adequate OH
- manageable pocket <4mm
Control modifying factors:
- reduce smoking and good diabetic control

CSP3 YR5- Restorative RESET (44 decks)

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