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BDS3 > Periodontitis > Flashcards

Periodontitis Flashcards

1
Q

True of false: attachment loss is normal in the ageing process

A

True, through a lifetime accumulation of attachment loss (e.g. recession, continuous tooth eruption).

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2
Q

Why is smoking a major risk factor for periodontitis? (very simplified MoA)

A
  1. Nicotine causes vasocontriction
  2. Less nutrition to the bone and gums
  3. Bone resorption over time
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3
Q

True or false: Biofilm is necessary for periodontitis to occur.

A

True. (The host also needs to be susceptible)

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4
Q

What causes destruction of periodontium in periodontitis?

A

Bacterial toxins and enzymes AND host-mediated immune response

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5
Q

What THREE bacteria are in the “Red Complex”?

A
  • Porphyromonas Gingivalis (Pg)
  • Tanerrella forsythus (Tf)
  • Treponema denticola (Td)

Bonus (in the orange complex):
- Aggregatibacter actinomycetemcomitans (Aa)

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6
Q

What are the x roles of JE?

LOOK AT OLD LECT NOTES TO ADD

A
  • Large intercellular spaces to let PMNs and biofilm products in (for detection)
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7
Q

What specifically activates the immune system to cause periodontitis?

A

Lipopolysaccharide (LPS) from the cell wall of gram negative bacteria together with other products of plaque/biofilm.

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8
Q

Describe TWO things that occur when the JE is reacting to LPS.

A
  • JE release cytokines (IL-8, TNFa, IL-1a, PGE2, MMP)

- Perivascular mast cells release histamine causing endothelium to release IL-8

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9
Q

What does Matrixmetaloproteinase (MMP) do?

A

Breaks down collagen and other soft tissues

NOTE: does not really break down hard tissue

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10
Q

How are macrophages recruited to the periodontal site and what do they do when they get there?

A
  • Recruited by serum proteins (eg. complement) that are released into the blood/CT via vascular reaction to plaque
  • Macrophages regulate activity of other cells (wbc, fibroblasts, osteoclasts) via cytokines (IL-1b, IL-6/10/12, TNFa, PGE2, MMP, IFNg) and chemotaxins (MCP, MIP, RANTES)
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11
Q

What are the FOUR stages of periodontitis pathogenesis?

A
  1. Initial reaction to plaque (JE and mast cells react to LPS, IL-8 attracts PMNs)
  2. Activation of Macrophage (monocytes recruited, turn into macrophages and release lots of cytokines. Leukocytes also recruited)
  3. Upregulation of inflammatory cell activity (plasma cells, T-cells, PMNs and fibroblasts release cytokines - plasma cells dominate)
  4. Initial loss of attachment (cytokines encourage macrophage -> preosteoclast, then RANKL from T-cell and osteoblast encourage preosteoclast -> osteoclast = net bone resorption)
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12
Q

What medication and dose/duration can be used to manage bone loss in periodontitis?

A

Doxycycline

- 20mg twice daily for six weeks

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13
Q

Name FOUR things that influence Macrophage activity.

A
  • Genetics (hyperresponsive Macrophage phenotype)
  • Smoking (same effect)
  • Uncontrolled diabetes
  • NSAIDS (suppresses PGE2 production)
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14
Q

What FOUR effects can antibodies have?

A
  • Aggregate microbes
  • Prevent adherence of bacteria to epithelium
  • Work with complement to kill microbes
  • Permit efficient phagocytosis by PMNs

NOTE: people who can mount an effective antibody response may be less susceptible to periodontitis

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15
Q

Name FIVE proinflammatory cytokines

A
  • IL-1b
  • TNFa
  • IFNg
  • PGE2
  • MMP
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16
Q

Name FOUR antiinflammatory cytokines

A
  • IL-1ra
  • IL-10
  • TGFb
  • TIMPs
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17
Q

What are FOUR main cytokines that regulate osteoclasts?

Which TWO are most relevant to periodontitis?

A
  • PTH
  • Calcitonin
  • PGE2
  • RANKL
    NOTE: PGE2 and RANKL are the most relevant to perio
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18
Q

What are TWO sources of RANKL?

A
  • T-cells

- Osteoblasts

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19
Q

What are TWO ways to decrease osteoclast activity?

A
  • Osteoprotegerin (OPG) from osteoblasts

- Bisphosphonates

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20
Q

What is the dentally related risk when pts are on bisphosphonates?
How long does this risk last for after stopping bisphosphonates?

A

On bisphosphonates, the bone becomes ‘frozen in time’ and has a tendency for necrosis after extractions.
The effect of bisphosphonates can last up to 10 years.

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21
Q

What is meant by infrabony and suprabony pockets?

A 
infrabony = vertical/angular bone loss 
suprabony = horizontal
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22
Q

Where are the THREE walls positioned in a 3-walled defect?

A

Interdentally, palatally/lingually and buccally.

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23
Q

Define grades of furcations.

A

Grade I - 1mm
Grade II - More than 2mm
Grade III - through and through

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24
Q

What walls are lost when progressing from a 3 walled defect to 2 and from a 2 to 1 walled defect?

A

3 –> 2 we lose the interdental wall.

2 –> 1 we lose the buccal wall (loss of cortical bone).

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25
Q

How much is normal/physiological tooth movement?

A

0.2mm

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26
Q

Link PDL, bone loss, occlusive force and tooth mobility

A

Occlusive force applies stress to the PDL which then relax upon force release, allowing for a certain degree of tooth mobility.
Normally this is not a significant amount of mobility because only the coronal third and apical third of PDL is affected. But when bone loss occurs, only the apical third of PDL is left over, producing more mobility.

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27
Q

True or false: generally it is a good idea to still splint teeth that are mobile but not increasing in mobility, to prevent worsening of mobility.

A

False. We mainly splint teeth that are worsening in mobility.

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28
Q

Name THREE types of tooth splints.

A
  • Wire splint
  • CR splint
  • acrylic splint
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29
Q

Wire splints are semi-rigid splints while CR splints are fully rigid. What is the risk of fully rigid splints?

A

Lack of PDL movement/use can lead to ankylosis of tooth roots to alveolar bone.

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30
Q

Define the THREE grades of mobility.

A

Grade I - up to 1mm horizontal movement
Grade II - >1mm horizontal
Grade III - horizontal and vertical movement

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31
Q

What positions are the roots and furcal entrances of upper first molars.

A

Roots: two buccal one palatal
Furcations: buccal, DP, MP

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32
Q

What positions are the roots and furcal entrances of lower first molars.

A

Roots: mesial and distal
Furcations: buccal, lingual

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33
Q

What positions are the roots and furcal entrances of two rooted upper first premolars?

A

Roots: buccal and palatal
Furcations: mesial and distal

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34
Q

What’s so bad about furcation involvement?

A

The area is extremely hard to clean -> entrypoint for bacteria

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35
Q

From where to where is root trunk measured?

A

CEJ to furcation

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36
Q

What’s so bad about a short root trunk?

A

Higher furcation meaning easier to get furcation involvement.

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37
Q

What is the difference between hemisection and root resection?

A

Hemisection = separate portions of root+crown

Root resection = removal of a root

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38
Q

How do we usually manage furcation involvements?

A
  • Root surface debridement

- OHI

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39
Q

What is a primary risk factor for periodontitis? (primary = direct cause)

A

Specific pathogens from plaque (ie. red complex)

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40
Q

What are THREE non-alterable secondary risk factors for periodontitis?

A
  • Genetics (e.g. IL-1 gene polymorphism)
  • Gender
  • Age
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41
Q

What are SIX alterable secondary risk factors for periodontitis?

A 
MHx
- Smoking
- Diabetes mellitus
- HIV/AIDS
DHx/SHx
- Stress
- Lack of recall
- Up bringing
42
Q

What is the difference between a predisposing factor and a modifying factor? (both are different types of risk factors)

A
  • Predisposing factor interferes with the operator/patient’s ability to remove plaque
  • Modifying factor may influence disease expression/progression by altering host protective mechanisms
43
Q

What are SIX predisposing factors to periodontitis?

A
  • Tooth anatomy
  • Restorations
  • Prostheses
  • Age
  • SES
  • Gender
44
Q

What are EIGHT modifying factors to periodontitis?

A
  • Diabetes
  • Smoking
  • HIV/AIDS
  • Neutrophil dysfunction
  • Hormones
  • Genetics
  • Stress
  • Medications
45
Q

True or false: poor OH allows mostly gram -ve anaerobes bacteria to migrate subgingivally to cause gingivitis +/- periodontitis.

A

False (not completely true), bacteria in general will migrate subgingivally if left there for long enough, but the gram -ve anaerobes will flourish in the oxygen poor subgingival environment.

46
Q

What are NINE things regarding tooth anatomy that can predispose someone to localised periodontal lesions?

A
  • Cervical enamel projections (CEJ migrating towards furcation)
  • Palatal invaginations
  • Accessory root canals
  • Close roots (<0.3mm apart, only separated by PDL not bone)
  • Root proximity (<0.8mm apart, thinner bone at greater risk of bone loss)
  • Furcation involvement
  • Root concavities
  • Enamel pearls
  • Overhang
  • Crowding
47
Q

What is plunger cusp and what does it cause?

A

Overerupted tooth (due to lack of opposing tooth) will occlude with teeth adjacent to missing tooth to form a plunger effect which will pack food into the gingiva of the missing tooth, leading to gingival irritation/inflammation.

48
Q

Why might periodontal disease incidence be different for different genders?

A

Difference in OH behaviour.

49
Q

What are the FOUR stages of HIV infection and the corresponding symptoms + timeframes?

A
  1. Primary (rash, myalgia, fever, mouth ulcers) [start]
  2. Early (asymptomatic) [at 10wks]
  3. Intermediate (minor infections, skin conditions, TB, pneumonia) [at 5yrs]
  4. Life (neoplasms) [at 10yrs]
50
Q

What is another name for hypertrophic candidiasis? (not thrush)

A

Pseudomembranous candidiasis.

51
Q

What are FIVE mechanisms through which smoking can cause periodontitis?

A
  • Bacterial flora (more pathogenic)
  • Host vasculature (vasoconstriction = less blood to gums -> less immune and nutrients)
  • Host immune response (decreased WBC function - PMN and T/B cells)
  • Host inflammatory response (increase proinflammatory cytokines PGE2 and TNFa)
  • Decreased healing of periodontal CT (nicotine decreases fibroblast adhesion to root surface)
52
Q

What is smoker’s keratosis and how does it occur?

A
  • White patch in oral cavity (in area not necessarily with friction)
  • Caused by smoking increasing proliferation of keratinocytes
53
Q

What are FOUR oral pathologies that occur more often in poorly controlled diabetes?

A
  • Periodontitis
  • Gingivitis
  • Xerostomia/Caries
  • Candida albicans infections
54
Q

What are the normal ranges for blood glucose and Hba1c?

A
  • Blood glucose: 4-8mmol/L

- Hba1c: 6.5-7%

55
Q

What are FIVE mechanisms through which poorly controlled diabetes can cause gingivitis/periodontitis?

A
  • Non-enzymatic glycosylation of collagen slows turnover rate (slower healing)
  • Advanced glycation end products (AGEs) increases collagen cross-linking (thickens basement membrane imparing O2 diffusion, waste elimination and leukocyte migration)
  • Altered microbiota (more P. gingivalis)
  • Altered immune response (altered macrophage phenotype, high glucose inhibits PMN respiratory burst and phagocytosis)
  • Pro-inflammatory cytokines (IL-1, PGE2, TNFa)
56
Q

True or false: there is a reciprocal relationship between diabetes and periodontitis.

A

True, periodontitis may worsen the degree of diabetic blood glucose control.

57
Q

What are THREE changes in the gingiva that may occur during menstruation? Why does this occur?

A

Increase in progesterone increases permeability of gingival vasculature -> bleeding, swollen gingivae and minor increase in tooth mobility.

58
Q

What is a pregnancy epulis?

A

Hypertrophy of the gingiva resulting in a lump, caused by increase in oestrogen/progesterone during pregnancy.

59
Q

True or false: Post-menopausal osteoporosis is linked with increase in periodontial attachment loss.

A

True

60
Q

What are TWO ways stress increases periodontitis?

A
  • HPA axis releases CRH and glucocorticoid hormones -> release pro-inflammatory cytokines (ILs, PGs, TNF)
  • Adrenaline/NA exerts immunosuppresive effect
61
Q

What are THREE medications that can cause gingival hypertrophy and how do we treat this?

A
  • Phenytoin, calcium channel blockers, cyclosporine

- Full debridement, OHI

62
Q

What are NINE factors to consider when determining prognosis of an individual tooth?

A
  • Percentage bone loss
  • Distribution and type of bone loss
  • Caries and pulpal involvement
  • Mobility
  • Crown to root ratio
  • Presence and severity of furcation
  • Root form
  • Strategic value
  • Tooth position (occlusal load)
63
Q

What are NINE factors to consider when determining overall periodontial prognosis?

A
  • Individual tooth prognosis
  • Age
  • Medical status (e.g. diabetes)
  • Oral habits (e.g. bruxing)
  • Risk factors (e.g. smoking)
  • Rate of progression
  • Patient cooperation
  • Economic consideration
  • Knowledge and ability of dentist
64
Q

What are Kaur’s THREE levels of perio prognosis?

A
  • Good (tooth can be saved)
  • Questionable/Guarded (not sure if it can be saved)
  • Poor/Hopeless (cannot be saved)
65
Q

What is ONE reason why people tend to lose more upper teeth than lower teeth?

A

People tend to concentration on lower teeth more when brushing (As stated by Kaur 2017)

66
Q

True or false: Studies show that tooth loss has bilateral symmetry.

A

True. (McGuire and coworkers)

67
Q

Fill in the blank:

1) Identify local and systemic risk factors
2) ________
3) Periodontal prognosis

A

Determine if local/systemic risk factors can be controlled.

68
Q

When would we consider LA for scaling?

A

When scaling subgingivally for pockets 5mm or deeper. Inject a few drops into the base of the interdental papillae.
- Topical anaesthetic is insufficient (only surface numbing)

69
Q

Should be give LA when removing overhang?

A

Yes (says Kaur 2017)

70
Q

What are the FIVE treatment phases for periodontitis?

A
  1. ROP (LA, endo/exo if required)
  2. Systemic phase (Abx cover, bleeding risk, assess risk factors for prognosis)
  3. Hygienic phase (OHI, full debridement)
  4. Corrective phase (surgical)
  5. Maintenance phase (3-6 monthly hygiene and charting)
71
Q

What is a good starting interval for supportive periodontal therapy?

A

3 months (to a max of 6 months)

72
Q

What is the main benefit of polishing after supragingival power scaling?

A

It smooths over little divets in the enamel that would have collected plaque.

73
Q

Why might age be an important patient factor when making a periodontitis diagnosis?

A

A 35yo with moderate bone loss might be diagnosed with aggressive perio while the same amount of bone loss in a 55yo would be classed as chronic.

74
Q

What are the THREE levels of diagnosis for periodontitis?

A
  • Patient factors
  • Oral factors
  • Site factors
75
Q

One of the three levels of perio diagnosis is patient factors.
What are SEVEN patient factors for perio diagnosis?

A
  • Age
  • Smoking
  • Medical conditions (e.g. diabetes)
  • Medications
  • Stress
  • Initial perio diagnosis (aggressive vs. chronic)
  • Genetics (e.g. IL-1 polymorphism)
76
Q

One of the three levels of perio diagnosis is oral factors.

What are FIVE oral factors?

A
  • Oral hygiene and access (e.g. prostheses)
  • Parafunction
  • Hx of tooth loss (caries vs. perio)
  • Bone levels and age
  • Gingival biotype
77
Q

One of the three levels of perio diagnosis is site/tooth factors.
What are SIX site/tooth factors for perio diagnosis?

A
  • Calculus
  • Probing depth (bone loss) + recession (attachment loss)
  • BOP
  • Furcation (nabers probe)
  • Suppuration
  • Mobility
78
Q

Link transseptal gingival fibres to the progression of periodontitis.

A

Alveolar bone loss from periodontitis causes transseptal gingival fibres to reform at a more apical level, manifesting as increased pocket depth.
As perio is treated, the transseptal fibres are allowed to reform more coronally, reducing pocket depth.

79
Q

What are TWO general MoAs for perio affecting the body on a systemic level?

A
  • Periodontal infection applies a chronic inflammatory burden at the systemic level
  • Bacteria & their products pass through pockets and into the blood stream causing systemic issues
80
Q

What is a focal infection?

A

A bacterial infection that is localised to a specific area (e.g. tooth) from which it may spread to other parts of the body. [ie. doorway infection?]

81
Q

What are TWO types of focal infection of oral origin?

A
  • Open foci (e.g. caries, perio pockets, pericoronitis)

- Closed foci (e.g. endodontic infections)

82
Q

True or false: Risk of bacteraemia correlates with the degree of gingivitis rather than periodontitis.

A

True (Kaur 2017)

83
Q

What are SEVEN systemic factors that have associations/causations with perio?

A 
Causality (more evidence)
- Diabetes
- Preterm low birth weight
- CVD
- Pulmonary disease
Associations (less evidence)
- Rheumatoid arthritis
- Osteoporosis
- Obesity
84
Q

What is the general consensus on periodontitis and CVD? (2009)

A

A direct causal relationship between periodontitis and atherosclerotic CVD is NOT established

85
Q

What are THREE mechanisms through which perio might cause CVD?

A
  • Perio bacteria similar to that found in atheromas (arterial plaques)
  • Increased inflammation (macrophage cytokines, C-reactive protein from liver)
  • Periodontopathogens may cause platelet aggregation
86
Q

What is ONE mechanism through which periodontitis may worsen diabetes?

A

Chronic inflammatory burden

87
Q

What are TWO mechanisms through which periodontitis may increase the likelihood of preterm low birth weight?

A
  • Increased inflammatory mediators (indirect)

- Bacterial assault on amnion (direct)

88
Q

True or false: There is no compelling evidence that treatment of periodontitis improves birth outcomes.

A

True (2011 JCP systematic review)

89
Q

What is ONE mechanism through which poor oral health may worsen respiratory disease?

A

Oral cavity can act as an important reservoir for bacteria that cause lung disease.

90
Q

What are two mechanisms through which RA can be linked to periodontitis?

A
  • Molecular mimicry

- Difficulty brushing teeth (due to bad joints)

91
Q

What are SIX causes of gingival recession?

A 
Classical (non-inflammatory)
- Tooth brushing (seen with wedged shaped abrasion lesions)
- Frenum pull
- Orthodontics
- Tooth morphology (dehiscence/fenestration)
Perio related
- Periodontitis
- Excessive scaling
92
Q

What are TWO situations where antibiotic prophylaxis may be indicated?

A
  • Immunosuppressed patients

- According to the infective endocarditis guidelines

93
Q

What are FOUR instances where antibiotics is indicated for treatment?

A
  • NUG
  • Periodontal abscess that has spread
  • Aggressive periodontitis
  • Refractory periodontitis
94
Q

How long does subgingival plaque take to mature?

A

3 months

95
Q

Antibiotics should not be used as a sole treatment for periodontitis, but as an adjunct with debridement. WHY is this and WHEN are appropriate times to use them?

A
  • Antibiotics unable to penetrate mature biofilm alone

- Use immediately after initial phase (aggressive) or at re-evaluation phase (refractory)

96
Q

What FOUR antibiotics can be used in periodontal treatment, what are their doses and which TWO can be used against A.a?

A
  • Amoxycillin (250-500mg tds for 5/7)
  • Metronidazole (200-400mg tds for 5/7)
  • Azithromycin (500mg od for 3/7, +A.a)
  • Tetracyclines (consult TG for dental doses, +A.a)
97
Q

What are SIX indications for short term CHX mouthwash?

A
  • After initial debridement if difficulty brushing (discomfort)
  • NUG
  • Severe chronic gingivitis
  • Aphthous ulcers
  • Rampant caries
  • After surgical procedures of the medically compromised
98
Q

What are TWO reasons why CHX is more effective than Cetylpyridinium Chloride (CPC - quarternary ammonion compound used in other common mouthwashes)?

A
  • CHX binds to bacterial cell membranes to leak intracellular components (effective MoA)
  • CHX has much higher substantivity (retained in pellicle for 12hrs vs. 3hrs for CPC)
99
Q

What is more effective, CPC (used in colgate Plax) or essential oils (used in listerine)?

A

Essential oils in Listerine (disrupts cell walls and inhibits enzymes)

100
Q

What is the MoA of tea tree oil?

A

Plaque inhibitory and anti-inflammatory

101
Q

Do mouthwashes reach subgingival plaque?

A

No, due to presence of calculus and area too tight for liquid to penetrate.

102
Q

What are the FOUR steps to a Supportive Periodontal Therapy (SPT) appt?

A
  1. Examination and re-evaluation (3 levels of Dx)
  2. Motivation, re-instruction and instrumentation
  3. Treatment of reinfected sites
  4. Polish, fluoride and determination of future SPT appt.

BDS3 (22 decks)

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