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MDENT110 > Periodontal disease > Flashcards

Periodontal disease Flashcards

1
Q

What is the difference between gram positive and gram negative bacterium?

A

Gram negative - 2 cell membranes with thin cell wall between creating a space called the perioplasm - more transport proteins, outer capsule is LPS
-don’t retain stain so appear pink

Gram positive - thick cell wall (peptidoglycan) retains stain (purple) and one cell membrane

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2
Q

What are polymicrobial infecfions?

A

Interactions between two or more organisms leading to disease,

  • sum of parts and their virulence factors cause disease and not one in isolation, -
  • interaction with host defences are key
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3
Q

Describe the arrangement of subgingival plaque

A

Microorganisms firmly attached at the bottom of the JE, more loosely attached towards the top, lots of polymicrobial attachments in the gingival crevicular fluid

  • Contains a predominantly Gram-positive layer attached to hard tissue
  • Overlying layers contain Gram-negative anaerobes and motile bacteria
  • All exist in close, mixed communities
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4
Q

Treatment for periodontal disease?

A

RSD, removing plaque, antimicrobial therapy

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5
Q

What changes a quiescent site into an active site?

A

Change in the host e.g. smoking, immune status, age, environmental factors
Change in microbial challenge - type, number, virulence factors

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6
Q

What bacteria dominates in ANUG?

A

Fuso-spirochaetal complex

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7
Q

What is amelogensisis imperfecta?

A

Enamel hasn’t formed properly - very sensitive teeth with rough enamel

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8
Q

Which teeth are probed in children?

A

6 teeth - UR6, UR1, UL6, LL6,LL1, LR1

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9
Q

Challenges to toothbrushing?

A

Retroclined teeth in cleft lip and palate, abnormalities of tooth, Orthodontic appliances, sensitive teeth, physical or learning disabilities

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10
Q

How do periodontal pockets develop?

A

When the junctional epithelium detaches from the enamel

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11
Q

Why is the JE thin?

A

This allows the transport of nutrients from the connective tissue to the tooth and outside of it as well (sulcus).

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12
Q

What is the depth of normal sulcus?

A

0.5-2.0mm

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13
Q

When do the inital changes of early gingivitis occur?

A

Occurs in the first week

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14
Q

When does the early lesion occur?

A

Occurs in second week

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15
Q

When does chronic marginal gingivitis occur: established lesion?

A

within 2-3 weeks

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16
Q

When does destructive periodontitis occur?

A

Timescale unknown

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17
Q

What is the initial response to plaque?

A

Increased blood flow (looks red)

oedema
development - plasma leaking out of blood, increased blood vessels

Migration of neutrophils

Loss of perivascular collagen of blood vessels - leaky

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18
Q

What changes occur in the early lesion?

A

Increase in neutrophils and crevicular fluid (macrophages and lyphocytes)

  • junctional epithelium starts to proliferate (hyperplastic - rete pegs) but still attached to tooth and ends at the ACJ

fibroblasts show signs of damage and get collagen loss but fibres inserting into cementum still attached

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19
Q

What happens in chronic marginal gingivitis: the established lesion?

A

Increased in vascularity and formation of GCF

Increase in lymphocytes and plasma cells (chronic cells now not acute cells)

JE becomes detached from tooth but still attached at ACJ

JE may be ulcerated

Marked loss of collagen but fibres into cementum still intact

sulcus may appear deepened but no true pocket formation

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20
Q

What happens in destructive periodontitis?

A

Loss of the collagen fibres inserting into cementum

Junctional epithelium migrates downwards onto cementum

Destruction of alveolar bone (due to inflammation damaging the bone)

True pocket formation

Quite a lot of PDL fibres lost

destruction is not continuous but occurs in bursts?

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21
Q

How do we manage destructive periodontitis?

A

RSD

Removal of plaque, calculus, debris

Inflammation subsides

Junctional epithelium proliferates

Attaches to tooth- long epithelial attachment

Little or no regeneration of bone or
collagen fibres inserting into cementum (fibroblasts)

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22
Q

What type of studies are the Loe studies?

A

Longitudinal studies

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23
Q

What do germ free animals show?

A

No bacteria, no disease

germ free animals + bacteria = disease but not all animals equally

periodontitis causing bacteria is transmissable but not for all animals - disease may or may not arise

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24
Q

How would you sample subgingival plaque?

A

Curette/paper point - perio probe (difficult)

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25
Q

Why can 16s rRNA be sequenced easily?

A

16s rDNA gene is very well conserved due to essential function -acts as molecular clock and species signature as evolves slowly in time.

16s = bacteria
18s = human/animal
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26
Q

What type of bacteria are raised in perio disease?

A

Anaerobic gram negative bacteria

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27
Q

What evidence for specific microbial aetiology?

A

High numbers of certain bacteria cultured from diseased sites and sequences identified in molecular studies

Can cause disease in certain animal models

Have demonstrable virulence factors

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28
Q

What is the evidence against specific microbial aetiology?

A

Potential pathogens present in health and in non-diseased sites

Do these indicate a pathogenic environment or are we missing a key organism?

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29
Q

Which 3 bacteria are always associated with increased probing depth, BOP in high numbers?

A

P.gingivalis
Ta.forsythia
T.denticola

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30
Q

What is the key nutritional source for tannerella and how do they get this?

A

Sialic acid - acquisition of this requires cleavage from host proteins

Inhibition with Tamiflu STOPS growth

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31
Q

What shape is T.denticola?

A

Small, thin spiral shaped bacrerium

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32
Q

Why are groups of organisms more important than single pathogens?

A

Different bacteria have different virulence factors

A combination of these factors is more likely to cause disease

The qualitative mixture of pathogens determines disease progression

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33
Q

What has p.gingivalis shown in mouse models?

A

Has been shown to shift the whole population from non- pathogenic to pathogenic even though itself only being present in low numbers

New idea of one pathogen causing a dysbiosis of a community is new and important theory also being noticed in other conditions e.g. obesity

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34
Q

What are some mechanisms of tissue damage by bacterium?

A
  • evasion of host defences
  • infuction of inflammation
  • soft tissue damage
  • bone resoprtion
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35
Q

Why does ANUG differ clinically and in aetiology?

A

Tissue invasion

selection of specific bacteria by host-derived nutrients - fuso-spirochaetal complex (treponema vincentii, other treponemes, fusobacteria, p.intermedia

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36
Q

Why would visible plaque be present in more 8 year olds than 5 year olds?

A

Parents stop helping with brushing at 8 years old but still helping at 5 years old

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37
Q

What percentage of 15 year olds had bleeding on probing in 2013 survey of childrens’ dental health in the UK?

A

40%

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38
Q

Why is gingivitis less prevalent on the left hand side of the mouth than the right hand side?

A

More right handed people better at brushing left side of mouth than right side

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39
Q

Which gender has lower plaque and calculus scores?

A

Females

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40
Q

Which BPE codes are used for 7-11 year olds?

A

0-2

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41
Q

Which BPE codes are used for 12-17 year olds?

A

0-4

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42
Q

What are the common gingival disorders in children?

A

Chronic gingivitis (plaque-induced)
Gingival hyperplasia
Traumatic lesions
Acute gingivitis (infective)

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43
Q

What can chronic gingivitis be exacerbated by?

A

exfoliating teeth, malocclusion or presence of orthodontic appliances

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44
Q

What is localised gingival recession in children ususally associated with?

A

Malaligned teeth, self inflicted injury, toothbrushing habits

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45
Q

What drugs can cause gingival hyperplasia?

A

Phenytoin (anti epileptic)
Cyclosporin (immunosuppresent)
Nifedepine (calcium channel blocker)

46
Q

What does cyclosporin do?

A

Selective immunosuppressent - inhibits t lymphocyte proliferation

used mainly to prevent graft rejection

gingival hyperplasia in 30% of cases and made worse by poor OH

affects fibroblasts promoting protein synthesis and collagen formation

47
Q

What systemic diseases can gingival hyperplasia indicate?

A

Sarcoid

cyclic neutopenia

48
Q

What are the 3 types of traumtic gingival injury - self inflicted>

A

TYPE A - injuries are superimposed upon a pre- existing source of irritation

TYPE B - injuries are secondary to another established habit

TYPE C - injuries are of complex aetiology and are a physical manifestation of an underlying emotional disturbance - resistant to
conventional treatment

49
Q

What acute gingival conditions are common in children?

A

Acute herpetic gingivostomatitis
Necrotising ulcerative gingivitis
Hand, foot & mouth
Herpengina

50
Q

What are the signs and symptoms of acute herpetic gingivostomatitis?

A 
Pyrexia, >39o C
lymphadenopathy
malaise & irritability
profuse salivation
refusal to eat
sore throat & mouth
symptoms for 7-10 days
clinical features:
multiple small irregular ulcers on gingiva, tongue and palate
erythematous gingiva
occasional extra-oral lesions
salivation
lymphadenopathy
recurrence as herpes labialis in 30%
51
Q

What is the management of AHGS?

A 
fluids and soft diet
analgesics and antipyrexics
isolation of eating/drinking utensils
OHI - chlorhexidine and sponges, soft toothbrush
rest
reassurance and review
Not acyclovir (unless immunocompromised)
52
Q

What systemic conditions may present with gingival changes?

A 
HIV
Chrons’ disease
leukaemia
Langerhans’ cell histiocytosis
scurvy
53
Q

What are the clinical features of aggressive periodontal disease in children?

A

Around 0.1% of white Caucasians and 2.6% of black Africans may suffer from localized aggressive forms of periodontitis
Onset around puberty
may present with tooth mobility, drifting or periodontal abscess
rapid periodontal attachment loss, usually incisors and first permanent molars
Often a positive family history
Healthy apart from periodontitis

Amounts of microbial deposits are inconsistent with the severity of destruction
Elevated proportions of A. actinomycetemcomitans and in some populations, P.gingivalis
Phagocyte abnormalities (host defence defects) Hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1β
Progression of attachment loss and bone loss may be self arresting

54
Q

What is NOMA characterised by?

A

Necrosis and ulceration - usually interdental papillae, gingivae bleed profusely, distinctive halitosis

Broad anaerobic infection

can spread rapidly to facial tissues

55
Q

How do you treat NOMA?

A

OH, hydrogen peroxide mouthwash, metronidazole 3 days

56
Q

How would you manage aggressive periodontal disease in children?

A
  • early diagnosis and interventions critical
  • standard mechanical perio therapy - RSD
  • systemic or local drug therapy (metronidazole AND amoxycillin tds 1 week)
  • maintenance therapy
  • periodontal surgery
  • chlorhexidine rinses
57
Q

What systemic or genetic conditions may exacerbate periodontal disease or in which perio is worse?

A 
Insulin-dependant diabetes
Down syndrome
Papillion-lefevre syndrome
Enlers-Danlos syndrome
Langerhans’ cell histocytosis
Neutropenias
Hypophosphatasia
58
Q

What are some of the symptoms of Papillon-Lefevre syndrome?

A

Itchy feet
Loose teeth - bone destruction and resorption of roots
generalised gingival recession
hyperkeratosis of palms and soles

59
Q

What antibacterial substances are in the saliva?

A

Lactoferrin
Thiocynate
Hydrogen peroxide

60
Q

What is the role of the epithelium

A 
1. Surface epithelium shed
together with any attached
bacteria.
2. Permeability barrier
3. Junctional epithelium may be
more permeable than oral
epithelium.
4. Epithelium can stimulate the
inflammatory and immune
response by releasing cytokines
e.g. IL-1
61
Q

What happens to igA as it gets secreted?

A

Turns from monomeric to dimeric form

62
Q

What is IL1?

A

pro- inflammatory cytokine

63
Q

What does GCF contain?

A
  • Complements C1-C9
  • Antibodies - opsonins
  • Contains clotting cascade- fibrin forms a barrier to
    spread of infection;
    thrombin & Hageman factor promote the
    inflammatory response.
    • Kininogens-converted to kinins by proteases.
    Bradykinin- similar to histamine, promotes
    inflammatory response
64
Q

What does c3a and c5a do?

A

vascular changes, stimulate histamine
release, promote formation of leukotrienes &
prostaglandins; attract phagocytes and aid
phagocytosis

65
Q

What does c9 do?

A

membrane attack complex, destroys microorganisms

66
Q

What can bacteria metabolise in the GCF?

A

complement, immunoglobins and other components partly consumed and degraded in the crevice

67
Q

What carbohydrate do neutrophils and macrophages bind to on the bacterium?

A

Manose sugars

68
Q

What is the function of neturophils?

A

Production of NETS- neutrophil extracellular traps. (sheds DNA and throws out like net)
• Kill microbes by antimicrobial peptides and is a signal for other neutrophils
• Neutrophils themselves die in the process

69
Q

What happens to patients with reduced number of neutrophils?

A

Increased priodontal destruction e.g. cyclic neutropenia

defeciency in cathepsin C - papillon lefevre syndrom

  • contribute to perio in diabetes and downs syndrome
70
Q

What can an activatd macrophage do?

A

Phoagocytosis
antigen presentation - stimulate immune response
growth factors - stimulation of fibroblasts + endocthelial cells to promote healing
- secrete cytokines and chemokines to attract inflammatory cells and regulate inflammatory response - secrete Il-1 and TNF

71
Q

What do macrophages do?

A 
Stimulate the immune
response
•Release cytokines
•Phagocytose
•Stimulate healing
72
Q

What can antibodies do for defence?

A 
•Acts as an opsonin
•Activates neutrophil enzyme secretion
•Prevents bacterial attachment
•Activates complement
•Directly inhibits bacterial metabolism
BIND TO SOLUBLE FACTORS
•Neutralises toxins
•Inhibits enzymes
73
Q

What is the cause of tissue damage and bone loss in periodontal disease?

A 
Bacterial products:
- endotoxins - may damage epithelium, fibroblasts
- bacterial enzymes e.g. collagenase, hyaluronidase break
down the connective
tissue
• Lipopolysaccharide,
capsular material,
Peptidoglycans,
muramyl dipeptide,
proteases may cause
bone resorption 
Host products:
• Release of enzymes
from neutrophils
• Complement
• Production on IL-1, IL-6
by macrophages stimulates
bone
resorption & epithelial
proliferation
• Inflammatory mediators, prostaglandins,
other
cytokines, leukotrienes
also stimulate bone
resorption
74
Q

What is the periodontal ligament protected by?

A

Saliva
Epithelium
Inflammatory response
Immune response

75
Q

When does periodontal disease occur?

A

when the balance between destruction and repair in the host response to bacteria is disturbed.
This may be due to alterations in bacterial pathogenicity or the host response.

76
Q

What is the old classification of periodontal diseases called?

A

Armitage 1999

77
Q

What is the Armitage 1999 classification?

A

I. Gingival diseases (non-plaque induced and plaque
induced)
II. Chronic periodontitis
III. Aggressive periodontitis
IV. Periodontitis as a manifestation of systemic diseases
V. Necrotising periodontal diseases
VI. Abscesses of the periodontium
VII. Periodontitis associated with endodontic lesions
VIII.Developmental or acquired deformities and condition.

78
Q

What is the classification of gingival diseases?

A 
- Developmental - Acquired or hereditary
• Infective
• Non-plaque induced or Plaque induced
• Allergic
• Modified by or attributable to systemic factors
• Inflammatory or non-inflammatory
• Traumatic
• Overgrowth (Hypertrophy, hyperplasia, oedema)
79
Q

What are the characteristics of chronic periodontitis?

A

Can be localised or generalised (30% of sites affected)
destruction is consistent with local factors
subgingival calculus is a frequent finding
variable microbial pattern
progression is low but rapid bursts can occur
breakdown of periodontal fibres at cervical margin,
alveolar bone resorption
apical proliferation of junctional epithelium beyond ACJ
Associated with local predisposing factors - overhangs, grooves, crowding
risk factors - genetics, age, gender, smoking, plaque levels, systemic disease (diabetes), stress

80
Q

What are the characteristics of aggressive periodontitis ?

A

Rarer but often severe
rapid attachement loss and bone destruction
possible familial aggregation of disease
patients are systemically healthy, usually non smokers
Onset - earlier age and less than 30 years
amount of plaque out of proportion with severtiy of disease
can be localised (1st molar and incisor involvement)
can be generalised (3 or more teeth involved)
destruction is greater than local factors
suggests elevated levels of aggregatibacter actinomycetemcomitans and prophyromonas gingivalis
- phagocytre abnormalities
attachement and bone loss may be self arresting

81
Q

What are the characteristics of generalised aggressive periodontitis?

A

Severe, generalised form, young adults , 30 years
interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors
episodic nature of destruction of alveolar bone and attachment
1-2% of western pop, increased in afro-carribeans

82
Q

What are the characteristics of localised aggressive periodontitis?

A

Severe, localised
onset around puberty
localised attachement loss of at least 2 permanent teeth one of which is a first molar and involving no more than 2 teeth other than first molars and incisors

83
Q

What systemic conditions can affect the periodontium?

A
  • Acquired neutropenia
  • Leukemias
Down syndrome
• Leukocyte adhesion deficiency syndromes
• Papillon-Lefevre syndrome
• Chediak-Higashi syndrome
• Histiocytosis syndromes
• Glycogen storage disease
• Infantile genetic agranulocytosis
• Cohen syndrome
• Ehlers-Danlos syndrome types IV and VIII
• Hypophosphatasia
84
Q

What are the symptoms of Ehlers-Danlos syndrome types IV and VIII?

A

Hyperflexibility of joints
• Increased bleeding and bruising
• Hyperextensible skin
• Underlying molecular abnormality of collagen
• Type IV – bleeding commoner
• Type VIII – aggressive periodontitis, early onset
• All types – pulp stones

85
Q

What are the symptoms of papillon-lefevre? (oral)

A

• Palmoplantar hyperkeratosis and AP
• Affects 10 and 20 dentition
• Normal dental development until hyperkeratosis
of palms and soles appears
Hyperkeratosis of palms and soles of feet appear in first few years of life.
• Mechanism poorly understood

86
Q

What are the symptoms of downs syndrome?

A

Bradycephaly, mid-face retrusion, small nose, flattened
nasal bridge, upward sloping palpebral fissures
• Macroglossia, delayed eruption of teeth
• Heart defects, atlanto-axial subluxation (C1-C2 disorder
causing impairment in rotation of the neck), anaenia,
increased risk of leukaemia

87
Q

What are the symptoms of Chediak-Higashi syndrome?

A

a rare autosomal recessive disorder that arises from a mutation of a lysosomal trafficking regulator protein, which leads to a decrease in phagocytosis. The decrease in phagocytosis results in recurrent pyogenic infections, albinism and peripheral neuropathy.

Combination of defective neutrophil function,
abnormal skin pigmentation and increased
susceptibility to infection

88
Q

What are the characteristics of Necrotising periodontal diseases?

A
  • NUG and NUP
    • Related to diminished systemic resistance to bacterial infection
    • Destructive inflammatory condition – rapid, debilitating, acute
    • Only differ in terms of tissue affected, with NUP extending into periodontal attachment
  • Painful ulcerated necrotic papillae & gingival margins,
    ‘punched out’ appearance
    • Ulcers with yellow-grey slough
    • Metallic taste, teeth feel wedged, foetor oris
    • Craters – interproximal, loss of crestal bone
    • Loss of attachment can lead to NUP
    • Regional increased LN, fever , malaise can occur
    • Associated with poor OH, stress, smoking
    • Gram –ve anaerobic infection
89
Q

What are the three types of abscesses in the periodontium?

A

Gingival

periodontal

pericoronal

90
Q

What developmental or acquired deformities and conditions associated with the periodontium exist?

A

Localised factors:
Developmental - groove, enamel pearl - difficult to keep clean, attracts calculus
Acquired - root fracture - infection going through this site

-recession
• abnormal gingival contour (incomplete eruption)
• aberrant fraenum

occlusal trauma

91
Q

What are the issues with the old classification?

A

Considerable overlap in disease categories
• Absence of a gingival disease component
• Inappropriate emphasis on age of onset of
disease and rates of progression
• Inadequate or unclear classification criteria

92
Q

What are the goals of periodontal therapy?

A

Restore health/eliminate disease
Improve patient’s quality of life
Clinical goals

93
Q

What is oral health?

A

such a state of health of the teeth and supporting tissues, and of efficiency, as is reasonable to safeguard general health” (General Dental Services Regulations)

94
Q

What are clinical goals of periodontal therapy?

A 
No progression.
Reduction in probing depths.
No probing depth > 5mm.
No bleeding on probing.
No smoking
Plaque score < 20% surfaces.
95
Q

What are factors that can affect the outcome of periodontal treatment?

A 
Susceptibility to disease / genetic factors
Plaque control
Previous periodontal disease
Smoking 
Stress
Some systemic diseases eg diabetes
Diet
96
Q

What are the 4 stages of the periodontal treatment strategy?

A

Initial treatment
Cause-related therapy
Non-surgical treatment
Surgical treatment (0ccasionally)

97
Q

What should initial treatment be based on?

A

Emergency treatment/ relief of pain (where necessary)

Extraction of teeth having a hopeless prognosis

Oral health education / oral hygiene advice

Plaque control including correction of plaque retention factors

Root surface debridement

Initial occlusal adjustment (where necessary)

Reassessment and monitoring

98
Q

What is cause-related therapy?

A

Oral health education and advice on plaque control - this is what has caused the perio/gingivitis

99
Q

What evidence was found to have a small but positive effect on reduction in gingivitis in adults from 2000 article?

A

A single oral hygiene instruction + toothbrush demonstration + scaling - a significant albeit small positive effect on the reduction of gingival inflammation in adults with gingivitis.

100
Q

What non-surgical treatment exists?

A

Removal of plaque retention factors (includes scaling and correction of restoration margins)
Root surface debridement of periodontal pockets ≥4mm) under LA
Review 3 months following the completion of treatment (review oral hygiene at 1 month) - symptoms, risk factors and plaque scores
Further treatment of non-responding sites.

can do it in quadrants or full mouth

101
Q

What are the indications for RSD?

A

≥ 4mm
removal of sub-gingival plaque & calculus
removal of surface toxins (endotoxin etc)
under LA usually
Predominantly ultrasonic

102
Q

What hand instruments are used for scaling?

A

periodontal hoes
files if needed
Langer universal curettes

103
Q

What should you review at 3 months?

A

Plaque scores, probing depths, bleeding indices, mobility scores

104
Q

What are the good and bad outcomes of RSD?

A

Reduced probing depths
Less bleeding
No suppuration
Improved tissue contour

Recession
Increased sensitivity
Other complications

105
Q

For what depths can periodontal treatment cause clinical attachment loss?

A

1-3mm

106
Q

When is periodontal treatment complete?

A

When probing depths are less than or equal to 4/5mm and BoP is less than 30%

107
Q

How would you monitor periodontal disease?

A 
Probing depths
Recession
Plaque control
Inflammation (bleeding)
Mobility
Drifting/migration
Dentine sensitivity
108
Q

What are the limitations of clinical measurements?

A 
Errors in probing depth measurements
Bleeding on probing:
Low sensitivity/specificity
Smoking
Medication
Flow between sites

Absence of bleeding:
Higher sensitivity/specificity

109
Q

What are the limitations of using radiographs to assess perio?

A

Show hard/calcified tissue only
Inter/intra operator variance, angulation
Patient factors, tolerance

110
Q

When would systemic antibiotics be used to treat perio?

A

Aggressive forms of disease

“Refractory” disease

Necrotising forms of periodontal
diseases

Severe disease

Abscesses

111
Q

What periodontal surgery may be carried out?

A

Flap surgery – open flap debridement

Gingivectomy

MDENT110 (26 decks)

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