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4th Year Revision > Periodontology > Flashcards

Periodontology Flashcards

1
Q

What is the criteria for the stages of periodontitis? (4)

A
  • stage 1 <15% bone loss
  • stage 2 coronal third of the tooth
  • stage 3 mid third of the tooth
  • stage 4 apical third of the tooth
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2
Q

What are the features of gingivitis dental plaque induced associated with the biofilm alone? (4)

A
  • no loss of supporting structures
  • rete pegs elongate
  • progressive collagen destruction
  • increase in inflammatory infiltrate
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3
Q

What are the causes of gingival diseases non dental plaque induced? (8)

A
  • genetic/developmental
  • specific infections
  • inflammatory/immune
  • reactive processes
  • neoplasms
  • endocrine, nutritional, metabolic
  • traumatic lesions
  • gingival pigmentation
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4
Q

What is primary occlusal trauma?

A

The effect of abnormal forces acting on a tooth with normal periodontal structures with no attachment loss

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5
Q

What is secondary occlusal trauma?

A

The effect of occlusal forces that may or may not be abnormal on a tooth which has already experienced attachment loss

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6
Q

What is the effect on the periodontal tissues if the force applied is of greater magnitude? (2)

A
  • necrosis of the periodontal ligament with decomposition of cells matrix and fibres occur
  • osteoclasts do not appear on bone surface but resorb bone in the marrow spaces until they reach tissue in the pressure zone
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7
Q

What are the tissue reactions under mild force in pressure zone 1? (4)

A
  • increased vascularisation
  • increased vascular permeability
  • thrombosis
  • osteoclasts on bone surfaces cause bone resorption
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8
Q

What occurs at the tension zone created by normal orthodontic forces causing primary occlusal trauma? (3)

A
  • PDL increases width
  • tooth becomes hyper mobile
  • bone is laid down to regain normal width of the PDL
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9
Q

What occurs when jiggling type forces are applied to the tooth causing primary occlusal trauma? (4)

A
  • increased PDL width around the whole tooth
  • bone resorption
  • tooth becomes progressively mobile
  • reduce bone height
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10
Q

What can occlusal trauma do? (2)

A
  • initiate physiological bone resorption

- may increase the rate of progression of periodontal disease but only in the presence of plaque induced inflammation

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11
Q

How do you make a permanent splint? (2)

A
  • acid etch techniques to place a custom made adhesive splint
  • need a silicone impression
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12
Q

What are the advantages of a permanent splint?

A

Thin, highly polished and comfortable while allowing efficient cleaning

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13
Q

What are the systemic risk factors in periodontal disease? (6)

A
  • genetic factors
  • behavioural
  • environmental
  • endocrine/metabolic
  • life style factors
  • haematological
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14
Q

Name 3 plaque retentive factors

A
  • deficient restorations
  • badly designed dentures and bridgework
  • carious cavities
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15
Q

What is smokings effect on calculus formation?

A

Smoking increases parotid flow which has raised pH, raised calcium concentration and raised precipitation of calcium phosphate thus calcium deposition occurs

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16
Q

What is smokings effect on blood flow? (5)

A
  • vasoconstrictor reducing blood flow
  • impairs the vascularity of periodontal tissues
  • fewer large blood vessels and more smaller blood vessels
  • less gingival redness
  • less bleeding on probing
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17
Q

How does smoking affect the host immune and inflammatory response? (3)

A
  • reduced fibroblast function
  • reduced chemotaxis and phagocytosis of neutrophils
  • reduced IgG immunoglobulin production
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18
Q

What is the result of reduced GcF? (3)

A
  • fewer Igs and other defence molecules
  • reduced microbial nutrients
  • reduced flushing out of the gingival crevice which would usually remove micros and their waste
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19
Q

What are the reasons for reduced pocket depth in non smokers? (3)

A
  • reduction in inflammatory swelling
  • improved tissue resistance
  • small possible gain in attachment
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20
Q

How do you differentiate between periradicular abscess and periodontal abscess?

A

In a periradicular abscess the tooth is non vital due to pulp necrosis and in a periodontal abscess the tooth is vital

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21
Q

What are the clinical features of ANUG? (5)

A
  • necrotic ulcers
  • halitosis
  • spontaneous bleeding
  • metallic taste
  • no systemic symptoms
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22
Q

What are the SDCEP recommendations for treating ANUG? (5)

A
  • use of oral hygiene tips
  • scale
  • 6% hydrogen peroxide or 0.2% chlorohexidine MW
  • review within 10 days and carry out further scaling if required
  • metronidazole 400mg 3 times a day for 3 days
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23
Q

What are the causes of a pocket blockage that can lead to a periodontal abscess? (3)

A
  • untreated periodontal disease
  • inadequate periodontal support
  • foreign body impaction into the pocket
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24
Q

What is the differential diagnosis of a periodontal abscess? (5)

A
  • periradicular abscess
  • perio endo lesion
  • vertical root fracture
  • gingival abscess
  • periocoronal abscess
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25
Q

What are the antibiotics for periodontal abscesses when drainage hasn’t occurred? (2)

A
  • amoxicillin 500mg 3 times a day for 5 days

- metronidazole 400mg 3 times a day for 5 days

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26
Q

What are the clinical features of a primary herpetic gingivostomatitis? (6)

A
  • sudden onset
  • vesicles all over the mouth
  • vesicles burst leaving superficial ulcers wit a grey/yellow base and red halo
  • ulcers coalesce and develop a fibrinous coating
  • cervical lymphadenopathy
  • fever
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27
Q

What are the clinical features of primary herpetic gingivostomatitis in young children? (3)

A
  • irritable
  • profuse salivation
  • refusal to eat
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28
Q

What is the treatment of primary herpetic gingivostomatitis? (6)

A
  • reassurance
  • dietary advice
  • paracetamol
  • chlorohexidine mouthwash
  • review in 1 week
  • if immunocompromised give systemic acyclovir 200mg 5x daily for 5 days
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29
Q

What are the causes of herpes labialise?

A

Reactivation of latent HSV in the trigeminal ganglion

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30
Q

What are the predisposing factors to herpes labialise? (4)

A
  • systemic disease
  • sunlight
  • stress
  • hormonal changes
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31
Q

What are the types of endo periodontal lesions with root damage? (4)

A
  • root fracture or cracking
  • root canal or pulp chamber perforation
  • external root resorption
  • endo periodontal lesions in periodontitis patients
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32
Q

What are the good indicators of prognosis of perio endo lesions? (3)

A
  • single rooted teeth
  • narrow pockets
  • straightforward endo
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33
Q

What are the poor indicators of prognosis of perio endo lesions? (3)

A
  • multi rooted teeth
  • re root treatments
  • unstable periodontal with LOA
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34
Q

What is the role of vitamin C? (3)

A
  • essential for collagen
  • defends against oxidative stress and free radicals
  • promotes chemotaxis
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35
Q

What do you see when there is a deficiency in vitamin C? (4)

A
  • red spots on mucosa
  • pain
  • non healing wounds
  • ulceration
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36
Q

What is the role of vitamin D? (2)

A
  • skeletal development

- modulation of immune system

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37
Q

How much vitamin D do we need a day?

A

100-125 micrograms

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38
Q

What is the definition of obesity?

A

Abnormal or excessive fat accumulation posing a risk to health

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39
Q

What does adipose tissue produce? (3)

A
  • TNF alpha IL6
  • cytokines
  • pro inflammatory mediators
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40
Q

What are the features of over nutrition? (3)

A
  • higher circulating glucose
  • more adipose tissue
  • greater inflammatory drive
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41
Q

What is the risk of periodontitis in patient with diabetes?

A

3x risk of periodontitis

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42
Q

What is the role of refined food/sugar in the inflammatory process? (2)

A
  • high HbA1c

- advanced glycation end products

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43
Q

What are the complications of obesity? (4)

A
  • more tissue makes surface harder to keep plaque free
  • high cho diet favours plaque formation
  • tissue and tongue spread make access difficult
  • safety and comfort in the dental chai
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44
Q

What are the adverse effects of alcohol? (5)

A
  • defective neutrophil function
  • altered clotting mechanism
  • increased bone resorption and decreased bone formation
  • reduced healing
  • direct toxic effect on periodontal tissues
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45
Q

What are the complications of diabetes?

A
  • atherosclerosis
  • retinopathy
  • nephropathy
  • neuropathy
  • impaired wound healing
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46
Q

What is the relationship between poor glycemic control and periodontitis?

A

Evidence suggests a dose dependent relationship between poor glycemic control with both the severity and risk of progression of chronic periodontitis

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47
Q

What are the consequences of diabetes? (4)

A
  • increased formation of advanced glycation end products
  • altered immune cell function
  • altered fibroblast function
  • poor wound healing
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48
Q

What are the consequences of diabetes on immune cell function? (2)

A
  • reduced neutrophil function
  • hyper responsive monocytes and macrophages results in increased secretion of pro inflammatory mediators such as cytokines and prostaglandins
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49
Q

How does diabetes effect fibroblast function? (2)

A
  • gingival fibroblasts produce less matrix and collagen and increase collagenase production
  • increased fibroblast cell death
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50
Q

What is the effect of uncontrolled diabetes on the periodontium? (6)

A
  • hyperglycaemia
  • elevated AGE/RAGE
  • oxidative stress
  • local immune dysfunction and local elevation of pro inflammatory cytokines
  • increased tissue breakdown and reduced tissue repair
  • exacerbation of diabetes periodontitis
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51
Q

What is the effect of periodontitis on diabetes? (3)

A
  • bacteria and bacterial antigens in the bloodstream
  • increased systemic inflammatory state
  • exacerbation of diabetes
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52
Q

What are the types of stress? (4)

A
  • emotional
  • physical
  • behavioural
  • psychological
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53
Q

What are the theories linking psycho social stress and chronic disease? (2)

A
  • psychoneurogenic model

- behaviour orientated model

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54
Q

What are the oral effects of stress? (4)

A
  • decreased salivary flow
  • increased glycoprotein content
  • increase salivary acidity
  • increased levels of stress hormones which reduce gingival blood flow
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55
Q

What is a pregnancy epulis?

A

A localised fibrogranulomatous growth

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56
Q

What changes result in the sensitisation of the periodontal tissues to the presence of plaque bacteria in pregnancy? (2)

A
  • high levels of the hormone progesterone in pregnancy affect the local vasculature
  • progesterone and oestrogen reduce the thickness of the keratin in the gingival epithelium. Therefore is less effective barrier to bacteria
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57
Q

How does puberty effect the gingiva?

A

Increase in steroid hormones results in a temporary increase in gingival inflammation

58
Q

How does the menstrual cycle affect the gingiva?

A

Increased gingival crevicular flow

59
Q

What systemic diseases are possible linked to perio disease? (3)

A
  • diabetes
  • cardiovascular disease
  • adverse pregnancy outcomes
60
Q

What mechanisms link CVD and periodontal disease? (5)

A
  • the common susceptibility model
  • direct bacterial effects on platelets
  • autoimmune responses
  • uptake of bacteria into endothelial cells and macrophages
  • inflammation
61
Q

What is the common susceptibility model linking CVD and periodontal disease?

A

Can inherit a hyper inflammatory monocyte phenotype. When stimulated these monocytes produce excessive amounts of pro inflammatory cytokines

62
Q

How does direct bacterial effects on platelets link CVD and periodontal disease?

A

Certain surface proteins on some oral bacteria mimic the host receptors that trigger thrombus formation within the vascular system. Thus, if these oral bacteria enter the bloodstream they may trigger inappropriate blood clotting leading to MI and stroked

63
Q

How do autoimmune responses link CVD and periodontal disease?

A

Some periodontal pathogens can cause a cross reaction which causes the host to produce antibodies against itself leading to damage to the host cells

64
Q

What mucogingival conditions can you get around natural teeth? (8)

A
  • gingival phenotype
  • gingiva/soft tissue recession
  • lack of gingiva
  • decreased vestibular depth
  • aberrant frenum/muscle position
  • gingival excess
  • abnormal colour
  • condition of the exposed root surface
65
Q

What does cyclic neutropenia result in?

A

Oral ulceration and rapid periodontal destruction associated with periods of low neutrophil numbers

66
Q

What is the appearance of necrotising gingivitis in HIV infections? (7)

A
  • painful red swollen gingiva
  • yellowish greyish marginal necrosis with loss of interdental papillae
  • gingival bleeding
  • halitosis
  • no loss of attachment
  • anterior gingiva mostly affected
  • can progress to NUP leading to severe damage
67
Q

What are the important features of necrotising periodontitis? (4)

A
  • severe deep pain localised to the jaw bone
  • widespread BOP
  • halitosis
  • several independent localised lesions
68
Q

What is the treatment for periodontal disease relating to HIV infection? (4)

A
  • conventional debridement
  • remove necrotic tissue
  • oral metronidazole 200-400mg three times a day for 7 days
  • twice daily 0.12% chlorohexidine mouthwash useful both in active treatment and maintenance
69
Q

What is the dental impact of systemic sclerosis? (2)

A
  • gingival recession common and increased prevalence of periodontitis
  • radiographically increased width of the periodontal ligament and gradual obliteration of the lamina dura
70
Q

What diseases present as desquamative gingivitis? (5)

A
  • lichen planus
  • benign mucous membrane pemphigoid
  • pemphigus vulgaris
  • plasma cell gingivitis
  • erythema multiform
71
Q

What is the treatment for a degree 1 furcation? (3)

A
  • scaling and polishing
  • root surface debridement
  • furcationplasty
72
Q

What is the treatment for a degree 2 furcation? (4)

A
  • furcationplasty
  • tunnel preparation
  • root resection
  • extraction
73
Q

Why do smokers have more gingival recession? (3)

A
  • alteration in immune response
  • reduction in gingival blood flow
  • increase in toothbrush abrasion from smokers trying to remove stain
74
Q

What is millers class I? (2)

A
  • marginal tissue recession not extending to the mucogingival junction
  • no loss of interdental bone or soft tissue
75
Q

What is millers class 2? (2)

A
  • marginal tissue recession extending to or beyond the mucogingival junction
  • no loss of interdental bone or soft tissue
76
Q

What is millers class 3?

A
  • marginal tissue recession extending to or beyond the mucogingival junction
  • loss of interdental bone or soft tissue is apical to CEJ but coronal to the apical extent of marginal tissue recession
77
Q

What is millers class 4?

A
  • marginal tissue recession extending to or beyond the mucogingival junction
  • loss of interdental bone extends to a level apical to the extent of marginal tissue recession
78
Q

What are the consequence of gingival recession? (6)

A
  • dentine hypersensitivity
  • aesthetic concerns
  • root caries
  • tooth abrasion
  • plaque retention
  • fear of tooth loss
79
Q

What is the treatment for recession? (4)

A
  • improve oral hygiene
  • scaling
  • root surface debridement
  • if condition deteriorates mucogingival surgery
80
Q

What does phase 2 cause related therapy do?

A

This phase identifies and controls risk factors for periodontal disease and then begins active therapy

81
Q

What are the sub sections of phase 2 cause related therapy? (4)

A
  • clinical checks
  • discussion of disease with patient
  • advices
  • debridement
82
Q

What are the clinical checks in phase 2? (5)

A
  • caries
  • restoration overhangs/deficiencies
  • furcation involvement
  • sensitivity testing
  • occlusal trauma
83
Q

What advices do you give a patient in phase 2? (5)

A
  • OHI
  • smoking cessation
  • dietary advice
  • dentine hypersensitivity
84
Q

What is the hands on therapy in stage 2? (5)

A
  • extraction of teeth of hopeless prognosis
  • management of faulty restoration margins
  • scaling and polishing
  • root surface debridement
  • treatment of furcation involvements
85
Q

What is involved in phase 4 definitive treatment? (3)

A
  • further RSD
  • periodontal surgery
  • advanced restorative and fixed/removable prosthetic treatment
86
Q

What bacteria are in the red complex? (3)

A
  • porphyromonas gingivalis
  • treponema denticola
  • tannerella forsythia
87
Q

What does proliferation of gingival connective tissue result in?

A

Root resorption

88
Q

What are the causes of treatment failure? (5)

A
  • inadequate plaque control
  • original assessment incorrect
  • inadequate debridement
  • patient is a poor responder
  • inadequate maintenance
89
Q

What are the favourable cases for non surgical periodontal therapy? (6)

A
  • dextrous motivated patients
  • early/moderate disease
  • lack of furcation involvement
  • cleanable restorations
  • non smokers
  • regular attenders
90
Q

When should a patient be referred for surgery? (5)

A
  • deep non responding pockets, >5mm in depth
  • documented consistently excellent plaque control
  • molars especially with furcation involvement
  • persistent bleeding or suppuration
  • treatable and useful teeth
91
Q

What is the half life for a non slow release intra crevicular drug?

A

1 minute

92
Q

What are the advantages of LDAs? (6)

A
  • site specific
  • locally high concentrations
  • prolonged exposure with slow release systems
  • lower systemic side effects compared with systemic antimicrobial agents
  • high patient compliance
  • lower risk of super infection
93
Q

What is the active ingredients in LDAs? (2)

A

Antimicrobial- tetracycline

Antiseptic- chlorohexidine

94
Q

What are the effects of tetracyclines? (2)

A
  • broad spectrum bacteriostatic antibiotic

- host modulation effect

95
Q

What are the LDA products on the market? (2)

A

Antimicrobial slow release gels- dentomycin and adjusan

Antiseptics- periochip and chlo site

96
Q

What type of drug is dentomycin?

A

Biodegradable 2% minocycline gel

97
Q

How long does dentomycin produce its MIC?

A

12-24 hours

98
Q

How do you use dentomycin?

A

Apply 3-4 applications at 14 day intervals

99
Q

What is in adjusan?

A

Biodegradable doxycycline gel

100
Q

Why are antiseptic systems better than antimicrobial gels?

A

Antiseptic systems are better than antimicrobial gels as these products are based on chlorohexidine therefore there is no risk of bacterial resistance

101
Q

What is the active component of periochip?

A

2.5mg chlorohexidine gluconate

102
Q

How long does it take periochip to biodegrade?

A

7-10 days

103
Q

What are the advantages of periochip? (2)

A
  • no bacterial resistance

- no staining of teeth

104
Q

What are the disadvantages of periochip? (2)

A
  • can only treat one site per chip

- relatively expensive

105
Q

What are the phases of release of chlorohexidine in periochip?

A

Initial burst effect of chlorohexidine in first 24 hours and then constant slow release over the next 7 days

106
Q

What forms of chlorohexidine does chlo site contain? (2)

A
  • 0.5% chlorohexidine digluconate which lasts 7 days

- 1% chlorohexidien dihydrochloride which lasts 7-15 days

107
Q

What are the problems with LDA? (3)

A
  • expensive with little evidence of long term benefits
  • potential of re infection by bacteria from untreated sites
  • safety issues (bacterial resistance, interaction with other medications, allergy and medical contra indications)
108
Q

When should you not use systemic antimicrobials in periodontology? (3)

A
  • gingivitis
  • periodontitis
  • non responding cases
109
Q

When can you use systemic antimicrobials? (4)

A
  • NG and NP
  • some cases of aggressive periodontitis
  • immuno compromised patients
  • periodontal abscess
110
Q

What systemic antibiotics do you give?

A

Combined amoxycillin 250mg capsules and metronidazole 400mg tablets both 3 times a day for 7 days

111
Q

What are the disadvantages of systemic antimicrobial treatment? (5)

A
  • hypersensitivity
  • bacterial resistance
  • drug interactions
  • super infections
  • poor compliance
112
Q

What is periostat and what is in it?

A

Tetracycline at such a low dose it is not acting as an antibiotic
20mg doxycycline hyclate

113
Q

What are the instructions for taking periostat? (3)

A
  • twice daily orally
  • 1 hour before food
  • 3 month treatment periods
114
Q

What are the functions of periostat? (3)

A
  • reduces collagen breakdown
  • promotes repair and healing
  • inhibits disease and progression
115
Q

What are the contraindications for the use of periostat? (3)

A
  • allergy to tetracyclines
  • pregnancy/breast feeding
  • children <12 years old
116
Q

What drugs do periostat interact with? (3)

A
  • warfarin
  • penicillin
  • photosensitivity
117
Q

How long does it take the dentinal surface to recover from acidic challenge?

A

2-7 hours

118
Q

What are the causes of dentine hypersensitivity? (6)

A
  • damaging tooth brush technique
  • poor oral hygiene
  • periodontal treatment removing dentine exposing tubules
  • dietary acids
  • excessive occlusal forces
  • physiological reasons such as over eruption of teeth leading to exposed root surfaces
119
Q

What are the dentine hypersensitivity preventative measures? (5)

A
  • reduction of dietary acid
  • non damaging brushing technique
  • timing of tooth brushing
  • use of de sensitising toothpaste
  • not rinsing after brushing
120
Q

What is nova min?

A

Calcium sodium phosphosilicate which is a particular bioactive glass composition

121
Q

What is the action of nova min? (3)

A
  • nova min reacts with saliva to release sodium ions
  • then binds to dentine and release calcium and phosphate which then form a layer within the dentinal tubules
  • this new layer is resistant to physical removal and is harder than the original exposed dentine
122
Q

What desensitising agents do you get in home products? (3)

A
  • CDP
  • arginine calcium carbonate
  • fluorides
123
Q

What do oxalates do?

A

Potassium oxalate chemically reacts with the calcium inside the tubules to form insoluble calcium oxalate crystals and block fluid flow

124
Q

What is the stepwise approach for dentine hypersensitivity? (3)

A
  • sensitivity toothpaste and preventative advice
  • once daily mouthwash at a separate time to brushing
  • review diagnosis
125
Q

What substances occlude tubules and treat localised dentine hypersensitivity? (3)

A
  • resins
  • glass ionomers
  • fluoride varnishes
126
Q

What are the histological characteristics of implant health? (3)

A
  • no cementum or periodontal ligament
  • peri implant epithelium zone longer
  • connective tissue does not have insertion fibres
127
Q

What is the microflora of peri implantitis (5)?

A
  • gram -ve anaerobes
  • p gingivalis
  • bactericides forsythias
  • p intermedia
  • fusobacterium nucleatum
128
Q

What other factors can cause peri implantitis? (4)

A
  • presence of cement
  • excessive occlusal force
  • poor positioning
  • bone necrosis
129
Q

How do you diagnose peri implantitis? (3)

A
  • BOP and/or suppuration
  • probing depths >6mm
  • bone levels >3mm apical to the most coronal portion of intraosseous part
130
Q

What is the chemical adjunct for the debridement of implants?

A

0.2% chlorohexidine gluconate bd for 3-4/52

131
Q

What can you use for the debridement of implants? (3)

A
  • vector system with carbon fibre tip
  • implant derider
  • ultrasonic with plastic tips
132
Q

What are the symptoms of a cracked tooth?

A

Patient has sharp, shooting pain on biting with it being sensitive to thermal, sweet and acidic foods. It can be difficult to localise

133
Q

What are the types of tooth cracks? (5)

A
  • craze lines
  • fractured cusp
  • cracked tooth
  • split tooth
  • vertical root fracture
134
Q

What are the true contraindications to root canal treatment? (4)

A
  • insufficient periodontal support
  • caries of root
  • vertical root fracture
  • condition of the remaining dentition
135
Q

What are the contents of the root apex? (4)

A
  • accessory canals
  • pulp stones
  • irregular secondary dentine
  • lack of dentinal tubules
136
Q

What are the injection techniques beside infiltration and block? (4)

A
  • PDL anaesthetic injection
  • intraosseous injection
  • intrapulpal injection
  • computer controlled anaesthetic
137
Q

What are the types of intra osseous injections? (2)

A
  • stabident

- x tip

138
Q

How do you do an intra osseous injection?

A

The cortical bone is perforated by creating a small hole between the roots of the teeth using a special rotary instrument, light pecking motion

139
Q

What is the duration for a PDL anaesthetic injection?

A

30-45 minutes

140
Q

What is the duration for a intraosseous injection?

A

60 mins with a vasoconstrictor

4th Year Revision (12 decks)

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