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Finals > Periodontology > Flashcards

Periodontology Flashcards

1
Q

What does a healthy gingivae look like clinically?

A
  • Coral/light pink in colour
  • Stippling
  • Knife-edge margins
  • Gingival groove
  • Pappilae fill space exactly
  • No BOP
  • Distinct demarcation
  • Good OH
  • Pockets ≤ 3mm
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2
Q

What is the histopathology of clinically healthy gingivae?

A
  • Little inflammatory infiltrate - mainly neutrophils - migrate through the JE to the gingival sulcus to address plaque biofilm
  • Small amount of GCF present
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3
Q

What are the 2 main types of risk factors involved in periodontitis?

A

Local and systemic

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4
Q

What are systemic risk factors?

A
  • Factors that affect the host response to the plaque biofilm, upsetting the host-microbial balance
  • Coming from within the body
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5
Q

What are examples of systemic risk factors?

A
  • smoking
  • diabetes
  • Age
  • Stress
  • Nutrition
  • Medications/immunocompromised
  • Genetics
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6
Q

What are local risk factors?

A
  • Factors local to the oral cavity, which may influence plaque accumulation or occlusal forces
  • Coming from within/around the mouth
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7
Q

What are examples of local risk factors?

A
  • Calculus
  • Lone standing molars
  • Tooth position
  • Anatomical features
  • Restorations
  • Xerostomia
  • Malocclusion
  • Ortho appliances/dentures
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8
Q

What are the clinical signs and symptoms of gingivitis?

A
  • erythema
  • oedema
  • bleeding
  • papillae over fill ID spaces
  • loss of stippling
  • rolled swollen margins
  • loss of obvious demarcation
  • plaque often seen at gingival margin
  • probing depths may increase due to swelling and false pocketing
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9
Q

what is the histopathology of gingivitis?

A
  • more inflammatory cells
  • increased GCF flow
  • reduction in number of fibroblasts
  • reduction in collagen
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10
Q

What are the 4 periodontal lesions?

A

initial lesion
early lesion
established lesion
advanced lesion

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11
Q

What is the name of classification used to grade tooth mobility?

A

Millers mobility index

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12
Q

What does Class 0 represent in the millers classification?

A

Normal (physiologic) movement when force is applied, <0.2mm

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13
Q

What does Class I represent in the millers classification?

A

Mobility greater than psycholgic, >0.2mm, <1mm

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14
Q

What does Class II represent in the millers classification?

A

Tooth can be moved up to 1mm or more in a lateral direction (buccolingual or mesiodistal), inability to depress the tooth in a vertical direction (apicocoronal), >1mm

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15
Q

What does Class III represent in the millers classification?

A

Ability to depress the tooth in a vertical direction

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16
Q

What classification is used to grade furcation?

A

HAMP et al

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17
Q

What is Grade 1 furcation?

A

Probe goes <1/3 of the way through

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18
Q

What is Grade 2 furcation?

A

Probe goes >1/3 of the way through but not all the way through

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19
Q

What is grade 3 furcation?

A

Probe goes all the way through

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20
Q

What are the concerns of furcation?

A
  • Difficult to clean
  • Abscesses can form - there are accessory canals in furcation area and bacteria can travel in and out
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21
Q

What does BPE stand for?

A

Basic Periodontal Examination

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22
Q

What screening tool is used to carry out a BPE?

A

WHO (World Health Organisation) probe

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23
Q

What does a BPE code 0 mean?

A

Healthy gingivae

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24
Q

What does a code 1 BPE score mean?

A

BOP

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25
Q

What does a code 2 BPE score mean?

A

Plaque retentive factor

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26
Q

What does a code 3 BPE score mean?

A

Pocket depth - first black band is partially visible, (>3.5mm,<5.5mm)

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27
Q

What does a code 4 BPE score mean?

A

Cant see the first black band, >5.5mm

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28
Q

What does * mean on a BPE

A

Furcation involvement

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29
Q

What is the tx for a code 1 BPE?

A

OHI

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30
Q

What is the tx for a code 2 BPE?

A
  • OHI
  • Removal of plaque retentive factors
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31
Q

What is the tx for a code 3 BPE?

A
  • Initial therapy
  • OHI
  • PMPR
  • Review OH after 12 wks, if no improvement do 6PPC of the areas with code 3 and carry out RSD on pockets ≥ 4mm
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32
Q

What are the 5 tootbrushing techniques?

A
  • Modified bass technique
  • Mini scrubb
  • Stillman
  • Roll technique
  • Charter brushing method
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33
Q

Describe the modified bass tehcnique

A
  • Most recommended brushing tehcnique
  • Place brush at a 45 degree angle to the gum line
  • Brush each tooth using a gentle circular movement
  • When finished flick the toothbrush down the root away from the gum line
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34
Q

Describe the stillman brushing method

A
  • Similarly to the bass method the stillman places bristles at a 45 degree angle in relation to the tooth
  • This method makes more effort to massage the gum tissue simultaneously
  • Great for massaging and stimulating the gingival tissue but less effective at removing plaque below the gum line.
  • Can be more risky for causing injury to gums if gentle motions not used
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35
Q

Describe the charter brushing method?

A

Brush is held at a 45 degree angle towards the chewing side of the teeth as opposed to being angled towards the gum line

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36
Q

Describe the mini scrub method

A
  • Often the standard method used to clean teeth
  • Rigorous vertical and horizontal motions on every surface of your teeth
  • Can lead to recession of the gums when too much force is used while brushing
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37
Q

Who came up with the bacteria complexes involved in the initiation and progression of periodontal disease?

A

Socransky

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38
Q

Which coloured complexes are most involved in periodontal disease?

A

Orange and red

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39
Q

What are the 3 bacterias in the red complex?

A
  • Porphyromonas gingivalis
  • Tannerella forsythia
  • Treponema denticola
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40
Q

What are the bacterias in the orange complex?

A
  • Fusobacterium nucleatum
  • Prevotella intermedia
  • Treponema vincentii
  • Aggregataebacter actinomycetemcomitans
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41
Q

What does NG stand for?

A

Necrotising gingivitis

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42
Q

What does NG look like?

A

The tips of the gums between the teeth appear punched-out and become sores (ulcers) covered with a gray layer of dead tissue

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43
Q

What are the signs and symptoms of NG?

A
  • Pain
  • BOP
  • Inflamed gums
  • Foetor oris
  • Metallic taste in mouth
  • Pseudomembranous slough - that can be removed
  • Loss of id papillae
  • Raised temp
  • Lymphadenopathy
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44
Q

What are the risk factors for NG?

A
  • Stress
  • Smoking
  • Immunocompromised
  • Poor OH
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45
Q

What is the treatment for NG?

A
  • Metranidazole, 3 days, 400mg, 3 times a day
  • USS to disturb the bacteria- cavitational effect- bubbles of oxygen kill bacteria
  • OHI
  • Smoking cessation
  • Address the stress
  • Review in 7-10 days
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46
Q

What is the bacteria involved in NG?

A
  • Fusobacterium nucleatum
  • Treponema vincentii
  • Prevotella Intermedia
  • Treponema denticolli
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47
Q

What does smoking do to the oral cavity?

A
  • Contributes to oral cancer
  • Reduces blood supply - vasoconstriction
  • Causes dry mouth
  • Masks effects of perio disease - less BOP
  • Reduces number of host cells (neutrophils and macrophages) and their ability to be mobile
  • Soft tissues can be pallor
  • Hyper keratosis
  • Damage fibroblasts - loss of collagen - loss of elasticity in the tissue
  • good healing is less likely post tx
  • increases production of inflammatory cytokines enhancing tissue breakdown
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48
Q

What are the 2 cells most worried about smoking affecting?

A
  • Neutrophils
  • Fibroblasts
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49
Q

What are the clinical signs of a smoker?

A
  • causes dry mouth
  • more calculus present
  • plaque
  • less BOP
  • staining
  • more/deeper pocketing
  • halitosis
  • more tooth loss than a non smoker
  • more alveolar bone loss
  • more vertical defects
  • refractory response to NSPT
  • impaired healing
  • hyperkeratosis
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50
Q

What does smoking do to the oral acvity?

A
  • Reduces gingival blood flow
  • Impairs white blood cells function
  • Impairs wound healing
  • increases production of inflammatory cytokines enhancing tissue breakdown
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51
Q

How do you work out a smokers pack years?

A

Number of packs you smoke per day x Number of years you have smoked

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52
Q

What are some examples of medical conditions affecting the periodontium?

A
  • Diabetes
  • Asthma
  • HBP
  • Epilepsy
  • Pregnancy
  • Leukamia
  • Bleeding Disorders
  • CVD
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53
Q

How does diabetes affect the periodontium?

A
  • slow healing process
  • pt at higher risk of disease/severe disease
  • if disease is not well controlled it will lead to higher blood sugar levels (glucose) in the fluids in the mouth, this promotes the growth of bacteria that contributes to disease
  • poorly controlled diabetes is associated with poorer response to perio treatment (impaired healing)
  • ^ only in poorly controlled diabetes
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54
Q

How does asthma affect the periodontium?

A
  • Candidiasis
  • Dry mouth from inhaler
  • Antifungals used to treat
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55
Q

How does HBP affect the periodontium?

A

Patients who take calcium channel blockers such as amlodipine can be prone to gingival englagement

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56
Q

What drugs can induce gingival enlargement?

A

calcium channel blockers - nifedipine, amlodipine. verapamil, diltiazem
antiepeleptic drugs - phenytoin, sodium valproate
Immunoregulators - cyclosporine

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57
Q

How does epilepsy affect the periodontium?

A

patients who take fenytoine can be at risk of gingival enlargement due to it stimulating fibroblasts to lay down collagen

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58
Q

What periodontal problems may a pregnant lady suffer from?

A
  • Gingivitis - progesterone causes vasodilation, and the reaction to plaque becomes an exagerrated response
  • Prengnancy Epulus - pyogenic granuloma appears in the oral cavity. Usually related to crowidng/rotated teeth and filling overhangs. It is a non-neoplastic, reactive gingival overgrowth occurring due to the influence of female sex hormones.
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59
Q

How does Leukaemia affect the periodontium?

A
  • Infiltration of the gingival tissue with leukaemia cells can cause gingival enlargement
  • ulcerations
  • spontaneous bleeding
  • oral mucosa pallor
  • chemotherapy can cause vomiting and oral mucositis
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60
Q

How does CVD affect the periodontium?

A
  • The bacteria that infect the gums and cause gingivitis/perio disease also travel to blood vessels elsewhere in the body where they can cause blood vessel inflammation and damage
  • The body’s immune response - inflammation - can set off a cascade of vascular damage throughout the body, including the heart and brain
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61
Q

How does HIV effect the periodontium?

A
  • dry mouth
  • hairy leukoplakia
  • weaker immune system - gum disease will be more severe and progress more rapidly
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62
Q

how do bisphosphonates effect the periodontium?

A
  • may reduce bone turnover and bone blood supply and lead to death of bone (osteonecrosis)
  • dead bone may show through the gum after an extraction
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63
Q

How does radiotherapy of the head and neck effect the periodontium?

A
  • xerostomia
  • salivary gland dysfunction
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64
Q

What is palliative care?

A
  • The study and management of patients with active, progressive, far-advanced disease in whom the oral cavity is compromised either by the disease directly or by its treatment
  • The pt can’t imporve their OH anymore or there wont be a good result from invasive care
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65
Q

What is a gingivectomy?

A

Gingivectomy is surgery to remove excess or overgrown gum tissue (gingiva)

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66
Q

What is a gingival graft?

A

Gum graft surgery is a dental procedure for treating thinning gums or gum recession. Gum grafting covers exposed teeth roots and adds volume to your gum line, improving overall oral health

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67
Q

What is furcation plasty therapy?

A

The dissection and elevation of a soft tissue flap. – to obtain access.

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68
Q

What is flap surgery?

A

The primary purpose of flap surgery is to remove or decrease the pocket. A flap-like incision in the gum tissue is created to access the pocket. This makes it possible to remove the diseased tissue from the pocket and adequately clean the root surfaces of the teeth, which aids in the removal of toxic plaque and tartar.

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69
Q

Why do PMPR on pockets ≥ 4mm (RSD)

A
  • Render root surface biologically compatible with healing
  • Reduce pocket depths and bleeding
  • Recession (not true) - gingival shrinkage - loss of ID papillae
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70
Q

How does the healing process after carrying out RSD work?

A
  1. within 24-48 hrs there is signs of acute inflammation - redness swelling, pain, heat, loss of function
  2. Over 1-12 wks new attachment of LJE. There is a decrease in inflammatory cell infiltrate therefore a decrease in redness, bleeding and swelling. There is an increase in fibroblast number and activity, increases collagen, increasing elasticity of the tissue and tightening the gingival cuff. Tightening of the gingival cuff and the LJE + shrinkage
  3. Why3/12? - granulation tissue in pocket - do not probe this, is like jelly, will break
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71
Q

What tissue do you not want to probe for 12 wks before its fully formed?

A

granulation tissue

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72
Q

Why might RSD not work?

A
  • Medical conditions
  • Poor OH
  • Smoker
  • Immunosuppressed
  • Clinician hasnt removed it all
  • OHI wasnt suffice
  • teeth may have hopeless prognosis
  • Original assessment/diagnosis incorrect
  • Inadequate maintenance
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73
Q

What to do next if RSD fails?

A
  • Repeat RSD
  • Get a specialist opinion - surgical tx
  • Chemical adjuncts
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74
Q

What are chemical adjuncts?

A

Given to areas that persisently will not heal post RSD tx

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75
Q

Name 2 examples of chemical adjuncts

A
  • Antiseptics - chlorohexidine
  • Antibiotics - would need to be prescribed for us
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76
Q

Name 2 types of USS scalers

A
  • Piezo electronic
  • Magnetostrictive
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77
Q

How does the magnetostrictive USS work?

A
  • Conduction through nickel stacks
  • allows an eliptical movement pattern of the working tip (both sides)
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78
Q

How does the piezoelectric USS work?

A

Small currents of electricty are used to alter the dimensions of quartz crystals which produces the vibration effect
back and forth movement

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79
Q

What are the 3 modes of action of the USS

A
  • Mechanical abrading action
  • Cavitational effects
  • Acoustic streaming
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80
Q

What is the mechanical abrading action?

A

Where the mixture of back, forth and ciruclatory movements of the woring tip mechanically abrades and chips away at the calculus deposits on the tooth surface

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81
Q

What is cavitational effects?

A
  • Produced onlu by the USS due to their high energy output
  • The coolant water contains air bubbles which are expanded by the energy at the vibrating tip, causing them to implode, thus releasing shock waves
  • These shock waves remove calculus and plaque biofilm
  • the air bubbles also release oxygen which kills anaerobic bacteria
82
Q

What is acoustic streaming?

A
  • All mechanicals scalers set up vigorous movements of water and around their tips known as acoustic streaming
  • This helps to remove some of the tooth surface deposits and disrupt plaque colonies
  • water flow flushes out debris
83
Q

What is supportive periodontal therapy/maintenance therapy?

A

Following completion of treatment and arrest of inflammation, supportive periodontal therapy is employed to reduce the probability of re‐infection and progression of the disease; to maintain teeth without pain, excessive mobility or persistent infection in the long term, and to prevent related oral diseases.

84
Q

What is the order of diagnosis?

A

Extent of disease - gen, loc
Type of disease - ging, perio
Stages - bone levels
Graded - % bone loss/pt age
Stability of disease
RF

85
Q

what is pericoronitis?

A

Partially erupted teeth - operculum - plaque gets trapped under - inflammation/infection
usually effecting wisdom teeth

86
Q

what is the aetiology of a periodontal abscess?

A

bacteria blocked in pocket - e.g. calculus, food, scaling

87
Q

what are the clinical signs and symptoms of a periodontal abscess?

A
  • rapid onset
  • spontaneous pain
  • TTP
  • pus formation
  • swelling
  • deep periodontal pocket
  • sensibility testing normal response
  • existing perio can be a RF
88
Q

What is the management of a periodontal abscess?

A
  • drainage
  • +/- antibiotics
  • scaling/PMPR
  • review
89
Q

What is the aetiology of acute herpetic gingivostomatitis?

A

Herpes simplex virus (HSV - 1)

90
Q

What are the clinical signs and symptoms of acute herpetic gingivostomatitis?

A
  • Generalised erythema
  • pain
  • all over mouth
  • vermillion border
  • ulceration ( yellow)
  • lymphadenopathy
  • fever
  • malaise
91
Q

What is the management of acute herpetic gingivostomatitis?

A
  • Analgesia - e.g. paracetamol (it’s viral not bacterial infection)
  • control temperature
92
Q

What are the complications of acute herpetic gingivostomatitis?

A
  • virus lies dormant in trigeminal ganglion
  • can be reactivated easily (clinically herpes labialis)
  • reactivated by stress, immunocompromised
  • exposure to UV light
93
Q

What is mechanical plaque control and list examples?

A

the removal of dental plaque on a regular basis and the prevention of its accumulation on the teeth and adjacent gingival surfaces
- Toothbrushing
- ID cleaning
- chemical agents
- PMPR

94
Q

What are the methods of chemical plaque control?

A
  • toothpaste
  • mouthwashes
  • antibiotics
95
Q

What are the 2 most important ingredients in tooth paste?

A
  • fluoride
  • triclosan - antimicrobial properties
96
Q

What mouthwashes can be used as chemical adjuncts?

A
  • chlorohexidine
  • phenol
  • oxidising
97
Q

what are the advantages and disadvantages of chlorohexidine mouthwash?

A

Advantages:
* antiseptic and disinfecting agent - helps with mouth infections, ulcers, gum disease
* reduces number of bacteria in mouth
Disadvantages:
* staining
* alters function of taste buds
* associated with calculus formation
* can affect efficiency of salivary glands

98
Q

What are the advantages and disadvantages of phenol mouthwash?

A

Advantages:
* slight antibacterial function - very short lasting
* cosmetic mouthwash - fresh breath
Disadvantages:
* using after brushing will wash Fl away
* Increasing alcohol content consumption in the mouth will increase the risk of oral cancer

99
Q

What are the advantages and disadvantages of oxidising mouthwash?

A

Advantages:
* cavitational effect which kills GNABs
* Good for patients with NG
Disadvantages:
* contains hydrogen peroxide which can increase sensitivity in teeth

100
Q

What antibiotics are commonly used as chemical adjuncts?

A

Tetracycline, metronidazole, doxycycline and amoxicillin

101
Q

What is the sequence of RSD tx?

A
  1. Pre USS - disrupt biofilm and break up large calculus deposits
  2. hand scale - fine tuning
  3. post USS - flush debris
102
Q

What type of patient is maintenance therapy for?

A

stable periodontitis patient

103
Q

In 3/12 post RSD what three outcomes may there be?

A

Stability
Partly responsive
Non responsive

104
Q

What is RSD?

A

Root Surface Debridement
* the removal of subgingival plaque and calculus deposits and ideally removing the bacterial toxin contaminated cementum whilst retaining the healthy cementum layer on the root surface
* leaving the cementum promotes regeneration of the periodontal tissues

105
Q

What is the criteria to carry out RSD?

A
  • True pockets 4mm or >
  • BOP and presence of subgingival calculus
  • adequate OH
106
Q

What is gingival shrinkage?

A
  • shrinkage occurs following periodontal therapy (when inflammation resolves and the gingival cuff tightens pulling the gums in an apical direction) so the whole gingivae shrinks back
  • shrinkage causes the ID papillae to be lost
107
Q

What is genetic susceptibility?

A
  • susceptibility describes an individuals host response to plaque
  • it varies greatly and is unique to each person
  • is determined by the level of disease and patients age
  • some people with severe disease have genetic factors that affect the immune factor interleukin - 1 (IL-1), a cytokine involved in the inflammatory response
108
Q

what is the dose of metronidazole?

A

400mg, 3-5 days, 3 times a day

109
Q

what is the dose of doxycycline?

A

can only be given as a perio subdose
3, 6, 9, 12 months at a time depending on severity
to avoid antibiotic Resistance

110
Q

what is palliative care?

A

patient cant improve their OH anymore or there wont be a good result

111
Q

when do you recall patients in the maintenance phase?

A

tailored to every individual, anywhere from 3-12 mths

112
Q

What cells are predominantly involved in acute inflammation?

A

Neutrophils

113
Q

What cells are predominantly involved in chronic inflammation?

A

Lymphocytes
Plasma cells
Macrophages

114
Q

What are the signs and symptoms of acute inflammation?

A

Redness
Swelling
Heat
Pain
Loss of function

115
Q

What are the signs and symptoms of chronic inflammation?

A

Persistent swelling
Redness
Mild or intermittent pain
No heat
No fever
No pus formation

116
Q

What is gingival crevicular fluid?

A
  • fluid found flowing from the JE into the gingival crevice
  • contains plasma proteins, antibodies and neutrophils
  • carries inflammatory cells to challenge bacteria
  • maintaining the structure of junctional epithelium and the antimicrobial defense of periodontium.
117
Q

How do you calculate LOA and what does this show you?

A

pocket depth + reccesion
shows disease progression/improvement, fixed point

118
Q

What are PDL fibres called?

A

Sharpey’s fibres

119
Q

what happens during periodontal breakdown?

A
  • apical migration of the je caused by damage to underlying PDL fibres
  • loss of collagen fibres due to fibroblast damage
  • loss of surface cementoblasts
  • resorption of alveolar bone - osetoclastic action - osteoclasts are present on surface of the bone and initiate bone resorption
  • secretion of host resorption factors from immune cells as well as osteoblasts, fibroblasts and endothelial cells
120
Q

several models have been proposed to describe the rate of periodontal disease progression, what are they?

A

continuous model - suggests that disease progression is slow and continuous, with affected sites showing a constantly progressive rate of destruction throughout the duration of the disease.
random burst model - proposes that periodontal disease progresses by short bursts of destruction followed by periods of no destruction. This pattern of disease is random with respect to the tooth sites affected and the chronology of the disease process.
asynchronous burst model - suggests that periodontal destruction occurs around affected teeth during defined periods of life and that these bursts of activity are interspersed with periods of inactivity or remission. The chronology of these bursts of disease is asynchronous for individual teeth or groups of teeth.

121
Q

what are the 3 proposed parts to the burst theory?

A
  1. gingivitis does not always inevitably lead to periodontal breakdown
  2. periodontal breakdown does not occur gradually and continuously
  3. pattern of destruction varies greatly between individuals and even in the same person over time
122
Q

why do we do a 6PPC?

A
  • helps guide tx
  • monitors improvement/deteriroation
  • allows LOA to be measured
  • Motivation for pt
123
Q

How do we screen for periodontitis?

A
  • risk assessment
  • probing (up to 3mm is healthy)
  • radiographs
124
Q

what is considered clinical gingival health?

A

<10% BOP

125
Q

What is taken into consideration when doing a diagnosis?

A

history
radiographic findings
pocket depth in detail (6ppc)
BOP or abscence in smokers

126
Q

What is required for a patient to be stable?

A

BOP < 10% overall and lack of bleeding at 4mm sites and no >4mm pockets

127
Q

what is required for a patient to be in remission?

A

BOP >10%, no bleeding at 4mm sites

128
Q

what is required for a patient to be unstable?

A

pockets of 5mm or more OR bleeding at sites of 4mm or deeper

129
Q

what is recession?

A

inflammation free condition = apical retreat of periodontium
ID papillae is at normal level
Teeth are never lost due to true recession

130
Q

What causes recession?

A

Incorrect TB technique
Quality of bone (fenestration and deniscence)
facitious injury
frenum pulls
ortho tx
excessive periodontal scaling
parafunction

131
Q

What are the problems with recession?

A
  • dentine hypersensitivity
  • root caries
  • toothbrush abrasion
132
Q

how do we treat recession?

A

modify tb technique
eliminate areas of mild chronic inflammation - replace faulty restoration margins
frenectomy
gingival grafts
tx hypersensitivity - fluoride, desensitising agents

133
Q

What roots on maxillary first premolars should be checked for furcation

A

2 roots (distal, mesial)

134
Q

where should be probed on maxillary to check for furcation?

A

3 roots (distal, mesial, buccal)

135
Q

Where should be checked on mandibular molars for furcation?

A

2 roots (buccal and lingual)

136
Q

Why does furcation reduce the prognosis of a tooth?

A
  • difficult to clean - more difficult to control disease in area
  • loss of vitality may occur due to accessory canals running from pulp chamber into furcation area - these act as a conduit for bacteria and their products
137
Q

How do we monitor furcations?

A

vitality testing should be carried out annually due to prognosis - use ethyl chloride, electric pulp test
regrade every 6/12 or 12/12 check up appt

138
Q

what is a furcation plasty?

A

bur used to widen lesion making it easier to clean

139
Q

what is a tunnel prep?

A

open furcation all the way up and make a grade 3

140
Q

what is root resection?

A

one root is cut off and removed therefore no furcation lesion to worry about

141
Q

what OHI should you give a furcation patient?

A
  • make pt aware of where furcation involvement is
  • explain why important to pay attention when cleaning the area
  • use single tufted, tepes etc
142
Q

what is the treatment for dentine hypersensitivity?

A

prevention - acid in diet? advise not to brush immediately after eating
remove cause if possible
occlude tubules e.g. sensodyne (K ions), desen
insulative restoration
may have to devitalise tooth

143
Q

what are the list of desensitising agents?

A
  • sodium fluoride
  • stannous fluoride
  • sodium monofluorophosphate
  • calcium hydroxide
  • strontium chloride
  • formaldehyde
  • resins and adhesives (seal and protect)
144
Q

what are the 5 As of smoking cessation?

A

Ask pt if they use tobacco
Advise on the benefits of quitting
Assess willingness to quit
Assist in quit attempt
Arrange follow up appt

145
Q

What are the 5 Rs in smoking cessation?

A

Relevance
Risks
Rewards
Roadblocks (stress, mental health etc)
Repetition

146
Q

what type of intervention do we do in dentistry with smokers?

A

brief
opportunistic way of appraching smoking cessation advice - almost a causal reference
should not last > 5 mins

147
Q

what are the types of nicotine replacement therapy (NRT)

A
  • patches
  • lonzenges
  • gum
  • inhalator
  • microtabs
  • nasal spray
  • e cigarettes
148
Q

what are non-nicotine products patients may use to help them quit?

A
  • champix
  • dummy cigarettes
  • complimentary therapy
  • hypnosis
  • diet and excercise
149
Q

what are the BPE guidelines for children?

A
  • from 7 onwards
  • only 6 teeth checked, UR6, UR1, UL6, LL6, LL1, LR6
  • 7-11 only check for BPE 0,1 and 2 as false pocketing can be a problem
  • 12-17 full range of BPE scores on the 6 teeth above
150
Q

how much force should be applied with a screening probe?

A

20-25g
parallel to long axis of tooth

151
Q

what is the main aim of palliative care?

A

to slow the disease down while attempting to keep patient comfortable with a functioning dentition

152
Q

what is the tx for a patient in palliative care?

A
  • s and p every 2-3wks
  • advise pt that in event of problem arising with a tooth on palliative care i.e. excessive mobility, abscess formation, extraction may be only optiom
  • a pt can go from palliative care to active tx
153
Q

what is in an active periodontal pocket?

A
  • the ulcerated epithelial lining of the pocket wall
  • the JE
  • the diseased root surface which is contaminated with subgingival calc deposits and a layer of dental plaque which contains perio pathogens
154
Q

what is involved in cause related therapy?

A

The objectives are to resolve the disease process and to create conditions that will mitigate against recurrence of the disease
hygiene phase
-prevention/OHI
NSPT
- instrumentation

155
Q

When should an USS not be used?

A
  • in patients with a pacemaker as the electromagnetic sound waves from the US interfere with the elctronic function of the pacemaker
  • patients with contagious disease
156
Q

what are the properties of porphyromonas gingivalis?

A

surrounded by a capsule - protective
produces gingipains - play a role in bacterial housekeeping and infection, including amini acid uptake from host proteins
produces enzymes toxins and acids

157
Q

what studies prove plaque accumulation causes gingivitis?

A

experimental gingivitis in man
12 male dental students with healthy gingivae were subjected to a 3 week period without oral hygiene
during this period 6 subjects rinsed their mouth 3 times a day with distilled water whilst the other 6 rinsed with vancomycin
plaque accumulated rapidly at the gingival margin and at the end of the 3 weeks all participants had developed gingivitis

158
Q

How would you describe RSD tx being successful?

A
  • pt is comfortable
  • all pockets are cleansable by the pt
  • 4mm with no BOP = closed pockets
  • consistenlty low BOP (<10%)
  • adequate plaque control
159
Q

How would you describe RSD tx being unsuccessful?

A
  • pt has discomfort
  • persisting pockets not manageable by at home OH measures
  • persistent BOP
  • persistent suppuration
  • increasing attachment loss
160
Q

what are the 4 stages of wound healing?

A
  • haemostasis
  • inflammation
  • proliferation
  • remodelling
161
Q

why is there usually more recession following RSD?

A
  • reduction in inflammatory swelling (tissue shirnkage - gingival margin moves apically)
162
Q

what does the term re-attachment mean?

A

reunion of tissue with a root separated by incision or injury

163
Q

what does new attachment mean?

A

reunion of tissue with a root which has been pathologically exposed

164
Q

why do we get reduced probing depths following RSD?

A
  • reduction in inflammatory swelling
  • improved tissue resistance - increases resistance to probing
  • formation of the LJE
165
Q

why is calculus bad?

A
  • has a coating layer of plaque
  • impedes toothbrushing and ID cleaning
  • porous - absorbs bacterial endotoxins
  • may impede perio probing
166
Q

what are the 5 phases of treatment planning?

A
  1. initial examination
  2. cause related (non-surgical) therapy
  3. re-examination
  4. definitive tx plan
  5. maintenance
167
Q

why must you remove the affected cemntum during RSD?

A

necrotic cementum is infiltrated with toxic materials of bacterial origin such as endotoxins

168
Q

how is full mouth disinfection perio tx carried out?

A
  • conventional instrumentation/RSD within 24-48hrs and OHI
  • Used along with an adjunct such as chlorohexedine or an antibiotic
  • only used in few cases that havent responsded to NSPT
169
Q

What is the role of a therapist in periodontal surgery?

A

pre surgery - provide OHI
make sure site is as clean as possible as well as whole mouth to help with healing
post surgery - POIG
remove sutures
recommend chlorohexedine

170
Q

what are the shapes of calculus under a microscope?

A

brushite, dicalcium phosphate dehydrate, hydroxypapetite, whitlockite, octacalcium phopshate

171
Q

what are the types of recession?

A

Fenestration
Dehiscence

172
Q

what is fenestration?

A

window of bone
bone will break away

173
Q

what is dehiscence?

A

a lack of bone

174
Q

what are you looking for when looking for recession?

A
  • stillman’s clefts - v shapes in gums
  • McCall’s festoons - gum has rolled margins
  • clinical reccession
175
Q

what can periodontal health, gingival diseases and conditions be broken into?

A

periodontal health
gingivitis: dental biofilm induced
gingival diseases: non dental biofilm induced

176
Q

what can periodontal disease be catergorised into?

A

necrotising periodontal disease
periodontitis as a manifestation of systemic disease
periodontitis

177
Q

what may a definitive tx plan include for a periodontal patient?

A

RSD
Periodontal surgery
endo tx
definitive retsorative and prosthetic tx

178
Q

what are the 5 stages of trearment planning?

A
  1. initial examination/pain relief
  2. cause related therapy
  3. re - examination
  4. definitive tx plan
  5. maintenance
179
Q

what is a risk marker and give an example of one?

A

implies the presence of the disease but is not the cause of the disease
BOP
Mobility

180
Q

what is the evidence for NSPT?

A
  • little improvement of shallow pcokets following RSD
  • shallow pockets lose some clinical attachment after instrumentation
  • pockets of 4-6mm shows average probing depth reductions of about 1mm and 0.5mm gain of attachment post tx
  • pockets >6mm show average probing depth reductions of about 2mm and 1mm gain of attachment after tx
  • deeper pockets show greater reduction of probing depths following tx than shallow pockets
181
Q

what is the sequence of a periodontal treatment plan?

A
  1. initial assessment and pain relief
  2. cause related therapy
    - hygiene phase
    - NSPT
  3. re-evaluation and make corrective tx plan
  4. definitive tx
    - further NSPT
    - local delivery of antimicrobials
    - periodontal surgery
  5. re-evaluation and maintenance
182
Q

what is involved in phase 1 of the treatment plan?

A

initial assessment and pain relief
- BPE, perio summary assessments etc
- tx of acute condition - if pt in pain

183
Q

what is involved of phase 2 of the treatment plan?

A

cause related therapy
- objectives are to resolve the disease process and to create conditions that will mitigate against recurrence of the disease
- involves controlling dental plaque supra and sub
- hygiene phase therapy
- NSPT

184
Q

What is oral hygiene TIPPS?

A

Talk
Instruct
Practice
Plan
Support

185
Q

what does standard prevention indicate?

A

standard risk

186
Q

what does enhanced prevention indicate?

A

increased risk

187
Q

why is calculus bad?

A

supra and sub
sterile
porous
layer of unmineralised plaque
plaque retentive
withholds cytoxins
impeded probing

188
Q

what causes stippling?

A

tightly bound collagen fibres

189
Q

what are the immunogloblins?

A

IGG
IGA
IGM
IGE
IGD

190
Q

what immunoglobulins are found in saliva and GCF?

A

GCF - IGA, IGG
saliva - IGA

191
Q

Why is the junctional epithelium leaky?

A

because it has larger intracellular spaces

192
Q

what are cytokines?

A

protein cell signalling molecules - pro inflammatory

193
Q

what is phagocytosis?

A

engulfing of bacteria

194
Q

what do immunoglobulins produce?

A

antibodies which attach to antigen presented cells (oponisation)
this marks for antigen destrcution and beutralises toxins from bacteria

195
Q

what are gingivapains?

A

proteases
break down proteins such as collagen and host response cells (impairs host response)

196
Q

what are fimbrays?

A

on porphyromonas gingivalis - legs

197
Q

what bacteria complex releases proteases?

A

red

198
Q

what type of bacteria is treponemas?

A

spirocheate
flagella (motile)
cork screw
very destructive

199
Q

what is the only way to stop host destruction?

A

remove bacteria

200
Q

what is a pellicle made of?

A

salivary glycoproteins

201
Q

what is meant by the term prognosis?

A

predicted outcome of disease

Finals (9 decks)

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