periodontology Flashcards

Question 1

Q

28-year-old patient fit and well patient has full mouth periapicals which show generalised bone loss.
What is your Diagnosis & explain (1 mark)

Answer

A

Stage 4, Grade C generalised periodontitis.
(We don’t know the status without Bleeding on probing or pocket depths & risk factors haven’t been mentioned)

Question 2

Q

What Clinical and lab investigations can we do for periodontitis? (3 marks)

Answer

A

Thorough history (including Dental/medical/social/family history and clinical examination )

Clinical tests- 6 point pocket chart. Plaque and bleeding scores.

Microbiological analysis of sample (swab of crevicular fluid)

Radiographs??

Question 3

Q

Your patient has periodontal disease.
How would you decide prognosis of individual teeth? (3 marks)

Answer

A

Loss of attachment
Mobility
Furcation involvement

(Could also argue:
Sensibility test- is it just a perio problem could there also be an endo problem which influences prognosis- perio endo lesion)

Question 4

Q

28-year-old patient fit and well patient has full mouth periapicals which show generalised bone loss.
Why would PMPR not be successful in eliminating pocket bacteria? (2 marks)

Answer

A

Failure to disrupt the biofilm- Deeper pocket depths & furcations are more resistant due to blind cleaning.

Necrotic pulp- This would reinfect the cleaned pocket. We need to treat the tooth before doing perio.

Local factors- unfavourable root anatomy, overhangs and crowns can cause plaque retention

Patient compliance- are they looking after their Oral Hygiene?

Question 5

Q

28-year-old patient fit and well patient has full mouth periapicals which show generalised bone loss.
Your treatment of the pocket with pmpr was unsuccesful. Why would antibiotics not be effective in this scenario? (3 marks)

Answer

A

The patient is currently fit and well. We don’t want to give antibiotics to all patients due to the increased antibiotic resistance risk.

Antibiotic are only given in combination with mechanical disruption of the biofilm ALONE they will not be effective.

Only when there is proof the bacteria is the problem- where periodontitis has not gone away despite HPT and excellent OH.

Question 6

Q

How would you manage a periodontal abscess with systemic involvement? (5 marks)

Answer

A

Careful subgingival instrumentation short of the pocket base. (Attachment is friable & easily damaged so aggressive cutting would cause recession instead of healing)
If pus is present- drain by incision or through the periodontal pocket.
0.2% chlorohexidine mouthwash until the acute symptoms subside.
Analgesia
Antibiotics- because there is systemic inolvement (MUST be used with mechanical therapy
Penicillin V 250mg 2 tablets 4 times daily for 5 days.

If allergic- Metrondiazole 400mg 3 times daily for 5 days.

Question 7

Q

What would be clinical signs of improved periodontal health?

Answer

A

● Currently stable
BOP <10%
PPD less than or equal to 4mm (with NO BOP at 4mm sites)

● Currently in remission
BOP greater than or equal to 10%
PPD less than or equal to 4mm (NO BOP at 4mm sites)

Question 8

Q

A picture showing a space between 13 and 14.
Investigations you should do and why? (6)

Answer

A

BPE - screen for periodontal cause

Plaque and bleeding scores

6 Point pocket chart - assess perio disease

Periapical radiographs- to assess bone levels/ prognosis of teeth/ any radiolucencies/cysts displacing

Assess occlusion - is there occlusal trauma (+plaque induced inflammation) causing migration/splaying etc

Study models- allow you to monitor the change over time.

Clinical photographs??
Sensibility testing??

Question 9

Q

Other than aesthetics. Why restoring this space between the 13 and 14 can be challenging? (1)

Answer

A

If 13 and 14 are of good prognosis we are more reluctant to remove healthy tooth tissue to place crowns or veneers (to reduce the gap)
Composite could be used to restore the gap by making one of the teeth bigger but this may be more noticeable to the patient and others.

13 - involved in canine guidance

Question 10

Q

The gap between 13 and 14 is very small- What could inpede the placement of implants in this case (3)

Answer

A

Inadequate space (need 7mm in the edentulous saddle)
and 3mm between roots/implants, 2mm from adjacent structures
Inadequate bone levels (height and width) and quality
active diease = Periodontal problem = periimplantitis

Question 11

Q

What bacteria are involved in Necrotising periodontal diseases ?

Answer

A

Fusiform e.g. Fusobacterium
Spirochetes e.g. Treponema

Question 12

Q

What are the clinical signs and symptoms of Necrotising periodontal disease? (6)

Answer

A

Loss of Papillae - papillae and gingival margins are ulcerated and necrotic

Ulcers are covered in sloughing (yellowish/white/grey slime made of necrotic tissue bacteria and cells)

Halitosis and bad taste

Deep pocket formation (gingival necrosis coincides with loss of crestal alveolar bone).

Bleeding easily provoked.

First lesions often seen interproximally in the mandibular anterior region.

Question 13

Q

List 5 risk factors involved with necrotising gingival diseases

Answer

A

Immunocompromised
Stress
Smoking
Bad diet
Poor oral hygiene.

Question 14

Q

Briefly outline management of necrotising periodontal diseases. (5)

Answer

A

Ultrasonic debridement (necrotic tissue is removed to facilitate healing)
Mouthwash-
0.2% chlorohexidine mouthwash twice daily (pain making it unbearable to brush) or 3% hydrogen peroxide mouthwash- This froths up producing oxygen (anaerobic bacteria in NG/NP)
Antibiotics (if systemically unwell patient (fever)
400mg metronidazole 3 times daily for 3 days.
If allergic or on warfarin amoxicillin 500mg 3 times daily for 3 days.
Advise ibuprofen if fever present
Smoking cessation/ vitamin supplementation/ dietary advice.
PMPR once acute symptoms subside (to treat the perio disease)

Question 15

Q

Mr Fothergill is a 65 year old obese reformed smoker with a history of ischaemic heart disease who has
successfully completed a course of cause related therapy.
However, despite excellent oral hygiene, he still has some teeth with pockets of 6 and 7 mm which bleed on probing.
He is keen to pursue further treatment and You elect to undertake open flap curettage.

What information would you give to the patient so he can give informed consent? (5 marks)

Answer

A

Whats involved in the procedure:
Create a cut in the gum to improve visibility and allow us to thoroughly remove calculus deposits & sharp bony edges.

Risks: gingival recession, Pain, Infection, Swelling, Bleeding, Bruising

Benefits: PMPR will be more effective as we will have direct vision = increased success rates and possible reduction of pocket depth

Alternative treatment options:
Repeat non-surgical periodontal treatment. Regenerative therapy.
Furcation resective treatment. Mucogingival therapy.

Risks of refusing treatment:
Increased likelihood of tooth loss (increase in mobility & increased pocket depth)

Likely outcome?

Question 16

Q

Mr Fothergill consents to treatment of his deep pockets with open flap curettage.

You give 2 mL of 2% lidocaine hydrochloride with 1:80,000 adrenaline as buccal and palatal infiltrations.

As you are placing the final sutures, Mr Fothergill complains of a central crushing pain across his chest and down his left arm.

What is the most likely diagnosis (1 mark) and what would be your immediate management of this patient? (4
marks)
Assume the patient remains conscious.

Answer

A

Unstable angina
Management-
400mg GTN spray (2 sublingual actuations)

If this doesn’t help the patient assume its an MI and provide:
Aspirin chewed/crushed 300mg

Give 15l oxygen with a rebreathing trauma mask

phone 999

Question 17

Q

You successfully manage Mr Fothergill’s medical emergency OF MI.
In what forms would you deliver the post-surgical advice (1 mark) and what do you want the patient to know to minimise the incidence of any post-operative complications? (5 marks)

Answer

A

Verbally to the patient & written

post op:
Reinforce mechanical plaque control
Post-operative soft toothbrush for operated area
Chlorhexidine mouthwash 1-2 weeks.
Analgesics 2-3 days.
Antibiotics if indicated ( while complications in healing)
Remove sutures after 1 week.

Post operative:
There will be pain- Start taking analgesia before the LA wears off (Ibuprofen & paracetamol switching every 2 hours)
Swelling- swelling should peak within the 48 hours and and dies. If it continues then it is more likely to be infected.
Bleeding- a bit of blood in saliva is normal. Ooozing is not. To avoid- don’t touch it with you tongue/brush/finger. Avoid hot food/drink. Avoid smoking or activities that increase your blood pressure.If it bleeds use wet gauze to apply pressure for 30 mins. If it doesn’t stop Then apply pressure again for 1 hour. If it still doesn’t stop (A&E)
Bruising- to help use a cold patch on for 5 mins off for 5.
Infection-
Avoid smoking & alcohol for as long as possible to aid healing.
Stiffness of the TMJ- should settle after a few days/ a week.
Antiseptic mouthwash- chlorohexidine start after a few days (not to be used in open wounds). A capful of 0.2% chlorohexidine 3 times a day.
Sutures have been put in to help the socket heal and make it stop bleeding. Tell the patient if they are dissolvable or that the pateint needs to come back to have them removed.

Question 18

Q

Mr Fothergill returns to your surgery after 1 week for suture removal and all is well.
When should you next review this patient and what is the rationale behind this time interval (2 marks).

Answer

A

Patient should be re-evaluated in 8 weeks to allow time for;

Healing of the periodontal tissue
Decreased pocket depth.
Decreased oedema causing gingival recession
Increased clinical attachment due to formation of the junctional epithelium & an increase in tissuetone (producing resistanceto probing)

Question 19

Q

What clinical findings indicate that Periodontal treatment had been successful (2 marks)

Answer

A

Pocket depth < or equal to 4mm (no bleeding)

BOP < 10%

Question 20

Q

Why might antibiotics not work for treatment of non-responding periodontal disease? (3)

Answer

A

Biofilm is resistant to antibiotics

Antibiotics have not been used alonsgide mechanical disruption.

Poor patient adherence to the OHI regimen.

Question 21

Q

What is SIRS?

Answer

A

Systemic Inflammatory Response Syndrome which is used to diagnose a systemic response to infection.

Any 2 or more of: temp <36°C or >38°C,
Elevated heart rate >90bpm
respiratory rate >20/min,
WBC <4000 cells/mm3
>12000 cells/mm3

Question 22

Q

What is a periodontal abscess?

Answer

A

An infection in the periodontal pocket.
This is usually related to a pre-existing deep pocket/food packing/ tightening of the gingival margin after HPT.

Question 23

Q

What are the signs and symptoms of a periodontal abscess

Answer

A

Pain
Swelling
TTP in a lateral direction
Deep periodontal pocket
Suppuration
Enlarged regional lymph nodes
Fever
Commonly pre-existing periodontal disease.

Question 24

Q

How would you decide if the abscess is a periodontal abscess or a periapical abscess?

Answer

A

Sensibility testing-
Vital tooth associated with periodontal abscess
Non-vital tooth associated with a periapical abscess.

PA radiograph- periapical lucency at the apex of the tooth = periapical abscess.

Question 25

Q

How do you manage occlusal trauma in a patient with periodontal disease? (3)

Answer

A

Control the plaque induced inflammation (OHI & HPT- we may need to splint the teeth to stabilise them for debridement)
Correct the occlusal relations (remove any high restorations. Can the parafunction be treated?
Splint it- To spread the load and get support from other teeth.

Question 26

Q

Occlusal trauma in a patient with periodontal disease

What factors can influence localised mobility?(5)

Answer

A

Existing periodontal disease,
Widening of the PDL due to occlusal trauma (PDL widens to dissipate the force but sometimes the force is too great- no stabilisation)
Decreased alveolar bone density
The number/shape/length of the roots
Resorption/ trauma

 Width of the PDL: increased width = increased movement
 Height of the PDL: too high = restricted movement, too low = increased mobility
 Inflammation – in health there is a tight collar of fibrous tissue and collagen = restricted movement, swollen gingiva filled with inflammatory fluid = increased movement.
 Number, shape and length of roots: small, short root = more mobile

Question 27

Q

A patient has tooth mobility- When might splinting be advised? (3)

Answer

A

When mobility is
* Due to advanced loss of attachment
* Causing discomfort or difficulty in chewing
* affecting our ability to provide PMPR (we need to stabilise the teeth)

Question 28

Q

Why is there a decrease in mobility after periodontal treatment? (2)

Answer

A

There is an increase in clinical attachment due to:
* formation of the long junctional epithelium
* An increase in tissue tone as inflammatory resolves

Question 29

Q

occlusal trauma in a patient with periodontal disease

What can you do if the PDL is still widened after successful periodontal treatment?

Answer

A

Reduce contact in occlusion (correct occlsual abnormalities)
splinting

Question 30

Q

How do we define localised and generalised in terms of periodontitis?

Answer

A

Localised <30% of teeth have periodontitis.
Generalised >30% of teeth have periodontitis

In terms of gingivitis As per BSP guidelines.
Gingival health <10%
Localised 10-30%
Generalised >30%

Question 31

Q

What are we looking for to decide if a tooth is of poor prognosis due to periodontitis & why? (4)

Answer

A

Tooth Mobility - This indicates reduced bone support,
Furcation involvement - more difficult to keep clean for patient,
Loss of Attachment - less supporting structures for tooth
Sensibility testing- is the tooth non-vital ?

Question 32

Q

2 further investigations can be carried out on a periodontal patient (2)

Answer

A

Plaque and Bleeding scores
6 point pocket chart.
Radiographs?

Question 33

Q

2 further bits of info needed from a periodontal patient before determining poor prognosis of teeth (2)

Answer

A

Smoking
Drug history
Systemic disease

UNSURE

Question 34

Q

Patient
- generalised severe gingival recession
- 60 yrs,
- mobile 21

Patient is complaning of mobility of the 21 and overall discomfort.
What can cause this and why (3)

Answer

A

Sensitivity due to exposed root dentine,
Perio-endo lesion
occlsual trauma

Mobility - bone loss (due to perio disease ) occlusal trauma (made worse by perio disease)

Question 35

Q

4 further investigations before treatment planning of a patient with generalised severe gingival recession (4)

Answer

A

6PPC
Periapical radiographs
MPBS
study models (to monitor gingival recession)
Clinical photographs (Calibrated by the inclusion of a probe)

Question 36

Q

How can we manage a patient with generalised severe gingival recession (3)

Answer

A

Fluoride varnish/sensitive toothpaste to manage sensitivity
PMPR
Oral hygiene instruction.

If recession type 1- we can refer for surgical intervention to make it easier to clean. Potentially gingival graft
Recession type 2 and Type 3 not much we can do about it.

Question 37

Q

List the classifications for periodontal disease

Answer

A

Health
- intact periodontium
- reduced periodontium (Causes other than periodontitis e.g. crown lengthening surgery)

Plaque induced gingivitis

Non-plaque induced gingival diseases and conditions (e.g. primary herpetic gingivostomatitis/ Vitamin C deficiency/ trauma)

Periodontitis

Necrotising periodontal diseases

Periodontitis as a manifestation of systemic disease (Down’s syndrome)

Systemic disorders affecting the periodontal tissues (Uncontrolled diabetes mellitus)

Periodontal abscesses

Periodontal-endodontic lesions

Mucogingival deformities and conditions. (Recession)

Question 38

Q

How is localised angular periodontitis caused? (2)

Answer

A

When pathway of inflammation travels directly into PDL space

Localised plaque retention factors e.g. overhang, crowding, malposition

Question 39

Q

How to classify localised angular periodontitis

Answer

A

1 walled defect
2 walled defect
3 walled defect

Question 40

Q

Following hygiene phase therapy this patient’s oral hygiene was excellent but pockets of >6mm persisted in the lower right quadrant. Open flap debridement was performed:

(a) What feature of this patient’s disease, observable on the radiograph, is most likely to limit the success of this treatment and why? (1 mark)

Answer

A

Furcation involvement- makes it harder for the patient to clean & more resistant to PMPR.

Question 41

Q

3 clinical/ radiographic signs of periodontal healing (3)

Answer

A

Gingival recession: black triangles,

Clinical reattachment = reduced probing depths

Reduced BOP

</=4mm PPD, <10%BOP, no bleeding at 4mm sites

Question 42

Q

Provide treatment options for localised angular periodontitis (5)

Answer

A

Management-
* Closed/open pmpr (Healing by repair)

Regenerative techniques- for new bone/ periodontal ligament and cementum - GTR and GBR (guided tissue/bone regeneration) and Emdogain (biological mediator)
Resective techniques:
Tunneling, Hemisection, furcationplasty, Pocket elimination with osseous resection (where the flap is repositioned apically )

Question 43

Q

What is the difference between horizontal and angular bone loss?

Answer

A

Horizontal = base of pocket is above the alveolar crest
Vertical(angular) = apical end of pocket is below with bone rest

Related to the width of the initial bone prior to the onset of plaque induced periodontal inflammation & the radius of the destruction from plaque.

When thin bone between two teeth resorbs in inflammation- the radius of destruction of plaque (2mm is greater than the bone width)
= horizontal bone loss (Loss of height of the crestal bone around the teeth)

When there is bone resorption from plaque induced inflammation in thick bone with teeth further apart = vertical bone loss. The radius of the destruction of plaque is < bone width. So if the interproximal bone is greater than 2mm then vertical/angular defects occur.

Question 44

Q

New classification = How do we define the severity of periodontal disease

Answer

A

By defining the patient’s STAGE.
1- Mild (<15% OR < 2mm)
2- moderate- bone loss to coronal 1/3
3- severe- mid 1/3 of root
4- apical 1/3 of root.

Question 45

Q

How does a healthy periodontium react to traumatic occlusion?

Answer

A

Primary occlusal trauma
Tissue changes from excessive occlusal forces on a dentition with normal periodontal support (no perio disease)

A health periodontium has normal PDL height and width, in areas of pressure = resorption and in areas of tension = bone deposition
This creates a wider PDL space without the present of periodontal disease

PDL width increases until forces are dissipated
- Width then stops increasing and stabilises when the force is adequately dealt with
- This is a successful adaptation
- Once the force is removed, the width should go back to normal = reversible

If excessive loading is more than the adaptive capacity
- Width increases until it becomes a functional problem = pathological problem (doesn’t stabilise)

No LOA or inflammation!!!
Will resolve once occlusion sorted = reversible

Question 46

Q

How does a healthy but reduced periodontium react to traumatic occlusion?

Answer

A

There is no plaque induced inflammation.
The trauma will not lead to further loss of attachment- just increased mobility.

Known as Secondary occlusal trauma:
Tissue changes from normal/excessive occlusal forces on a dentition with a reduced but healthy periodontium (has less PDL and bone support)

Question 47

Q

Describe the effect of occlusal trauma in a patient with perio/plaque induced inflammation.

Answer

A

= Bone loss and loss of attachment

Why is there more bone loss?
There are Zones of co-destruction;
- Bone resorbed from plaque induced inflammation
- Bone resorbed from excessive occlusal loading

When these happen at the same time = more attachment loss

LARA ANSWER
There is greater attachment loss &bone loss due to combination of:
* Plaque induced inflammation
* Excessive load on the teeth.
CO-Destruction

Question 48

Q

What is chlorhexidine?

Answer

A

Bisbiguanide antiseptic.

Question 49

Q

What is CHX’s mode of action?

Answer

A

Dicationic -> 1 cation adheres to pellicle and 1 cation disrupts bacterial membrane. It is antibacterial and antiseptic,
therefore, bacteriostatic and bacteriocytic. It works against Gram +ve and –ve bacteria, fungi & viruses

Question 50

Q

What is the substantivity of CHX?

Question 51

Q

Give 2 common doses of CHX.

Answer

A

0.2% 10ml/20mg 2x daily OR 0.12% 15ml/18mg 2x daily

Question 52

Q

Give 4 side effects of CHX

Answer

A

staining

taste disturbance

salivary gland enlargement

anaphylaxis

interacts with SLS

Question 53

Q

Give 8 uses of chlorohexidine

Answer

A

Testing rubber dam seal prior to endo

Endo irrigant

Management/treating candidia infections

Used for oral hygiene in paediatric trauma i.e. DAF

Used to carry out OH in patients with intellectual impairment when effective oral hygiene cannot be carried out

Treating ANUG

Use after minor surgical procedures if cannot carry out tooth brushing

Management of mucositis in patients undergoing chemo/radiotherapy

OHI patients with jaw fixation

Recurrent oral ulceration

Denture stomatitis

Treatment of dry socket

Question 54

Q

How is HPT provided? (5)

Answer

A

Follow BSP s3 guidelines
Education

Regular reinforcement of OHI using TIPPS

Non-surgical periodontal therapy
- supra and subgingival PMPR

Diet advice

control risk factors: Removal of plaque retentive factors, Smoking cessation

Question 55

Q

What is TIPPS?

Answer

A

Talk – about causes of periodontal disease and any barriers to plaque removal

Instruct – best ways to perform effective plaque removal

Practice – practice cleaning teeth and using interdental aids in surgery

Plan – put into place a plan of how the patient OH fits in with daily life

Supports – follow up with patient

Question 56

Q

What 7 things are recorded on a periodontal pocket chart?

Answer

A

Teeth missing

gingival margin height

pocket depth

loss of attachment

mobility

furcation

bleeding on probing.

Question 57

Q

Give 2 disadvantages of a 6 point pocket chart (4)

Answer

A

assumes all pts have same root length/morphology so may appear worse than they are
Probing depths are subjective/variation between operators
True pocket depth may not be measured accurately if subgingival calculus is blocking the probe from gaining full access to the periodontal pocket
Cannot carry out a full mouth chart in children 12-18 since they have immature gums and false pocketing is common

Question 58

Q

What are the local factors for gingival recession?***

Answer

A

Periodontal disease.

parafunctional habits

traumatic tooth-brushing and abrasive toothpastes

poor restoration margins

high frenal attachment

crowding/malpositioned teeth

traumatic overbite

plaque/calculus deposits

smoking - not local

fixed ortho appliances/orthoodntics

Question 59

Q

How can you measure recession?

Answer

A

measure using a PCP12 probe the distance from the CEJ to the gingival margin (poss duirng 6ppc)

and then classify Using the gingival recession indices;
Recession type 1
No loss of inter-proximal attachment
(recession is narrow and localised)

recession type 2
Apical attachment loss is greater than interproximal

recession type 3
Papilla completely lost
Interproximal attachment loss is greater than apical. (Nothing interproximal left)

Clinical pics??
study models??

–> millers classification

Question 60

Q

How is localised recession managed? (6)

Answer

A

Adress the underlying cause (e.g. OHI for atraumatic toothbrushing/ management of parafunctional habits)

Monitor

Treat the sensitivity (fluoride varnish/ sensodyne toothpaste/ fluoride mouthwash/ seal and bond)

minimise risk factors (e.g. periodontal disease/ smoking cessation)

Surgery- Muco-gingival therapy
- pedicle soft tissue graft
- coronal advancement flap
- gingival graft

gingival veneer

Question 61

Q

Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.
Give 3 differential diagnoses

Answer

A

endo - perio with root damage
- root fracture
- perforation
- external RR

endo - perio with NO root damage
- in perio px (3 grades)
- in non-perio px (3 grades)

occlusal trauma (+ plaque induced inflammation = enhanced bone loss)

Question 62

Q

Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.

What special investigations would you carry out?

Answer

A

Take a thorough history - endo symptoms

examine - sinus tract (+/- pus), crown discolouration

Special Tests:
6PPC
Localised deep pockets (this tooth only) or generalised throughout mouth
- mobility
- bleeding

TTP

percussion tests

Question 63

Q

Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.

What is your initial treatment for the tooth? **

Answer

A

Re-RCT

Recommend analgesia
(Only prescribe antibiotics if systemic or persistent)

Prescribe a Chlorhexidine mouthwash until acute symptoms subside

If the tooth is primarily affected by endo = endo treatment is enough for resolution and this stage and PMPR isn’t always required.

Once endo initiated review the patient within 10 days and carry out PMPR (perio treatment)

Question 64

Q

Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.
Your treatment fails and the tooth is extracted. Give 2 options for replacement

Answer

A

Bridge
- resin retained or conventional
- fixed fixed or centilever

Implant

RPD

Answer 64

A

If active perio present
Assess the stage&grade and extent of the periodontal disease - generalised or localised.

Bone quality - width and height

space available 7mm between crowns

Assess pt motivation, attendance and OH

assess risk factors e.g. smoking, uncontrolled diabetes, stress and non-modifiable risk factors e.g. genetics

assess medical history e.g. on bisphosphonates

Answer 65

A

regeneration techniques:
1. selective tissue repopulation e.g. GTR/GBR
By placing a barrier between the gingival epithelium and the tooth this facilitates repopulation of the area by PDL and bone cells instead of epithelial cells

Biological mediator = Emdogain
an enamel matrix protein derived from the porcine tooth germ.
Function- forms a matrix on the root surface that mediates the production of cementum.

Implants:
Bone grafts +/- guided tissue regeneration

Answer 66

A

The radius of destruction of plaque determines the defect-
The radius is approximately 1.5-2mm and if the interproximal bone is
greater than this radius then the pattern is vertical/angular (not all of the bone is destructed)

Answer 67

A

By number of walls: 1, 2 or 3 wall defects → 2 and 3 wall defects heal better.

Answer 68

A

SDCEP:
PPD <4mm
plaque scores <15%
bleeding scores <10%
or 50% reduction in each

BSP:
PPD < OR = 4mm (with no bleeding on probing)
BoP <10%

plaque scores < 20%
bleeding scores <30%
or 50% reduction in each
This is BSP measurement of patient engagement

Answer 69

A

Infrabony defects - 2 and 3 walled defects

Grade 2 furcation in mandibular teeth

Grade 2 buccal furcation in maxillary molars.

Type 1 gingival recession.

Answer 70

A

palliative care - Non-surgical PMPR & maintaining plaque control

Resective treatment:
1. root resection/hemisection - get rid of the furcation (chop a root off) & make the area easier to clean.
2. tunnel preparation - makes the furcation big enough to enable cleaning with an interdental brush
3. furcation plasty - mainly at buccal and lingual furcation

extraction

Answer 71

A

Poor/Inadequate subginigval PMPR by the practitioner
- complex root anatomy/furcations/angular defects that are difficult to effectively debride

Motile anerobes moving into tissues.

Poor/inadequate control of supragingival deposits by the patient (poor OH)
- unmotivated and non-compliant patient

Poor control of risk factors; smoking, uncontrolled diabetes mellitus, stress, nutrition, hormones etc.

Answer 72

A

Glucose tolerance test.
Patient should fast.
Patient given a fixed amount of sugar.
Patients blood sugar levels tested 2 hours after.
In health:
Fasting = < 6.1 normal
After 2 hours: < 7.8 normal
Diabetes:
Fasting = > 7
After 2 hours = > 11.1

Random plasma glucose (RPG)
> 11.1 mmol/l on 2 occasions = diabetes
(less than this is normal/in health)

Answer 73

A

Hb1ac - glycated haemoglobin - this is the amount of glucose stored in RBCs.
This is used instead of measuring glucose levels as HbA1 gives us information about the patients diabetes over 8-12 weeks.

Answer 74

A

HBA1c
diabetes = 48Mmol/mol (6.5%) or more
normal = < 42 mmol/mol (5.7%)

a prediabetic person is between 42-47mmol/mol

Answer 75

A

Alters the oral microbiota which triggers the immune system to attack.
The vasoconstriction of blood vessels in gums decreases the healing capacity as it decreases oxygen and nutrients supply to the gums.
(Smokers can also have active periodontal disease with no bleeding the smoking just suppresses the symptoms by the above mechanism)
Smokers also have increased amount of inflammatory mediating cytokines (Causing tissue breakdown)

wtf is this??
CCEB → 1. Impaired Chemotaxis and phagocytosis 2. inc Cytokine production (tx breakdown) 3. Affects Enzyme catalases 4.Blood flow restricted.

Answer 76

A

A pro-inflammatory cytokine produced by epithelial cells,
macrophages, dendritic cells, endothelial cells and B cells.
Stimulates the release of enzymes and osteoclasts causing increased tissue destruction.

Answer 77

A

lichen planus

mucous membrane pemphigoid

pemphigus

Answer 78

A

Calculus

Ortho/pros appliances

overcrowding/malposition of teeth

Answer 79

A

Topical steroids e.g. Betamethasone or beclomethasone, Tacrolimus m/w.

Answer 80

A

Phenytoin = anti-epileptic

Cyclosporine = immunosuppressant

amlodipine = Ca channel blocker

Answer 81

A

Plaque is still the primary aetiological factor, therefore, OHI and pmpr should be the first port of call.

If there is no improvement and pt still has good OH liaise w/GMP to discuss changing medications.

or consider surgery approaches (once the causative factor controlled) such as a gingivectomy
= Reduction of gingival excess to:
* Facilitate plaque control
* Facilitate restorative dentistry
* Improve appearance.

Answer 82

A

● 0- PPD <3.5mm, no BOP, no PRF
● 1- PPD <3.5mm, BOP, no PRF (plaque can be present)
● 2- PPD <3.5, BOP, plaque retentive factors (calculus and overhangs)
● 3- PPD between 3.5-5.5mm
● 4- >5.5mm
● *- furcation involvement

Answer 83

A

0 = physiological movement
1 = up to 1mm movement
2 = 1-2mm movement
3 = >2mm severe movement that impacts function
can depress or rotate

Answer 84

A

1 = < 1/3rd (<3mm)
2 = > 1/3rd but not all the way through (>3mm)
3 = through and through

Answer 85

A

Recession type 1
No loss of inter-proximal attachment
(recession is narrow and localised)

recession type 2
Apical attachment loss is greater than interproximal

recession type 3
Papilla completely lost
Interproximal attachment loss is greater than apical. (Nothing interproximal left)

6PPC with a PCP12 probe
Clinical photographs
study models

Answer 86

A

generalised - stage 4 - grade c - stability? - RF?

Answer 87

A

Age

MH: fit and well

extent of interproximal bone loss at worst site

risk factors - local and systemic

Answer 88

A

P&G scores - assess OH

6PPC

plaque sample to lab

possible blood test to check for host factors

swab cervicular fluid

Clinical photographs

Study models.

Answer 89

A

3.5-5.5mm probing depths (partially visible black band)
With bleeding on probing and plaque retentive factors.

Answer 90

A

You should complete a simplified BPE- You probe 16, 11, 26, 36, 31, 46

Answer 91

A

junctional epithelium = 1mm

connective tissue attachment = 1mm

= 2mm total biological width/supracrestal attachment

Answer 92

A

Genetic causes:
- Papillion lefevre syndrome
- Chediak Higashi syndrome
- LAS syndrome
- Downs syndrome
- Chronic granulomatous disease

Diseases that cause;
- (acute myeloid) Leukaemia
- Agranulocytosis
- Neutropenia
- HIV infections
- Liver disease
- poorly controlled/undiagnosed Diabetes
- Infections (bacterial and viral)

Malnutrition

medications:
(Epilepsy) phenytoin
Immunosupression e.g. Cyclosporine
Calcium channel blockers e.g. Amlodipine

Answer 93

A

puberty

malnutrition

Genetic causes:
- Papillion lefevre syndrome
- Chediak Higashi syndrome
- LAS syndrome
- Downs syndrome
- Chronic granulomatous disease

Diseases that cause;
- (acute myeloid) Leukaemia
- Agranulocytosis
- Neutropenia
- HIV infections
- Liver disease
- poorly controlled/undiagnosed Diabetes
- Infections (bacterial and viral)

medications:
(Epilepsy) phenytoin
Immunosupression e.g. Cyclosporine
Calcium channel blockers e.g. Amlodipine

Answer 94

A

Plaque and bleeding scores

6 point pocket chart of the full mouth after initial treatment

Radiographs (bitewings or Periapicals- to establish if pocketing is true or false)

Refer - blood work (diabetes and leukaemia)

Answer 95

A

Plaque and bleeding scores
6 point pocket chart of the full mouth after initial treatment
Radiographs (bitewings or Periapicals to establish if pocketing is true or false.)

then stage 1:
Plaque control
Explain disease, risk factors, treatment alternatives/ risks and benefits (Including not getting treatment)

b.OHI (showing & motivating) & supra and subgingival PMPR on the crown.

c. Reduce risk factors & Plaque retentive factors e.g.
Calculus and overhanging rx

d. Using their risk factors decide the recall period.

e. Other infection control may include- caries treatment & endodontic therapy.

re-evaluate
engaging = step 2
non-engaging = repeat step 1

Step 1 plus- Subgingival PMPR
a. Reinforce oral hygiene/ risk factor control/ behaviour change.
b. Subgingival PMPR on the root
c. Use of adjunctive systemic antimicrobials (Chlorohexidine)

Re-evaluate after 3 months
engaging = supportive
- Continuous monitoring of local and systemic risk factors.
- PMPR

non-engaging = step 3
a. Treating the areas not responding
b. Reinforce OH/ risk factor control and behaviour change.
c. Repeat subgingival PMPR on root of Moderate residual pockets (4-5mm)
d. May also include
i. Access flap periodontal surgery
ii. Resective periodontal surgery
iii. Regenerative periodontal surgery.
e. Refer any deep >6mm pockets

Answer 96

A

Patient is aged 13 (likely to have 7s. Won’t have 8s so total = 28)

Stage- 1 (largest bone loss- 10%)
Grade- B moderate 10/13 = 0.7%
E- Generalised 7/28= 30%
Risk factors (don’t know yet)

Stage 1 Grade 3 Generalised periodontitis (don’t know stability) With no risk factors.

Answer 97

A

PA radiographs

6 point pocket chart

Answer 98

A

Related to the width of the initial bone prior to the onset of plaque induced periodontal inflammation
When there is bone resorption from plaque induced inflammation in thick bone with teeth further apart = vertical bone loss

The radius of destruction from plaque determines this pattern.
It is approximately 1.5-2mm and if the interproximal bone is greater than 1.5-2mm then vertical/angular defects occur.

Answer 99

A

1 wall defect (1 wall left)

2 wall defect (2 wall left) - will heal better
3 wall defect (3 wall left) - will heal better

Answer 100

A

Management-
* Closed/open pmpr (Healing by repair)

Regenerative techniques- for new bone/ periodontal ligament and cementum - GTR and GBR (guided tissue/bone regeneration) and Emdogain (biological mediator)
Resective techniques:
Tunneling, Hemisection, furcationplasty, Pocket elimination with osseous resection (where the flap is repositioned apically )

Answer 101

A

Loss of attachment – less supporting structures for the tooth and harder to clean at home (esp PPD> 4mm) = increased risk of
tooth loss

Mobility – reduced bone support; increased risk of tooth loss

Furcation involvement – more difficult to keep clean, increasing risk of caries
etc.

Answer 102

A

Smoking

OHI and motivation

Systemic disease – e.g poorly controlled diabetes, immunosuppression, pregnancy

Drug history

Answer 103

A

Loss of perio attachment from perio disease
unfavourable soft tissue profile
Unfavourable occlusal forces (+ plaque induced gingivitis)

Answer 104

A

History - identify risk factors
examination - assess local risk factors
BPE - screening
Radiographs - show the extent of bone loss
P&G scores - assess OH
6PPC

Treatment:
BSP S3 guidelines step 1 = educate on the disease, provide OHI, diet diary, smoking cessation (if applicable), Reduce risk factors & Plaque retentive factors and provide PMPR of clincial crown (supra&sub).
review and repeat stage 1 or progress to stage 2 etc.

once periodontal disease is stabilised;
accepting the position and splint

correct abnormal occlusal relationships

Answer 105

A

Periodontal abscess

Periapical abscess

endo-perio lesion/abscess

Answer 106

A

sensibility test:
Endo involvement= negative/altered response
no endo involvement = tooth usually vital

PA radiograph to assess PA pathology

6ppc to assess for associated deep pockets

Answer 107

A

Drain the pus by dilating the pocket
incise and drain

Answer 108

A

Don’t aggressively instrument – will inhibit repair of the pocket - careful, subgingival instrumentation short of the base of the pocket.
Drain the pus by dilating the pocket – if no oose of pus then just make an incision
Recommend analgesia
Only give antibiotics if the abscess is persistent or the patient has systemic signs e.g. Penicillin V 250mg 2 tablets 4 times daily for 5 days.
Chlorhexidine mouthwash use until the acute symptoms subside
Review when they’re not in pain and carry out more thorough instrumentation

Answer 109

A

Crater like ulcers
loss of papillae
sloughing of ulcers
halitosis
Deep pocket formation associated with the ulcers (gingival necrosis coincides with loss of crestal alveolar bone)
Readily provoked bleeding .

Answer 110

A

Stress, immunocompromised, smoking,
severely malnourished, poor OH,
sleep deprivation
Underlying viral conditions (HIV/ AIDS)

Answer 111

A

Ultrasonic debridement (the necrotic tissue is removed to facilitate healing)
Mouthwash
a. 0.2% Chlorhexidine mouthwash twice daily

(3% hydrogen peroxide mouthwash- Anaerobic bacteria are involved & the mouthwash froths up producing oxygen)

Antibiotics if we have systemically unwell pt. (fever)
400mg Metronidazole 1 tablet 3 times daily for 3 days.
b. If allergic or on warfarin-
Amoxicillin or doxycycline
Smoking cessation, vitamin supplementation and dietary advice
Hygiene phase therapy/PMPR (to treat the perio disease) once acute symptoms subside

Answer 112

A

Periodontal abscess:

Periodontal abscess- A 10mm pocket is too large. forthe patient to clean.
This causes the build up of bacteria and food inside the pocket.
Without adequate treatment - pocket becomes inflamed (neutrophils come to the area and engulf the invading pathogens) But this can get further infected pridcing pus which the abscess forms around to prevent spread

If PMPR recieved- Food can pack into the pocket after gingival cuff has tightened post HPT. Less flow of fluid and debris out of hte gingival crevice causing infection.

Acute infection with suppuration causes rapid destruction of perio tissues = negative prognosis for the tooth

Answer 113

A

Secondary occlusal trauma:
Tissue changes from normal/excessive occlusal forces on a dentition with a reduced but healthy periodontium has less PDL and bone support.
There is no plaque induced inflammation
The trauma will not lead to further loss of attachment, just increased mobility

physiological:
A health periodontium has normal PDL height and width, in areas of pressure = resorption and in areas of tension = bone deposition
This creates a wider PDL space without the present of periodontal disease
PDL width increases until forces are dissipated
- Width then stops increasing and stabilises when the force is adequately dealt with
- Once the force is removed, the width should go back to normal = reversible

Pathological:
If excessive loading is more than the adaptive capacity
- Width increases until it becomes a functional problem = pathological problem = width continues to increase and doesn’t stabilise.

OT IN ACTIVE PERIO
Plaque induced inflammation (periodontitis) and excessive occlusal loading
= More bone loss than a healthy individual.
Why is there more bone loss?
There are Zones of co-destruction;
Bone resorbed from plaque induced inflammation and bone resorbed from excessive occlusal loading
When these happen at the same time = more attachment loss.

Answer 114

A

Control plaque induced inflammation - BSP S3 guidelines
HPT (diet adv, smoking cessation, OHI etc) /PMPR to stabilise the perio
Correct abnormal occlusal relations/parafunction
Use of a bite raising appliance
Splinting healthy teeth to spread the load and allow the healthy teeth to support

Answer 115

A

Width of the PDL: increased width = increased movement

Height of the PDL: too high = restricted movement, too low = increased mobility

Inflammation (existing perio) – in health there is a tight collar of fibrous tissue and collagen = restricted movement, swollen gingiva filled with inflammatory fluid = increased movement.

Number, shape and length of roots:
small, short root = more mobile

Answer 116

A

When there is increased mobility due to advanced loss of attachment making it
difficult/uncomfortable for the patient to eat or clean.

Splinting can also facilitate HPT/PMPR as the teeth will be stabilised.

Answer 117

A

Due to increased tissue tone and long junctional epithelium attachment with successful HPT

Answer 118

A

Reduce contacts within the occlusion that is causing the traumatic occlusion initally

then splinting to healthy teeth to spread occlusal load evenly

Answer 119

A

Incisors – 6.3mm
Canines – 8.5mm
Premolars – 10mm
Molars – 12.8mm

Answer 120

A

Modifiable & systemic:
* Smoking
* Poorly controlled diabetes
* HIV
* Leukaemia
* Osteopenia
* Osteoporosis
* Stress
* Medications
* Hormonal changes
* Poor nutrition
* Poor SIMD

Answer 121

A

Monogenetic syndromes – Sickle cell; CF; PKD

Down’s syndrome

papillion lefere

Answer 122

A

Poor control causes high glucose level. The body needs something to do with it so it gives glucose to the proteins = changing the conformation.
This activates the immune system:
Increased adhesion of the endothelial cells & permeability. (allowing migration)
Increased chemotaxis (more neutrophils are directed to the infection site)
Impaired neutrophil function (problems with the first response)
Increased macrophage release of IL-6 and TNF-alpha (cytokines which co-ordinate the immune response)
Increased MMP (excess causes damage)
Decreased collagen production by fibroblasts (helps with healing)

ADV. Glycation products infiltrate the blood vessels (causing inflammation- smaller lumen & less blood flow) We get less oxygen & nutrients. This causes poorer wound healing.

Hyperglycaemia can alter the balance between RANKL and OPG = increased bone destruction.

Answer 123

A

The reduction or elimination of gingival inflammation achieved through complete removal of all factors responsible for gingival inflammation e.g. Plaque retentive factors

Achieving a clean and infection free dentition.

This initial stage aim is to motivate the patient to perform optimal OH.

Answer 124

A

To preserve for a patient’s lifetime a dentition which, although affected by periodontitis, has levels of appearance and function that are acceptable to the patient.

Answer 125

A

Drug induced:
§ Anti-epileptic = phenytoin
§ Calcium channel blocker – amlodipine
§ Immunosuppressant – cyclosporine

leukaemia

hormones e.g. puberty and preganancy

chronic granulomatous disease

Answer 126

A

Starts at the interdental papillae and develops to include up to the entirety of the attached gingivae

Answer 127

A

Plaque control becomes increasingly difficult which results in an additional oedematous inflammatory component to the overgrowth. (Classified as plaque induced gingivitis)
but there is no evidence to suggest overgrowth predisposes periodontitis

Answer 128

A

Periodontal abscess:

Periodontal abscess- A 10mm pocket is too large. forthe patient to clean.
This causes the build up of bacteria and food inside the pocket.
Without adequate treatment - pocket becomes inflamed (neutrophils come to the area and engulf the invading pathogens) But this can get further infected pridcing pus which the abscess forms around to prevent spread

If PMPR recieved- Food can pack into the pocket after gingival cuff has tightened post HPT. Less flow of fluid and debris out of hte gingival crevice causing infection.

Acute infection with suppuration causes rapid destruction of perio tissues = negative prognosis for the tooth
A periodontal abscess. A 10mm pocket is too large for the patient to clean. This causes the build up of bacteria and food inside the pocket.
Without adequate cleaning & subgingival PMPR this pocket becomes inflamed
(Neutrophils come to the area to engulf the invading pathogens)
But this can get further infected producing pus (bacteira with dead/dying neutrophils) .
An abscess forms around this to wall off the pus & prevent pottential spread.

Answer 129

A

Careful subgingival instrumentation short of the pocket base. (Attachment is friable & easily damaged so aggressive cutting would cause recession instead of healing)
If pus is present- drain by incision or through the periodontal pocket.
0.2% chlorohexidine mouthwash until the acute symptoms subside.
Analgesia
No antibiotics as there is no systemic involvement
Follow up. withperiodontal treatmetn (S3 guidelines)

Answer 130

A

Vertical bony defects are generally V shaped and sharply outlined.

Answer 131

A

Localised affects <30% of sites.
Generalised affects >30% of sites.

Answer 132

A

For the bony defect- Tissue guided regeneration- Placement of a barrier between the gingival epithelium and the tooth facilitates repopulation of the area by the PDL and bone cells instead of epithelial cells.
For the furcation region- Tunnelling which makes the furcation big enough to enable cleaning with an interdental brush.

Answer 133

A

mobility will decrease as there is an increase in tissue tone and decrease in probing depth due to an increase in junctional epitheliu????

Answer 134

A

6PPC to assess LOA, mobility and furcation
OPT to assess bone loss and rule out pathology
investigation of occlusion - is occlusal trauma present
history of loss of other teeth - FH of perio disease, reason for loss of posterior teeth

RPD, bridgework, implants

??

Answer 135

A

TTP- laterally or vertically ???

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periodontology Flashcards

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