periodontology Flashcards
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)
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)
2
Q
What Clinical and lab investigations can we do for periodontitis? (3 marks)
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??
3
Q
Your patient has periodontal disease.
How would you decide prognosis of individual teeth? (3 marks)
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)
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)
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?
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)
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.
6
Q
How would you manage a periodontal abscess with systemic involvement? (5 marks)
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.
7
Q
What would be clinical signs of improved periodontal health?
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)
8
Q
A picture showing a space between 13 and 14.
Investigations you should do and why? (6)
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??
9
Q
Other than aesthetics. Why restoring this space between the 13 and 14 can be challenging? (1)
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
10
Q
The gap between 13 and 14 is very small- What could inpede the placement of implants in this case (3)
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
11
Q
What bacteria are involved in Necrotising periodontal diseases ?
A
Fusiform e.g. Fusobacterium
Spirochetes e.g. Treponema
12
Q
What are the clinical signs and symptoms of Necrotising periodontal disease? (6)
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.
13
Q
List 5 risk factors involved with necrotising gingival diseases
A
Immunocompromised
Stress
Smoking
Bad diet
Poor oral hygiene.
14
Q
Briefly outline management of necrotising periodontal diseases. (5)
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)
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)
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?
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.
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
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)
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.
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).
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)
19
Q
What clinical findings indicate that Periodontal treatment had been successful (2 marks)
A
Pocket depth < or equal to 4mm (no bleeding)
BOP < 10%
20
Q
Why might antibiotics not work for treatment of non-responding periodontal disease? (3)
A
Biofilm is resistant to antibiotics
Antibiotics have not been used alonsgide mechanical disruption.
Poor patient adherence to the OHI regimen.
21
Q
What is SIRS?
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
22
Q
What is a periodontal abscess?
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.
23
Q
What are the signs and symptoms of a periodontal abscess
A
Pain
Swelling
TTP in a lateral direction
Deep periodontal pocket
Suppuration
Enlarged regional lymph nodes
Fever
Commonly pre-existing periodontal disease.
24
Q
How would you decide if the abscess is a periodontal abscess or a periapical abscess?
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.
25
How do you manage occlusal trauma in a patient with periodontal disease? (3)
1. Control the plaque induced inflammation (OHI & HPT- we may need to splint the teeth to stabilise them for debridement)
2. Correct the occlusal relations (remove any high restorations. Can the parafunction be treated?
3. Splint it- To spread the load and get support from other teeth.
26
Occlusal trauma in a patient with periodontal disease
What factors can influence localised mobility?(5)
* 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
27
A patient has tooth mobility- When might splinting be advised? (3)
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)
28
Why is there a decrease in mobility after periodontal treatment? (2)
There is an increase in clinical attachment due to:
* formation of the long junctional epithelium
* An increase in tissue tone as inflammatory resolves
29
occlusal trauma in a patient with periodontal disease
What can you do if the PDL is still widened after successful periodontal treatment?
Reduce contact in occlusion (correct occlsual abnormalities)
splinting
30
How do we define localised and generalised in terms of periodontitis?
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%
31
What are we looking for to decide if a tooth is of poor prognosis due to periodontitis & why? (4)
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 ?
32
2 further investigations can be carried out on a periodontal patient (2)
Plaque and Bleeding scores
6 point pocket chart.
Radiographs?
33
2 further bits of info needed from a periodontal patient before determining poor prognosis of teeth (2)
Smoking
Drug history
Systemic disease
| UNSURE
34
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)
* 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)
35
4 further investigations before treatment planning of a patient with generalised severe gingival recession (4)
* 6PPC
* Periapical radiographs
* MPBS
* study models (to monitor gingival recession)
* Clinical photographs (Calibrated by the inclusion of a probe)
36
How can we manage a patient with generalised severe gingival recession (3)
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.
37
List the classifications for periodontal disease
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)
38
How is localised angular periodontitis caused? (2)
When pathway of inflammation travels directly into PDL space
Localised plaque retention factors e.g. overhang, crowding, malposition
39
How to classify localised angular periodontitis
1 walled defect
2 walled defect
3 walled defect
40
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)
Furcation involvement- makes it harder for the patient to clean & more resistant to PMPR.
41
3 clinical/ radiographic signs of periodontal healing (3)
Gingival recession: black triangles,
Clinical reattachment = reduced probing depths
Reduced BOP
42
Provide treatment options for localised angular periodontitis (5)
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 )
43
What is the difference between horizontal and angular bone loss?
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.
44
New classification = How do we define the severity of periodontal disease
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.
45
How does a healthy periodontium react to traumatic occlusion?
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
2. 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
46
How does a healthy but reduced periodontium react to traumatic occlusion?
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)
47
Describe the effect of occlusal trauma in a patient with perio/plaque induced inflammation.
= 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
48
What is chlorhexidine?
Bisbiguanide antiseptic.
49
What is CHX's mode of action?
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
50
What is the substantivity of CHX?
12 hours
51
Give 2 common doses of CHX.
0.2% 10ml/20mg 2x daily OR 0.12% 15ml/18mg 2x daily
52
Give 4 side effects of CHX
staining
taste disturbance
salivary gland enlargement
anaphylaxis
interacts with SLS
53
Give 8 uses of chlorohexidine
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
54
How is HPT provided? (5)
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
55
What is TIPPS?
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
56
What 7 things are recorded on a periodontal pocket chart?
Teeth missing
gingival margin height
pocket depth
loss of attachment
mobility
furcation
bleeding on probing.
57
Give 2 disadvantages of a 6 point pocket chart (4)
1. assumes all pts have same root length/morphology so may appear worse than they are
2. Probing depths are subjective/variation between operators
3. True pocket depth may not be measured accurately if subgingival calculus is blocking the probe from gaining full access to the periodontal pocket
4. Cannot carry out a full mouth chart in children 12-18 since they have immature gums and false pocketing is common
58
What are the local factors for gingival recession?***
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
59
How can you measure recession?
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
60
How is localised recession managed? (6)
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
61
Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.
Give 3 differential diagnoses
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)
62
Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.
What special investigations would you carry out?
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
63
Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.
What is your initial treatment for the tooth? ****
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)
64
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
Bridge
- resin retained or conventional
- fixed fixed or centilever
Implant
RPD
65
Tooth 15 has been root treated, has a 9mm pocket and a vertical bony defect radiographically.
The patient wants an implant: what would you look for? (6)
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
66
Give types of intervention for inadequate bone levels
a) Perio
b) Implant
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
2. 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
67
A patient presents with generalised horizontal bone loss and vertical and furcation bone loss of 46. What is the mechanism of a vertical bone on the mesialdefect? ****
| 2020 paper 1 Q4
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)
68
A patient presents with generalised horizontal bone loss and vertical and furcation bone loss of 46. How may they be further classified?
By number of walls: 1, 2 or 3 wall defects → 2 and 3 wall defects heal better.
69
Following HPT- how is success determined clinically
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
70
The patient is deemed to be suitable for regenerative periodontal surgery/treatment.
What are the indications. (3)
Infrabony defects - 2 and 3 walled defects
Grade 2 furcation in mandibular teeth
Grade 2 buccal furcation in maxillary molars.
Type 1 gingival recession.
71
If regenerative periodontal surgery fails- how else can the tooth be managed? (3)
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
72
Why might non-surgical management of periodontal disease be unsuccessful? (4)
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.
73
Give 2 tests to test for diabetes
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)
74
What test is used to monitor diabetic control?
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.
75
what is the normal value for Hba1c - glycated haemoglobin?
HBA1c
diabetes = 48Mmol/mol (6.5%) or more
normal = < 42 mmol/mol (5.7%)
a prediabetic person is between 42-47mmol/mol
76
How does smoking affect the periodontal tissues? (3)
- 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.
77
What is interleukin-1?
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.
78
A patient attends with erythematous, inflamed gingiva extending beyond the mucogingival junction.
Name 3 oral conditions associated with this.
lichen planus
mucous membrane pemphigoid
pemphigus
79
A patient attends with erythematous, inflamed gingiva extending beyond the mucogingival junction. What 2 local factors that may exacerbate this?
Calculus
Ortho/pros appliances
overcrowding/malposition of teeth
80
A patient attends with inflamed gingiva extending beyond the mucogingival junction.
Give 2 topical treatments. *****
Topical steroids e.g. Betamethasone or beclomethasone, Tacrolimus m/w.
81
Name 3 medications associated with gingival hyperplasia
Phenytoin = anti-epileptic
Cyclosporine = immunosuppressant
amlodipine = Ca channel blocker
82
how is gingival hyperplasia managed? (3)
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.
83
What do the values mean for BPE?
● 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
84
How is mobility graded?
0 = physiological movement
1 = up to 1mm movement
2 = 1-2mm movement
3 = >2mm severe movement that impacts function
can depress or rotate
85
How is furcation graded?
1 = < 1/3rd (<3mm)
2 = > 1/3rd but not all the way through (>3mm)
3 = through and through
86
How is gingival recession graded? (3)
how can this be measured? (3)
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
87
A 28 year old who is fit and well presents with severe bone loss in her full mouth periapicals.
What is your diagnosis?
generalised - stage 4 - grade c - stability? - RF?
88
A 28 year old who is fit and well presents with severe bone loss in her full mouth periapicals.
Give 3 features that lead to this diagnosis of stage 4 grade C periodontitis.****
Age
MH: fit and well
extent of interproximal bone loss at worst site
risk factors - local and systemic
89
A 28 year old who is fit and well presents with severe bone loss in her full mouth periapicals. What further clinical and laboratory investigations could you carry out? (5)
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.
90
A 13-year-old new patient turns up to your surgery. BPE Score of 3 3 3/ 332
What does a BPE score of 3 mean? (1)
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3.5-5.5mm probing depths (partially visible black band)
With bleeding on probing and plaque retentive factors.
91
A 13-year-old new patient turns up to your surgery. BPE Score of 3 3 3/ 332
What teeth should you probe to obtain the BPE score? (1)
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You should complete a simplified BPE- You probe 16, 11, 26, 36, 31, 46
92
What is the normal depth from CEJ to alveolar bone crest? (1)
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junctional epithelium = 1mm
connective tissue attachment = 1mm
= 2mm total biological width/supracrestal attachment
93
A 13-year-old new patient turns up to your surgery. BPE Score of 3 3 3/ 332. What medical condition could the patient have?
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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
94
A 13-year-old new patient turns up to your surgery. BPE Score of 3 3 3/ 332. If the child is not on any medications what else might have caused this?
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
95
A 13-year-old new patient turns up to your surgery. BPE Score of 3 3 3/ 3 3 2.
What 4 other further investigations should you do?
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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)
96
A 13-year-old new patient turns up to your surgery. BPE Score of 3 3 3/ 3 3 2. What is the treatment plan
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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
97
A 13-year-old new patient turns up to your surgery. BPE Score of 3 3 3/ 3 3 2.
Plaque score 10/10/10
10/10/8
The radiograph found 9 teeth with bone loss and the worst site is 10%. Give diagnosis.
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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.
98
Periodontal disease vertical bone defects (infrabony pockets) - what investigations would you use to identify vertical bony defects? (2)
PA radiographs
6 point pocket chart
99
Periodontal disease vertical bone defects (infrabony pockets)
How does an infrabony defect occur?
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.
100
Periodontal disease vertical bone defects (infrabony pockets)
How do we classiy vertical bone defects.
1 wall defect (1 wall left)
2 wall defect (2 wall left) - will heal better
3 wall defect (3 wall left) - will heal better
101
Periodontal disease vertical bone defects (infrabony pockets)
What are the treatment options for vertical bone defects? (3)
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 )
102
In a perio chart, what results would show teeth with worst prognosis? (3)
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.
103
In terms of perio, What patient factors affect prognosis of teeth? (4)
Smoking
OHI and motivation
Systemic disease – e.g poorly controlled diabetes, immunosuppression, pregnancy
Drug history
104
Elderly patient presets with anteriors drifting and increase in over jet
- What could be causing this movement? (3)
- Loss of perio attachment from perio disease
- unfavourable soft tissue profile
- Unfavourable occlusal forces (+ plaque induced gingivitis)
105
Elderly patient presets with anteriors drifting and increase in over jet - what are the treatment options? (3)
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
106
Susan is a 29 year old patient who is a regular attendee at your practice, she has
previously undergone periodontal treatment, she attends as an emergency
complaining of pain in her upper front tooth. On examination you notice a swelling
pertaining to the 11, TTP and there is associated lymphadenopathy.
- Give 2 differential diagnoses for what this condition could be
Periodontal abscess
Periapical abscess
endo-perio lesion/abscess
107
Susan is a 29 year old patient who is a regular attendee at your practice, she has
previously undergone periodontal treatment, she attends as an emergency
complaining of pain in her upper front tooth. On examination you notice a swelling
pertaining to the 11, TTP and there is associated lymphadenopathy.
Give 2 special investigations you would undertake to confirm your diagnosis
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
108
Susan is a 29 year old patient who is a regular attendee at your practice, she has
previously undergone periodontal treatment, she attends as an emergency
complaining of pain in her upper front tooth. On examination you notice a swelling
pertaining to the 11, TTP and there is associated lymphadenopathy.
State 2 ways that you could drain the swelling
* Drain the pus by dilating the pocket
* incise and drain
109
Susan is a 29 year old patient who is a regular attendee at your practice, she has
previously undergone periodontal treatment, she attends as an emergency
complaining of pain in her upper front tooth. On examination you notice a swelling
pertaining to the 11, TTP and there is associated lymphadenopathy.
Give your initial management of this patient’s swelling if not endodontically
involved
* 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
110
A 22 year old presents at your surgery complaining of pain. You can smell his
halitosis from the waiting room,
On examination it is clear that he has ANUG.
Describe 4 intra oral signs of ANUG
* 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 .
111
What 4 risks factors pre-dispose someone to ANUG?
Stress, immunocompromised, smoking,
severely malnourished, poor OH,
sleep deprivation
Underlying viral conditions (HIV/ AIDS)
112
A 22 year old presents at your surgery complaining of pain. You can smell his
halitosis from the waiting room,
On examination it is clear that he has ANUG.
Outline your treatment for this patient
1. Ultrasonic debridement (the necrotic tissue is removed to facilitate healing)
2. Mouthwash
a. 0.2% Chlorhexidine mouthwash twice daily
(3% hydrogen peroxide mouthwash- Anaerobic bacteria are involved & the mouthwash froths up producing oxygen)
3. 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
4. Smoking cessation, vitamin supplementation and dietary advice
5. Hygiene phase therapy/PMPR (to treat the perio disease) once acute symptoms subside
113
Susan is a 29 year old patient who is a regular attendee at your practice, she has
previously undergone periodontal treatment, she attends as an emergency
complaining of pain in her upper front tooth. On examination you notice a swelling
pertaining to the 11, TTP and there is associated lymphadenopathy.
There is a 10mm probing depth on palatal side of tooth. What may have caused the swelling?
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
114
Describe the response of a healthy (but reduced) periodontium to occlusal trauma.
Describe the physiological response & the pathological responses to occlusal trauma in a healthy periodontium.
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.
115
How do You manage traumatic occlusion in a patient with periodontal disease? (3)
1. Control plaque induced inflammation - BSP S3 guidelines
HPT (diet adv, smoking cessation, OHI etc) /PMPR to stabilise the perio
2. Correct abnormal occlusal relations/parafunction
Use of a bite raising appliance
3. Splinting healthy teeth to spread the load and allow the healthy teeth to support
116
What factors can influence localised mobility? (4)
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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
117
- Mobility is not routinely be treated or managed, list 2 circumstances when mobility is to be intervened (2)
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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.
118
Occlusal trauma: Why is there a decrease in mobility after treatment of the periodontitis/plaque induced inflammation? (2)
Due to increased tissue tone and long junctional epithelium attachment with successful HPT
119
occlusal trauma: What can you do if the PDL is still widened after successful treatment? ** unsure
Reduce contacts within the occlusion that is causing the traumatic occlusion initally
then splinting to healthy teeth to spread occlusal load evenly
120
What are the values of average horizontal bone loss for incisors, canine, premolars and molars?
Incisors – 6.3mm
Canines – 8.5mm
Premolars – 10mm
Molars – 12.8mm
121
What are the modifiable systemic factors that can cause periodontitis?
Modifiable & systemic:
* Smoking
* Poorly controlled diabetes
* HIV
* Leukaemia
* Osteopenia
* Osteoporosis
* Stress
* Medications
* Hormonal changes
* Poor nutrition
* Poor SIMD
122
What are the genetic systemic factors that can cause periodontitis? (3)
Monogenetic syndromes – Sickle cell; CF; PKD
Down’s syndrome
papillion lefere
123
Describe why diabetes is a risk factor for periodontal disease. (7)
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.
124
What are the initial aims of HPT? (3)
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.
125
What is the overall aim of periodontal therapy
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.
126
List causes of gingival hyperplasia.
Drug induced:
§ Anti-epileptic = phenytoin
§ Calcium channel blocker – amlodipine
§ Immunosuppressant – cyclosporine
leukaemia
hormones e.g. puberty and preganancy
chronic granulomatous disease
127
What is the classic pattern of gingival hyperplasia?
Starts at the interdental papillae and develops to include up to the entirety of the attached gingivae
128
How does gingival overgrowth influence periodontal status?***
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
129
Patient has arrived with a swelling above the 11 with no systemic symptoms.
There is a 10mm probing depth on the palatal side of the tooth. What could have caused the swelling ?
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.
130
Patient has arrived with a swelling above the 11 with no systemic symptoms.
There is a 10mm probing depth on the palatal side of the tooth.
How will 11 be treated.
1. Careful subgingival instrumentation short of the pocket base. (Attachment is friable & easily damaged so aggressive cutting would cause recession instead of healing)
2. If pus is present- drain by incision or through the periodontal pocket.
3. 0.2% chlorohexidine mouthwash until the acute symptoms subside.
4. Analgesia
5. No antibiotics as there is no systemic involvement
6. Follow up. withperiodontal treatmetn (S3 guidelines)
131
Tooth 46 shows generalised Horizontal bone loss, a vertical defect and furcation involvement. Describe the pattern of bone loss that will be seen on a radiograph?
Vertical bony defects are generally V shaped and sharply outlined.
132
Define localised and generalised bone loss
Localised affects <30% of sites.
Generalised affects >30% of sites.
133
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:
**Give two alternative options for the management of the lower right second molar (47). **
| 2020 paper Q4
* 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.
134
Patient complains of gap of front teeth which gradually increases over time. 21 mobile and cause discomfort. Charting (and photo) given
7 321 123
54321 1234
List 4 bits of information you would like to know about this case. (4)
135
Patient complains of gap of front teeth which gradually increases over time. 21 mobile and cause discomfort. Charting (and photo) given
7 321 123
54321 1234
After sucessful perio treatment is the mobility of the 21 likely to increase or decrease and why? (2).
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mobility will decrease as there is an increase in tissue tone and decrease in probing depth due to an increase in junctional epitheliu????
136
Patient complains of gap of front teeth which gradually increases over time. 21 mobile and cause discomfort. Charting (and photo) given
7 321 123
54321 1234
List 4 bits of information you would like to know about this case.
List 3 management options after successful periodontal treatment (3)
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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
??
137
9mm suppuration pocket, radiolucent area from mid root to apex distally, tooth is endodontically treated, vertical root fracture was ruled out
- 3 differential diagnoses (3)
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138
9mm suppuration pocket, radiolucent area from mid root to apex distally, tooth is endodontically treated, vertical root fracture was ruled out
- What is another clinical information you would like to know to help with diagnosis (1)
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TTP- laterally or vertically ???
139
9mm suppuration pocket, radiolucent area from mid root to apex distally, tooth is endodontically treated, vertical root fracture was ruled out
- What are your initial treatment options for the tooth? (2)
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