Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BDS4 > Restorative - Periodontology > Flashcards

Restorative - Periodontology Flashcards

1
Q

What clinical and lab investigation can you do to help with periodontal diagnosis?

A
  • history and exmaination
  • 6PPC
  • Full mouth OPT or PA
  • Microbiological analysis of sample (swap of cervicular fluid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How would you decide on the prognosis of individual teeth that have periodontal disease

Do in systemical way like new patient assessment to make sure dont miss anything

A
  • Facial swelling due to periodontal abscess
  • Loss of attachment
  • Tooth mobility
  • furcation involvement

What you assess on 6PPC bascially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. What bacteria are implicated in periodontal disease?
A

P.ginigvalis
AA aggregtibact actinomycomitans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. 2 further investigations to be carried out for perio patients to aid diagnosis ? (2)
A

6PPC
MP&BS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Give 4 reasons tooth may have a poor prognosis in a periodontal patient?

A
  • LOA (less supporting structures)
  • Mobility (loss of bone support)
  • furcation involvement (difficult to keep clean for patient, increase risk of caries
  • Non longer vital
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. What patient factors affect prognosis of teeth? (2)
A
  • Smoking
  • diabetes
  • family history of periodontal disease
  • Stress
  • Levels of OH
  • Immunosuppressed and pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Risk Factors-
1. Why is diabetes a risk factor in periodontal disease?

A
  • In patients with poorly controlled glucose levels there are increased advanced glycation end products (AGE) (due to reaction of glucose and other glycating compounds) which causes microvascular changes (including increased inflammatory cytokine release and chemotaxis such as TNF &interleukins, increased permeability and adhesion of endothelial cells and increased MMPS) this increases systemic inflammation therefore increasing risk of periodontal disease
  • Also, implications of poor wound healing and immunosuppression (as a result of impaired neutrophil function) and alteration of collagen metabolism in poorly controlled diabetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What tests are carried out to tests for diabetics?

A
  • Fasting plasma glucose
  • Random plasma glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. What is the normal value for this? Fasting and random plasma glucose.
A
  • RPG- normal < 11.1mmol/L, diabetes > 11.1mmol/L on 2 separate occasions
  • FPG- normal <7mmol/L, diabetes >7mmol/L on 2 separate occasions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Give 1 test for diabetic control?
A
  • Hb1aC- glycated haemoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. What is it normal value for a Hb1aC in a patient who has well controlled diabetes.
A
  • <7% (treatment aims for 6.5%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. How does smoking affect the periodontal tissues?
A
  • Smoking impairs the vasculature of the gingival and periodontal tissues resulting in reduced blood flow (shown through less gingival erythema and bleeding on probing- masking effect on gingivitis and periodontitis)
  • It also alters the recruitment (via chemotaxis) and function of various inflammatory cells including neutrophils
  • Shifts the inflammatory balance towards tissue destruction through increased production and expression of pro-inflammatory mediators such as cytokines
  • Can also result in impaired wound healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. What is interleukin 1 and what does it do?
A
  • Pro-inflammatory cytokine which plays a role in the regulation of immune responses
  • Produced by a range of cells including epithelial cells, macrophages, endothelial cell and B cells
  • Stimulated the release of enzymes and osteoclasts causing increased tissue destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. What do the values mean for BPE?
A
  • 0- black band showing completely, no BoP or plaque retentive factors (no Tx, OHI)
  • 1- black band visible, BoP, no plaque retentive factors (Tx- OHI)
  • 2- black band visible, BoP, supra or sub-gingival calculus or plaque retentive factors (Tx- OHI, remove plaque retentive factors, supra-gingival scaling and RSI as required)
  • 3- black band on partially visible pocket 3-5-5.5mm (Tx- OHI, remove plaque retentive factors, supra-gingival scaling and RSI as required, 6ppc at review)
  • 4- black ban no longer visible pocket >5.5mm (Tx- OHI, remove plaque retentive factors, supra-gingival scaling and RSI as required, 6PPC full mouth)
  • *- furcation involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. How is mobility graded?
A
  • 0- physiological movement 0-0.2mm
  • 1= <1mm horizontal movement
  • 2= 1-2mm horizontal movement
  • 3= >2mm horizontal and vertical movement (rotations and depression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. How if furcation graded?
A
  • 1=<3mm horizontal involvement
  • 2= >3mm horizontal involvement but not through and through
  • 3= through and through defect
17
Q
  1. How is gingival recession graded?
A
  • Millers classification
  • 1= marginal tissue recession that does not extend to the mucogingival junction
  • 2= marginal tissue recession that extends to or beyond the mucogingival junction with no PD attachment loss in interdental area
  • 3= marginal tissue recession that extend to or beyond the mucogingival junction with PD attachment loss in the interdental area of malposition of teeth
  • 4= marginal tissue recession that extends to or beyond the mucogingival junction with sever bone or soft tissue loss in the interdental area and/or sever malpositioning of teeth
18
Q
  1. Why would mechanical root surface debridement not be successful in limiting pocket bacteria/ Why would NSPD be unsuccesful? (2)
A
  • Inadequate RSD due to poor technique or lack of operator experience
  • Specific pocket sites may be inaccessible to instrumentation meaning bacteria persist and may further invade for example dentinal tubules (e.g. deep furcation lesions and angular defects)
  • Patient not adhering to OH requirements
  • Failure to disrupt biofilm
  • Patient immunocompromised (HIV diabetes etc.)
  • Patient smoking
  • Associated endodontic lesions/perforation causing continual reinfection of pocket
19
Q

What are some possible reasons as to why antibiotics should not be prescribed for periodontal disease?

A
  • AB should only be prescribed if systemic involvement, spreading infection or patient is immunocomproimised.
  • Systemic AB also may not reach the site of disease
  • May be inactived by 1st pass metabolism so drug is in too small of a concentration
  • Cannot penotrate the biofilm
  • Poor patient adherence to the regimen
20
Q
  1. How would you manage a periodontal abscess with systemic involvement? (5)
A
  • Gentle debridement just short of the base of the pocket to avoid damage(and flushing out cells involved in healing)
  • If pus present then drain through the pocket or via incision
  • Recommend analgesics
  • Recommend chlorohexidine mouthwash until acute symptoms subside
  • AB of Pen V (250mgx2 500mg 4x a day for 5 days). Metronidazole (400mg 3x daily for 5 days)
  • Following acute management then review (within 10 days) carry out definitve periodontal instrumentation and HPT
  • XLA if tooth is hopeless
21
Q
  1. What would be clinical signs of stable periodontal health?
A
  • No pockets of greater than 4mm
  • Any pockets of 4mm have no BOP
22
Q
  1. What would be clinical values would be given for plaqye and bleeding in an engaged patient?
A

An overall 50% reduction from the baseline reading
MPS - <20%
MBS - <30%

23
Q

What is involved in step one of the S3 BSP guidelines?

A

I: Explain disease, risk factors & treatment alternatives, risks & benefits including no treatment
II: Explain importance of Oral Hygiene (OH), encourage and support behaviour change for OH improvement
III: Reduce risk factors including removal of plaque retentive features, smoking cessation and diabetes control interventions
IV: Provide individually tailored OH advice including interdental cleaning, + / - adjunctive efficacious toothpaste & mouthwash,
+ /- Professional Mechanical Plaque Removal (PMPR) including supra and subgingival scaling of the clinical crown
V: Select recall period following published guidance and considering risk factors such as smoking and diabetes

24
Q

What does TIPPS stand for in terms of periodontal treatment

A

Talk
Instruct
Practise
Plan
Support

25
Q

What are 7 things recorded on a 6PPC?

A
  • Recession
  • Pocket depth
  • Loss of attachment
  • Mobility
  • Furcation involvement
  • teeth present
  • BOP
26
Q

Give two disadvantages with a pocket chart in general?

A

Assumes everyone has the same length of roots
Probing depths are subjection and operator dependant

Time-consuming and can be uncomfortable for the patient?

27
Q

What is SIRS?

Sepsis

A

Systemic inflammatory response syndrome. Need 2 or more of the following.
4 things
BR > 20/min
HR -90bpm
WBC - <4000 cell/mm3 or >12,000 cell/mm3
Temperature - less than 36 or greater than 38

28
Q

Patient presents with generalised severe gingival recession, 60 years old and with a mobile 21 and experiencing discomfort.
1. Give a cause for this and explain why?

A
  • Due to the recession their is exposed root dentine which causes sensitivity

Dentine has tubules, or narrow channels, that lead to the pulp of the tooth, where the nerve fibres are located. When external stimuli can reach these tubuli, they can stimulate the nerve fibres and are registered as pain. The major cause for exposed dentine is recession of gum tissue.

29
Q

Angular bone loss
2. How is this caused? (2)

A
  • Alveolar bone loss occurs in response to an inflammatory biofilm which does not extend along the length of bone it is adjacent to
  • Angular/vertical bone loss will occur is the zone of destruction (2mm radius) is less than the width of bone
  • Pathway of inflammation travels directly into the PDL space following plaque pattern generally caused by localised plaque retention factors and poor Oh and interdental cleaning
30
Q
  1. What is the limitation of treating this lesion? (1) (furcation involvment) and why is this a problem.
A

This is difficult for the patient to clean themselves
Furcation has reduced blood supply so there is reduced healing
Cannot treat 1 walled defect

31
Q

Give 2 clinical or radiographic signs of healing (perio disease)?

A
  • Reduction in probing depth as reattachment of long junctional epithelium
  • Reduced BOP
  • Ginigval recession - formation of black triangles between the teeth
32
Q
  1. What is the difference between horizontal and angular bone loss?
A
  • The radius destruction of plaque is approximately 2mm
  • Horizontal bone loss is found where plaque and inflammatory process destroys bone completely between 2 roots (bone dimension <2mm between roots)
  • Angular bone loss occurs where the 2mm radius is less than the width of the bone between the two teeth resulting in bone being left on one side. So there is more than 2mm of bone between the two teeth.
33
Q

What is the radius of destruction for plaque?

A

2mm

34
Q
  1. Define localised and generalised bone loss?
A
  • Localised < 30% of teeth affected
  • Generalised >30% of teeth affected

BDS4 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions