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BDS 3 CDS > Periodontology > Flashcards

Periodontology Flashcards

(63 cards)

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1
Q

what extent can periodontitis be classified

A

localised - less than 30%
generalised - more than 30%
molar incisor pattern

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2
Q

what stages are used in classification

A

maximum bone loss in the worst area on radiograph
1 - early/mild - less than 15%, or 1-2mm
2 - moderate - coronal third, 3-4mm
3 - severe - mid-third, more than 5mm
4 - very severe - apical third, more than 5mm

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3
Q

what grades are used in classification

A

% bone loss over age, rate of destruction
a - slow - less than 0.5
b - moderate - 0.5-1.0
c - rapid - more than 1.0

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4
Q

what systemic risk factors are present in periodontitis

A

diabetes, smoking, obesity, stress, alcohol consumption

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5
Q

what defines stable periodontitis

A

bleeding on probing less than 10%
pocket depth less than or = to 4mm
no bleeding at 4mm sites

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6
Q

what defines periodontitis in remission

A

bleeding on probing greater than 10%
pocket depth less than or = to 4mm
no bleeding at 4mm sites

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7
Q

what defines unstable periodontitis

A

pocket depth more than or = to 5mm
bleeding at 4mm pockets

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8
Q

why is the 4mm pocket depth important

A

patients cannot clean pockets greater than 4mm themselves, if a pocket is 4mm and is bleeding, it is unable to heal and needs further RSD

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9
Q

what defines a healthy periodontium

A

absence of bleeding on probing, erythema, oedema, pocket depth 1-3mm, no radiographic bone loss or interdental recession

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10
Q

what defines plaque induced gingivitis

A

bleeding on probing greater than 10%, no radiographic bone loss, no recession, pockets no greater than 4mm

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11
Q

give 3 uses of chlorhexidine

A

necrotising ulcerative gingivitis - after debridement, too painful for patients to brush, instead use chlorhexidine mouthwash 2 times a day
periodontal patients - respond well to hygiene phase therapy but some persistent pockets of 5mm or more - can be put in these pockets when carrying out RSD
trauma patients - should use mouthwash for a week after trauma

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12
Q

what is the advantages and disadvantages of local microbials

A

advantages - not systemic, higher concentration, no drug interactions, no patient compliance, can use chlorhexidine
disadvantages - expensive, still require disruption of biofilm

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13
Q

why are antibiotics not first line use for periodontitis patients

A

bacteria in perio is in a biofilm, surrounded by extra cellular matrix, antibiotics cannot penetrate through the layers of this, so need mechancial disruption of biofilm, bacteria is then vulnerable and can use antibiotics after this - only in patients with rapid disease - grade b or c

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14
Q

what cohort of patients is necrotising gingivitis/periodontitis in

A

malnourished children or immunosuppresed - HIV positive

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15
Q

give clinical signs of necrotising gingivitis

A

painful bleeding gums, ulceration and necrosis of interdental papilla, rapidly destructive, halliotosis, yellowish white plaque (Slime)

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16
Q

what treatment would be given to patients with NUG

A

ultrasonic debridement of necrotic tissue, painful to brush teeth so need chlorhexidine mouthwash - 0.1% 10ml twice a day

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17
Q

what kind of antiboitic is given to patients with NUG and when is it given

A

200mg metronidazole 3 times a day for 3 days (TID - 3 times daily)

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18
Q

how does chlorhexidine work

A

group of biguanides one cation invades the cell and the other alters the cell wall, this increases permeability leading to precipitation of cytoplasm and cell death

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19
Q

what is the relationship between smoking and periodontitis

A

smoking alters the microbiome - more pathogenic and destructive as it reduces the level of oxygen in the mouth. Therefore more anaerobic bacteria survive - P. gingivalis, A.A, more destructive. it also alters the immune system to increase pro-inflammatory cytokines. additionally, it is a vasoconstrictor which reduces blood flow and reduces healing capacity

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20
Q

what is the relationship between diabetes and periodontitis

A

sub-optimally controlled diabetes results in hyperglycaemia. Increase in glycotoxin, which increases the level of proinflammatory mediators such as IL. This alters the ratio between OPG and RANKL - resulting in more alveolar bone loss. Also, increases advanced glycation end products which increases pro-inflammatory cytokines and desctructive inflammatory mediators. Results in more inflammation which is destructive to the periodontium

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21
Q

what is medication is linked with risk of periodontitis

A

anti-convulsants - phenytoin
immuno-suppressants - cyclosporin
calcium channel blockers - nifidepine

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22
Q

what other systemic diseases are linked with periodontitis

A

an increase in chronic inflammation has an effect on the overall wellbeing of the patient. Increase systemic inflammation, by inflammatory mediators.
cardiovascular disease - hypertension and artherosclerosis
rheumatoid arthritis
alzheimer’s dementia

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23
Q

who requires supportive periodontal care

A

every periodontal patient, for the rest of their life. Always at risk of disease recurring.

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24
Q

when should supportive periodontal care be carried out.

A

Depends on every individual patient. Need to risk assess to see how likely they are for disease recurring, therefore, how often they should be seen and supported to prevent this happening. Risk assessment dependant on - bleeding on probing, probing depth, bone levels per age, tooth loss, systemic disease and environmental factors (e.g. smoking)

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25
what is done in supportive periodontal care
part 1 - examination. Need to check medical history, plaque and bleeding scores, probing depth, can use this to inform oral hygiene and motivation levels. evaluation of caries, restoration, prosthesis. compare this to last visit part 2 - treatment, depending on what is found. remove any supra gingival plaque and calculus, want to provide patient with a polished surface easy to clean. If any pockets larger than 4mm - RSD. pockets 1-3mm - unless there is visible calculus, no subgingival scaling - can effect attachment, and cause attachment loss.
26
what do you do if patient disease recurs
need to find the reason why - and sort this out first. re-motivate patient.
27
what are ramjford's teeth
16,21,24,36,41,44
28
what are the scores for modified bleeding score
measured at 4 points around ramjford's teeth, 0 - no bleeding, 1 - bleeding on probing present
29
what are the scores for modified plaque score
measured at 3 points around ramjford's teeth, 0 - no plaque present even with a probe, 1 - plaque present with a probe, 2 - plaque visibly present
30
what modified plaque and bleeding scores show a non-compliant patient
plaque score > 30% bleeding score > 35%
31
where is bleeding measured from for MBS
marginal bleeding around 4 points on ramjford's teeth
32
what is the pulpal diagnosis of a patient presenting with pain on hot and cold, when cold test, only lasts a few seconds after stimulus applied
reversible pulpitis
33
what is the pulpal diagnosis of a patient presenting with pain on eating and spontaneous, sharp, positively responds to EPT and thermal test, pain lasting after stimulus removed
symptomatic irreversible pulpitis
34
what would a patient be complaining of with asymptomatic irreversible pulpitis
no pain on eating, normal response to EPT and thermal testing, but deep restoration or caries, pulpal exposure if removal
35
what is the diagnosis if a pulp responds negatively to EPT
pulpal necrosis
36
what are the diagnostic categories available if a tooth has previously been root treated
previously treated - complete root canal treatment previously initiated - pulpectomy or pulpotomy, incomplete RCT
37
what is the diagnostic requirement for normal apical tissues
no TTP or pain on biting, no radiolucency evident on radiograph, lamina dura is intact and space is uniform
38
if a patient presents with TTP or pain on biting/palpating, what is your differential diagnosis
symptomatic apical periodontitis
39
if a patient presents with a large apical radiolucency, widened PDL space but no TTP, what is your differential diagnosis
asymptomatic apical periodontitis
40
what is the difference between a chronic apical abscess and an acute apical abscess
both in response to pulpal infection and necrosis chronic - no pain associated, small pimple, pus discharged through sinus tract acute - rapid onset, painful, extreme tenderness of tooth to pressure, fever also associated
41
what is condensing osteitis
radiopaque lesion at apices, bony reaction to inflammatory stimulus
42
what is a periodontal abscess
abscess in periodontal space, in patient with periodontitis, deep pockets, food packing in here and build up of bacteria causing infection. causes rapid destruction to periodontal structures. symptoms - pain, but not as painful as periapical periodontitis,
43
how is a periodontal abscess treated
removal of bacteria with scaling, mustnt go too deep or will cause more attachment loss. antibiotics only given if systemic infection - 250mg penicillin v
44
how does pulp and periodontal tissue communicate
dentinal tubules - porous, bacteria can travel through here to reach pulp and cause infection of pulp. only if gap between enamel and cementum in which dentine is exposed to bacteria accessory/lateral canals - bacteria travel through here apical foramen furcal canals
45
how are perio-endo lesions classified
if had root damage or not - perforation or trauma if patient has periodontal disease or not - this could be the cause of the endodontic lesion then the size of the lesion grade 1 - on one surface, narrow deep pocket grade 2 - on one surface, wide deep pocket grade 3 - wide pocket on more than one surface
46
how are perio-endo lesion treated
endodontic treatment first - RCT review in 10 days - periodontal treatment review and check for healing if not - surgical treatment
47
give 4 reasons for tooth mobility
periodontitis, trauma, occlusal trauma, dental abscess
48
when must tooth mobility be intercepted
if giving rise to symptoms, if interfering with restorative treatment, if it's getting progressively worse
49
how does mobility come about
width of PDL space, height of PDL space, inflammation, size shape and number of roots
50
how does occlusal trauma increase PDL space
pressure on PDL, increases vascularisation, results in necrosis of PDL and alveolar bone resorption - increases mobility
51
what is secondary occlusal trauma
when excessive occlusal force results in increased tooth mobility in a dentition already with periodontitis - increased probing depth, reduced clinical attachment levels
52
what is fremitus
visible or palpable movement when teeth come into occlusal contact. tooth movement caused by occlusal forces
53
what is the issue with splinting
appropriate when mobility due to advanced loss of attachment, causing issues with eating, need stabilised for debridement. will not treat cause, if already periodontitis will be a plaque retentive factor but makes patient comfortable, treatment of last resort
54
what is supracrestal attachment
from alveolar crest to gingival sulcus, includes junctional epithelium and connective tissue. restorative margins should not lie here
55
what is recorded in a 6PPC
teeth missing, gingival margin, bleeding on probing, probing depth, loss of attachment, mobility, furcation
56
what is the classification of mobility
0 - normal physiological mobility, 0.1-0.2 1- increased mobility, less than 1mm, only horizontal 2 - increased, more than 1mm but only horizontal 3 - increased, in both horizontal, vertical or rotational
57
what is the classification of furcation involvement
1 - less than one third of the tooth support 2 - more than one third 3 - through and through
58
what is recorded on the abbreviated 6PPC
BOP, probing depth, mobility, furcation
59
what is an example of non-plaque induced gingivitis
gingival herpetic stomatitis - herpes simplex virus 1 infection, common in young children, systemic infection associated with fever, treated with acyclovir 200mg 5 times a day
60
what is step 1 of periodontal treatment
control of local risk factors - calculus, overhangs - PMPR and OHI control of systemic risk factors - diabetes, smoking cessation
61
what is step 2 of periodontal treatment and when do patients move on to this
step 1 (OHI and PMPR) plus subgingival instrumentation (with or without local antimicrobials i.e. chlorhexidine). patients only move from step 1 when they have adequate OH (plaque less than 15% and BOP less than 10%) but pockets more than 4mm persist (or BOP at 4mm sites)
62
what is step 3 of periodontal treatment and when do patients move on to this
periodontal surgery - only in specific cases. when residual pockets persist even after step 1 and 2
63
what is step 4 of periodontal treatment and when do patients move on to this
supportive periodontal care, review appts every 3-12 months depending on risk factor of patient - patients never cease to be periodontal patients. patients only move on to this when good plaque control, pocket depth less than 4mm, BOP less than 10% and no bleeding at 4mm sites - stable

BDS 3 CDS (7 decks)

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