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BDS3 CDS > Periodontology > Flashcards

Periodontology Flashcards

1
Q

What are the 10 periodontal disease classifications 2017?

A
  1. health
  2. plaque induced gingivitis
  3. non plaque induced gingival disease and conditions
  4. periodontitis
  5. necrotising periodontitis
  6. periodontitis as a manifestation of systemic disease
  7. systemic diseases of conditions effecting the periodontal tissue
  8. periodontal abscess
  9. periodontal endodontic lesion
  10. mucogingival deformities and conditions
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2
Q

What determines whither the periodontitis is generalised of localised?

A

localised <30% of teeth
generalised >30% of teeth

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3
Q

What information do you need in a perio diagnosis?

A
  • extent
  • stage
  • grade
  • stability
  • risk factors
    ie localised periodontitis stage 3, Grade B, currently unstable with uncontrolled diabetes
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4
Q

What are the 4 stages of periodontitis?

A

At worst site:
1. less than 15% or 2mm bone loss (mild)
2. coronal 1/3 bone loss (moderate)
3. middle 1/3 bone loss (severe)
4. apical 1/3 bone loss (very severe)*

  • or if known to have lost teeth due to perio
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5
Q

How is someone’s periodontitis Grade calculated?

A
  • max % bone loss divided by patient age (measures progression of the disease)
    Grade A = <0.5 (slow)
    Grade B = O.5-1 (moderate)
    Grade C = >1 (rapid)
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6
Q

What are the indications that someone’s periodontal disease is currently stable?

A

BoP < 10%
PPD < or = 4mm
no BoP at 4mm sites

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7
Q

What are the indications that someone’s periodontal disease is in remission?

A

BoP > or = 10%
PPD < or = 4mm
no BoP at 4mm sites

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8
Q

What are the indications that the periodontal disease is active?

A

PPD> or = 5mm
PPD> or = 4mm and BoP

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9
Q

Describe the action you would take if a patient had BPE scores of 1?

A

OHI and DHE

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10
Q

Describe the treatment you would provide if a patient had BPE scores of 2?

A

OHI and removal of plaque retentive factors including all supra and subgingival calculus

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11
Q

Describe the treatment you would provide if a patient had BPE scores of 3?

A
  • periapical radiographs of involved sextants
  • same as code 2 and RSD if required
  • 6ppc in involved sextants after treatment
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12
Q

Describe the treatment you would provide if a patient had BPE scores of 4?

A
  • periapical radiographs
  • same as code 2 and RSD
  • full mouth 6ppc before and after treatment
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13
Q

what are the clinical signs of gingival health?

A
  • no BoP, erythema, oedema, attachment loss or bone loss
  • bone levels range from 1mm-3mm from the cemento-enamel junction
  • <10% BoP
  • pocket depths <3mm
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14
Q

What causes plaque induced gingivitis?

A
  • bacteria in the dental biofilm alone irritating the soft tissue producing inflammation
  • mediated by systemic and local risk factors
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15
Q

What are the clinical signs of plaque induced gingivitis?

A
  • still stippling of the papilla
  • inflammation of the papilla giving rolled appearance
  • plaque and calculus build up
  • no radiographic bone loss
  • no interdental recession
  • BPE 2 or less
  • BoP > 10%
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16
Q

What are the clinical signs for a patient with gingival health but a reduced periodontium?

A
  • probing attachment loss
  • pocket depths < or = 3mm
  • <10% BoP
  • radiographic bone loss possible
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17
Q

What are the clinical signs for a patient with gingivitis and a reduced periodontium?

A
  • probing attachment loss
  • pocket depths < or = 3mm
  • BoP > or =10%
  • ## radiographic bone loss
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18
Q

What are the signs for a successfully treated periodontitis patient with gingival health?

A
  • stable
  • pocket depths <4mm or no site > or = 4mm with BoP
  • <10% BoP
  • radiographic bone loss
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19
Q

What are the signs of a successfully treated periodontitis patient with gingivitis?

A
  • in remission
  • pocket depths <4mm or no site > or = 4mm with BoP
  • > 10% BoP
  • radiographic bone loss
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20
Q

What are some systemic modifying factors of plaque induced gingivitis?

A

A: sex steroid hormones
- puberty
- menstrual cycle
- pregnancy
- oral contraceptives
B: Hyperglycaemia
C: leukaemia
D: Smoking
E: malnutrition

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21
Q

What are the oral modifying factors enhancing plaque accumulation?

A
  • prominent subgingival restoration margins
  • hyposalivation
  • drug influenced gingival enlargements
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22
Q

What can cause non-plaque induce gingival diseases and conditions?

A
  • genetic/developmental disorders
  • specific infections
  • inflammatory and immune conditions
  • reactive processes
  • neoplasms
  • endocrine, nutritional and metabolic diseases
  • traumatic lesions
  • gingival pigmentations
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23
Q

Name a genetic developmental condition causing gingival disease?

A

hereditary gingival fibromatosis
- overgrown fibrotic gingivae that is treated by removal

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24
Q

Name a specific infection causing gingival disease?

A

Herpetic gingival stomatitis (candida albicans)

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25
Q

Name an inflammatory/immune condition causing gingival disease?

A

lichen planus or benign mucous membrane pemphigoid

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26
Q

Name a nutritional deficiency that can cause gingival disease?

A

Vit C deficiency

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27
Q

What are some of the clinical signs of necrotising gingivitis?

A
  • necrosis and ulcer in the interdental papilla
  • gingival bleeding
  • pain
  • pseudomembranous formation
  • halitosis
  • extra-oral lymphadenopathy/ fever
  • in children pain and halitosis less frequent where as lymphadenopathy and sialorrhea more frequent
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28
Q

What are some of the clinical signs of necrotising periodontitis?

A

In addition to the signs of necrotising gingivitis:
- necrosis progression into the PDL and alveolar bone leading to attachment loss
- frequent extra-oral signs
- in severely immuno-compromised patients bone sequestrum might occur

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29
Q

What are the clinical signs of necrotising stomatitis?

A
  • when the necrosis progresses to deeper tissues beyond the mucogingival line, including the lip or cheek mucosa, the ton- gue, etc.
    -bone denudation extending through the alveolar mucosa
  • larger areas of osteitis and bone sequestrum
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30
Q

What are the predisposing conditions for necrotising periodontal disease in severely immunocompromised adults and children?

A

in adults:
- HIV/Aids with CD4 counts < 200 and detectable viral load
- other severe systemic conditions (immunosuppression)
In children:
- severe malnourishment
- extensive living conditions
- severe viral infections

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31
Q

What are the predisposing factors for necrotising periodontal disease in temporary or moderately immunocompromised patients?

A
  • stress, nutritional, smoking habits
  • Previous NPD (residual craters)
  • root proximity or tooth malposition
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32
Q

What is the classification of periodontitis as a manifestation of systemic disease?

A
  • rare diseases that affect the course of periodontitis resulting in early presentation of severe periodontitis
  • based on the primary systemic disease
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33
Q

Name systemic diseases that cause periodontitis as a manifestation?

A
  • papillon lefevre syndrome (advanced bone loss in deciduous dentition)
  • leucocyte adhesion deficiency
  • hypophosphatasia
  • downs syndrome
  • Ehlers-danlos
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34
Q

What is the classification for systemic diseases or conditions affecting the Periodontal tissues?

A
  • Mainly rare conditions affecting the periodontal supporting tissues independently of dental plaque biofilm‐induced inflammation.
  • mimic the clinical presentation of periodontitis
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35
Q

Name a disease which would come under the classification: systemic diseases or conditions affecting the periodontal tissues?

A

diabetes mellitus

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36
Q

What can cause a periodontal abscess in a non-periodontal patient?

A
  • impaction (dental floss, rubber dam, orthodontic elastic)
  • harmful habits (nail biting and clenching)
  • orthodontic factors ( orthodontic forces or crossbite)
  • gingival over growth
  • alteration of root surface
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37
Q

When can a periodontal abscess form in a periodontal patient?

A

Acute Exacerbation:
- untreated periodontitis
- unresponsive periodontitis patient
- supportive periodontal therapy
After treatment:
- post scaling
- post surgery
- post medication

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38
Q

What are the 2 classification for periodontal Endodontic lesions?

A
  • periodontal endodontic lesions with root damage
  • periodontal endodontic lesion without root damage
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39
Q

What causes mucogingival deformities and conditions?

A
  • lack of keratinised gingiva/ insufficient frenal attachment
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40
Q

Describe Type 1 gingival recession?

A
  • gingival recession with no loss of interproximal attachment
  • Interproximal CEJ is clinically not detectable at mesial and distal aspects of the tooth
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41
Q

Describe Type 2 Gingival Recession?

A

Gingival recession associated with loss of interproximal attachment. The amount of interproximal attach‐ ment loss (measured from the interproximal CEJ to the depth of the interproximal sulcus/pocket) is less than or equal to the buccal attachment loss (measured from the buccal CEJ to the apical end of the buccal sulcus/pocket).

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42
Q

Describe Gingival recession Type 3?

A

Gingival recession associated with loss of interproximal attachment. The amount of interproximal attach‐ ment loss (measured from the interproximal CEJ to the apical end of the sulcus/pocket) is greater than the buccal attachment loss (measured from the buccal CEJ to the apical end of the buccal sulcus/pocket).

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43
Q

What is step 1 in the BSP Guidelines for treatment of periodontal disease?

A
  • oral health, risk assessment, diagnosis and care plan
    step 1 - education, OHI, risk factor control, PMPR of all accessible plaque and calculus
  • re evaluate and if engaged move on to step 2 or refer. If not engaged repeat step 1
44
Q

What is Step 2 in the BSP guidelines for treatment of periodontal disease?

A

Step 2 - reinforce OH, risk factor control and behaviour change
- subgingival root instrumentation (hand or power)
- use of adjunctive systemic antimicrobials
- revaluate in 3 months: if patient is stable proceed to step 4 or proceed to step 3 if patient is unstable

45
Q

What is step 3 in the BSP guidelines for treatment of periodontal disease?

A

Step 3
- reinforce OH, risk factor control and behavioural change
- moderate 4-5mm pockets repeat subgingival scaling
- deep pockets > or = 6mm consider alternative causes
- consider referral for pocket management or regenerative surgery
- if referral not possible re- perform subgingival instrumentation
- proceed to step 4 once stable

46
Q

What is the step 4 BSP guidelines for treatment of periodontal disease?

A

Step 4
- maintenance
- supportive periodontal care
- Reinforce OH, risk factors and behaviour
- regular targeted PMPR
- consider adjunctive efficacious tooth paste or mouth wash to control inflammation

47
Q

What are the BSP guidelines to determine an engaging periodontal patient?

A
  • improved OH indicated by > or = 50% improvement in plaque and bleeding scores OR
  • plaque levels < or = 20% and bleeding levels < or = 30% OR
  • patient has met targets as outlined in there personal self care plan as determined by the healthcare practitioner
48
Q

What are the BSP guidelines to determine an non-engaging patient?

A
  • insufficient improvement in OH (plaque and bleeding not improved by >50%)
  • Plaque levels >20% and bleeding levels >30%
  • patient states preference to a palliative approach to periodontal are
49
Q

What factors influence the decision to whither someone is suitable for periodontal surgery?

A
  • Smoking
  • Compliance
  • Oral hygiene (<20% plaque score)
  • Systemic disease
  • Suitability of site (access, soft and hard tissue factors)
  • Prognosis of tooth, importance of tooth
  • Availability of specialist treatment
  • Patient preference
50
Q

What is the ideal endpoint for a periodontal patient?

A

No pockets > 4mm
No pockets = 4mm with BOP
BOP < 10%
Functional and comfortable dentition
Plaque scores < 20% (or target for patient)

51
Q

Who should receive supportive periodontal care?

A

patients that have had periodontal treatment

52
Q

Why is it important that periodontal patients receive supportive periodontal care?

A
  • to prevent recurrent periodontitis (increased pocket depth, bone loss or tooth loss)
  • figures show if they are 5.6 times more lightly to lose teeth if they don’t return for supportive perio care
  • Patients with inadequate SPT after successful regenerative therapy have a fiftyfold increase in risk of probing attachment loss compared with those who have regular recall visits
53
Q

How often should a perio patient return for supportive perio treatment?

A
  • depends on the risk assessment of each individual patient
  • Pocket depth, genetic, age, BOP, environment, and tooth loss
54
Q

What would you do during a supportive perio care visit?

A
  1. examination
    - update MH
    - Oral pathologic examination Oral hygiene status (plaque and bleeding chart)
    -Gingival changes, Pocket depth changes, Mobility changes, Occlusal changes, Dental caries, Restorative, prosthetic, and implant status (6ppc)
  2. Treatment
    - Oral hygiene reinforcement
    - Supra gingival scaling
    - Root surface debridement
    - Polishing
  3. Report, Clean up and scheduling
    - write report in chart and discuss with patient
    - schedule next re call visit
    - schedule further treatment
    - schedule or refer for restorative periodontal treatment
55
Q

What are some of the reasons for reoccurrence of periodontal disease?

A
  • inadequate plaque control
  • failure to comply with the recommended SPT
  • failure of treatment to remove all plaque retentive factors
  • incomplete calculus removal in areas with difficult access
  • inadequate restorations placed post perio treatment
  • ## presence of systemic disease that may be affecting hosts resistance to previously acceptable plaque levels
56
Q

What are the challenges of Periodontal care?

A
  • patients with perio are at risk of reoccurrence for the rest of there life
  • pockets in furcation areas may not be eliminated by initial treatment
  • the only way to determine areas that are losing attachment is a well defined charting system
  • no test to accurately predicts disease activity therefore have to rely on plaque and bleeding scores, probing depths and radiographs
57
Q

What type of periodontal disease can result in denudation of the bone leading to osteitis and oro-antral fistulas?

A

necrotising stomatitis

58
Q

What is Cancrum oris (noma)?

A

is a necrotizing and destructive infection of the mouth and face, and therefore not strictly speaking a periodontal disease. In modern times, this condition usually occurs almost exclusively in malnourished children in developing countries. It may be disfiguring and is frequently fatal. It has been suggested that all cases of cancrum oris develop from pre-existing NG, but this is not confirmed.

59
Q

What is vincents Angina?

A
  • commonly called ANUG
  • acute bacteria infection of the throat caused by spirochetes
  • NPD and VA occur independently of each other
60
Q

How would you diagnose necrotising gingivitis?

A
  • based on symptoms only
  • Ulcerated and necrotic papillae and gingival margin resulting in a characteristic punched-out appearance
  • The ulcers are covered by a yellowish, white or greyish slaim (sloughthing) – no coherence only slime made of fibrin, necrotic tissue, leucocytes, erythrocytes and mass of bacteria. When this ‘membrane’ is removed, the underlying connective tissue becomes exposed and bleeds.
  • Lesions develop quickly
  • Lesions are very painful – severe pain
  • Bleeding readily provoked
  • The first lesions are most often seen interproximally in the mandibular anterior region
  • Foetor ex ore
61
Q

How would you diagnose necrotising peridontitis?

A
  • diagnosis based on symptoms
  • may take radiographs
  • ulcerations associated with deep pockets
  • alveolar bone loss
  • ## submandibular lymph node involvement if severe
62
Q

How would you diagnose denture stomatitis?

A
  • diagnosis is symptom based
  • bone denudation extends through the alveolar mucosa, larger bone sequestra may occur, with large areas of osteitis and oral–antral fistulae. These lesions are of greater severity in patients with severe systemic compromise, including patients with AIDS and patients with severe malnutrition
63
Q

Why is diagnosis for NG, NPD and DS purely symptom based and not tests?

A
  • the histopathology is not pathogenic
  • spirochetes and fusobacteria are isolated from a large number of necrotic disease but they are not always found in primary lesion therefore are of no histological importance
64
Q

How can you differentiate NPD from herpetic gingivostomatitis?

A

Aetiology: NPD=bacteria and HG= herpes simplex virus
Age: NPD= 15-30 and HG = children
Site: NPD = interdental papillae and HG = gingiva and entire oral mucosa
Symptoms: NPD = ulceration, necrotic tissue and yellowish white plaque, Foetor ex ore and moderate fever and HG = number of vesicles which disrupt, leaving small round fibrin covered ulcerations, Foetor ex ore, fever
Duration: NPD = 1-2 days if treated and HG = 1-2 weeks
Contagious: NPD = no and HG = yes
Immunity: HG = partial
Healing: NPD = destruction of periodontal tissue remains and HG = no permanent destruction

65
Q

how may the clinical characteristics of NPD in a HIV positive patient differ from a seronegative patient?

A
  • in HIV patient lesions tend not to be associated with a large amount of plaque and calculus
66
Q

What would be the acute treatment of a patient with necrotising periodontitis?

A
  1. arrest disease process and tissue destruction
  2. control pain and discomfort that is interfering with nutrition and oral hygiene practices
    - superficial debridement to remove the soft mineralised deposits
    -ultrasonic device recommended but exerting minimal force over the ulcerated tissue
    - this should be preformed every day for 2-4 days (acute phase) gradually getting deeper as patient tolerance improves
    - mechanical oral hygiene measure should be limited as it may impair healing
    - instead patient should use chlorohexidine based mouth rinse (0.12-0.2% twice daily) or 3% hydrogen peroxide diluted 1:1 in warm water (antibacterial effect)
    -Patients have to be followed up very closely (daily, if possible) and as the symptoms and signs improve, strict mechanical hygiene measures should be enforced, as well as complete debridement of the lesions.
67
Q

If NPD is showing unsatisfactory response to debridement or showing systemic effects (fever and/or malaise) how would you treat this?

A

Prescribe patient with antibiotic (Metronidazole 400mg TID 3 days)

68
Q

NPD usually occurs over a pre-existing condition (periodontitis or chronic gingivitis). Once the acute phase has been controlled how would you treat the pre-existing condition?

A
  • professional prophylaxis and/or scaling and root planing.
    -Oral hygiene instructions
    -motivation
  • Existing predisposing local factors, such as overhanging restorations, interdental open spaces and tooth malposition, should be carefully evaluated and treated
  • control of the systemic predisposing factors, including smoking, adequate sleep, reduction of stress, dietary advice ( vitamin supplementation) or treatment of involved systemic conditions.
69
Q

After someone has had gingival disease what corrective treatment may you offer them?

A

Gingivectomy and/or gingivoplasty procedures may be helpful for treatment of superficial craters; periodontal flap surgery, or even regenerative surgery, are more suitable options for deep craters
- deep craters act as plaque traps

70
Q

What is an appropriate course of treatment in a patient with a periapical abscess?

A
  • 5 day course of amoxicillin
  • 500mg capsule x 3 daily in adults
  • 6-11months 125mg x 3 daily
  • 1- 4 years 250mg x 3 daily
    or
    metronidazole 400mg 5 days
71
Q

What are some genetic conditions associated with the impairment of the immune system?

A

Papillon-Lefevre syndrome, Chediak-Higashi syndrome, LAS syndrome, Down’s syndrome, chronic granulomatous disease

72
Q

What are some diseases leading to impairment of the immune system?

A

Leukaemia, agranulocytosis, neutropenia, HIV infection,

73
Q

Name some acquired local risk factors that may contribute to periodontal disease?

A

Acquired: plaque, calculus, overhanging and poorly contoured restorations and prosthetic crowns, orthodontic appliances, occlusal trauma

74
Q

Name some non-modifiable systemic risk factors that may contribute to periodontal disease?

A

Non-modifiable: aging, genetic factors, gender (males), genetic disorders: Down syndrome, Papillon-Lefevre syndrome.

75
Q

Name some modifiable systemic risk factors that may contribute to periodontal disease?

A

Modifiable: smoking, poorly controlled diabetes, HIV, leukaemia, osteopenia, osteoporosis, stress, medications, hormonal status, poor nutrition, socioeconomic status

76
Q

Name some anatomical local risk factors contributing to periodontal disease?

A

Anatomical: malpositioned teeth, root groves, concavities and furcations, enamel pearls

77
Q

What effect can occlusal trauma have on periodontitis?

A
  • The ratio of OPG and RANKL is changed
  • Occlusal trauma on top of periodontitis further progresses the disease and leads to more bone loss but it does not cause periodontitis
78
Q

Why can smoking be a risk factor of periodontal disease?

A
  • alters oral microbiota favouring gingivitis
  • increases activation of immune system by releasing chemicals
  • reduced blood flow therefore slower heeling
79
Q

Why can sub-optimally controlled diabetes mellitus be a risk factor in periodontal disease?

A
  • Hyperglycaemia in diabetes may modulate
    RANKL ( the receptor activator of nuclear factor-kappa 𝛃): OPG (osteoprotegerin) ratio and thus contribute to alveolar bone destruction
  • In hyperglycaemia production of AGE (advanced glycation end products) increases which leads to exacerbation of inflammation (production of pro-inflammatory cytokines and destructive metalloproteinases)
80
Q

What test cam be done to determine degree of diabetic control in a patient?

A

HbA1c
- haemoglobin average blood glucose levels

81
Q

what is a normal range of HbA1c in mmol/mol?

A

42 or less (below 6%)

82
Q

What is a prediabetic range in a HbA1c test?

A

42 - 47 mmol/mol (6-6.4%)

83
Q

What result is considered to be a diabetic patient in a HbA1c test?

A

48mmol/mol (6.5% or over)

84
Q

Why is obesity a risk factor for periodontal disease?

A
  • adipocytes secrete a variety or metabolically and immunologically active molecules termed adipokines
  • these adipokines have a proinflammatory effect
85
Q

Why is a nutrition deficiency a risk factor of periodontal disease?

A
  • Severe vit. C deficiency effects collagen production – scorbutic gingivitis - scurvy
    Lack of nutrients - decrease function of the immune system
86
Q

What drugs can cause hyperplasia?

A

Anticonvulsant: phenytoin
Immunosupresants: cyclosporin (transplant patients)
Calcium channel blockers (nifedipine,amlodipine)

87
Q

How do certain drugs such as calcium channel blockers cause an increased risk of periodontal disease?

A

Interaction between the drug and host fibroblasts resulting in a increased deposition of connective tissue supporting a hyperproliferative epithelium.
- patients struggle to clean teeth and remove plaque due to large amount of swelling

88
Q

How is osteoporosis a risk factor in periodontal disease?

A

Contributes to alveolar bone resorption and will accelerate bone loss in periodontitis
- may also increase the release of pro -inflammatory mediators and lead to enhanced destruction of the periodontal tissues

89
Q

How can stress be a risk factor of periodontal disease?

A
  • increased production of cortisol via pituitary gland results in stimulation of the immune system
  • ANS also stimulated leading to production of catecholamine and substance P that can also regulate the immune/inflammatory response
90
Q

Why it is difficult to document cause-effect association between cardiovascular diseases and periodontitis ?

A

The same risk factors for both diseases (smoking, diabetes, stress, obesity)
Common pathomechanisms associated with systemic inflammation and activation of the immune system

91
Q

What are possible mechanisms of periodontitis being risk factor for cardiovascular diseases?

A

Activate cells in the immune system which can play significant role in site of cardiovascular pathology

92
Q

What are the mechanisms of diabetes being a risk factor for periodontitis?

A
  • increased deposition of advanced glycation end products (AGEs) in the periodontal tissues
  • interaction between AGEs and their receptors RAGE lead to local immune and inflammatory response
  • this upregulated response leads to an increased secretion of cytokines (IL-1B, TNF-alpha, IL-6) which increase oxidative stress and disruptions of the receptor activator RANK/OPG axis to favour bone resorption
  • causes local tissue damage, periodontal connective tissue breakdown and resorption of the alveolar boen
93
Q

What is the mechanisms for periodontitis exacerbating diabetes mellitus?

A
  • periodontal bacteria and their products, together with inflammatory cytokines and other mediators produced locally in the inflamed periodontal tissues, enter the circulation and contribute to upregulated systemic inflammation. This leads to impaired insulin signalling and insulin resistance, thus exacerbation of diabetes.
94
Q

What is the mechanisms that makes periodontitis a risk factor to Rheumatoid arthritis?

A
  • activation of the immune system (periodontitis)
  • p. gingivalis - enzyme: PPAD peptidyl arginase deminase
  • circulation of the host proteins results in changing of the proteins conformation which stimulates immunological response to unrecognised compounds which destroys surface cartilage
95
Q

Why is periodontitis a risk factor for respiratory system?

A

Periodontal bacteria debilitate immune protection of the respiratory epithelium making colonisation by other respiratory viruses and bacteria easier

96
Q

According to the SDCEP guidelines how would you treat a periodontal abscess?

A
  • LA and subgingival instrumentation just short of the pocket base
  • if pus present in abscess drain by incision or through the periodontal pocket
  • recommend optimal analgesia
  • recommend 0.2% chlorohexidine mouth rinse twice a day until acute symptoms subside
  • following acute management carry out definitive periodontal instrumentation and arrange recall visit
97
Q

According to the SDCEP guidelines how would you treat a endo-periodontal abscess?

A
  • LA and endodontic treatment
  • 0.2% chlorohexidine mouth rinse until acute symptoms subside
  • recommend optimal analgesia
  • following acute symptoms review within 10 days and carry out supra and subgingival instrumentation if necessary
98
Q

What is the classification of an endodontic lesion?

A
  • primary carious lesion in the pulp which secondarily effects the periodontium
  • destruction of the periodontium which secondarily effects the root canal
  • or by both events occurring at the same time
99
Q

What is excessive occlusal force?

A

forces applied to tissues which are greater than the reparative capacity of the supporting periodontal apparatus and cause occlusal trauma and or excessive tooth wear

100
Q

What is occlusal trauma?

A
  • an injury which results in tissue changes within the attachment apparatus of the tooth as a result of occlusal forces
101
Q

What factors can effect tooth mobility?

A
  • height of PDL
  • width of PDL
  • inflamation
  • Shape, length and number of roots
102
Q

Describe 3 therapies that can be used to reduce tooth mobility?

A
  • removal/control of plaque induced inflammation (PDT)
  • correction of occlusal relations
  • splinting if none of the above have worked
103
Q

What is primary occlusal trauma?

A
  • tissue changes resulting from excessive occlusal forces applied to a tooth with healthy periodontium
104
Q

What is the response of a healthy periodontium to occlusal trauma?

A
  • increase in PDL width until force can be adequately dissipated and then the PDL should stabilise
  • tooth mobility will be increased as a result
  • when forced removed pdl width should return to normal
  • physiological response
105
Q

What occurs if occlusal force exceeds the reparative capacity of the supporting apparatus of the tooth?

A

PDL width will continue to increase
PDL width and tooth mobility fail to reach a stable phase
failure to adaptation is pathological

106
Q

What is secondary occlusal trauma?

A

injury resulting in tissue changes from normalor excessive occlusalforces applied to a tooth or teeth with reducedperiodontal support.
It occurs in thepresenceofattachment loss, boneloss, and normal/excessive occlusal force(s).

BDS3 CDS (6 decks)

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