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BDS3 > Periodontology > Flashcards

Periodontology Flashcards

1
Q

Localised

A

<30% of teeth

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2
Q

Generalised

A

> 30% of teeth

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3
Q

Why must diseases be classified?

A

To properly diagnose and treat patients as well as for scientists to investigate aetiology, pathogenesis and treatment

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4
Q

10 types of periodontal conditions

A

Health
Plaque induced gingivitis
Non plaque related gingival diseases and conditions
Periodontitis
Necrotising periodontal diseases
Periodontitis as a manifestation of systemic disease
Systemic diseases or conditions affecting the periodontal tissues
Periodontal abscesses
Periodontal-endodontic lesions
Mucogingival deformities and conditions

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5
Q

Stage 1 meaning and bone loss

A

Early/mild <15% or 2mm

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6
Q

Stage 2 meaning and bone loss

A

Moderate, coronal third of root

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7
Q

Stage 3 meaning and bone loss

A

Severe, mid third of root

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8
Q

Stage 4 meaning and bone loss

A

Apical third of root

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9
Q

What is perio stage used for?

A

To describe the severity of disease

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10
Q

What value is used to work out periodontitis stage?

A

Maximum bone loss at worst site

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11
Q

What is perio grade used for?

A

Estimate the disease rate of progression

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12
Q

What are the periodontitis grades and what are their values?

A

A - slow - <0.5 bone loss/age
B - moderate - 0.5-1.0
C - rapid - >1.0

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13
Q

BSP guidelines for next step for BPE code 0,1,2

A

Diagnose if gingivitis
<10% BOP - clinical gingival health
10-30% BOP - localised gingivitis
>30% BOP - generalised gingivitis
Also make comment on plaque retentive factors where BPE 2 is given
PMPR for calculus deposits

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14
Q

What is the difference between BSP and SDCEP guidelines for BPE 3?

A

SDCEP - localised 6ppc BEFORE AND AFTER initial treatment
BSP - localised 6ppc after initial treatment

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15
Q

What mucogingival deformity can occur in pregnancy?

A

Pregnancy epulis

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16
Q

Gingival fibromatosis

A

Hereditary non-plaque induced gingival disease

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17
Q

Cause of herpetic gingival stomatitis

A

Candida albicans

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18
Q

Properties of necrotising gingivitis

A

Necrosis and ulcer in interdental papilla (94-100%)
Gingival bleeding (95-100%)
Pain (86-100%)
Pseudomembrane formation (73-88%)
Halitosis (84-97%)
Extraoral regional lymphadenopathy (44-61%)
Fever (20-39%)

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19
Q

Properties of necrotising periodontitis

A

in addition to the signs of necrotising gingivitis, there is bone destruction and loss of attachment
Frequent extraoral signs
In immunocompromised patients, potential bone sequestrum

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20
Q

Necrotising stomatitis

A

Bone destruction extended through the alveolar mucosa
Larger areas of osteitis and bone sequestrum (than in necrotising periodontitis patients)

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21
Q

Examples of diseases that can effect periodontal health

A

Papillon Lefevre Syndrome
Leucocyte adhesion deficiency
Hypophosphatasia
Down’s syndrome
Ehlers-Danlos

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22
Q

Function of periodontium

A

Attach the teeth to the jaws
To dissipate occlusal forces

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23
Q

Examples of horizontal forces applied to teeth

A

Orthodontics - constant
Occlusal (jiggling) - intermittent

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24
Q

Excessive occlusal force

A

Occlusal force that exceeds the reparative capacity of the periodontal attachment apparatus, which results in occlusal trauma and/or causes excessive tooth wear

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25
Q

Occlusal trauma

A

Injury resulting in tissue changes within the attachment apparatus, including periodontal ligament, supporting alveolar bone and cementum, as a result of occlusal forces
Occlusal trauma may occur in an intact periodontium or in a reduced periodontium cause by periodontal disease

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26
Q

Factors affecting tooth mobility (4)

A

Width of PDL
Height of PDL
Inflammation
Number, shape and length of roots

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27
Q

When can tooth mobility NOT be accepted

A

It is progressively increasing
It gives rise to symptoms
It creates difficulty with restorative treatment

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28
Q

Therapy to reduce tooth mobility

A

Control of plaque-induced inflammation
Correction of occlusal relations
Splinting

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29
Q

Primary occlusal trauma

A

Injury resulting in tissue changes from excessive occlusal forces applied to a tooth or teeth with normal periodontal support.
It occurs in the presence of normal clinical attachment levels, normal bone levels and excessive occlusal forces

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30
Q

Response of the healthy periodontium to primary occlusal trauma - physiological vs pathological

A

PDL width increases until forces can be adequately dissipated, the PDL width should then stabilise - tooth mobility increased - successful adaptation to increased demand and therefore physiological
If demand is subsequently reduced, PDL width should return to normal
If demand of occlusal forces is tooth great or the adaptive capacity of the PDL reduced - width may continue to increase, tooth mobility fails to reach a stable phase and the failure of adaptation is regarded as pathological

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31
Q

Secondary occlusal trauma

A

Injury resulting in tissue changes from normal or excessive occlusal forces applied to a tooth or teeth with reduced periodontal support
Occurs in the presence of attachment loss, bone loss and normal/excessive occlusal forces

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32
Q

Fremitus

A

Palpable or visible movement of a tooth when subjected to occlusal forces

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33
Q

Bruxism

A

Habit of grinding, clenching or clamping the teeth
The force generated may damage both tooth and attachment apparatus

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34
Q

Factors considered in tooth migration

A

Loss of periodontal attachment
Unfavourable occlusal forces
Unfavourable soft tissue profile

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35
Q

Options for management of tooth migration

A

Treat the periodontitis
Correct occlusal relations
Either:
a) accept the position of the teeth and stabilise
b) move the teeth orthodontically and stabilise

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36
Q

Characteristics associated with abnormal occlusal contacts

A

Significantly deeper probing depths, greater clinical attachment loss and increased assignment to a less favourable prognosis

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37
Q

Methods to correct occlusal relations

A

Occlusal adjustment (selective grinding)
Restorations
Orthodontics

38
Q

What should be done to the occlusion of a periodontitis patient?

A

The occlusion should be examined and recorded before and after treatment
Occlusion of periodontally compromised teeth should be designed to reduce the forces to be within the adaptive capabilities of the reduced periodontal ligament

39
Q

What effect can occlusal therapy have on periodontitis?

A

May slow the progression and improve the prognosis

40
Q

When might splinting be the appropriate treatment in a periodontitis patient?

A

Mobility is due to advanced loss of attachment
Mobility is causing discomfort or difficulty in chewing
Teeth need to be stabilised for debridement

41
Q

Is there a correlation between mobility and gingival recession?

A

No

42
Q

Characteristics of necrotising periodontal diseases

A

Most severe inflammatory periodontal disorder caused by plaque bacteria
Rapidly destructive and debilitating
Not contagious
Painful, bleeding gums
Ulceration and necrosis of the interdental papilla
Opportunistic infection - caused by bacteria inhabiting healthy oral cavity

43
Q

Necrotising gingivitis

A

Only the gingival tissues are affected

44
Q

Necrotising periodontitis

A

Necrosis progresses into the PDL and the alveolar bone, leading to attachment loss

45
Q

Necrotising stomatitis

A

When the necrosis progresses to deeper tissues beyond the mucogingival line, including the lip or cheek mucosa, tongue, etc
Mostly in malnutrition or HIV
Can lead to destruction of bone leading to osteitis and oro-antral fistula

46
Q

Cancrum oris

A

Necrotising and destructive infection of the mouth and face - not strictly a periodontal disease

47
Q

Where are the first lesions in necrotising gingivitis usually seen?

A

Interproximally in the anterior mandibular region

48
Q

How are diagnoses of necrotising periodontal diseases diagnosed?

A

Based on symptoms
Ulcerated and necrotic papillae giving characteristic ‘punched out’ appearance
Ulcers covered in yellow/white/grey sloughing layer, when removed lesions bleed
Lesions develop quickly and are very painful

49
Q

Necrotising periodontal diseases should be differentiated from..

A

Oral mucositis
HIV associate periodontitis
Herpes simplex virus
Scurvy
Gingivostomatitis
Desquamative gingivitis
Invasive fungal disease
Illicit drug related gingival disease
Agranulocytosis
Leukaemia
Chronic periodontitis

50
Q

Differences between NPD and herpetic gingivostomatitis

A

Bacteria/Herpes simplex virus etiology
Age: 15-30, frequently children
Interdental papilla Entire oral mucosa
Necrotic tissue, ulcerations with yellw/white layer Multiple vesicles which burst leaving small, non fibrin covered round ulcerations

1-2 days if treated 1-2 weeks
Destruction of PDL remains, no permanent destruction

51
Q

Necrotising periodontal disease risk factors

A

Young adults with predisposing factors such as stress, sleep deprivation, poor OH, smoking, immunosuppression
(in developing countries, mostly malnourished children)

52
Q

Two main objectives for NPD therapy

A

Arrest the disease process and tissue destruction
Control the patient’s general feeling of discomfort and pain that is interfering with nutrition and OH

53
Q

What is the first task in NPD therapy?

A

Careful superficial debridement of the soft and mineralised deposits, done daily for the acute phase (usually 2-4 days), done deeper as patient tolerance improves

54
Q

Why should mechanical oral hygiene measures be limited during acute phase of NPD? What should be done instead?

A

Brushing in wounds may impair healing and induce pain
Chlorhexidine based mouth rinses (0.12-0.2%, twice daily)

55
Q

What treatment should be considered in NPD with systemic effects, or does not respond to debridement?

A

Systemic antimicrobials
Metronidazole 400mg 3x daily 3 days

56
Q

Aesthetic consequence following NPD, and what can be done?

A

Gingival craters
Gingevectomy, gingivoplasty

57
Q

Genetic conditions associated with impairment of the immune system

A

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

58
Q

Diseases leading to impairment of immune system

A

Leukaemia
Agranulocytosis
Neutropenia
HIV

59
Q

Acquired local risk factors for periodontal disease

A

Plaque
Calculus
Overhanging restorations
Ortho appliances
Occlusal trauma

60
Q

Anatomical local risk factors for periodontal disease

A

Malpositioned teeth
Root grooves
Concavities and furcations
Enamel pearls

61
Q

Non-modifiable systemic risk factors for periodontal disease

A

Aging
Genetic factors
Gender (males)
Genetic disorders (Downs, papillon lefevre syndrome)

62
Q

Modifiable systemic risk factors for periodontal disease

A

Smoking
Poorly controlled diabetes
HIV
Leukaemia
Osteopenia
Osteoporosis
Stress
Medication
Hormonal status
Poor nutrition

63
Q

Occlusal trauma may cause ____ but not ____

A

Bone loss
Periodontitis

64
Q

Why is smoking a risk factor for periodontitis?

A

Effect on oral microbiota
Increased activation of the immune system
Decreased healing capacity due to reduced blood flow

65
Q

How does sub optimally controlled diabetes act as a risk factor for periodontal disease?

A

Hyperglycaemia in diabetes may modulate RANKL:OPG ratio and thus contribute to alveolar bone destruction
Also, production of AGE increases, exacerbating inflammation

66
Q

Drugs that are risk factors for periodontal diseases

A

Phenytoin - anticonvulsant, used in epilepsy
Cyclosporin - immunosuppressant, used in transplant patient
Nifedipine, amlodipine - calcium channel blockers

67
Q

Explain how stress is a risk factor for periodontal disease

A

Hypothalamus-pituitary-adrenal axis is stimulated, leading eventually to increased production and secretion of cortisol, which stimulates the immune system

68
Q

Periodontal disease is a risk factor for diseases of which organ system?

A

Cardiovascular

69
Q

Long term clinical complications of hypertension

A

Heart failure
Renal failure
Dementia/stroke
Vascular disease

70
Q

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

A

Same risk factors for both
Common pathomechanisms associated with inflammation and activation of the immune system

71
Q

Gingival abscess

A

Localised to gingival margin

72
Q

Periodontal abscess

A

Usually related to pre-existing deep pocket, also associated with food packing and tightening of the gingival margin post HPT

73
Q

Pericoronal abscess

A

Associated with partially erupted tooth, most commonly 8s

74
Q

Endodontic-periodontal lesion

A

Tooth is suffering from varying degrees of endodontic and periodontal disease

75
Q

Periodontal abscess

A

Infection in a periodontal pocket which can be acute or chronic and asymptomatic if freely draining
Rapid destruction of periodontal tissues, with a negative effect on the prognosis of the affected tooth

76
Q

Signs and symptoms of periodontal abscess

A

Swelling
Pain
Tooth may be TTP in lateral direction
Deep periodontal pocket
Bleeding
Suppuration
Enlarged regional lymph nodes
Fever
Tooth usually vital
Commonly pre-existing periodontal disease

77
Q

SDCEP management of acute periodontal abscess

A

Careful subgingival instrumentation, short of the base of the periodontal pocket, to avoid iatrogenic damage - LA may be required
If pus present, drain by incision or through periodontal pocket
Recommend analgesia
Do not prescribe antibiotics unless signs of spreading infection/systemic involvement
Recommend 0.2% chlorhexidine mouthwash
Follow with review, periodontal instrumentation and recall

78
Q

What antibiotics would you prescribe if periodontal abscess showed signs of spread or systemic effects?

A

Penicillin V 250mg or amoxicillin 500mg 5 days
Metronidazole 400mg 5 days

79
Q

Two potential routes of infection to the periapical tissues

A

Infection via carious cavity or traumatised crown
Infection via periodontal ligament

80
Q

Symptoms and signs of chronic periodontal abscess

A

Deep periodontal pockets reaching or close to apex
Negative or altered response to pulp vitality tests
Bone resorption in apical or furcation region
Spontaneous pain
Pain on palp and percussion
Tooth mobility
Purulent exudate
Sinus tract
Crown, gingival colour alterations

81
Q

Lateral and accessory canals

A

Found in 30-40% of teeth, usually in the apical third of the root

82
Q

What is the main route of communication between the pulp and the periodontium?

A

Apical foramen

83
Q

What is the result of a perforation?

A

Communication between the root canal system and either peri-radicular tissues, periodontal ligament or the oral cavity

84
Q

Potential causes of perforation

A

Extensive caries
Resorption
Operator error e.g root canal instrumentation

85
Q

3 potential classifications of endo-periodontal lesions with root damage

A

Root fracture or cracking
Root canal or pulp chamber perforation
External root resorption

86
Q

What are the grades of endo periodontal lesions in endo-periodontal lesions without root damage? and what are the two classifications of these?

A

Grade 1 - narrow deep periodontal pocket in 1 tooth surface
Grade 2 - wide deep periodontal pocket in 1 tooth surface
Grade 3 - deep periodontal pockets in more than one tooth surface
Classified by whether in periodontitis patient or non-periodontitis patient

87
Q

SDCEP recommended management of perio-endo lesions

A

Carry out endodontic treatment
Recommend analgesia
Do not prescribe antibiotics unless signs of systemic involvement
0.2% chlorhexidine mouthwash until acute symptoms subside
Review 10 days and carry out supra/subgingival instrumentation as necessary

88
Q

Pulp is not usually significantly affected by periodontal disease until…?

A

Recession affects a lateral or accessory canal to the pulp

89
Q

What can lateral or accessory canals be protected by, and what does this usually prevent?

A

Cementum
Necrosis

90
Q

What can happen if bacteria enters the pulp chamber through lateral or accessory canals?

A

Chronic inflammation
Possible necrosis

BDS3 (20 decks)

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