Periodontology Flashcards
1
Q
Localised
A
<30% of teeth
2
Q
Generalised
A
> 30% of teeth
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
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
5
Q
Stage 1 meaning and bone loss
A
Early/mild <15% or 2mm
6
Q
Stage 2 meaning and bone loss
A
Moderate, coronal third of root
7
Q
Stage 3 meaning and bone loss
A
Severe, mid third of root
8
Q
Stage 4 meaning and bone loss
A
Apical third of root
9
Q
What is perio stage used for?
A
To describe the severity of disease
10
Q
What value is used to work out periodontitis stage?
A
Maximum bone loss at worst site
11
Q
What is perio grade used for?
A
Estimate the disease rate of progression
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
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
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
15
Q
What mucogingival deformity can occur in pregnancy?
A
Pregnancy epulis
16
Q
Gingival fibromatosis
A
Hereditary non-plaque induced gingival disease
17
Q
Cause of herpetic gingival stomatitis
A
Candida albicans
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%)
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
20
Q
Necrotising stomatitis
A
Bone destruction extended through the alveolar mucosa
Larger areas of osteitis and bone sequestrum (than in necrotising periodontitis patients)
21
Q
Examples of diseases that can effect periodontal health
A
Papillon Lefevre Syndrome
Leucocyte adhesion deficiency
Hypophosphatasia
Down’s syndrome
Ehlers-Danlos
22
Q
Function of periodontium
A
Attach the teeth to the jaws
To dissipate occlusal forces
23
Q
Examples of horizontal forces applied to teeth
A
Orthodontics - constant
Occlusal (jiggling) - intermittent
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
25
Occlusal trauma
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
26
Factors affecting tooth mobility (4)
Width of PDL
Height of PDL
Inflammation
Number, shape and length of roots
27
When can tooth mobility NOT be accepted
It is progressively increasing
It gives rise to symptoms
It creates difficulty with restorative treatment
28
Therapy to reduce tooth mobility
Control of plaque-induced inflammation
Correction of occlusal relations
Splinting
29
Primary occlusal trauma
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
30
Response of the healthy periodontium to primary occlusal trauma - physiological vs pathological
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
31
Secondary occlusal trauma
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
32
Fremitus
Palpable or visible movement of a tooth when subjected to occlusal forces
33
Bruxism
Habit of grinding, clenching or clamping the teeth
The force generated may damage both tooth and attachment apparatus
34
Factors considered in tooth migration
Loss of periodontal attachment
Unfavourable occlusal forces
Unfavourable soft tissue profile
35
Options for management of tooth migration
Treat the periodontitis
Correct occlusal relations
Either:
a) accept the position of the teeth and stabilise
b) move the teeth orthodontically and stabilise
36
Characteristics associated with abnormal occlusal contacts
Significantly deeper probing depths, greater clinical attachment loss and increased assignment to a less favourable prognosis
37
Methods to correct occlusal relations
Occlusal adjustment (selective grinding)
Restorations
Orthodontics
38
What should be done to the occlusion of a periodontitis patient?
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
What effect can occlusal therapy have on periodontitis?
May slow the progression and improve the prognosis
40
When might splinting be the appropriate treatment in a periodontitis patient?
Mobility is due to advanced loss of attachment
Mobility is causing discomfort or difficulty in chewing
Teeth need to be stabilised for debridement
41
Is there a correlation between mobility and gingival recession?
No
42
Characteristics of necrotising periodontal diseases
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
Necrotising gingivitis
Only the gingival tissues are affected
44
Necrotising periodontitis
Necrosis progresses into the PDL and the alveolar bone, leading to attachment loss
45
Necrotising stomatitis
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
Cancrum oris
Necrotising and destructive infection of the mouth and face - not strictly a periodontal disease
47
Where are the first lesions in necrotising gingivitis usually seen?
Interproximally in the anterior mandibular region
48
How are diagnoses of necrotising periodontal diseases diagnosed?
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
Necrotising periodontal diseases should be differentiated from..
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
Differences between NPD and herpetic gingivostomatitis
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
Necrotising periodontal disease risk factors
Young adults with predisposing factors such as stress, sleep deprivation, poor OH, smoking, immunosuppression
(in developing countries, mostly malnourished children)
52
Two main objectives for NPD therapy
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
What is the first task in NPD therapy?
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
Why should mechanical oral hygiene measures be limited during acute phase of NPD? What should be done instead?
Brushing in wounds may impair healing and induce pain
Chlorhexidine based mouth rinses (0.12-0.2%, twice daily)
55
What treatment should be considered in NPD with systemic effects, or does not respond to debridement?
Systemic antimicrobials
Metronidazole 400mg 3x daily 3 days
56
Aesthetic consequence following NPD, and what can be done?
Gingival craters
Gingevectomy, gingivoplasty
57
Genetic conditions associated with impairment of the immune system
Papillon-lefevre syndrom
Chediak-Higashi syndrome, LAS syndrome, Down's syndrome, chronic granulomatous disease
58
Diseases leading to impairment of immune system
Leukaemia
Agranulocytosis
Neutropenia
HIV
59
Acquired local risk factors for periodontal disease
Plaque
Calculus
Overhanging restorations
Ortho appliances
Occlusal trauma
60
Anatomical local risk factors for periodontal disease
Malpositioned teeth
Root grooves
Concavities and furcations
Enamel pearls
61
Non-modifiable systemic risk factors for periodontal disease
Aging
Genetic factors
Gender (males)
Genetic disorders (Downs, papillon lefevre syndrome)
62
Modifiable systemic risk factors for periodontal disease
Smoking
Poorly controlled diabetes
HIV
Leukaemia
Osteopenia
Osteoporosis
Stress
Medication
Hormonal status
Poor nutrition
63
Occlusal trauma may cause ____ but not ____
Bone loss
Periodontitis
64
Why is smoking a risk factor for periodontitis?
Effect on oral microbiota
Increased activation of the immune system
Decreased healing capacity due to reduced blood flow
65
How does sub optimally controlled diabetes act as a risk factor for periodontal disease?
Hyperglycaemia in diabetes may modulate RANKL:OPG ratio and thus contribute to alveolar bone destruction
Also, production of AGE increases, exacerbating inflammation
66
Drugs that are risk factors for periodontal diseases
Phenytoin - anticonvulsant, used in epilepsy
Cyclosporin - immunosuppressant, used in transplant patient
Nifedipine, amlodipine - calcium channel blockers
67
Explain how stress is a risk factor for periodontal disease
Hypothalamus-pituitary-adrenal axis is stimulated, leading eventually to increased production and secretion of cortisol, which stimulates the immune system
68
Periodontal disease is a risk factor for diseases of which organ system?
Cardiovascular
69
Long term clinical complications of hypertension
Heart failure
Renal failure
Dementia/stroke
Vascular disease
70
Why is it difficult to document cause-effect association between cardiovascular diseases and periodontitis?
Same risk factors for both
Common pathomechanisms associated with inflammation and activation of the immune system
71
Gingival abscess
Localised to gingival margin
72
Periodontal abscess
Usually related to pre-existing deep pocket, also associated with food packing and tightening of the gingival margin post HPT
73
Pericoronal abscess
Associated with partially erupted tooth, most commonly 8s
74
Endodontic-periodontal lesion
Tooth is suffering from varying degrees of endodontic and periodontal disease
75
Periodontal abscess
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
Signs and symptoms of periodontal abscess
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
SDCEP management of acute periodontal abscess
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
What antibiotics would you prescribe if periodontal abscess showed signs of spread or systemic effects?
Penicillin V 250mg or amoxicillin 500mg 5 days
Metronidazole 400mg 5 days
79
Two potential routes of infection to the periapical tissues
Infection via carious cavity or traumatised crown
Infection via periodontal ligament
80
Symptoms and signs of chronic periodontal abscess
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
Lateral and accessory canals
Found in 30-40% of teeth, usually in the apical third of the root
82
What is the main route of communication between the pulp and the periodontium?
Apical foramen
83
What is the result of a perforation?
Communication between the root canal system and either peri-radicular tissues, periodontal ligament or the oral cavity
84
Potential causes of perforation
Extensive caries
Resorption
Operator error e.g root canal instrumentation
85
3 potential classifications of endo-periodontal lesions with root damage
Root fracture or cracking
Root canal or pulp chamber perforation
External root resorption
86
What are the grades of endo periodontal lesions in endo-periodontal lesions without root damage? and what are the two classifications of these?
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
SDCEP recommended management of perio-endo lesions
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
Pulp is not usually significantly affected by periodontal disease until...?
Recession affects a lateral or accessory canal to the pulp
89
What can lateral or accessory canals be protected by, and what does this usually prevent?
Cementum
Necrosis
90
What can happen if bacteria enters the pulp chamber through lateral or accessory canals?
Chronic inflammation
Possible necrosis
