Periodontics Flashcards
(94 cards)
1
Q
Why do we need a classification system for gingivitis?
A
The classification systems are necessary in order to provide a framework in which to scientifically study the aetiology, pathogenesis and treatment.
2
Q
What is gingivitis?
A
It is generally regarded as site-specific inflammatory condition initiated by dental biofilm accumulation and characterized by gingival redness and oedema and the absence of periodontal attachment loss
3
Q
How is gingivitis diagnosed?
A
It is a purely diagnosed condition. Use signs and symptoms. Look, feel and SMELL it. Listen to the patient – do their gums bleed? Are they experiencing soreness in gums? Increased BOP? Halitosis smell? Discomfort on probing?
4
Q
What if you see any bone loss in the radiograph and think it is gingivitis?
A
NO IT IS PERIODONTITIS. Any attachment loss = periodontitis (except for reduced periodontium).
5
Q
Compare and Contrast reduced periodontium and bone loss.
A
- Reduced periodontium refers to a condition where the supporting structures of the teeth (including bone, periodontal ligament, and gingiva) are diminished in quantity or quality, but not necessarily due to active disease. This can result from factors like orthodontic treatment, remodeling after extractions, or natural variation. It implies less periodontal support but may not involve ongoing pathological bone loss.
- Bone loss specifically refers to the destruction or resorption of alveolar bone supporting the teeth, typically due to periodontal disease (e.g., periodontitis) or other pathological processes like trauma or tumors. Bone loss is often progressive if untreated and is a hallmark of periodontitis, detected via radiographs or clinical probing.
6
Q
What is the prevalence of gingivitis and periodontitis?
A
Gingivitis of some degree – 95% of the population
Periodontitis – 60-65% of over 65 population
7
Q
How do we define cases of gingivitis in an intact periodontium?
A
Localised gingivitis : Probing attachment loss – No, Radiographic bone loss – No, BOP score – between 10% and 30%
Generalised gingivitis: Probing attachment loss – No, Radiographic bone loss – No, BOP score – above 30%
8
Q
How do we define cases of gingivitis in a reduced periodontium without history of periodontitis?
A
Localized gingivitis: Probing attachment loss – Yes, Radiographic bone loss – Possible, Probing depth all sites – less than 3mm, BOP score – between 10% to 30%
Generalised gingivitis: Probing attachment loss – Yes, Radiographic bone loss – Possible, Probing depth all sites – less than 3 mm, BOP score – above 30%
9
Q
How do we write diagnostic statement for gingivitis?
A
- Extend - localised of generalised
- Disease - gingivitis
- Specification - biofilm induced, mediated by pregnancy or leukaemia
10
Q
What is the pathogenesis of gingivitis? (Initial reaction)
A
- Biofilm accumulates
- Biofilm produces metabolites (fatty acids), peptides (FMLP) and LPS
- Junctional epithelium cells stimulated to synthesize inflammatory mediators (cytokines)
- Free nerve peptides produce neuropeptides and histamine in response to cytokines
- Perivascular mast cells release even more histamine
- This cause an increase in local vascular activity
- Endothelium releases IL-8 into vessels to attract PMNs
11
Q
What is the pathogenesis of gingivitis? (PMNs migration)
A
- Mast cells release histamine
- Direct activation – LPS or OMP react with endothelial cells
- Indirect activation – after contact with LPS/OMP macrophages release proinflammatory cytokines
- ELAM-1 is expressed
- Contact between leucocytes adhesion receptor integrin beta 2 with endothelial Integrin ICAM-1
- PMNs leave vessel by amoeboid diapedesis
- PMNs follow gradient of chemotactic factors
12
Q
What is the pathogenesis of gingivitis? (Post PMNs migration)
A
- Biofilm stimulates JE cells to produce cytokine IL-8
- IL-8 is a chemo-attractant for PMNs
- PMNs follow IL-8 concentration gradient
- PMNs reach the sulcus
- Complement and antibodies support phagocytosis of bacteria and their products
13
Q
What is the pathogenesis of gingivitis? (Early gingivitis)
A
- PMNs form dense layer over biofilm
- PMNS and tissues release pro-inflammatory cytokines nad enzymes
- Activation of macrophages (more proinflammatory things)
- Lymphocytes infiltrating connective tissues (T cells mostly)
- Increase in vascular dilation
- Lateral proliferation of junctional epithelium basal cells
14
Q
What is the pathogenesis of gingivitis? (Established gingivitis)
A
- Intense PMN infiltration in junction epithelium
- Lymphocytes dominate the infiltrate
- Activated T cells coordinate the response via cytokines
- B cell differentiation and conversion to plasma cells
- Plasma cells produce Igs and cytokines
- Activated fibroblasts produce MMP and TIMP instead of collagen
- Loss of collagen fibres to provide space for expanding infiltrate
- Lateral proliferation and apical migration of junction epithelium (creation of pseudopocket)
15
Q
Why do we say that gingivitis “takes two” factors?
A
Because gingivitis take 2 important factors to develop –1 the microbes and 2 the host response to the microbes
16
Q
What is a risk factor?
A
It is something that increases the chance of developing a disease or disorder
17
Q
What are the two categories of risk factors of gingivitis?
A
- Systemic
- Local
18
Q
What are the systemic risk factor for gingivitis?
A
It is something that modifies disease expression and may influence disease progression by altering the host’s immune response
19
Q
What are some of the systemic risk factors for gingivitis?
A
- Smoking
- Hyperglycemia
- Nutritional factors
- Pharmacological agents
- Sex hormones
- Hematological conditions
20
Q
What are the impacts of smoking on gingival tissues
A
- Decrease immunoglobulin G2 production
- Chronic reduction in blood flow and vascularity – THIS ALSO REDUCES THE BOP AND POTENTIALLY REDUCING POCKET DEPTH
3Increase prevalence of potential periodontal pathogens
- Shift in neutrophil function towards destructive activities
- Negative effects on cytokine and growth factor production
- Inhibition of fibroblast growth attachment and collagen production
21
Q
How does hyperglycaemia impact gingivitis?
A
Hyperglycaemia causes a production of advanced glycation end products or (AGE) which causes immune disfunction, cellular stress & increase of proinflammatory cytokines.
22
Q
What is the local risk factor for gingivitis?
A
It is the retention biofilm or prevent its removal and predispose for disease progression
23
Q
What are some of the local factor for gingivitis?
A
- Dental plaque retention
- Oral dryness
24
Q
What is DIGO?
A
Drug Induced Gingival Overgrowth
25
What are some of the medication associated with DIGO?
1. Calcium channel blocker
2. Immuno-suppressants
3. Anticonvulsants
26
How do you treat patients with DIGO?
1. Biofilm control
2. Surgical excision
3. Drug substitution
27
What are signs of necrotising gingivitis?
1. Necrosis of papilla
2. HELLA BOP
3. Pain on probing
4. Halitosis
5. Lympadenopathy
28
What causes necrotising gingivitis?
It is caused by opportunistic bacteria but it is also influenced by systemic factors
29
What are the treatments of necrotising gingivitis?
1. Debriment under LA
2. Local Irrigation with Chlorhexidine 0.2%
3. Antibiotic Therapy – Metronidazole 400mg orally, 12-hourly, 3-5 days
4. Analgesics
5. Review
6. potentil referral to a Specialist or GP
30
What are some of the classifications of the non-biofilm induced gingival disease
1. Genetic developmental disorders
2. Specific infections
3. Inflammatory and immune conditions and lesions
4. Reactive processes
5. Neoplasms
6. Endocrine nutritional and metabolic diseases
7. Traumatic lesions
8. Gingival pigmentation
31
What is supra- and subgingival debridement?
It is the removal or disruption of dental deposits and plaque-retentive calculus from tooth surfaces and within the periodontal pockets space without deliberate removal of cementum as done in root planning and often in dental scaling
32
What is the relevance of debridement in treating periodontal disease?
As biofilm matures, the opportunities to shift from healthy biofilm to pathogenic increases.
Debridement allows for removal of the biofilm or destruction of the bio-environment which encourages the growth of less pathogenic species of bacteria within the biofilm.
33
What is the rationale of removal of supra and subgingival calculus?
1. This eliminate a potential colonisation site for the pathogenic bacteria
2. This allows the patient to perform oral hygiene techniques appropriately
34
What are the instruments available for debridement at the ADH for supragingival removal?
1. Sickle Scaler – anterior
2. McCall's Scaler – universal
3. Ultrasonic scaler – regular or fine tip
4. Gracey Curettes – with limitations around the contact point
35
What instruments can be used for debridement at the ADH for subgingival removal?
1. Ultrasonic scaler – XF tip
2. Gracey Curettes
36
What are the part of the scaler?
1. Handle
2. Terminal Shank
3. Working end
37
How does the power scaler work at the ADH?
1. The alternating current is connected to a quartz crystal in the scaler
2. The current makes the quartz crystal to expand and contract
3. The resulting vibration is passed to the working tip at the end of the scaler
4. Ossilating generates hit – thus scaler is in constant use of water
5. The blade is oscillating back and forward
38
What is the benefit of having constant water flow in the power scales on top of cooling?
It flushes the dental deposits that are broken down – this is called lavage
39
What are some of the other ways power scalers are able to aid in removal of dental deposits?
1. Cavitation - build-up of microscopic bubbles
2. Acoustic Microstreaming – creation of currents from sound made by the vibrations
40
What are the steps of debridement?
1. Detect biofilm and calculus (dry area, use mirror from different angles, use Tri Plaque Gel, use radiographs)
2. Use 11/12 explorer probe by going around the tooth if needed
3. Use a systematic stroke technique to clean subgingivaly
4. Use ultrasonic scalers
41
What is recession?
It is the apical shift of the gingival margin. It is common in adult population. The instances of recession increase with age.
42
What does recession lead to in terms of patient concerns?
1. Dentine hypersensitivity
2. Impaired Oral Hygiene
3. Esthetical concerns
4. Easier development of caries
5. Non-carious cervical lesions
43
What can cause recession
1. Anatomical component – tooth position, periodontal phenotype, alveolar bone fenestration, frenal attachment
2. Inflamatory component – biofilm build up, trauma (chronic or physical or post periodontal treatment)
44
What is periodontal phenotypes?
It is both the natural thickness of the gingiva as well as the bone. Thin gums are determined when a perioprobe can be seen when inserted into the gingival sulcus.
45
What is alveolar bone dehiscence/fenestration?
It when the alveolar bone does not fully surround the entirety of the tooth. Fenestrations can be seen and radiographs display bones as thin.
46
What are frenal attachment?
Places where frenums attach. They may pull on tissues making it hard to clean in the pulled areas.
47
What are supracrestal attached tissues or biological width?
Thes upracrestal attached tissues are the junctional epithelium + the underlying connective tissue attachment. It is 2 mm wide in general. We need to consider this area when performing restoration, because if the area is violated this could lead to gingival inflammation.
48
What are Stillman clefts?
They are small, slit like recessions that are usually fast.
49
What are McCall's festoon?
They are more rounded and slow progressing recessions.
50
How do we measure the recession?
1. Dry teeth
2. Feel with probe
3. Find CEJ
4. Measure from CEJ to GM
51
How many recession types are there?
There are 3 recession types
52
What is recession type 1?
It is gingival recession with no loss of inter-proximal attachment.
53
What is recession type 2?
It is gingival recession with some loss of inter-proximal attachment. The inter-proximal attachment loss is less than the true buccal attachment loss.
54
What is recession type 3?
It is gingival recession with loss of inter-proximal attachment. The inter-proximal attachment is more than the recession on true buccal attachment loss.
55
What is the treatment plan for recession?
1. Assessment/documentation
2. Identify and Modify Etiologic Factors
3. Adress the consequences of root surface exposure
4. Monitor progression
5. Potential interventions like ortho or surgery if needed
56
What can we classify as necrotising gingivitis?
Necrotising gingivitis is only when gingival tissues only are involved.
57
What can we classify as necrotising periodontitis?
Necrotising periodontitis is when gingival tissues are involved as well as attachment loss can be observed.
58
What can classify as necrotising stomatitis?
When lesions are 1 cm away from the gingival margin, we can classify a disease as necrotising stomatitis.
59
What is the most sever type of necrotising stomatitis?
It is the NOMA.
60
What is periodontitis?
It is a multifactorial inflammatory disease associated with dysbiotic microbial dental biofilms and characterized by non-reversible progressive periodontal tissue destruction.
61
What are the symptoms of periodontitis?
1. All sympotms of gingivitis
2. Receding gums
3. Gaps between teeth
4. Increased food debris
5. Mobile teeth
6. Change in teeth position
7. Speech alteration
8. Tooth loss
9. Pain in acute conditions
62
What are the signs of periodontitis?
1. Periodontl pocketing
2. Recession
3. Clinical attachment loss
4. Evidence of radiographic bone loss
5. Increased mobility
6. Tooth loss
63
What can we classify as a patient with periodontitis?
If a patient has clinical attachment loss interdentally at 2 non-adjacent teeth
Or
Buccal or oral clinical attachment loss with pocketing 3 mm at 2 or more teeth
64
How to classify the staging of periodontitis?
1. Severity and extent
2. Complexity
65
How to classify the grading of periodontitis?
1. Future risk
2. Estimate potential health impact of periodontitis
66
How many stages of periodontitis are there?
There are 5 stages
67
What is stage 1 periodontitis?
1. 1-2mm attachment loss
2. Coronal third bone loss
3. No tooth loss
4. Maximum probing depth of below 4mm
5. Mostly horizontal bone loss
6. Extent variable
68
What is stage 2 periodontitis?
1. 3-4mm attachment loss
2. Coronal third bone loss
3. No tooth loss
4. Maximum probing depth of below 5mm
5. Mostly horizontal bone loss
6. Extent variable
69
What is stage 3 periodontitis?
1. 5mm or more attachment loss
2. Bone loss extending to middle or apical third of the root
3. Tooth loss due to periodontitis of 4 or less teeth
4. Probing depth of 6 mm or more
5. Vertical bone loss of 3 mm or more
6. Class II or III furcation
7. Moderate ridge defect
70
What is stage 4 periodontitis?
1. 5mm or more attachment loss
2. Bone loss extending to middle or apical third of the root
3. Tooth loss due to periodontitis of 5 or more
4. Probing depth of 6 mm or more
5. Vertical bone loss of 3 mm or more
6. Class II or III furcation
7. Moderate ridge defect
8. Mastication disfunction
71
How many grade of periodontitis are there?
3 grades
72
What is Grade A periodontitis?
When there are no evidence of loss over 5 years
73
What is Grade B periodontitis?
When there is a below 2 mm loss over 5 years.
74
What is Grade C periodontitis
When there is an above 2mm loss over 5 years
75
What are the steps for diagnostic treatment of periodontitis?
1. Use the algorithm for new patients
2. For patients suspected to have periodontitis proceed to the next algorithm
3. Establish stage for periodontitis patient
4. Grading for patient with existing previous records
76
How to write diagnosis for periodontitis?
1. Types of periodontal disease
2. Disease extent
3. Stage
4. Grade
5. Curretn disease status
6. Risk profile
77
What do we need for a full periodontal examination?
1. We need a visual examination of the soft tissues
2. A full periodontal chart
3. A series of radiographic images
78
What is a healthy alveolar crest shape?
It is usually pretty flat and is about 1-3 mm below the CEJ. Remember that little "steps" are possible if the adjacent teeth sit in a little bit of a different position.
79
How can we grade periodontal disease using a radiograph?
1. Healthy - not bone loss
2. Mild - less than 15% bone loss
3. Moderate - 15-33% bone loss
4. Sever - above 33% bone loss
80
What is horizontal bone loss?
When the entire alveolar crest shift down
81
What is vertical bone loss?
When only part of the alveolar crest shift down
82
What is the normal periodontal ligament space?
A thin black line. It gets thicker if disease is present.
83
What is the disadvantage of radiographs?
The early stages of periodontitis cannot be detectable using just radiographs, as usually they underestimate bone loss.
84
Which radiograph is the best?
Depending on patient needs. But only take it after the gingival assessment and perioprobing.
85
What is the timeline for periodontal disease therapy?
1. Emergency treatments
2. Evaluation
3. Systemic phase
4. Phase I – debridement and non-surgical treatment
5. Reevaluation
6. Phase II and III – corrective and restorative
7. Phase IV
86
Describe the Phases/Steps of Periodontal Treatment.
**At any phase: Specialist Referral**: Refer to a periodontist, OMS, oral pathologist, or other specialist if needed.
1. **Emergency Treatment**: Address urgent periodontal issues at any stage.
2. **Evaluation**: Conduct oral health and risk assessment, diagnosis, and treatment planning.
3. **Systemic Phase**: Manage systemic disease and address modifying factors (e.g., smoking counseling).
4. **Initial Phase**: Perform causative, hygienic, non-surgical addressing of predisposing factors.
5. **Re-evaluation**: Assess progress after 8-12 weeks.
6. **Surgical Phase**: Perform surgical interventions if necessary.
7. **Restorative Phase**: Conduct restorative procedures as needed.
8. **Maintenance Phase/SPT**: Implement ongoing maintenance and supportive periodontal therapy.
87
What is Phase I therapy?
Phase I therapy is the initiation of a comprehensive daily plaque or biofilm control regimen, management of periodontal-systemic interrelationships as needed, and thorough removal of supragingival and subgingival bacterial plaque or biofilm and calculus. It also includes addressing other problems such as the use of chemotherapeutic agents as necessary, and local factors like elimination of defective restorations and treatment of carious lesions. These procedures are a required part of periodontal therapy, regardless of the extent of disease present. In many cases, only Phase I therapy is required to restore periodontal health, or it serves as the preparatory phase for surgical therapy. The results of Phase I therapy in two patients with chronic periodontitis demonstrate its effectiveness, aimed at removing pathogenic biofilms, toxins, and calculus, and reestablishing a biologically acceptable root surface.
88
The EFP S3 Level Guidelines outline periodontal treatment in a stepped approach with the following steps:
1. **Step 0 - Prerequisite to Therapy**: Educate, classify, diagnose, assess risk, and create a care plan.
2. **Step 1 - Risk**: Control risk factors, improve oral hygiene (OH), manage adjuncts for gingivitis (GI), periodontitis-associated marginal periodontitis (PMPR), and perform supra-gingival scaling.
3. **Step 2 - Intervene**: Remove sub-gingival biofilm and calculus, with additional adjuncts as needed.
4. **Step 3 - Check**: Assess non-responder sites and apply re-scaling/debridement (Re-RSD) or surgery if necessary.
5. **Step 4 - Exit**: Plan long-term care, focusing on supportive care and rehabilitation.
This approach accepts a basic underpinning phase (Step 0) and follows the "PRICE" framework (Steps 1–4), recognizing the human and financial costs of periodontitis.
89
What can cause a treatment failure?
- Incorrect diagnosis
- Insufficient debridement
- Poor oral hygiene
- Systemic factors
- Local factors
90
What is Step 1 in Periodontal Treatment?
Step 1 in periodontal treatment involves building foundations for optimal outcomes by explaining disease, risk factors, treatment alternatives, risks, and benefits, including no treatment; emphasizing oral hygiene (OH) importance, encouraging behavior change, and reducing risk factors like plaque retentive features, smoking, and diabetes; providing tailored OH advice, including interdental cleaning, +/- adjunctive toothpaste/mouthwash, +/- professional mechanical plaque removal (supra- and subgingival scaling); setting recall periods based on risk factors; and involving an Oral Health Educator, Hygienist, Therapist, Dentist, or accredited practitioner. Diagnosis identifies periodontal health, gingivitis, or periodontitis, with extraction for hopeless or unsalvageable teeth (e.g., grade III mobile). After re-evaluation, non-engaging patients repeat Step 1, engaging patients proceed to Step 2, or referral is considered.
91
How to redcue the risk factors including removal of plaque retentive features, smoking cessation and diabetes control intervention?
- Removal of calculus
- Removal of overhangs
- Recontouring of restorations
- Restoration (temp. / perm) of open caries lsions
- Restoration of open contacts
92
**What is Step 2 in Periodontal Treatment?**
Step 2: Subgingival instrumentation (root surface debridement/PMPR on root) involves reinforcing oral hygiene (OH), risk factor control, and behavior change; performing subgingival instrumentation with hand or powered (sonic/ultrasonic) tools, either alone or combined; and using adjunctive systemic antimicrobials as determined by a practitioner accredited for Level 2 and 3 care.
93
What is Step 3 in Periodontal Treatment?
Step 3: Managing non-responding sites includes reinforcing OH, risk factor control, and behavior change; moderating (4-5mm) residual pockets with re-performance of subgingival instrumentation; addressing deep residual pockets (≥6mm) by considering alternative causes; referring for pocket management or regenerative surgery if needed; and re-performing subgingival instrumentation if referral is not possible, proceeding to Step 4 if all sites are stable after re-evaluation at 3 months.
94
What is Step 4 in Periodontal Treatment?
Step 4: Maintenance focuses on supportive periodontal care, strongly encouraged alongside reinforcing OH, risk factor control, and behavior change; regular targeted PMPR as required to limit tooth loss; considering evidence-based adjunctive efficacious toothpaste and/or mouthwash to control gingival inflammation; and scheduling maintenance recalls (Step 4) with individually tailored intervals from 3-12 months.
