Periodontics Flashcards
1
Q
What findings should you search for in a perio exam?
A
Pocket Depth BOP Calculus Plauqe index Furcation Mobility Vitality test (if suspect perio-endo lesion)
2
Q
What are the 5 major categories of what to look for when checking radiographs for perio disease?
A
Remaining bone support Bone loss Calculus Crown/Root morphology Evidence of Endo involvement
3
Q
When looking examining a radiograph for bone loss on radiographs, what features should you look for?
A
Size
Extent/progression (in order this is):
- Breakdown of lamina dura
- Wedge shaped lesion on mesial/distal aspect of interdental septum
- Loss of interdental septum bone height
- Crater formation in interdental septum (cupping effect)
- Disparate buccal/lingual height of cortical plate
- Vertical bone loss
- Furcation involvement
- Formation of two distinct margins due to difference in height of buccal and lingual cortical plate
Shape:
- Vertical (infrabony)
- Horizontal (suprabony)
- Hemiseptal (3 wall), 2 wall, 1 wall, cup shaped
4
Q
When checking for crown/root morphology for perio disease on radiographs, what should you search for?
A
- Crown: root ratio
- Crown/root fractures
- Interproximal spacing (can be influenced by convexity of crown/greater convexity=greater spacing)
- Size, shape, position of root
- Signs of resorption
- Convergence/divergence of roots
- Length of root trunk
- Any remaining root fragments
5
Q
When looking for evidence of endo involvement in perio disease on radiographs, what should you look for?
A
- Widening of PDL (though this could indicate occlusal trauma)
- Pulpal anatomy/evidence of pathology
6
Q
What are the grades of mobility? What is the normal range for tooth mobility?
A
Grade I: up to 1mm of movement in horizontal direction
Grade II: up to 2mm of movement in horizontal direction
Grade III: greater than 2mm-3mm movement in horizontal and vertical direction
Elasticity of bone and PDL allows 0.2mm of movement in normal/healthy person, varies throughout day
7
Q
What can cause mobility, and how can it be managed?
A
Occlusal trauma:
- Widening of PDL space
- Mobility evident with no bone loss due to rigidity of PDL fibres
- Can treat by adjusting occlusion/lowering tooth surface to reduce load (may be done to natural tooth or restorations)
Bone loss: Splint teeth, options include: -Removable acrylic splint -Wire splint (semi-rigid) -Composite resin splint (rigid, risk of ankylosis/ tooth fusion to bone occurring)
8
Q
What is can cause furcation involvement?
A
- Periodontal bone loss
- Cervical projections/enamel pearls
- Iatrogenic endo damage
- Endodontic lesion with accessory canals into furcation area
9
Q
What are the management options for furcation?
A
Class I, II, III:
Non-invasive approach:
-OHI re. use of tufted brush to clean furcation area
-Scaling/cleaning of area
Class II or higher
- Tunnel prep (change furcation from class II to III to allow easier access)
- Furcation plasty: smooth the surfaces involved in furcation with a bur to allow easier cleaning
- Guided tissue regeneration
- Gingivectomy: surgical removal of a portion of gingiva to allow access for cleaning
- Root resection: Remove a root to allow for easier access, particularly if that root has heavy bone loss
- Hemisection: For lower molars, divide the tooth in half and convert it into two premolars
- Replacement with implant
10
Q
What are the grades of furcation?
A
Class I: Probe can be inserted up to 1mm into furcation
Class II: Probe can be inserted 2mm or more into furcation but can not pass all the way through
Class III: Probe can pass straight through furcation (through and through destruction)
11
Q
True or false: furcation involvement has both horizontal and vertical components
A
T
12
Q
What are the considerations for root resection?
A
- Vitality of tooth
- Size and length of root (if small don’t bother)
- Remaining bone support on other roots
- If heavily restored crown
- Convergence/divergence of roots
13
Q
What are the indications for root resection?
A
- Heavily restored crown (depending on situation)
- If remaining roots have good bone support
- Root fracture
14
Q
What are contra-indications for root resection?
A
- Heavily restored crown (depending on situation)
- Difficult endo on remaining roots/tooth still vital
- Fused roots
- Heavy bone loss on remaining roots
- Cost
- Small roots
15
Q
What is meant by a 3-walled defect, and what is it’s prognosis vs 1 walled defect?
A
3-walled defect means the lesion is surrounded by bone on 3 sides, far better prognosis than 1 wall defect
16
Q
What are some issues with the old studies involved in perio disease? (in particular with epidemiology)
A
- Considered perio to be inevitable progression of gingivitis without considering susceptibility of pt
- Considered perio would worsen with age
- Considered tooth loss inevitable without treatment
17
Q
What improvements have been made with modern studies of perio epidemiology? What issue still remains?
A
- Consider gingivitis and periodontitis separately and takes into account susceptibility of patient
- Measures actual attachment loss rather than using an index
- Correlates clinical findings with radiographs and histories
- However considers perio to the be the cause of all attachment loss
18
Q
What can cause attachment loss other than periodontitis?
A
Over-eruption of teeth: if radiograph will find bone is completely intact
19
Q
In terms of periodontic aeitology, what is a necessary cause and what is a sufficient cause?
A
Necessary cause: Necessary to cause the disease but will not cause disease on its own, in this case the bacteria
Sufficient cause: Enable to the necessary cause to cause disease, in this case host resistance/susceptibility and environmental factors
20
Q
What are the three main elements of chronic disease?
A
- Bacteria
- Host resistance/susceptibility (e.g. systemic disease, genetics)
- Nature/environment (upbringing, stress, social factors, habits)
21
Q
What is the red complex of bacteria in periodontitis?
A
- T.denticola
- P.gingivalis
- B.forsythus
22
Q
What are socransky’s postulates for perio disease?
A
- Bacteria capable of reproducing disease in animals
- Removal of bacteria leads to improvement of condition
- Virulence factors can be detected
- Bacteria able to activate host defence systems
23
Q
T/F junctional epithelium attaches onto enamel
A
T: attaches via epithelial attachment consisting of hemidesmosomes
24
Q
Describe 2 different ways of classifying gingival fibres and the types of fibres present in each category.
A
By direction:
- Alveolar crest fibres: Travel apically from just apical of junctional epithelium to alveolar crest of bone
- Horizontal fibres: Travel at right angles to long axis of tooth to bone
- Oblique fibres (most numerous): travel in obliquely and coronally to insert into bone
- Apical fibres: radiate from apex of root to insert into bone
- Interradicular fibres: Travel from furcation area of multi-rooted teeth to insert into bone (interradicular septum)
By origin/insertion:
- Dentogingival: From cementum to lamina propria of gingiva
- Alveologingival: From alveolar bone to lamina propria of gingiva
- Dentoperiosteal: From cementum to periosteum of alveolar bone
- Transseptal: Travel from cementum of one tooth to cementum of adjacent tooth just apical to junctional epithelium (travel over alveolar crest)
- Circular: Encircles tooth and acts as anchors for other fibres
25
Give a brief summary of the clinical presentation of the stages of gingivitis and periodontitis.
```
Healthy
Plaque: minimal
JE/pocket depth: minimal
PMN's: Few PMN's migrating through JE to gingival sulcus
CT: Dense fibres and intact fibroblasts
```
Initial gingivitis:
Plaque: Heavier than in healthy mouth
JE/pocket depth: slight deepining of sulcus
PMN's: Migrate through JE and palisade around plaque bacteria in attempt to wall off and engulf
CT: Early lymphocyte infiltration
Established Gingvitis:
Plaque: Heavy levels present
JE/Sulcus depth: breakdown of JE and apical migration
PMN's: as with initial gingivitis
CT: inflammatory infiltrates protect deeper structures
Periodontitis:
- Attachment loss of CT mediated by cytokines
- Apical migration + ulceration of JE
- Apical migration of transseptal fibres
- Acute infection phase may cause gingival abscess
26
Describe the steps to the pathogenesis of gingivitis/periodontitis
1. Initial reaction to plaque/PMN migration
- Plaque bacteria produce LPS, fatty acids, peptides
- Trigger JE cells to secrete: IL-1 alpha, MMP, IL-8, TNF-alpha, PGE2
- Mast cells release histamine, triggering release of IL-8 from endothelial cells as well
- IL-8 acts as chemoattractant for PMN's
2. Macrophage activation
- Vascular changes cause leakage of complement protein into CT, thus establishing inflammatory reaction and recruiting leukocytes and monocytes
- Macrophages secrete pro-inflammatory cytokines:
- IL-1beta, 6, 10, 12
- MMP
- PGE2
- TNF-alpha
- IFN-gamma
- Chemotaxins (MCP, RANTES, MIP)
- These regulate activity of other inflammatory cells, fibroblasts and osteoclasts
* IL-10 is anti-inflammatory
```
3. Upregulation of inflammation (lymphocyte stage)
T-cells enter and produce
-IL 2-6, 10-13
-TNF-alpha
-Interferon-gamma
-TGF-beta (anti-inflammatory)
PMN's produce:
-cytokines, leukotrienes, MMP
B Cells produce Ig's which:
-Agglutinate bacteria
-Increase efficiency for phagocytosis
-Kill bacteria with complement
-Prevent adhesion
Fibroblasts:
-Produce MMP and TIMPS instead of collagen (these two antagonise each other)
```
4. Initial attachment loss:
Continued production of:
-IL-1beta, IL-6, IL-8, MMP, TNF-alpha, PGE2, MMP, TIMPs
-Increased macrophage activity, plasma cells dominate infiltrate
-Initial destruction of CT, collagen and bone resorption
27
Describe the process of bone loss
1. T cells upregulate production of RANKL
2. RANKL binds to receptors in pre-osteoclasts
3. Binding causes increased osteoclast differentiation and proliferation
4. Also increases osteoclast activity and prevents apoptosis
28
Describe the process that modulates excessive bone loss
1. OPG produced by osteoblasts bind to RANKL with high affinity
2. Prevents binding of RANKL to RANK receptor
3. Causes reduction in osteoclast differentiation and proliferation
4. Also increases apoptosis and decreases activity
29
What two major categories can risk factors in periodontics be divided into? What are the subcategories of each one?
Primary/Secondary:
- Primary risk factors (plaque bacteria/red complex)
- Secondary risk factors (alterable): smoking, diabetes, HIV, oral hygiene, stress, upbringing, lack of recall
- Secondary risk factors (non-alterable): age, genetics, IL-1 polymorphism, ethnic origin, gender
Predisposing/modifying:
- Predisposing: Factors that affect operator's/patient's ability to clean, thus resulting in plaque accumulation
- Modifying factors: Factors that modify disease by changing host protective mechanisms
30
What are the major categories for pre-disposing factors?
- Tooth anatomy/positioning
- Restorations
- Prostheses (if OH not maintained, especially abutment teeth)
- Plaque/calculus
- Gingival contour
- Gender (increased prevalence in males)
- Age (accumulation of attachment loss + change in microflora)
- SE status
31
What factors involved in tooth anatomy/positioning can predispose to perio disease?
- Crowding can cause difficulty in accessing ares to clean
- Proximal bone size
- Furcation involvement
- Root fractures
- Endo involvement
- Subgingival caries
- Grooves, invaginations, concavities
- Palatal invaginations (dens in dente)
- Enamel projections/pearls (can create ecological niche)
32
What factors involved in plaque/calculus can pre-dispose to perio disease?
- Subgingival plaque has gram (-) anaerobes particularly harmful to perio apparatus
- Supragingival may not have direct affect on perio, but may affect bacterial quantity and quality
- Calculus rough surface can harbor bacteria
33
What restorative factors can pre-dispose to perio disease?
- Overhanging margins (especially with interproximal restorations
- Margins close to the gingival sulcus associated with greater inflammation
34
How can gingival contour pre-dispose to perio disease?
- High/low frenal attachment can cause recession and can also cause difficulty in retracting lip for cleaning
- Gingival recession may also interfere with hygiene procedures due to sensitivity
35
What are the major modifying factors to perio disease?
Environmental
- Smoking
- Stress
Medical
- Systemic disease
- Medications
- Neutrophil dysfunction (increase susceptibility to infection)
Physiological
- Genetics
- Hormones
36
How does smoking modify perio disease?
Plaque: increase red complex
Immune
Host resistance: Decreased host resistance to disease
PMN's: Increased in circulation but fewer in sulcus and decreased function
Lymphocytes: Decreased IgG to AA, increased IgE and pro-inflammatory cytokines, decreased T cell proliferation thus affecting B cells and lowering Ig levels
Cytokines: increased inflammatory cytokines
Epithelium
Epithelium: Increased keratinocytes
Fibroblasts: reduced adhesion and altered morpholgy: affects regeneration
Vasculature: decreased blood flow, less bleeding but less nutrients and waste removal
Periodontal therapy: lowered quality of outcome
37
What main two systemic diseases are involved in modifying perio disease? How do they do this?
Diabetes:
Epithelium
- AGES: hyperglycaemia causes collagen uptake of sugar, producing AGE's (faulty collagen) that has greater cross-linking and differing turnover rate
- Basement membrane: AGE's induce basement membrane thickening, affecting nutrient supply, waste removal and PMN migration
- Vascular changes also cause issues with nutrient supply and waste removal
- Fibroblasts: Decreased growth, proliferation and collagen synthesis
Immune
- Macrophages: Decrease proliferation of reparative macrophages
- PMN's: Inhibit respiratory burst, phagocytotsis, chemotaxis
- Cytokines: increased production of pro-inflammatory cytokines
-Perio therapy: Decreased chance of good result except in well controlled patients
HIV
- Associated with NUG and localised perio as well as linear gingival erythma
- Particular danger if CD4+ cells below 200
38
How can genetics modify perio disease?
-Affects innate and adaptive immunity
39
How can stress modify perio disease?
-Release corticotropin releasing hormone (hypothalamus)--> corticotropin (anterior pituitary)-->cortisol (adrenal cortex)
-->Increased pro-inflammatory cytokines
--> Adrenaline release: immunosuppressive response
-->increased incidence of NUG and perio
40
How can hormones modify perio disease?
Puberty: Release of sex hormones increase prevalence of gingivitis
Menstruation: Increased progesterone production leads to:
- Change in vascular and collagen production
- Increased prostaglandins
- Increased PMN's: increased bleeding, swelling, minor tooth mobility
Pregnancy: Increased estrogen and progesterone
Menopause: Estrogen withdrawl leads to increased osteoclast activity and increased pro-inflammatory cyotkines
41
What medications can modify perio disease?
- Phenytoin (dilatin), calcium channel blockers, cyclosporin, can cause gingival enlargement
- May make it more difficult to clean due to tenderness
42
What factors should be considered for prognosis of individual teeth?
Practicality
- Strategic value (e.g. use for abutment teeth)
- Tooth position and occlusal relationship
Root
- Root form
- Furcation
Caries
- Endo involvement
- Presence of caries
Bone
- Remaining bone support
- Probing depth
- Distribution of bone loss
- Mobility
Crown to root ratio.
43
What factors should be considered for an overall prognosis?
- Age
- MHx
- Patient compliance
- Risk factors (e.g. smoking, stress)
- Oral Habits (e.g. bruxism, lip chewing, anything that interferes with treatment)
- Social factors (including economic considerations)
- Knowledge + skill of dentist
- Individual tooth prognosis
- Progression rate
44
What possible prognosis categories are there?
Good:
- systemic + local factors can be controlled
- Periodontium can be brought into a stable state through treatment and maintenance
Questionable:
- Systemic + local factors may or may not be able to be controlled
- May be possible for perio status to be stabilised through treatment and maintenance
Unfavourable:
- Systemic + local factors can not be controlled
- Unlikely to stabilise perio status with treatment and maintenance
Hopeless
45
What are the goals of perio treatment?
- Control infection
- Remove the cause, modifying and predisposing factors
- Reduce the signs and symptoms
- Prevent progression of disease
- Regenerate lost tissue
- Maintenance of long term aesthetics, function, lifespan
46
What phases of the treatment plan of perio are there and what do they involve?
ROP
Systemic Phase:
-Advise patient to reduce risk factors and assess MHx
Hygienic phase:
- OHI: Provide OHI catered to patient (use of flossettes, IP brushes, etc.)
- Patient education: role of plaque in perio disease
- Supra+ sub scaling to remove calculus
- If necessary antimicrobials (antibiotics, doxycycline, chlorhexidine)
```
Corrective Phase:
Management of local factors and further treatment, including:
-Removal of overhangs
-GTR
-Gingvectomy
-Root resection/hemisection
-Resective surgery
```
47
What are the possible outcomes of treatment (predictable and less predictable)?
Predictable:
- Reduction in symptoms
- Decreased pocket depth
- Decreased mobility
Less predictable
- Prevention of tooth loss
- Stop disease progression
- Maintain health over long term
48
What factors should you take into consideration at SPT (maintenence) recall appointments?
```
Pt factors
Background
-Age
-MHx
-Patient compliance
Risk factor (matrix)
-Stress
-Smoking
-Diet
Clinical
-Initial diagnosis
-IL-1 polymorphism
```
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Oral factors
Oral features/factors
-OH/access to sites for cleaning
-Parafunctional habits
-Gingival biotype
Disease
-Mucocutaenous disorders
-Current bone loss
-History of tooth loss
```
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Tooth factors
-Calculus/plaque
-BOP
-Pocket depth/bone loss/recession (attachment loss)
-Mobility
-Furcation
-Suppuration
(similar to what to look for in perio exam)
```
49
What should be done at SPT appointments?
- Re-evaluate previously infected sites
- Treatment of newly infected sites
- Assessment of future SPT/recalls
- Reinforce and re-motivate patient to follow OHI
- Can also use radiographs and additional tests
