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1
Q

Patient motivation - how to encourage a patient

A

Motivation stemming from patient but support from dentist

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2
Q

What are TIPPS

A

TALK - Patient education and motivation (barriers and facilitators to care)
INSTRUCT - the patient into how to perform effective plaque removal
PRACTICE - in the surgery(ID brush) prior to going home
PLAN - how this can fit into daily life
SUPPORT - susequent appointments

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3
Q

OH advice

How to advise

A 
Clean 2x daily - at least 30 s per quadrant
Manual or electric toothbrush
Fluoride toothpaste (1450ppm)
Use modicied base technique
Interdental cleaning at least once daily

Tell show do approach

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4
Q

Aspects of NSPT

A

regular OHI reinforcement
regular NS instrumentation - supra/subgingival
smoking cesssation
dietary advice
Root surface debridement of >4mm pockets with subgingival deposits

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5
Q

Goal of NSPT

A

Reduced BOP <10%
Reduced pocket depth <4mm
Reduced plaque scores <15%

Stabilisation NOT cure of disease
Emphasise patient’s role in their own care

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6
Q

Warnings to patient prior to scaling/RSD

A

Sensitivity
gingival recession
LA - Bite cheek/lip/tongue

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7
Q

Why is it not advised to redebride a pocket in a followiing appointment if not finished

A

This is because initial healing, after the gross deposits have been removed, can make re-accessing the pocket more difficult and partial removal of deposits leaves behind rough areas which are ideal for bacterial
proliferation. It is advised that the clinician concentrates on as many teeth, sextants or quadrants as can be thoroughly instrumented in the time available.

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8
Q

Why would a patient be prescribed systemic antibiotics

A

In adjunct to RSD to supress bacterial species, ONLY in cases where patient will benefit from them.
Aggressive perio

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9
Q

How does a perio pocket repair

A

• Fibrin clot adheres to the root surface
• Progenitor cells from surrounding tissue proliferate,
migrate and differentiate
• Formation of bone, PDL and cementum

(Fibrin clot - fails to adhere to root surface, Downgrowth of epithelium between root and clot, Epithelial attachment to root)

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10
Q

Why do periodontal pockets fail to heal

A

Not full detoxification of root surface
Mechaniclal stress disrupts clot formation
LAck of space to accomodate regenerating tissue

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11
Q

Strategies for periodontal regeneration

A

Space maintenance and clot protection
• Selective cell repopulation
• Provision of progenitor cells
• Use of biological mediators

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12
Q

Indication for periodontal regeneration

A

ndications for Periodontal Regeneration

  1. Two and three-walled proximal defects
  2. Grade II mandibular furcation defects
  3. Grade II buccal maxillary furcation defects
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13
Q

Objective of bone grafts

A 
Space maintenance and clot protection
• Osteoconduction
Scaffold
• Osteoinduction
Promoting osteoblast activity
• Osteogenesis
Osteoblasts present in the graft
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14
Q

Types of bone grafts

A

Human - Allograft/Autograft
Xenograft - bovine/equine
synthetic - Polymer/hydroxyapatite/bioactive glass

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15
Q

Types of root resorption

A

Internal resorption
-inflammatory replacement

External resorption - pathological/physiological

  • External surface resorption
  • External inflammatory
    a) External apical resorption
    b) External periodontal (cervical) resorption
  • External replacement resorption
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16
Q

Aetiology of root resorption (2)

Detailed explanation

A

Trauma - injury/ortho/oral surgery
Stimulation - pulp/periapical infection

Injury -> Predentinumand odontoblasts (internal resorption) / Precementum (external)

Denuded mineralized tissue is colonized by odontoclast/ cementoclasts/dentinoclasts (tooth resorbing cells)

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17
Q

Internal resorption -
Initiated by
Aetiology

A

Initiated within pulp chamber/cana;
Aetiology - caries/trauma/fracture/idiopathic
- chronic pulpal inflammation / Bacterial extension into pulp
OCCURS WHEN PULP IS VITAL, dentine replaced by granulation tissue

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18
Q

Internal resorption - clinical presentation

Investigations and findings

A

Often asymptomatic, detect on Rg
Rg - Uniform round radiolucent area in canal (enlarged - like a snake digesting something)
Pulp tests - variable results
+ve - Apical pulp necrotic, coronal vital
-ve - Apical pulp vital, coronal necrotic
May progress to symptoms/increased mobility

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19
Q

Management of internal root resorption
Non perforated
Perforated

A

Non perforated - PULPECTOMY, remove granulation tissue (sodium hypochlorite and ultrasonic)

Perforated - PULPECTOMY, ns CaOH/MTA
XLA
Resection
Periodontal surgery - crown / ortho

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20
Q

External surface resorption aetiology

A

Post traumatic
masticatory forces (physiological)
self limiting - not detectable
Excessive ortho forces

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21
Q

External inflammatory resorption
Cause
Investigations and findings
Treatment

A 
NECROTIC PULP
-trauma (luxation/avulsion) / caries 
-ve sensibility tests
TTP
Mobility if extensive resorption

Rg - PDL space widens, loss of lamina dura, root surface irregular

Treatment - RCT,
CaOH placement as intracanal medicament 6-24mths
Periradicular surgery

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22
Q

Apical resorption - Rg features

A

Moth eaten appearance, canal anatomy unaltered

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23
Q

Orthodontic induced root resorption

A

Shortening/rounding of roots

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24
Q 
External cervical (priodontal) resorption
Origin
Aetiology
Clinical features
Rg
A

Originates in periodontium
trauma / ortho / periodontal disease / periodontal therapy
- Asymptomatic
-+ve sensibility tests

Clinically - Pink spot cervically (highly vascular granulation tissue)
Rg - moth eaten irregularity superimposed on RC

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25
External Cervical resoption treatment
1. No treatment - XLA as symptoms appear 2. Immediate XLA 3. Debridement and resorption - RCT if near pulp
26
External replacement resorption 1. Aetiology 2. Action 3. Clinical features 4. Rg features
1. Luxation/avulsion - severe trauma, causes destuctionof cementum and root contact with bone - resorbed Ortho treatment 2. tooth gradually replaced by bone 3. Metallic percussion note, -ve sensibility tests, colour change, lack of physiological mobility, infraocclusion 4. Lack of PDL space,
27
function of periodontium
Force dissipation / attachment to jaws
28
Horizontal forces source
Orthodontic forces | Intermittent
29
Response of healthy periodontal to occlusal forces
PDL width increased until forces dissipation of forces Slight increase in tooth mobility Successful adaptation - physiological Demand eventually reduced - return to original width Demand too much - continuing increase in PDL width, increase in mobility
30
Occlusal trauma - definition | Rg evidence
Tooth mobility that is gradually increasing Symptoms Rg evidence - Increased PDL width In association with plaque induced inflammation
31
Occlusal trauma - associated with ------ bone defect
VERTICAL Plaque induced inflammation Trauma induced inflammation
32
Significance of tooth mobility Treatment Spliniting reasons?
1.Progressive Symptoms Interrupting restorative treatment 2. Controlled plaque induced inflam Correct occlusal relations Splinting - mobility - adv LoA Causing difficulty chewing Need to be stabilised for debridement LAST RESORT - OH difficulties
33
Deep traumatic overbite | -treatment
Treat plaque induced inflammation, relieve trauma - splint/ortho, restorative - occlusal stops
34
What is periodontal disease
A chronic inflammatory condition caused by anaerobic gram negative bacteria causing irreversible loss of attachment of teeth
35
Periodontal aetiology Systemic/Local Drugs - gingival hyperplasia
Systemic - Age/Race/Pregnancy(hormone imbalance)/puberty Local poor OH/malpositioned teeth/crowded/calculus/iatrogenic - restorative margins/denture Drugs - gingival hyperplasia 1. Cicclosporin 2. Phenytoin 3. ACE Inh
36
1. How can pregnancy gingivitis occur. | 2. Clinical features
1.Pregnancy can accentuate the response to plaque 2.Profuse bleeding • Increased ease of bleeding • Inflamed gingiva • Bright red-bluish red colour gingiva • oedematous interdental papilla • Papilla may pit on pressure • Smooth, shiny and soft (raspberry like appearance) • Marked vascularity • Sometimes present with raspberry like masses ‘pregnancy tumours Not in healthy gingivae
37
Pregnancy Gingivitis onset
2nd/3rd month greater erythema and inflammation greater bleeding tendency Greatest severity between 2/3 trimester
38
Histological features of pregnancy gingivitis
Non-specific vascularising, proliferative inflammation • Marked inflammatory cell infiltration • Oedema and degeneration of gingival epithelium and CT • Hyperplastic epithelium • Accentuated rete pegs • Reduced surface keratinisation • Various degrees of intracellular and extracellular oedema • Leukocyte infiltration • Copious newly formed engorged capillaries
39
Pathophysiology of periodontitis in diabetic patients
Hyper-inflammatory trait • Cytokines/Adipokines • AGE/RAGE deposition in gingivae • Microvascular changes in the periodontal tissues • Deficiencies in the innate and adaptive immune system • Increased inflammatory bone destruction • Reduced capacity for repair/remodelling (RANKL/OPG)
40
What is HbA1 and its significance in diabetes
Haemoglobin A1c - average blood glucose levels over a few months
41
Prevention for diabetic patients
Achieve and maintain healthy body weight; • Be physically active – at least 30 minutes of regular, moderate-intensity activity on most days. More activity is required for weight control; • Eat a healthy diet of between three and five servings of fruit and vegetables a day and reduce sugar and saturated fats intake; • Avoid tobacco use – smoking increases the risk of cardiovascular diseases
42
Smokers and periodontal disease - Effect on periodontium
Long term chronic effect | Impair vasculature of periodontal tissues (masks the signs of gingivitis) -
43
What are the features of aggressive periodontitis
``` Neutrophil function defects Root abnormalities Hyper-responsive macrophage phenotype LOW fetures of bacterial plaque > proportion of A.A ```
44
Localised Aggressive perio features
Localised Pubertal onset 6's and incisors Robust antibody response
45
Generalised aggressive perio features
Generalised (GAgP) • Usually affecting subjects under 30 yrs but may be older • Generalised pattern AL affecting 3 teeth other than 6s and incisors • Clear episodic nature of destruction of periodontal attachment and associated structures • Poor serum antibody response to infecting agents
46
Microbiology of aggressive perio
In relation to A.A - disease progression | High level of serum antibodies
47
Microbiology of aggressive perio
In relation to A.A - disease progression High level of serum antibodies A.A virulence factor - leucotoxin/collagenase
48
What are the virulence factors of A.A in Ag perio
1. Leucotoxin - affects PNM function by suppressing chemotaxis 2. Collagenases - breakdown of connective tissue and encourages loss of attachment 3. Endotoxins - drives inflam response in gingival tissues 4. fibroblast inh factor - prevent fibroblast attachment, affecting clot and attachment to root surface 5. Soluble heat labile factor - inhibit groeth and proliferation of other microorganisms redcing competition
49
Factors in Ag perio
Family history Smoking Papillion-Lefevre Syndrome
50
What is Papillion Lefevre syndrome Name some features How is the oral cavity affected
Rare genetic disorder Develop dryscaly patches of skin on palm of hands and soles of feet (hyperkeratosis) Oral cavity - teeth form and erupt normally but they exhibit chronic severe inflammation and degredation of periodontal tissues. - Gingivititis/stomatitis - Regional lymphadenopathy - greater pocketing - Halitosis and chewing painful
51
Candidate genes for Ag Perio
``` Cytokines e.g. IL-1, IL-10, TNF • Receptors e.g. FMLP, Fc receptors • Enzymes e.g. Cathepsin C • HLA antigens e.g. HLADQ1 • Structural proteins Meng et al 2007 ```
52
what can a dentist - tell patient about Ag perio | -factors
Genetic Poor OH Smoking related MUST monitor other family members
53
How to treat patients with Ag perio
``` Referral to specialist patient advised Adjunct antibiotics with RSD Plaque samples - lab Encourage good OH Full mouth debridement and CHX 0.2% mw Systemic antibiotics -early in treatment ```
54
Features of ANUG (Acute Necrotising Ulcerative Gingivitis)
-Blunt papillae -Painful erythematous gingivae underneath grey slough of necrotic mucosa/neutrophils -Bleeding and halitosis -Punched out crater like ulcers -Necrosis of gingival tissue - eventually leads to PDL and bone
55
Risk factors for ANUG
``` Poor OH Malnourished Stress Hormonal imbalance (Young adults) Smoking Impaired immunity - HIV/Immunosuppressed ```
56
What is necrotising stomatitis
Extension of necrosis beyond the mucogingival junction | Especially in those with HIV/Malnourished
57
Pathology of ANUG
Fusobacterium P intermedia Treponema
58
Treatment of ANUG and follow up
Gentle ultrasonic debridement Improve OH Smoking cessation CHX/ Oxidising Mw ``` If systemic symps - Metronidazole 400mg (9 tablets) 1 tablet 3x daily for 3 days ``` Follow up - continuation of HPT and supportive therapy, tends to recur if all factors not addressed. Can progress to NP
59
What is a periodontal abscess, | How can they be caused
A localised excaccerbation of a pre existing perio (chronic) pocket. Trauma or blockage of an existing pocket.
60
What are the symptoms of a periodontal abscess
``` Pain on biting Swelling adjacent to tooth Drainage to sinus Discharge and halitosis TTP Tooth mobility ```
61
Differential diagnosis for a periodontal abscess
Periapical abscess | Chronic perio - vital/non vital
62
Treatment of a periodontal abscess | Follow up plan?
Incision and drainage Gentle debridement of periodotal pocket warm salt mw XLA of teeth of poor prog Antibiotics if systemic involvement - metronidazole Follow with HPT and supportive therapy
63
Periodontal Surgery - when Indications
Indications: At re-eval 4-6 weeks after completion of NSPT. Persistant pockets of >5mm Good OH Between re-eval and reconstruction -If good plaque control but persistant deep pockets and BOP
64
Treatment for patients with: - Poor OH and inflammation - Good OH and inflammation resolved
1. Repeat HPT/cause related therapy | 2. Supportive therapy and proceed with treatment plan
65
Aims of periodontal surgery
Arrest disease process - complete RSD | Regenerate lost perio tissue
66
Post op care of periodontal surgery
``` CHX mw 0.2% for 1-2 weeks Analgesia - 2-3 days Antibiotics? Remove sutures Review and reappraise mechanical plaque control ```
67
Healing process after open flap currettage
Formation of blood clot and organisation of collagenout tissue Attachment of epithelium to root surface Reduction in pocket depth - gaining of clinical attachment and gingival recession
68
Types of bony defects
Infrabony - focal bone loss extends along root surface apically - 'Three walled' - buccal/lingual cortices preserved - 'Two walled' - buccal OR lingual cortex effaced - 'single walled' - both lingual/buccal cortices effaced Intrabony
69
Infrabony defect management
Closed/open RSD - healing by repair | Pocket elimination - osseous resection
70
Perio surgery outcomes
NSPT/SPT show clinical improvement reduced probing depths SUpportive perio care needed for long term success
71
How can periodontal therapy assist in restorative treatment
``` Improves soft tissue management Establishes stable gingival margin position Improves aesthetics Reduced tooth mobility Informs prognosis ```
72
Issues with an inflamed gingival margin
Difficult moisture control Poor aesthetics Unstable margin position - subgingival crown margin
73
Where should crown margins be ideally placed (measurements)
Within the gingival sulcus (0-0.5mm) AVOID the biological width (2-3mm) - junctional ep(1mm) and Connective tissue (1mm) Between crown margin and bone
74
What are the issues with an overhanging restoration
Plaque retention, inflammation and bone loss
75
What is ante's law
The combined periodontal area of the abutment teeth should be equal to or greater than the periodontal area of the tooth or teeth to be
76
What damage can be caused by FRP (crown/bridge)
Plaque retention Poor location and fit of margins Unfavourable transmission of occlusal forces Pulpal damage
77
What damage can be caused by RPDs
Plaque retention Unfavourable transmission of occlusal forces Direct trauma from components
78
How can communication between the pulp and oral cavity/periodontal tissues occur
``` Dentinal tubules Iatrogenic damage - perforation Lateral canals Fractures Resorption Apical foramen ```
79
Consequences when pulp becomes necrotic (periodontal tissues)
Direct inflammatory response from PDL at apical foramen | Leakage of necrotic tissue into periodontal tissues causing an inflammatory response
80
Consequences to pulp if periodontal disease occurs
Pulp not usually directly affected until recession causes lateral canals to become exposed to oral cavity (not protected by sound cementum)
81
How does a Primary Endodontic lesion with secondary periodontal involvement occur? Treatment
-Suppurating endodontic disease left untreatment, leaks into periodontal tisseus Plaque formed at gingival margin of sinus tract -Both periodontal and endo treatment Effective endo treatmetnt, perio determines the prognosis
82
Primary periodontal lesion with secondary endodontic involvement - What gives a better prognosis
Apical progression of periodontal pocket, infection able to enter pulp via lateral canals/apical foramen - pulp becomes necrotic - Pulp vitality maintained by blood supply through apex
83
What is a combined lesion - Features - Treatment
When coronally progressing endo lesion meets up with an apically progressing perio lesion - Tooth NON VITAL - periapical bone loss - Perio elsewhere in mouth - Large volume of attachment lost -RCT- periapical healing Periodontal therapy Surgical exploration to confirm diagnosis
84
Gingival recession symps
Poor aesthetics Sensitivity Tooth loss Cervical lesions/root caries
85
Recession treatment
1. Monitoring and prevention 2. Use of desensitizing agents, varnishes and dentine bonding agents 3. Composite restoration 4. Pink porcelain or composite 5. Removable gingival veneers 6. Orthodontics 7. Surgery
86
Recession aetiology
``` Mechanical - vigorous toothbrushing Tramatic occlusion Trauma - lip piercing Iatrogenic - poor crown margins Teeth out of arch alignment High frenal attachment ```
87
what can be detected in a 6ppc (7)
pocket depth/gingival margin/tooth mobility/furcation involvement/BOP/LOA/
88
idela HbA1c value
Ideal 48mmol/mol (6.5% or below)
89
What occurs when a pulp becomes necrotic | -PDL response
When the pulp becomes necrotic, there is a direct inflammatory response by the periodontal ligament at the apical foramen and/or opening of accessory canals • Inflammatory byproducts of pulpal origin may leach out through the apex, lateral and accessory canals and dentinal tubules to trigger an inflammatory vascular response in the periodontium. • Among those are living pathogens such as bacteria and their toxic byproducts, fungi and viruses as well as nonliving pathogens • Many of these are similar pathogens encountered in periodontal infections.

Perio (1 decks)

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