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Periodontology > Other > Flashcards

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1
Q

Necrotising periodontal disease

A

Distinct smell, ulceration
Depends if immunosuppression is temporary (smoking, stress, nutrition, previous necrotising ulcerative perio/gingivalis) or chronic (severe malnourishment, AIDS, extreme living conditions)

We should understand why are they immunocompromised and include this is the referral letter

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2
Q

Endo perio lesions

A

Root damage- Can be due to root/pulp chamber perforations, external root resorption, root fracture, cracking

No Root damage-
1. Perio pt-
grade 1: narrow/deep pocket on 1 tooth surface
Grade 2: wide/deep pocket on 1 tooth surface
Grade 3: deep pocket in more than one tooth surface

Non perio pt-
Grade 1: same
Grade 2: same
Grade 3: same

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3
Q

What is prestine gingivae

A

There is not histology possible
It is free from histological inflammation
Called conical gingival health
Pink knife edged stippled gingivae

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4
Q

Initial lesion

A

Inflammation nwothin 24 h hours of plaque accumulation- vasodilation happens and increase in GCF
Neutrophils migrate into gingival sulcus as well as small number of lymphocytes/macrophages
Lymphocytes bind to CT
Cellular response develops in 2-4 days

Defined as clinical gingival health

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5
Q

Early lesion (1 week)

A

Inflammatory infiltrate increases
Vessels become dilated/more vessels
Increase in lymphocytes and neutrophils- shows as BOP
Very few plasma cells
Fibroblasts show cell damage
Loss of gingival collagen
Proliferation of basal cells of junctional and sulcular epithelium
Rete ridges proliferation
Some coronal epithelium are lost- plaque starts to extend subgingival
Can persist without progression to established gingivitis

Can be diagnosed as gingivitis
If BOP- between 10-30%- localised
If BOP- above 30% -generalosed gingivitis

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6
Q

Established lesion

A

More GCF and inflammatory infiltrate
Neutrophils dominate and increased migration of them
Plasma cells form 10-30% of infiltrate
Fibroblasts continue to show cell damage
Loss of gingival collagen both laterally and apically
Rete ridges extend further
Junctional epithelium is no longer closely attached to the tooth( giving a false pocket but no LOA
Gingivae is red and swollen
This stage can remain stable or progress to periodontitis

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7
Q

Advanced lesion

A

Inflammatory infiltrate extends apically and laterally
Plasma cells predominate ( more than 50% of all cell types)
Loss of periodontal connective tissue attachment
Apical migration of junctional epithelium - true pocket formation
Alveolar bone loss

This is periodontitis

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8
Q

Models of periodontal disease progression /theories

A

Linear/continuous theory-

Random Burst model

Asynchronous multiple burst theory

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9
Q

Use of chemotherapeutics and antimicrobials

A

Rationale is to be used as adjuncts in certain cases of periodontitis - severe, if perio is not responding to treatment, if perio due to systemic disease (e.g. uncontrolled diabetes)
Can be used for medically compromised patients, and to reduce risk of infective endocarditis in susceptible individuals

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10
Q

Antibiotics in perio

A

It Has Very little importance in perio therapy
Antimicrobial resistance is on the rise -we are part of antimicrobial stewardship
Small risk of anaphylaxis in response to antibiotics

Keep it:
1. Drainage of the infection
2. Removal of the cause of infection - perio treatment -plaque removal

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11
Q

Systemic use of antimicrobials

A

Should be based on the infectious nature of disease- identification of bacterial agent and antibiotics sensitivity tests

Clinical benefits should outweigh possible risk of adverse reactions- allergy/anaphylaxis, development of resistant organism or opportunistic bacteria; interaction with other medication should be considered as well as general side effects of antibiotics (nausea, vomiting)

Antibiotics should not be used as monotherapy- always as adjunct to standard periodontal therapy (can include local drug delivery and antimicrobial rinsing)

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12
Q

Serial vs combination therapy

A

Perio infection contains a wide range of organisms and are not affected by any single antibiotic
So we need serial and combination antibiotic therapies

Serial- one is bactericidal and other is bacteriostatic antibiotics given serially (static given first to reduce the further growth/multiplication and cidal after to kill bacteria that is left- e.g. metronidazole and doxycycline

Combination - synergistic activity reduces lethal dose ( two drugs given together to increase their action or complement their action
E.g. amoxicillin and metronidazole
Amoxicillin and potassium clavulante and metronidazole
Ciproflaxacin and tinidazole

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13
Q

When to prescribe antibiotics in periodontitis

A

In normal perio -no
In severe perio- at the end of periodontal treatment, for duration of 7-10 days
Shorter course of antibiotics is preferred due to compliance

Necrotising periodontitis - quite rare but metronidazole is recommended as painful and severe inflammation (200 mg for 3 days)

Perio abscess - antibiotics only if systemic involvement - fever, malaise, facial swelling

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14
Q

Local drug delivery in clinical periodontology

A

Rationale is that antimicrobial agents are targeted to the site of infection e.g. perio pocket

It is sustaining local concentration at effective levels for a sufficient time and can eliminate or reduce pathogenic microorganisms

It will evoke minimal or no side effects

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15
Q

Local drug delivery system available

A
  1. Actisite ( tetracycline)
  2. Atridox (doxycycline)
  3. Periocline (minocycline)
  4. Elyzol (metronidazole)
  5. Periochip (chlorhexidine)
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16
Q

Indications for local delivery drugs

A

Isolated perio pockets (5mm or more), with successful perio therapy(scaling and RSD)
In medically compromised patients where surgical therapy is contraindicated or not suggested
In pt suffering from recurrent or refractory period
As an adjunct to perio regenerative procedures

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17
Q

Host modulation therapy

A

It does not switch off normal defense mechanism or inflammation

It ameliorates/reduces excessive or pathologically elevated inflammatory processes to enhance the opportunities for wound healing and periodontal stability

It will affect by:
Modulation of arachidonic acid metabolites-
Modulation of matrix metalloproteinases
Modulation by bone remodeling
Regulation of immune and inflammatory response

18
Q

Subantimicrobial dose doxycycline

A

Not used as monotherapy- but as an adjunct to SRP
20mg taken twice daily for 3 months and up to max of 9months
Only FTA approved HMT (host modulating therapy)

At this dose doxycycline does not kill bacteria but modulates the host without having an antimicrobial effect.

It targets MMPs, down regulation of key inflammatory cytokines, reduces osteoclast activity.and bone resorption, stimulates osteoblast activity

Contraindicated - Risk of allergy, pregnancy, breastfeeding, children under 12 y of age, can reduce effectiveness of oral contraceptives

19
Q

Bisphosphonates for perio

A

Affect osteoclast activity and cause bone resorption
Not FTA approved or routinely used

20
Q

Chemical plaque control agents

A

1st generation - capable of of reducing plaque up to 20-50%. Exhibit poor retention within the mouth- antibiotics (penicillin, erythromycin, metronidazole), phenolic compounds, essential oils, herbal extracts, oxygenating agents

2nd generation - produce an overall plaque reduction of about70-90% . Better retained than 1st generation. Chlorhexidine, alexinide…

3rd generation - they block binding of microorganisms to the tooth or to each other. Have poor retention capacity when compared to 2 ND generation. E.g. delmopinol

21
Q

Criteria for using mouthwash/chemical plaque control agents

A
  1. Substantivity- ability to bind to pellicle and tooth surface and to be released over period of time
  2. Stability- ability to remain stable within product formulation and to enzyme degradation
  3. Safety
  4. Efficacy
  5. Cost effectiveness
  6. Appropriate vehicle design
22
Q

Chlorhexidine mouthwash

A

Bacteriostatic and bactericidal effect
For plaque inhibition, oral candidiasis, gingivitis, management of aphthous ulcers

Side effects - risk of allergy, hypersensitivity, anaphylaxis, mucosal irritation, parotid gland swelling, staining of the composite restorations and teeth-reversible!, Taste disturbance, tongue discolouration

23
Q

Dental varnishes

A

Applied in thin layer/coating to the tooth surface
They form a continuous and solid film after undergoing chemical or physical changes
Can be chemical or mechanical adhesion(by irregularities on tooth surface) to tooth surface

24
Q

Most important part of varnishes?

A

Functional additives -active ingredients

25
Q

Three main tasks of dental varnishes

A
  1. Protection of teeth from caries- they contain fluoride or antimicrobials as active ingredient to reduce the demineralization process of teeth (e.g Duraphat, Fluor protector…)
  2. Enhancing aesthetics by alteration in tooth shades-some varnishes contain bleach agents as active ingredients and it removes discoloration on teeth surface and aids in whitening (e.g. VivaStyle Pain on Plus)
  3. Desensitization of the exposed dentinal or root surfaces- active ingredient in desensitizing agents forms a physical layer/coating onto the exposed dentinal tubules and seals them (e.g. VivaSens)
26
Q

What are Dentifrices

A

They contain:
1. Polishing/abrasive agent- mild abrasive action-aids in eliminating plaque and stains

  1. Binding/thickening agents- control stability and consistency of tooth paste
  2. Detergent/surfactants- produce foam that aid removal of food debris and desperation of a product within the mouth
  3. Humectants- aids in reducing loss of moisture from toothpaste
27
Q

What is 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

28
Q

Alveolar bone- some facts about normal

A

It is dynamic tissue continually forming and resorbing in response to functional requirements. It is a bone and bone’s metabolism is under hormonal control. It can be easily resorbed under the influence of inflammatory mediators at either the periapex or the marginal attachment.
In health, the crest of the alveolus lies about 2 mm apical to the cementoenamel junction

29
Q

What is occlusal trauma

A

It is a term used to describe injury resulting in tissue changes within the attachment apparatus, including periodontal ligament, supporting alveolar bone- and cementum, as a result of occlusal force

Oclcusal trauma may occur in healthy or reduced periodontium that is caused by periodontal disease

The definition and diagnosis of occlusal trauma is based on histological changes in the periodontium, therefore a definitive diagnosis of occlusal trauma is not possible without block section biopsy

Clinical and radiographic indicators and it used as surrogates to assist the presumptive diagnosis of occlusal trauma
These include progressive tooth mobility, fremitus, occlusal discrepancies, wear faucets, tooth migration, tooth fracture, thermal sensitivity, discomfort or pain on chewing, root resorption, cemental tear, widening of the PDL space on radiographs

30
Q

Histology of periodontal tissues undergoing occlusal trauma

A

Distinct zone of tension and pressure are seen within the periodontium. The location and severity of the lesion my vary based on the magnitude and direction of applied forces

On the pressure side - increased vascularization and permeability, hyalinization/necrosis of the PDL, haemorrhage, thrombosis, bone resorption and sometimes root resorption and cemental tears

On the tension side- elongation of PDL fibres, apposition of alveolar bone- and cementum

These histological changes reflect an adaptive response within the periodontium of occlusal trauma

Sustained occlusal trauma result in decreased density of the alveolar bone while the width of the PDL space increases. That leads to increased tooth mobility and often a radiographic widening of the PDL space, either limited to the alveolar crest or through the entire width of the alveolar bone

Clinical sign of occlusal trauma are: fremitus or palpable functional mobility of the affected tooth/teeth

31
Q

Primary occlusal trauma

A

Is 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

32
Q

Secondary occlusal trauma

A

Is injury resulting in tissue changes from normal to excessive occlusal forces applied to a tooth or teeth with reduced periodontal support.

Specific criteria to distinguish between normal and reduced periodontal support have not been identified
It was shown in some studies that PDL stress increases after reducing 60%of bone support

It is a trauma that happens in the presence of attachment loss, bone loss, and normal/, excessive occlusal forces

33
Q

What is fremitus

A

It is a palpable or visible movement/functional mobility of the tooth when subjected to occlusal forces

This may result from occlusal interference causing occlusal trauma, normal occlusion and occlusal forces but with reduced periodontium

34
Q

What is bruxism or tooth grinding

A

A habit of grinding, clenching or clamping the teeth

The force generated may damage both tooth and attached apparatus

35
Q

Effects of excessive occlusal load

A

There is a combined effect of occlusal trauma and bacterial plaque induced inflammation causing periodontal destruction - co-destruction.

When there is a presence of plaque induced periodontitis and occlusal trauma, there is a greater loss of the bone volume and increase mobility.
The loss of connective tissue attachment stays the same.

So there will be further progression of periodontitis but occlusal force does not cause initiation of the periodontitis/ not a causative agent of periodontitis (without plaque induced inflammation, occlusal trauma does not cause irreversible bone loss or loss of connective tissue attachment)

36
Q

How are perio and occlusion linked together

A

They both cause injury to the attachment apparatus because the periodontium is unable to cope with the pathological insult which it experiences

37
Q

What are acute and chronic traumas

A

Acute trauma from occlusion occurs following an abrupt increase in occlusal load such as a result of biting unexpectedly on a hard object

Chronic trauma from occlusion is more common and has greater clinical significance

38
Q

How does orthodontic (unilateral force) and jiggling (multidirectional displacement) force affect periodontium

A

Orthodontic force- does not lead to progression of perio in plaque-induced periodontitis

Jiggling force:
Healthy periodontium: increased PDL space but no LoA

Reduced by healthy periodontium: increased PDL space, no gingival inflammation, no further LoA

Plaque induced periodontitis: gradual widening of PDL space, progressive mobility, angular bone loss

39
Q

What are the most common clinical signs of occlusal trauma?

A

Increasing tooth mobility and migration or drifting
Fremitus
Persistent discomfort on eating

40
Q

What are common radiographic signs of occlusal trauma?

A

Discontinuity and thickening of lamina dura
Widening of PDL space
Radiolucency and condensation of alveolar bone/or root resorption

41
Q

What is considered as normal physiological tooth mobility

A

Between 10 microns and 150 microns

More than that, clinically detectable means there is some change in periodontal tissues that cause mobility

42
Q

How does PDL adapts to increased occlusal load

A

By resorption of the alveolar crest resulting in increased tooth mobility
This is called occlusal trauma and it is reversible if the occlusal trauma is rediced

Periodontology (5 decks)

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