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bds4 perio > Perio Revision > Flashcards

Perio Revision Flashcards

1
Q

What are the aims of periodontal therapy

A

To arrest the disease process

Ideally, to regenerate lost tissue

To maintain periodontal health long term

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2
Q

What is periodontal disease

A

A group of diseases affecting the periodontal tissues, representing an immune reaction (innate and adaptive) to adjacent microbial plaque

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3
Q

How could perio aid in restorative dentistry

A

Improves soft tissue management

Establishes stable gingival margin position

Contributes to aesthetics

Reduces tooth mobility

Informs prognosis

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4
Q

If you are treating a periodontitis pt who also has high aesthetic demands for there teeth, what do you do

A

if aesthetic demands are high the gingival margin should be monitored for at least 3-6 months
AFTER completion of periodontal treatment to check that it is stable

Once stability confirmed THEN place restorations

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5
Q

In a perio pt would removable or fixed prostheses be favorable

A

Fixed

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6
Q

What is meant by supracrestal tissue attachment and how long is it

A

It is the junctional epithelium and supracrestal connective tissue of the gingivae

2mm

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7
Q

Where should your restorative margins not encroach on

A

Supracrestal tissue attachment

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8
Q

What are overhangs asociated with

A

associated with more inflammation and bone loss
than non-restored sites (Gilmore 1971)

larger the overhang - greater the bone loss (Jeffcoat et al 1981)

development of pathogenic flora (Lang 1983)

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9
Q

What are the keys to periodontally successful indirect lesions

A

Start with healthy tissue

Adequate tooth preparation

Precise margin location

Excellent provisional restorations

Careful tissue handling and impression technique

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10
Q

What in Antes law

A

The combined periodontal area of the abutment teeth supporting a fixed dental prosthesis should be equal to or greater than the periodontal area of the tooth or teeth to be replaced

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11
Q

What is meant by 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

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12
Q

What is meant by occlusal trauma

A

injury resulting in tissue changes within the attachment apparatus, including periodontal ligament, supporting alveolar bone and cementum, as a result of occlusal force(s)

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13
Q

What is primary occlusal trauma

A

Injury resulting in tissue changes from excessive occlusal forces appliedto a tooth or teeth with normal periodontal support. It occurs in the presence of normal clinicalattachment levels, normal bone levels, and excessive occlusal force(s)

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14
Q

What is the response of the healthy periodontium to increased occlusal force

A

PDL width increases until forces can be adequately dissipated, the PDL width should then stabilise

Tooth mobility will be increased as a result

This can be regarded as successful adaptation to increased demand and therefore physiological

If demand is subsequently reduced, PDL width should return to normal

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15
Q

What is the histological basis of the adaptation of the periodontium to increased occlusal force

A

zones of tension and pressure within the adjacent periodontium

location and severity of the lesions vary based on the magnitude and direction of applied forces

on the pressure side, these changes may include increased vascularization and permeability, hyalinization/necrosis of the periodontal ligament, hemorrhage, thrombosis, bone resorption, and in some instances, root resorption and cemental tears

on the side of tension, these changes may include elongation of the periodontal ligament fibers and apposition of alveolar bone and cementum

Collectively, the histologic changes reflect an adaptive response within the periodontium to occlusal trauma

As a result of sustained occlusal trauma, the density of the alveolar bone decreases while the width of the periodontal ligament space increases, leads to increased tooth mobility

Radiographic widening of the periodontal ligament space, either limited to the alveolar crest or through the entire width of the alveolar bone

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16
Q

What is secondary occlusal trauma

A

Injury resulting in tissue changes from normalor excessive occlusal forces applied to a tooth or teeth with reduced periodontal support

It occurs in the presence of attachment loss, boneloss, and normal/excessive occlusal force(s)

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17
Q

What is fremitus

A

Palpable or visible movement of atooth when subjectedto occlusal forces

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18
Q

When would splinting be appropriate with perio cases with mobile teeth

A

Mobility is due to advanced loss of attachment

Mobility is causing discomfort or difficulty in chewing

Teeth need to be stabilised for debridement

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19
Q

periodontal health is determined by the balance of what

A

The outcome of the balance between bacteria of the dental plaque and the host Immune system

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20
Q

What are the 2 different local risk factors to perio and what falls under them

A

Acquired:
-plaque
-calculus
-overhanging and poorly contoured restorations and crowns
-ortho appliances
-occlusal trauma

Anatomical:
-malpostioned teeth
-root groves
-concavities and furcations
-enamel pearls

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21
Q

What are the 2 different systemic risk factors to perio and what falls under them

A

Non-modifiable:
-Aging
-Genetic factors
-Gender (males)
-Genetic disorders eg. papillon lefevre, downs

Modifiable:
-Smoking
-Poorly controlled diabetes
-HIV
-Leukameia
-Osteopenia
-Stress
-Hormonal status
-Nutritonal defficencys

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22
Q

What causes the connective tissue matrix degradation in perio

A

Matrix degradation is largely a result of MMP’s secreted by host inflammatory cells

Matrix metalloproteinases are a family of zinc and
calcium dependent proteolytic enzymes, which include collagenases

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23
Q

What is involved in the oral enviroment and what do they contain

A

Gingival crevicular fluid:
-AMP
-Cytokines
-Chemokines
-Lactoferrin
-IgG

Oral mucosa:
-AMP
-Cytokines
-Chemokines

Saliva:
-S IgA
-Lysozyme
-Peroxidase
-Lactoferrin
-Mucins
-Agglutinins
-Cystatins
-Histatins

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24
Q

What is in the red complex of socranskys model

A

P gingivalis

T forsythia

T denticola

25
Q

What is in the orange complex of socranskys model

A

Fusobacterium species
-F periodonticum
-F nuc. nucleatum
etc

Prevotella species
-P intermedia
-P nigrescens

Campylobacter species
-C rectus
-C showae
etc

26
Q

What is meant by polymicrobial dysbiosis

A

community of micro-organisms that work together to actively disrupt the normal homeostatic balance in the oral cavity for their own benefit

27
Q

What are the virulence factors of P gingivalis

A

Asaccharolytic– nutrients from breakdown of proteins and peptides

Gingipains– proteases with broad specificity

Atypical LPS–TLR4 antagonist (blocks signalling)

Inflammophilic–Inflammatory environment favours expression of virulence

Drives dysbiosis (in susceptible hosts)

28
Q

What is the aetiology of perio associated with

A

Accumulated plaque bacteria

Presence of periodontal pathogens

Polymicrobial dysbiosis

In susceptible hosts

29
Q

What happens in gingivitis

A

Increased TLR stimulation

Increased production of pro-inflammatory mediators

Triggers acute inflammatory response
Redness, swelling, bleeding

Increased vasodilation, cell migration

Neutrophils remain the predominant cell type in the initial lesion

Monocytes are recruited, activated and differentiate into macrophages

Lymphocytes are recruited to fine-tune the immune response

30
Q

What is the role of neutrophils in perio tissue destruction

A

Numbers increase in gingivitis

Excessive infiltration associated with chronic inflammation

Microbial subversion

Degradative enzymes (Major source of matrix metalloproteinases)

Inflammatory cytokines and oxygen radicals contribute to hypoxic environment

Connective tissue destruction manifests clinically as loss of attachment

31
Q

How does inflammation lead to bone loss

A

High levels of sRANKL

Low levels of OPG

Monocytes recruited in large numbers

Differentiate into osteoclasts

32
Q

What are the celluar and molecular events linking bacterial-induced inflammation with pathologic tissue destruction

A

Bacertial products bind to TLR’s on epithelium causes secretion of cytokines, chemokines and AMP’s

Vasodilation occurs and selective recruitment of leukocytes (predominantly neutrophils, also monocytes and lymphocytes)

bacterial products activate neutrophils causing further release of pro-inflammatory mediators and creating a amplification loop of neutrophil inifltration

Activated lymphocytes express RANKL disturbung the RANKL/OPG balance

RANKL binds RANK on osteoclast precursors (monocytes) activating osteoclastogenesis leading to alveolar bone resorption

Pro-inflammatory cytokines contribute to bone resorption by inhibiting bone foramtion

Elevated and dysregulated MMP acvtivation contributes to connective tissue destruction manifesting as attachement loss

33
Q

How may stress cause perio

A

In response to stressful events increased production and secretion of cortisol, which stimulates the immune system, the ANS is aslo stimulated leading to secretion of catecholamine and substance P which can regulate immune/inflam. response

mediating perio

34
Q

How can diabetes increase risk of periodontitis

A

Hyperglycaemia can modulate RANKL/OPG ratio and in HG production of AGE increases leading to exacerbation of inflam.

Increased AGE deposition in perio tissues

Interactions of AGE and its receptor RAGE leads to activation of the local immune and inflam. response

These unregulated responses lead to increased secretion of cytokines e.g. IL-1β, TNF-α, IL-6 and oxidative stress

This all disrupts the RANKL/OPG balance to favour bone resorption

Leading to local tissue damage, increased breakdown of the periodontal connective tissues and resorption of alveolar bone, thus exacerbation of periodontitis

35
Q

How can periodontitis affect diabetes

A

Bidirectional interaction

periodontal bacteria and products, together with inflammatory cytokines and other mediators produced locally in the inflamed periodontal tissues, enter circulation and contribute to upregulated systemic inflammation, also causing increased HbA1c levels

This leads to impaired insulin signalling and insulin resistance

Resulting inexacerbation of diabetes

36
Q

How can periodontitis be a risk factor of rhematoid arthiritis

A

Activation of immune system

P gingivalis- enzyme : PPAD peptidyl arginine deiminas

Cytrulination of the host proteins – changing of the proteins conformation – which stimulates immunological response to unrecognized compounds which destroys surface of cartilage

37
Q

How can perio be a risk of alzheimers

A

Activation of immune system

Increased production of plaques and tangles

Plaquesare deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells

Tangles are twisted fibers of another protein called tau that build up inside cells

38
Q

What are the limitations of BPE

A

Relies of pocket depth so where there is gingival enlargement or, as in young people, incomplete eruption, codes 3 or 4 may be recorded this may represent false
pocketing rather than true loss of attachment

In older individuals, there may be recession or furcation involvement but very little pocketing. The BPE will, in this case, lead to an underestimation of the loss of attachment

BPE is that it fails to indicate the extent of disease

39
Q

When should a pt recall appt be

A

Most pt’s recall appointment once every three months

For high-risk pt’s more frequent recall may be indicated, while lower risk pt’s may require less frequent recall

40
Q

What is the true measure to severity of periodontitis

A

loss of connective tissue attachment to the root surface

41
Q

What gracey curettes are there and what sites are they used

A

Gracey 1-2: anterior teeth (grey)

Gracey 7-8: buccal/lingual surfaces (green)

Gracey 11-12: posterior teeth, mesial surfaces (orange)

Gracey 13-14: posterior teeth, distal surfaces (blue)

42
Q

Why can pregnancy lead to pregnancy gingivitis

A

Because of the hormones
-increased Progesterone levels

43
Q

What alternative therapies are there for treating perio

A

Periostat

Periowave, photodisinfection

44
Q

What is periostat, how long is it taken and what does it do

A

20 mg of doxycycline

twice a day for 3 months systemically as an adjunct to supra-/sub-gingival instrumentation

Considered to be sub-antimicrobial as it does not inhibit the growth of bacteria but it is a collagenase inhibitor

45
Q

What are the 2 steps in periowave

A
  1. Irrigate: photosensitizing solution is topically applied to the gums at treatment site where It attaches to harmful bacteria and toxins associated with perio
  2. Illuminate: A thin, plastic light diffusing tip is painlessly placed into the treatment site and then illuminated with a specifically calibrated laser light activating the photosensitizing solution and destroying the harmful bacteria and toxins
46
Q

What happens in open flap debridement

A

An intracrevicular incision made through the base of the gingival pocket and entire gingivae

Muco-periostal full thickness flap formation

Removal of granulose tissue and instrumentation of the root surface flaps replaced to their original position

No attempts to reduce the pre-operative depth of the pockets

47
Q

What type of incision is made in open flap debridement

A

Intracrevicular through base of gingival pocket

48
Q

Following open flap debridement what are the post-op instructions

A

Reinforce mechanical plaque control

Post-operative soft toothbrush for operated area

Chlorhexidine mouthwash 1-2 weeks

Analgesics 2-3 days

Antibiotics if indicated ( while complications in healing)

Remove sutures after 1 week

49
Q

What are the indicatioins for a gingivectomy

A

Gingival enlargement or overgrowth

Idiopathic gingival fibromatosis

Falls pockets (enlargement of the gingival tissue without apical migration of the junctional epithelium attachment)

Minor corrective procedures

Procedure done during lengthening of the crowns before prosthetic treatment

50
Q

What is the purpose of a gingivectomy and how does the exposed tissue heal

A

reduction of gingival excess to facilitate plaque control, restorative dentistry and to improve apperance

Heals by secondary intention

51
Q

What is the gingivectomy procedure

A

Identification the bottom of the pocket with the probe

Marking the outer aspect of the gingivae creating a bleeding point

Scalloped external bevel incision apical to the bleeding points to terminate at the level slightly to the bottom of the pockets

Removal of detached gingiva

Gingivoplasty to create a better aesthetic contour

Root surface instrumentation

Periodontal dressing

52
Q

What are the aims of regenerative perio therapy

A

An increase in periodontal attachment of severe compromised teeth

A decrease in deep pockets to a more maintainable range

Reduction of the vertical and horizontal component of furcation defects

53
Q

What infrabony defects are there and when does it classify as one

A

1 wall

2 wall

3 wall

intrabony defect when the subcrestal component involves the root surface of only one tooth

54
Q

How are infrabony defects managed

A

Closed/open root surface debridement – healing by repair

Regenerative techniques:
-Space maintenance and clot protection

-Selective cell repopulation

-Provision of progenitor cells

-Use of biological mediators – signaling molecules

55
Q

What biological mediators are used in regenitive techniques

A

Platelet-derived growth factor

Insulin growth factor

Bone morphogenetic proteins

Prostaglandin

Fibronectin

Enamel matrix proteins

56
Q

Name a enamel matrix protein where its derived from and what it does

A

Emdogain
-derived from the porcine tooth germ

Forms a matrix on the root surface that mediates the production of cementum

57
Q

What significantly worsen the tooth prognosis and how is it graded

A

Furcation involvement

Grade I
-an early lesion, less than one third of horizontal attachment loss

Grade II
-more than one third horizontal attachment loss but not through and through

Grade III
-‘through and through’ from one furcation entrance to another

58
Q

What are indications for perio regeneration

A

Two and three-walled proximal defects

Grade II mandibular furcation defects

Grade II buccal maxillary furcation defects

59
Q

What resective treatment is there to eliminate furcation

A

Furcation plasty (mainly at buccal and lingual furcation)

Tunnel Preparation (to treat deep degree II and III furcation defects in mandibular molars) allows interdental cleaning

Root resection/separation

bds4 perio (5 decks)

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