Perio Revision Flashcards
What are the aims of periodontal therapy
To arrest the disease process
Ideally, to regenerate lost tissue
To maintain periodontal health long term
What is periodontal disease
A group of diseases affecting the periodontal tissues, representing an immune reaction (innate and adaptive) to adjacent microbial plaque
How could perio aid in restorative dentistry
Improves soft tissue management
Establishes stable gingival margin position
Contributes to aesthetics
Reduces tooth mobility
Informs prognosis
If you are treating a periodontitis pt who also has high aesthetic demands for there teeth, what do you do
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
In a perio pt would removable or fixed prostheses be favorable
Fixed
What is meant by supracrestal tissue attachment and how long is it
It is the junctional epithelium and supracrestal connective tissue of the gingivae
2mm
Where should your restorative margins not encroach on
Supracrestal tissue attachment
What are overhangs asociated with
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)
What are the keys to periodontally successful indirect lesions
Start with healthy tissue
Adequate tooth preparation
Precise margin location
Excellent provisional restorations
Careful tissue handling and impression technique
What in Antes law
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
What is meant by excessive occlusal force
occlusal force that exceeds the reparative capacity of the periodontal attachment apparatus, which results in occlusal trauma and/or causes excessive tooth wear
What is meant by occlusal trauma
injury resulting in tissue changes within the attachment apparatus, including periodontal ligament, supporting alveolar bone and cementum, as a result of occlusal force(s)
What is primary occlusal trauma
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)
What is the response of the healthy periodontium to increased occlusal force
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
What is the histological basis of the adaptation of the periodontium to increased occlusal force
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
What is secondary occlusal trauma
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)
What is fremitus
Palpable or visible movement of atooth when subjectedto occlusal forces
When would splinting be appropriate with perio cases with mobile teeth
Mobility is due to advanced loss of attachment
Mobility is causing discomfort or difficulty in chewing
Teeth need to be stabilised for debridement
periodontal health is determined by the balance of what
The outcome of the balance between bacteria of the dental plaque and the host Immune system
What are the 2 different local risk factors to perio and what falls under them
Acquired:
-plaque
-calculus
-overhanging and poorly contoured restorations and crowns
-ortho appliances
-occlusal trauma
Anatomical:
-malpostioned teeth
-root groves
-concavities and furcations
-enamel pearls
What are the 2 different systemic risk factors to perio and what falls under them
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
What causes the connective tissue matrix degradation in perio
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
What is involved in the oral enviroment and what do they contain
Gingival crevicular fluid:
-AMP
-Cytokines
-Chemokines
-Lactoferrin
-IgG
Oral mucosa:
-AMP
-Cytokines
-Chemokines
Saliva:
-S IgA
-Lysozyme
-Peroxidase
-Lactoferrin
-Mucins
-Agglutinins
-Cystatins
-Histatins
What is in the red complex of socranskys model
P gingivalis
T forsythia
T denticola
What is in the orange complex of socranskys model
Fusobacterium species
-F periodonticum
-F nuc. nucleatum
etc
Prevotella species
-P intermedia
-P nigrescens
Campylobacter species
-C rectus
-C showae
etc
What is meant by polymicrobial dysbiosis
community of micro-organisms that work together to actively disrupt the normal homeostatic balance in the oral cavity for their own benefit
What are the virulence factors of P gingivalis
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)
What is the aetiology of perio associated with
Accumulated plaque bacteria
Presence of periodontal pathogens
Polymicrobial dysbiosis
In susceptible hosts
What happens in gingivitis
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
What is the role of neutrophils in perio tissue destruction
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
How does inflammation lead to bone loss
High levels of sRANKL
Low levels of OPG
Monocytes recruited in large numbers
Differentiate into osteoclasts
What are the celluar and molecular events linking bacterial-induced inflammation with pathologic tissue destruction
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
How may stress cause perio
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
How can diabetes increase risk of periodontitis
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
How can periodontitis affect diabetes
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
How can periodontitis be a risk factor of rhematoid arthiritis
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
How can perio be a risk of alzheimers
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
What are the limitations of BPE
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
When should a pt recall appt be
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
What is the true measure to severity of periodontitis
loss of connective tissue attachment to the root surface
What gracey curettes are there and what sites are they used
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)
Why can pregnancy lead to pregnancy gingivitis
Because of the hormones
-increased Progesterone levels
What alternative therapies are there for treating perio
Periostat
Periowave, photodisinfection
What is periostat, how long is it taken and what does it do
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
What are the 2 steps in periowave
- Irrigate: photosensitizing solution is topically applied to the gums at treatment site where It attaches to harmful bacteria and toxins associated with perio
- 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
What happens in open flap debridement
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
What type of incision is made in open flap debridement
Intracrevicular through base of gingival pocket
Following open flap debridement what are the post-op instructions
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
What are the indicatioins for a gingivectomy
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
What is the purpose of a gingivectomy and how does the exposed tissue heal
reduction of gingival excess to facilitate plaque control, restorative dentistry and to improve apperance
Heals by secondary intention
What is the gingivectomy procedure
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
What are the aims of regenerative perio therapy
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
What infrabony defects are there and when does it classify as one
1 wall
2 wall
3 wall
intrabony defect when the subcrestal component involves the root surface of only one tooth
How are infrabony defects managed
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
What biological mediators are used in regenitive techniques
Platelet-derived growth factor
Insulin growth factor
Bone morphogenetic proteins
Prostaglandin
Fibronectin
Enamel matrix proteins
Name a enamel matrix protein where its derived from and what it does
Emdogain
-derived from the porcine tooth germ
Forms a matrix on the root surface that mediates the production of cementum
What significantly worsen the tooth prognosis and how is it graded
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
What are indications for perio regeneration
Two and three-walled proximal defects
Grade II mandibular furcation defects
Grade II buccal maxillary furcation defects
What resective treatment is there to eliminate furcation
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
