Periodontics Flashcards
(21 cards)
Periodontitis
Multifactorial disease caused by 1. Genetic predisposition, 2. Environmental factors: a dysbiotic dental biofilm → excessive host immunological response.
Chronic inflammation leads to irreversible, progressive periodontal tissue destruction, manifesting through CAL (increased PPD and gingival bleeding), radiographically-assessed alveolar bone loss, and eventual tooth mobility and loss.
Pathogenesis models
Ecological plaque hypothesis
Keystone pathogen hypothesis
IMPEDE model.
Ecological plaque hypothesis:
Disease is a result of imbalance in microflora due to ecological stress which enriches oral pathogens
Microenvironment is modified to favour pathogens
Keystone pathogen hypothesis
Keystone pathogens (P. gingivalis) trigger inflammation even if present in low numbers
Cause normal microbiome to become dysbiotic and disease-provoking in susceptible host
Manipulates native immune response
Inflamm byproducts (degraded collagen peptides & heme-containing cmpds) sustain dysbiotic microbiota - must modulate host in adjunct to AB measures
IMPEDE: inflammation-mediated polymicrobial-emergence and Dysbiotic-exacerbation model
Inflammation as the principal driver of periodontitis
Inflammation
Polymicrobial diversity
Dysregulated inflammation & pocket formation
Inflammation-mediated dysbiosis & further tissue damage
Pathogenesis microbiology
factors
Bacterial biofilm composition
Disruptive bacterial virulence factors
Gingipains, Cysteine proteases, chemokines
Gingipains produced by P.g. lys-x and arg-x - surface adhesins that degrade collagen, fibrinogen, fibronectin, lamelin and host protease inhibitors TIMPs
Host tissue cells
Gingival epithelial cells
sense microbes by MAMP (microbial associated molecular patterns), using their PRRs, tolerate commensals,
maintain tissue integrity (tissue repair factors), & produce antimicrobial proteins, cytokines
Fibroblasts produce cytokines and amplify inflammation
Neutrophils early stage
Source of destructive enzyme granules
Extracellular and intracellular killing,- collateral damage
Direct role in osteoclastogenesis
Late stage: Monocytes produce cytokines IL-6 and IL-8 and also differentiate into macrophages, DCs and osteoclasts
Angiogenesis and dvpt of HEV (high endothelial-like venules)
HEV are specialised blood vessels which allow lymphocytes to enter lymph nodes directly
Role in migration and recirculation of immune cells
Proinflammatory
Present in disease states
Innate immune defence
Toll-like receptors recognise microbe components and activate immune response
Immune cells: leukocytes and lymphocytes
Immune mediators
Defensins - soluble & memb-bound
Complement
Chemokines
Cytokines
Increased inflammatory Interleukins:
IL-1B
Increase BV permeability
TNF alpha
IL-6
B cell differentiation
IL-8
Recruit PMNs
PGE2
Prostaglandin E2 mediates osteoclastic activity by inhibiting OPG (the RANKL inhibitor) → increased bone resorption
MMP and TIMP
Fibroblasts produce Matrix metalloproteinases and tissue inhibitor metalloproteinases instead of collagen
MMPs: endopeptidases which degrade extracellular matrix proteins by cleaving cell surface receptors and releasing apoptotic ligands.
Acquired immune defence
Genetic predisposition
Congenital deficiencies (PMN, LAD)
Environment
⇒ Degradation of the PDL from proteases
⇒ Bone loss from osteoclasts - RANKL up OPG down
Diagnostic statement for periodonal diseases
Type of periodontal disease
Extent: Localised/generalised/MI pattern
Stage I-IV
Grade A-C
Stability
Stable: BOP<10%, PPD<=4m, no BOP at 4mm sites
Remission: BOP>=10%, PPD<=4mm, no BOP at 4mm sites
Unstable: PPD>5mm, or PPD>=4mm and BOP at 4mm sites
Risk factors (diabetes, smoking)
Risk factors of periodontitis
Tobacco smoking
Increase risk by 85%
Qualitative difference in subgingival biofilm
Highly diverse, commensal-poor, pathogen-rich, anaerobic microbiome
Disease severity is Dose-dependent - pack years
Smoking cessation is beneficial on therapy outcome and disease progression
Diabetes
Both T1 and T2DM have 3-4x risk
Prevalence, severity and extent ↑ in uncontrolled diabetes
Glycemic control effects the tx outcome and disease progression
Pathogenic bacteria and microbial tooth deposits
Smoking
Tobacco leaf combustion causes
Rapid dissolution of toxins which is taken up by the oral and airway epithelial lining fluids, as well as systematically uptaken
Produces ROS - reactive oxidative substances which destroy tissues and trigger inflammation
Induces Humoral response
Inflammatory mediator release: activating IL8 and TNFa
Chronic immune cell recruitment & inflammation: Th2 and Th17-type
Triggers epithelial cell intracellular signalling cascades
Activates corticosteroid-resistant type inflammation
Production of Advanced glycation end products (AGEs) which cause intracellular damage and apoptosis
Decreased Cellular response
Decreased TLR modulation and decreased gingival cell production of antimicrobial peptides
Decreased NK (anti-tumour and viral) → produce less Interferon gamma (which regulates cellular immunity by upregulating APC activity and trigger differentiation of cytotoxic T cells) →
→ Decreased APC function and Th1 responses
→ decreased immunity to infection
Decreased phagocytic uptake of bacteria and apoptotic cells → Impaired healing and accumulation of apoptotic/cellular debris
Increase in autoimmunity
Generation of auto-antibodies
Activates signalling pathway of Ras → promote cell growth and division → cancer
Despite Heightened constitutive inflammation, persistent mucosal epithelial activation leads to diminished antimicrobial functions
Impaired response to infectious pathogens
Suppressed anti-tumour immune cell functions
Sustained exposure leads to
Chronic inflammatory processes
Promotes enhanced microbial colonisation and infection
Intraoral clinical manifestation:
Masking of clinical signs of gingival inflamm, ↓BOP
↑ CAL, PPD, bone loss, furcation, mobility
↑ lost teeth
Conditions and diseases associated with causing periodontitis
Genetic disorders
Neutrophil disorders (inherited neutropenia, abnormal neutrophil function)
Metabolic, structural or immune protein defects
Leukocyte adhesion deficiency syndrome
Genetic polymorphism eg for for IL-1
Down Syndrome - increased T cell migration and MMPs, higher incidence congenital heart disease → predisposition to infections
HIV → infections
Atherosclerotic/Coronary Vascular Disease (AVD): endothelial dysfunction and bracial artery stiffness increases in pts w periodontitis. Viable invasive A.a. and P.g. can be recovered from human atheromas.
Stress
Psychological: poor OH, smoking&alcohol, nutritional choices, disturbed sleep
HPA axis: Cortisol increase + ANS: increase adrenaline → increase glucose, altered immune-inflamm response, poor wound healing
⇒ increased susceptibility to periodontitis
Obesity
1.35OR. Dose-response relationship
Adipose tissues actively produce hormones and proinflammatory cytokines (TNFa, IL-6)
Low-grade state of systemic inflammation
Osteoporosis
Low dietary Ca and vitD
Supplement
Intraoral manifestations of diabetes
Intraoral manifestations:
Pronounced clinical and radiographic signs of periodontitis
Progression, esp in children and adolescents
Multiple recurring periodontal abscesses
Unpredictable response to therapy (pts w poor glycemic control)
3x risk of future attachment and tooth loss
Conditions that are worsened by periodontitis
Pregnancy
Associated w preterm birth and bacteraemia transmission oral-utero
Periodontal therapy is safe during gestation and results in some improved obstetric outcomes
Renal disease
Faster progression
Dementia/Alzheimer’s
Greater risk
Cancer
Possible association
The direct and indirect pathway linking periodontal and systemic diseases
Direct pathway
The periodontal pocket is a gateway for viable bacteria & their toxins/components (LPS, outer memb vesicles, fimbriae)
Frequent transient bacteraemia in daily life
Indirect pathway
Local inflammatory response - pro-inflammatory cytokines released, causing differentiation of monocytes → macrophages
Bidirectional relationship between periodontitis and diabetes
Diabetes → periodontitis
Hyperglycemia-induced non-enzymatic glycation of complement components reduces their activation
Poorly functional PMN: DM reduces chemotaxis and phagocytosis, but induces enhanced NETosis
Increase numbers of M1 macrophages (IL-1 and TNFa elevation)
Differentiation of native CD4+ T cells into Th17 cells
High glucose conc reduces proliferation of PLSC and differentiation into osteoblasts
DM increases apoptosis of osteoblasts and PDL fibroblasts
AGE (advanced glycation end-products) alter collagen struc and increase collegenase activity
Via AGE-RAGE axis: RANKL expression ↑, OPG expression ↓
↑ osteoclastogenesis
PMNs produce more MMP-8
Periodontitis → diabetes
Periodontal infection causes elevation of serum pro-inflamm cytokines/prothrombotic mediators
Systemic inflammation leads to insulin resistance in hepatic and adipose tissues → hyperglycemic state
Bacteria
Altered insulin production and secretion
P.g. induces B-cell de-differentiation
Enzymes produced by P.g. reduce glucose-induced insulin production
Induced insulin resistance
Inhibition of glycogen synthesis in liver
Blocking insulin receptor substrate
Induced gut dysbiosis
Increase in endotoxins
P.g. reduces intestinal barrier function
Changes in blood small molecule chemicals
Periodontal treatment assists in diabetic control
Lowers HbA1c by 0.4%, equivalent to adding a second medication
But, Note that pts w poorly-controlled diabetes have increased risk of postoperative infections.
Prognostic factors for an individual tooth
General
Genetic, systemic, acquired risks
Age wrt attachment loss
Pt OHI compliance
Pt expectations and values
Local
Tooth position
Remaining % root attachment
Bone loss patterns (number of walls left)
Mobility
Root proximity
Site PPD, BOP
Plaque retentive factors
Accessibility for treatment
Stages of prognosis
Good prognosis
Control of etiological factors
Adequate periodontal support - relatively easy to maintain by pt and clinician.
Fair prognosis
25% attachment loss and/or Class I furcation
Where Location and depth of furcation allows proper maintenance w gd pt compliance
Poor prognosis
50% attachment loss w Class II furcations that allow maintenance, but with difficulty
Questionable prognosis
>50% attachment loss
Poor crown:root ratio & poor root form, significant root proximity
Uneasily accessible Class II furcations, or Class III.
Hopeless prognosis
Inadequate attachment to maintain tooth
PPD>7mm, Bone loss >65%, Class III furcations
Mobility 3
Recurrent periodontal abscesses, perio retreatment, failed RCT
Extraction performed or suggested
Do now if So mobile that function becomes painful
Conserve temporarily if maintains support until it can be replaced by implant/other pros ; anterior aesthetic zone, perform perio therapy first, then remove
Explain the goals of periodontal treatment
END POINT OF THERAPY:
No PPD>/4mm w BOP
or
No deep PPD >/6mm
1 - Immediate goals (weeks)
Absence of pain
Reduction and elimination of infection and inflammation
Removal of predisposing factors, control of modifiable factors
Reduction/resolution of gingival inflammation w full-mouth mean BOP=<20%
Reduction in PPD w no residual pockets PPD >5mm
Elimination of open furcations (>=2)
2 - Intermediate goals (months to years)
Cessation of attachment loss, Gain of attachment
Restoration of physiologic bone and gingival contour to aid in plaque control.
Restoration of health, function, aesthetic and longevity of dentition
3 - Long-term (rest of life)
Maintenance of health thru prevention and professional supportive therapy
Periodontal treatment plan
Emergency treatment
Eg extraction of hopeless prognosis teeth
Initial MHX Evaluation:
Pt medical history: active infectious, lifethreatening diseases?
Allergies - drugs.
Complications of invasive procedures (subgingival scaling - infective endocarditis; bleeding issues - anticoags)
Initial phase - causative, hygienic, nonsurgical
Risk assessment
Tooth prognosis
PerioRisk method (bone loss/age, smoking, diabetes, #PPD>=5, BOP%)
Bacterial testing - for more targeted AB choice
OHI
SRD (Scaling & Root Debridement) (Adjunctive AB does not work well on intact biofilm. Ensure disruption of biofilm in all quadrants)
Systemic phase
Eg Control of T2DM by constant contact with GP
Re-evaluation 12 weeks post
Possible retreatment
Full mouth SPT, OHI
Surgical phase?
Open flap debridement of II/III furcations
Removal of enamel pearls
Root separations, resections
Restorative phase? (splinting?)
Maintenance phase - assumed 3 monthly /SPT
Pt Hx and Data collection
221: comprehensive periodontal exam
First assessment, re-evaluation, 1x/yr during SPT, deterioration
All pts 1x/yr: under 011 - PSR - periodontal screening & recording - sextant measuring
Revisit OHI, Motivation, Instrumentation
Treatment of active sites
Polish
Retentive factors, fluoride app, update tx plan, risk assessment
→ schedule next appt
PSR
Periodontal screening and recording
0
No BOP
No calc
PPD<=3mm
Preventive tx
1
BOP
No calc
PPD<=3mm
OHI
Supra Debridement
2
BOP
Calc
PPD<=3mm
OHI
Sub Debridement
3
PPD 3.5-5.5mm
+ Full perio exam & radiographs - possible referral to specialist
4
PPD>=6mm
+ more extensive tx, possibly surgery
Refer to specialist
4*
PPD>=7mm or furcation probable
Adjunctive treatment and rationale
Winkelhoff’s cocktail:
Amoxicillin: 500mg, orally 3/d for 7d
Metronidazole: 400mg orally 2/d for 7d
Rationale
Adjunctive AB
Young pt (<36) or aggressive periodontitis (grade C rapid attachment loss) with no medically-contributing factors
Generalised severe periodontitis (stage III/IV) with PPD 5mm in >35% of sites
Pt immunocompromised
Periodontitis unresponsive to mechanical therapy
NPD (after emergency debridement under LA)
Local antimicrobials
Acute periodontal infections (NPD)
Post periodontal tx
Pain and tenderness after initial debridement
Unable to touch area after surgery
Handicapped pts (mentally/physically can’t clean interdentally)
Medically compromised eg during chemo or radiotherapy
Types of healing following root instrumentation
Healing process: JE + GE → CT → PDL → bone
Possibilities of healing:
=> PPD reduction/CAL gain
Complete regeneration: de novo formation of cementum, PDL, bone and JE
Repair of junctional epithelium
‘New’ attachment - synthesis of new perio tissues, attachment to previously treated root surface
Re-attachment - perio tissues that were partially destroyed but not yet infected reattach to hard tissues.
Alveolar bone fill - new cementum and PDL
Root resorption - CT repair
Ankylosis - aggressively regenerating bone resorbs and fills segments of root dentin, lack of PDL
Side effects of non-surgical therapy
Gingival recession, black triangles
Exposed dentine - treat w sensitive toothpaste first, sensodyne - after that consider blocking with varnishes/bond/restorations
‘Too good’ OH - aggressive brushing → abrasion
Configuration of boney defects
Supraboney pocket- pocket base coronal to alveolar Infraboney- pocket base apical to alveolar crest
Horizontal (parallel alv bone crest)
Vertical bone loss (V-shaped)
3wall
2wall (interdental crater)
1wall
Splinting procedure
Determine teeth involved, check occlusion for ideal lingual/labial placement, moisture control
Use 3M strip to clean contact points
Measure teeth w floss and cut Ribbond
Prepare surface and interproximal w 37% orthophos acid, apply thin later adhesive and LC 20s
Wet Ribbond with adhesive and place thin band of low viscous CR on teeth above contact point
Place Ribbond adapting into interproximal contacts. Remove excess and tack-cure Ribbond for 5s/tooth
Cover Ribbond w thin later flowable CR (using microbrush) and LC 30s/tooth
Check occlusion, finish & polish
