BDSIII: Periodontics

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PATHOGENESIS
Gingivitis = ? Periodontitis = ? Recession = ? PPD = ? CAL = ?
Understand the definitions of the terms used in periodontal
assessment, i.e mobility, furcation, defects
Periodontal status Cellular/tissue changes
Healthy gingiva plaque, normal JE, sulcus depth, PMNs, dense
collagen; PPD inhibited by JE
Early gingivitis biofilm, PMNs transmigrate JE and create
palisading wall, early infiltrate of LC, JE
Established gingivitis biofilm, JE apically displaced by pocket,
LCs/PMNs
Periodontitis CT attachment loss, bone, ulceration of JE,
bacterial invasion into CT spaces, EC matrix and
collagen; PPD inhibited by supported collagen
DX

Highfield, 2009. Diagnosis and classification of

periodontal disease. ADJ 54:1: S11-S26
DX
In summary
Ch vs Ag, Gen vs Loc, necrotising, abscesses, plaque-induced vs non, systemic
mod (incl drugs, malnutrition, hormones, allergy, disease), etc
Systemic factors are MODIFYING FACTORS, they influence how the host
responds to bacterial insult; whereas PRECIPITATING FACTORS influence
the number and/or type of pathogens by creating a niche.

AgP ChP
Plaque
Progress of disease, BL
Age of onset
Familial aggregation
Associated w PGE2, IL-1B, hyper-responsive macrophages
Vertical vs horizontal BL
MHx
Smoking, diabetes, stress
PREDISPOSING RFs

Tooth anatomy =
Dental restns =
Dental prosthesis
OH/plaque levels
Calculus
Tooth malposition
Gingival contours = recession, high frenal
attachment
Age/gender = ?
MODIFYING RFs
Smoking = nicotine w psychoactive effect +
cholinergic effect, ie stimulates SNS and adrenal
medulla to release catecholamines -> induce
vasoconstriction in peripheries + effects on flora +
effects on host (PMNs, IgE)

Uncontrolled DM = non-enzymatic glycosylation

and oxidation of proteins, ie alters structure and
turnover of collagen, basement membrane +
chemotaxis/PMNs effects

Others: neutrophil dysfx, hormones, osteoporosis,

genetics, stress (HPA-axis), drugs, disease
(immunosuppression)
ANTIBIOTICS & ANTISEPTICS
Considerations in AB therapy when balancing the effect on the individual vs
the effect on the community w RESISTANCE.
Also consider Adverse Effects (AE)
Common = hypersensitivities, nausea/diarrhoea, opportunistic infections
(pseudomembranous colitis, ie w Clindamycin), candidiasis
Drug interactions = warfarin and alcohol (need to be careful w erythromycin
and metronidazole)
Toxicity: teratogenicity, breastfeeding

Prophylaxis = Therapeutic Guidelines, Oral and Dental 2012 v2

Therapeutic = Therapeutic Guidelines, Oral and Dental 2012 v2

Plaque control = mechanical, chemical (mainly indicated for gingivitis;

gingivitis is a poor indication of periodontitis)
Mouthrinses: alcohol content, surfactants (remove debris and
antibacterial)

Two gold standard Tx

CHX 0.12 or 0.20% = bisbiguanide, cationic antiseptic, binds to negative

molecules
30mins post sodium lauryl sulphate
12hr slow release, prevents plaque formation
Rivacol 0.2% CHX, 11.8% alcohol; Chlorofluor 0.2% CHX, 8.9%
alcohol; Savacol 0.2%, 11.5%; Chlorofluor gel
Indications = when OH limited, aphthous ulcers, Ch gingivitis,
rampant caries
AE = unpleasant taste, external staining, enhanced calc formation
Essential Oils = thymol and eucalyptol
Disrupts cell walls and inhibits enzyme activity, prevents
aggregation and slow prolif
High alcohol content, up to 27%
Others
Tea-tree oil
H202
Iodine
Supportive Periodontal Therapy (SPT)

Monitoring and maintenance once periodontitis has been stabilised in

remission; a lack of SPT, biggest RF for TL! 3-5x, vs smoking 2-3x

TMT GOALS
Control infection
Remove predisposing factors
Regulate/control modifying factors
Regenerate to their original form and fx
Maintain the lifespan, fx and aesthetics

Pt risk profile + disease

=> Dx => + C/C, long term objective => Tx plan
Prognosis of indvl teeth

R/v: PPD assessment, changes in CAL, BOP, changes in MHx, TL, etc,
every 3monthly initially, slowly extend to 6monthly appts once stable.

Tooth Px: %BL, PPD, mobility, caries, crown:root ratio, furcations, pulpal
involvement, tooth position and occlusal relaitonship
Overall Px: age, medical status, individual tooth px, rate of progression, pt
coop, economic, operator-ability, RFs, oral habits
Pt expectation/realistic benefits post Tx
---- Resolution of signs & symptoms, reduced PD, reduction in tooth mobility
Not always achieved: stopping the progression, preventing tooth loss,
maintaining a healthy periodontium long-term

Long-term goals of perio therapy: predictable regen of lost perio attachment

IF those are the goals of Tx, then the goals of SPT are to maintain Tx goals
Appts are to r/v these aspects, continue subgingival root debridement (SRD),
preventive strategies, smoking cessation, etc

TMT: ROP, systemic phase (address RFs, MHx, AB cover), hygienic phase
(non surgical therapy, intensive OHI, motivation, debridement), corrective
phase (surgical tmt to address tissue destruction, to decrease likelihood of
progression)
(1) A 75yo pt comes into the clinic w moderate to severe ChP. Explain in
language theyll understand why they need treatment, what kind of
treatment they should expect and what they should expect post treatment.

(2) A patient presents informing you that subgingival debridement can cause
rheumatoid arthritis. Discuss (in dot points) the relationship bw
systematic diseases and periodontitis.

(3) Discuss the importance of Supportive Periodontal Therapy (SPT) and what
a maintenance appointment involves?

(4) Discuss ABs in periodontal management.

(5) Differences bw ChP and AgP

(6) Discuss through examples the differences bw modifying and predisposing

factors

(7) Discuss recession, in reference to definition, aetiology, clinical symptoms,

gingival biotype, measurements, classification and diagnosis.
RESOURCES

Therapeutic Guidelines: Oral and Dental, Version 2

Lindhe (2008), Clincial Periodontology and Implant Dentistry, 5th Ed,

Blackwell Publising Ltd, Oxford

Wolf & Rateitschak (2011), Color Atlas of Dental Medicine: Periodontology,

3rd Ed, Thieme

Journal of Periodontology