ACCUTE PERIODONTAL CONDITIONS

Periodontology: Semester 2, 2012

Definition
Clinical conditions of rapid onset that involve the periodontium and
associated structures and are usually associated with pain or discomfort
and infection.
May or may not be associated with gingivitis and periodontitis.
May be localized or generalized with possible systemic manifestations.
International Workshop for a Classification of Periodontal Diseases and
Conditions, 1999 I.
I. Gingival Diseases
II. Chronic Periodontitis
III. Aggressive Periodontitis
IV. Periodontitis as a Manifestation of Systemic Diseases
V. Necrotizing Periodontal Diseases
VI. Abscesses of the Periodontium
VII. Periodontitis Associated with Endodontic Lesions
VIII. .Developmental or Aquired Deformities and Conditions
Gingival Diseases
a) Dental plaque-induced gingival diseases
b) Non-plaque-induced gingival diseases
Gingival Diseases
Non-plaque-induced gingival lesions
o Gingival diseases of specific bacterial origin
Neisseria gonorrhea
Troponema pallidum
Streptoccocal species
Others
Gingival diseases of viral origin
o herpes virus infectionso primary herpatic gingivostomatitis,
o recurrent oral herpes,
o varicella- zoster infections
Gingival diseases of fungal origin
o Candida
o Histoplasmosis
Gingival lesions of genetic origin
Herpatic gingivostomatitis
o Characterized by generalized pain in the gingiva and oral mucous
membranes.
o Inflammation
o Vesiculation

o Ulceration
o Lymphadenopathy
o Fever and malaise
Herpatic gingivostomatitis
Treatment
Aimed at relief of pain to maintain nutrition, hydration and basic oral
hygiene.
Gentle debridement
Topical anaesthetic
Antiviral medication
Reassurance of self-limiting nature of disease.
Treatment of primary herpetic gingivostomatitis (Mell, 2008)

Abbreviation: BID, two times daily.

Gingival Diseases
Non-plaque-induced gingival lesions
o Gingival manifestations of systemic conditions
mucocutaneous disorders eg.
Lichen planus,
pemphigoid, pemphigus vulgaris
allergic reactions
o dental materials
o toothpastes, mouthwashes, chewing gum, food additives
Traumatic lesions
o Chemical
o Physical
o Thermal
Foreign body reactions
Not otherwise specified (NOS)

Lichen planus
Relatively common-1% incidence
Occurs on skin and orally
Itching/dry mouth
Most common is radicular manifestation
Common gingival form is erosive desquamative gingivitis
Erosive lichen planus

Pemphigoid
Autoimmune disease
Bullous lesions
Chlohexidine rinses
Local corticosteroid use

Pemphigus vulgaris
Autoantibodies agains epithelium

 Formation of bullae
Can be fatal
Systemic corticosteroid therapy
IX. Periodontitis as a Manifestation of Systemic Diseases
Associated with hematological disorders
acquired neutropenia
leukemia
Associated with genetic disorders
Cyclic neutropenia
Down syndrome
Leukocyte adhesion deficiency syndrome
Papillon-Lefevre syndrome
Hystocytosia
Cohen syndrome
Hypophosphotasia
Glycogen storage disease
Infantile genetic agranulocytosis
Ehlers-Danlos syndrome (Types IV and VIII)
Papillon-Lefevre

V. Necrotizing Periodontal Diseases

a) Necrotizing ulcerative gingivitis (NUG)
b) Necrotizing ulcerative periodontitis (NUP)
c) Necrotizing ulcerative gingivitis (NUG
a. accute infection of the gingiva
b. characterized by gingival necrosis, punched out papillea, gingival
bleeding and pain.
c. associated with fusiform bacteria and spirochetes.
d. predisposing factors critical in aetiology and include emotional
stress, poor diet, smoking and HIV infection.

Necrotizing Ulcerative Gingivitis

Treatment
Debridement under LA
OHI
Pain control
Antibiotics (Metronidazole) in conjunction with debridement
Investegation of possible systemic causes
Lifestyle counceling (smoking, nutrition, OH)
With NUG, appropriate therapy and patient complience results in
rapid improvement
Necrotizing ulcerative periodontitis (NUP)
characterized by necrosis of gingival tissues,
periodontal ligament, alveolar bone.
patients usually have systemic predisposition such as HIV infection, severe
malnutrition and
immunosuppression.

Necrotizing Ulcerative Periodontitis

VI.Abscesses of the Periodontium

a) Gingival abscess localized to marginal gingiva and interdental papilla
b) Periodontal abscess localized to the periodontal attachment
c) Pericoronal abscess localized to tissue surrounding partially or fully

erupted crown
Characterized by redness, swelling, pain and possibly purulent
disharge
Treatment involves debridement and drainage with surgical
access if necessary
Antibiotics only used if systemic symptoms are present.
Assessment of predisposing/modifying factors in order to prevent
recurrence.
Diagnosis (perio vs endo) is crutial
Gingival abscess

Periodontal abscess

Periapical VS periodontal lesions

Endo
Sharp, continuous pain
Well localized,
intense Swelling at muccobuccal fold
Swelling over apex of tooth
Non vital pulp
Very tender to touch
Discoloured tooth
Perio
Dull,
absent ache Poorly localized Swelling in attached gingiva
Perio elsewhere in mouth Pulp usually vital Slight tenderness Large
plaque/calculus deposits
Generalized caries problem

Pericoronal abscess
o Usually affects wisdom teeth
o Dull but increasing pain over 2-3 days
o Exacerbated by trauma from opposing tooth
o Foul odour, bad taste

VII. Periodontitis Associated With Endodontic Lesions

Combined periodontic-endodontic lesions
o localized, circumscribed areas of infection originating in the
periodontal and/or pulpal tissues.
o Symptoms include swelling, pain, purulant exudate, rapid loss of
attachment, draining fistula.
Perio-endo lesions
Treatment is based on primary aetiology
Pulpal necrosis requires endodontic
treatment
Periodontal lesion requires debridement
Verical root fracture usually requires
extraction
Antibiotics are only used when systemic
symptoms are present.
Perio-endo lesion

Perio-endo lesion
Vertical root fracture
Usually presents as a localized,
narrow, deep pocket
Usually associated with
RCT, post, heavily restored teeth
Often associated with swelling,
draining sinus
Tooth is usually not salvageable.

Learning objectives
What is an acute periodontal condition?
How do we manage acute non-plaque associated gingival lesions?
How do we manage NUG?
How do we manage periodontal abscesses?
How do we differentiate between periodontal and pulpal abscesses?
How do we manage perio-endo lesions?

Documenting periodontal Patients & intra-oral

photography
Periodontology, semester 2, 2012
Contents:
History of periodontal patients
Signs & symptoms of periodontal disease
Oral hygiene status
Additional dental examination
Intra-oral photography
History of periodontal patients:
Chief complaint
o Optimal Tx outcomes can only be achieved if the patients demands
& expectations are in balance with objective evaluation of the
disease & projected tx outcomes.
Medical history & medications
o CVD- circulatory risks
o Diabetes
o Bleeding disorders
o Infective risks (HIV/HepC)
o Allergic reactions (penicillin)
o Medications: Bisphosphonates, induce gingival hyperplasia.
Dental history:
o Migration
o Increase mobility
o Bleeding gums
o Food impaction
o Difficulties in chewing
o Bad taste in the mouth (morning)
o History of previous periodontal & orthodontic treatment
o Missing teeth- yes then why (caries, periodontitis, trauma
Social & family history
o SES
o Diagnosis: aggressive periodontitis
o Familial aggregation
Oral hygiene habits
o Routing
o Frequency
o Duration
o Interdental cleaning device
o Additional chemical supportive agents.
Smoking history
o Risk of periodontal disease
o Systemic local effects
o Treatment outcomes
o Exposure duration & quantity

Inflammation:
1. Swelling
2. Heat
3. Redness
4. Pain
5. Loss of function
The gingiva
Colour: Redness
Texture of the gingival margin: Swelling
Bleeding on probing
Supra- & subgingival plaque and calculus
Pain
Loss of function: Tooth loss

Histopathology:

measurements
Probe
o Thickness/ Diameter (0.4-0.5mm)
o Graduation scale
o Angulation and position
o Probing force (0.25N)
Degree of inflammation
Up to 1.0mm histological difference between healthy and inflamed gingiva
Intra-& Inter-operator reproducibility
PPD Measurements
Basic Periodontal Examination; BPE (or Periodontal Screening Record; PSR)
To identify patients with periodontitis and in need of periodontal therapy
6 points periodontal pocket charting
To evaluate the amount of periodontal tissue loss in periodontitis

6 Point Charting (6 PPT)

1. PAL: PPD and Recession
2. Furcation Involvement (FI)
3. Mobility
4. Bleeding on Probing (BoP)
5. Full Mouth Bleeding Score (FMBS)
6. Full Mouth Plaque Score (FMPS)
Furcation Involvement
Class I
Class II
Class III

Mobility
Degree 0: Physiological movement (0.1-0.2mm horizontal movement)
Degree 1: Up to 1mm of horizontal displacement within the alveolus
Degree 2: Visually increased mobility of the crown of the tooth exceeding 1mm in
a horizontal direction
Degree 3: Severe mobility in both horizontal and vertical directions
Bleeding on Probing
Bleeding arising from the bottom of the periodontal pockets, which provoked by
the insertion of the periodontal probe
Presence of bleeding = inflammation
Dichotomous manner (+/-)
Full-Mouth Bleeding Score: Presented in % (25% of FMPS)
Absence of bleeding is a good indicator of periodontal stability
Full Mouth Plaque Score
Biofilm (Plaque) as a risk factor
Dichotomous manner
Disclosing agents
Presented in %
Monitor patients oral hygiene status throughout the treatment
Additional Dental Exams
Dental Radiographs: Amount and nature of bone loss - horizontal and/or vertical
bone loss
OPG
PAs (Parallel technique)
EPT (Electric pulpal testing)
Cold Test
Intraoral Photography

Why to take clinical photograph?

Diagnosis and treatment planning
Documentation - legal and professional
Communication
Patient - education and progress
Colleagues, technicians and specialists
Communication

Camera Setting
1. Aperture
regulate the volume of light
depth of field
measure in f-number
The Smaller the f-number, the smaller the depth of field
2. Shutter speed
3.Z oom
Depth of Field
DOF = The distance range over which objects are acceptably sharp
Camera Setting
2. Shutter speed
regulates exposure time
1/1000 (fast) 1/1 seconds (slow)
Slower than 1/60s results in blurred
Camera Setting
3. Zoom lens: enable to vary focal lengths
Extraoral
f-number: f-30
Shutter speed: 1/100-200s
Zoom: 1:4-1:3.5
Full Mouth
f-number: f-30
Shutter speed: 1/100-200s
Zoom: 1:3
Occlusal
f-number: f-30
Shutter speed: 1/100-200s
Zoom: 1:3
Focusing few teeth
1-2 teeth
f-30
S:1/125s
Zoom 1:1
4-6 teeth
f-30
S: 1/125s
Zoom: 1:2 - 1:1.5

Accessories
Retractors
Intraoral mirrors
Objectives
Know the sequence of patient history taking....
What are the clinical signs and symptoms of periodontal diseases and how do we
clinically measure them?
Difference between PSR and 6-PPT.....
Considerations during probing....
What are the aims of clinical photography?

RATIONALE FOR PERIODONTAL SURGERY

Periodontology Semester 2,2012

RATIONALE FOR PERIODONTAL SURGERY

1. Why do we do periodontal surgery?
2. Periodontal flap surgery for the management of periodontitis
3. Mucogingival surgery for correcting periodontal defects
4. Regenerative surgery for regenerating periodontal structures
5. Implant surgery
Treatment sequence
1.EMERGENCY
a. Abscess
b. ANUG
2. SCREENING PSR IF 2 OR MORE SEXTANTS WITH SCORE 3 OR ABOVE =
FULL PERIODONTAL CHARTING AND RISK ASSESSMENT
3.DIAGNOSIS/RISK ASSESSMENT -TREATMENT PLAN
4.TREATMENT PHASE
a. OHI - WHAT, WHERE, WHEN, HOW, VERIFY
b. DEBRIDEMENT - WHICH TEETH, WHEN, LA? d. REVIEW (6-12
weeks)
Traditional treatment philosophy
Deep periodontal pockets (>6mm) can only be adequately treated by
surgical therapy.
RATIONALESurgicaltherapyis required to remove all residual calculus
AND contaminated (infected) root surface.
Residual Calculus (Buchanan and Robertson 1987)
Teeth scheduled for exo due to perio
Debrided with hand and/or ultrasonic instruments
Operators = randomly chosen periodontists
Examined under 10x magnification
% Surfaces with Residual Calculus (Buchanan and Robertson 1987)

% of Furcation Dome with residual calculus

50 teeth
with
Class II
and III
furc and
>=
5mmPD

Both surgical and non-surgical

debridement leave behind some
calculus.
In deep pockets and furcations,
surgical debridement may result
in less residual calculus than non
surgical debridement.

1986 Nyman et al Study on dogs

Produced similar contralateral defects then Flap surgery for access
o 1 side received SC and removal of cementum with diamond burs
o 1 side received prophy
Both sides had the same clinical response to treatment
1988 Nyman et al did a similar study to 1986 but in humans
Same improvement in periodontal health removal of exposed cementum
o Suggested that either
Endotoxins within the cementum has been neutralised by
the inflammatory response
or
Cytotoxic bacterial products are located on the surface of
the cementum
Need to consider the possible advantages of leaving cementum eg. less
sensitivity.
Smart et al 1990
o Light pressure from U/S scaler is enough to reduce LPS to the level
of uninvolved root surfaces in vitro
o Aim of treatment should be to remove plaque and predisposing
factors (especially calculus) to levels compatible with health.
o Total removal of plaque and calculus neither possible nor
necessary in many cases.
Results should not be interpreted to mean the removal of cementum in
periodontal therapy must necessarily be avoided. In fact elimination of calculus
cannot be performed without removal of some cementum.
Is surgical periodontal therapy more effective than non-surgical therapy?
Numerous longitudinal studies evaluating various periodontal therapies
carried out between early 70s and late 80s
o Ramfjord, Knowles et al (Michigan)
o Lindhe, Rosling, Nyman et al (Sweden)
o Pihlstrom et al (Minnesota)
o Kaldahl, Kalkwarf et al (Nebraska)
Non surgical therapy
Good oral hygiene + good debridement + regular maintenace recalls
can be successful even in deep (7-12mm) pockets in non-molar teeth.

Scaling and Root-planing (debridement !) results after 2 years: 12 adult periodontitis patients, 1682 sites, 139 molar
furcations
non-molar sites
o moderate and deep sites gain attachment and (decrease) pocket
depth
o 7% showed attachment loss
deep molar sites
o return to baseline after 24 months
o 10% showed attachment loss
moderate and deep furcations
o return to baseline after 24 months
o 25% showed attachment loss
Conclusion:
Molar furcations, premolar grooves, and inaccessible anterior sites may not
respond well to conservative scaling.
These sites should be reassessed at review. Access surgery should be
considered for non-responding sites.
Periodontal Flap Surgery
Non resective Replaced access flap, Mod Widman flap
Resective flap - Apically Repositioned flap/pocket elimination flap +/- bone
removal
Allow access to root surfaces, even infrabony (vertical bone defects)
Allow access to bone for osteoplasty if required
Different parts of flap can have separate characteristics (e.g. MWF + ARF)
Types of flaps Apically repositioned flap

Types of flaps Modified Widman Flap

Changes in Attachment Levels

(Ramfjord et al 1987)

Sites: >7mm
Review 3mths
Similar results for both tx
Data >5yrs no major difference

even though surgery results in greater

probing depth reduction this was greater
probing depth reduction this was no
protection against later breakdown.

Changes in sites >7mm

Private practice
Only PM and Molars
Initial Tx of Sc/Rp for 2 hours
Review Supra and SubG every 3 months
Although slightly greater reduction in pocket depth with surgery
No differ wrt attachment

Clinical Attachment Levels

over 3 years
.......Showed no difference among the three treatments nor was there any
difference in the distribution of sites gaining or losing attachment.
It is concluded that.....the three treatment modalities tested similarly.
Becker et al 1988 JDR 67:272
Surgical vs non surgical periodontal therapy
Both surgical and non-surgical therapy produced improvement in
periodontal health
Surgery results in greater short-term probing depth reduction than nonsurgery; however, in most studies, the advantage is lost over time
In shallow pockets, surgery produces greater loss of attachment than nonsurgery.
A small number of sites show continued loss of attachment following all
forms of Tx
No long term differences in mean attachment level change between
surgical and non- surgical therapy
No evidence supporting routine surgery for the treatment of periodontal
disease
BUT Studies looked at mean values, however we treat individuals and sites
that dont respond like the average.
The use of periodontal surgery must be based on a sound scientific
rationale

AIM OF PERIODONTAL THERAPY

Periodontal destruction occurs as a result of the host response to the
causative factor (dental plaque)
The principal aim of treatment is the removal of the causative factor

(dental plaque) to a level that is compatible with health, as defined by a

lack of bleeding after probing.
When do we need surgical access?
Logical therapeutic approach to access surgery
o Plaque control Non surgical debridement
o Assessment of response
o If response is unsatisfactory WHY?
o If the position and depth of the site prevent it from being
adequately debrided using a non-surgical approach, then surgery
is indicated as long as it improves the access to this particular site.
Furthermore, there may be predisposing factors (eg grooves) that
need to be addressed.
Pre treatment

After surgical treatment

Contraindications for Surgery:

Any contraindication for elective surgery is a contraindication for
periodontal surgery consult with GP if in doubt.
RELATIVE CONTRAINDICATIONS:
o Medical conditions
o Psychological conditions
o Smoking
o Poor plaque control
Patients and sites have to be assessed individually
WHY NOT? - Possible Contraindications
Anterior areas in patients with a thin morphotype where recession will
result in significant aesthetic problems
Smoking due to compromised healing
Patients suffering from aggressive periodontitis
Smoking and Surgical Response

Learning objectives
What are the different indications for periodontal surgery?
Is surgical access superior to non-surgical debridement for the
management of deep periodontal pockets?
What is the role of residual calculus in periodontal disease?
When do we use periodontal surgery for the
management of periodontitis?
What are the different periodontal surgery techniques that we can use?
What factors may influence our response to surgery?

Periodontology Wound Healing & Regeneration

Periodontology: Semester 2, 2012

PERIODONTITIS
Conventional periodontal treatment
Before Treatment

After Treatment

The Nature of Healing following Treatment

i. The inflammatory lesion resolves
ii. A long junctional epithelium of variable length is formed
iii. Bone may be laid down or remineralised
iv. The inflammatory lesion resolves
v. A long junctional epithelium of variable length is formed
vi. Bone may be laid down or remineralised
Periodontal treatment
The ultimate aim of periodontal treatment is the regeneration of the
affected tissues to their original architecture and function.
DEFINITIONS (AAP Glossary, 1992)
Repair is the restoration of new tissue that does not replicate the structure
and function of the lost tissue, and is analogous to scar tissue formation.
Reattachment is the reunion of connective tissue to the root surface
(separated by incision or injury) on which viable periodontal ligament is
still present, eg. pericision.
New attachment is the reunion of connective tissues with a pathologically
exposed root surface that is deprived of its periodontal ligament and may
or may not include new cementum
Regeneration is defined as a reproduction or reconstitution of a lost or
injured part in such a way that architecture and function are completely
restored. Periodontal regeneration is histologically characterized by the
restoration of all of the tooths supporting tissues, including alveolar
bone, periodontal ligament, and cementum over a diseased root surface.

Periodontal wound healing

Complex process due to the involvement of
o Four distinct soft and hard tissues:
1. Gingiva
2. Periodontal ligament
3. Cementum
4. Bone
Gingiva
Gingival epithelium and connective tissue have good regenerative potential
Epithelium divides rapidly
Epithelium attaches readily to root surface
Gingival connective tissue regenerates with little scarring
Recession and lack of attached gingiva can be a problem
Bone
In contrast to the gingiva, in the context of the periodontium, bone is
difficult to regenerate
Bone regeneration is achieved by osteoblasts, osteoclasts and cells of the
periosteum (progenitor cells)
Variability in periodontal wound healing depends on type of defect one,
two or three wall
Bone defect anatomy
Cementum
Four types:

1. Acellular afibrillar cementum

2. Acellular extrinsic fiber cementum*
3. Cellular intrinsic fiber cementum
4. Cellular mixed stratified cementum*
Cementum is critical in the periodontal regeneration process.

Periodontal ligament
The periodontal ligament is very important in periodontal regeneration,
because the progenitor cells required for cementum formation (and
hence new attachment formation) reside in the periodontal ligament and
not bone.
Furthermore, deposition and resorption of bone from the periodontal
surface of the bone is accomplished by cells that arise in the periodontal
ligament.
Regenerative procedures historical perspective
Conventional therapy
Root conditioning
Grafting
Guided tissue regeneration
Emdogain
Conventional treatment - scaling and surgery
Results in apical migration of the junctional epithelium along the root

surface, extending to the level of instrumentation

Epithelium adheres to the root surface
This can still be considered a healthy situation but it isnt regeneration
Root conditioning
1. Citric acid
2. Tetracycline
3. Fibronectin
4. Detergents
Aimed more at new attachment formation rather than true regeneration
Bone Grafting - definitions
1. Osteogenic - The formation of new bone from osteoblasts that are
transplanted as a viable component in autogenous bone grafts.
2. Osteoinductive - The formation of new bone through proliferation of
mesenchymal cells which differentiate into osteoblasts under the
influence of inducing agents.
3. Osteoconductive - The process by which host osteoblast precursors
infiltrate, proliferate, differentiate and form new bone in a favourable
environment. Osteoconductive agents act as a scaffold on which bone
matrix can be deposited.
Grafting - types

i.
ii.
iii.
iv.

Autografts: Intraoral/ extraoral

Allografts DFDBA
Xenografts BioOss
Alloplastic materials: beta tricalcium- phosphate,
hydroxyapatite, ceramic (perioglass)
The re-establishment of a connective tissue attachment to the root surface
and regeneration of the alveolar bone are unrelated phenomena

Guided tissue regeneration (GTR)

Based on the concept of using a barrier membrane to facilitate the repopulation of the periodontal defect with cells derived from PL and bone
at the expense of gingival epithelium and connective tissue.
GTR surgery

GTR
Complications due to: - membrane exposure and infection

- open wound
- membrane collapse
- lack of wound stability
Overall, clinically unpredictable
GTR
Case selection is essential:
o attachment loss > 4mm
o 2 or 3 wall bony defects
o class II furcations
o adequate attached gingiva
o Very technique sensitive
Guided bone regeneration (GBR)
Same principle as GTR
Aims to exclude faster proliferating soft tissues in preference to slower
proliferating bone
Very predictable
Closed wound (GBR) vs open wound (GTR)
Emdogain (GEL)
Based on embryological observations
EMDOGAIN
Enamel matrix proteins, predominantly amelogenin
Sourced from pigs
Results similar to GTR, no additive effect
Emdogain
Current status
Current periodontal regeneration techniques are
clinically unpredictable.
Why?
Procedures are very clinically sensitive
Complex structure of periodontium
o Gingiva
o Periodontal ligament
o Cementum
o Alveolar bone
A lack of understanding of the biological mechanisms involved
i. Growth factors
ii. Tissue engineering

Growth factor
Growth factor is a general term to donate a class of polypeptide hormones
that stimulate a wide variety of cellular events such as proliferation,
chemotaxis, differentiation and production of extracellular matrix.
i. Platelet-derived growth factor and insulin-like growth factor-1
(PDGF/IGF-1)
ii. Fibroblast growth factor (FGF)
iii. Bone morphogenetic proteins (BMPs)
Tissue engineering
Emerging interdisciplinary field which applies the principles of biology and
engineering to the development of viable substitutes which restore,
maintain, or improve the function of human tissues.

Periodontal Defect Filled with Engineered Matrix

Learning objectives
How does the periodontium heal following conventional periodontal
treatment?
What is the definition of periodontal regeneration and how does it differ
from other types of periodontal healing?
What are the biological principles behind the currently available
regenerative techniques using GTR and EMD?
What clinical situations are conducive to regeneration?
How predictable are currently available periodontal regeneration
techniques?
How may novel biological advances using growth factors and tissue
engineering be useful in achieving regeneration?

Chemical plaque control

Periodontology Semester 2, 2012
Rationale for plaque control
Plaque is the primary causative factor in the major dental diseases, dental
caries and periodontal disease (gingivitis and periodontitis).

Rationale for plaque control

Plaque is essential for the development of gingivitis ie. No plaque=no
disease.
Plaque is essential, but insufficient for the development of periodontitis, a
susceptible patient is also required.
Control of plaque is important in primary prevention of gingivitis.
Control of gingivitis is important in primary prevention of periodontitis.
Experiment of gingivitis in Man:
Abstained from OH for 3 weeks.
After 2-3 weeks all subjects had developed gingivitis
This was resolved after the introduction of OH measures
The accumulation of plaque precedes the onset of clinical signs, which
resolve after removal of plaque

Plaque control

 Control/modification of risk factors is a fundamental goal of prevention

and management of periodontal disease.
As primary etiological factor in gingivitis and periodontitis, adequate
plaque control remains a fundamental requirement for the prevention of
these diseases.
Dental plaque is a biofilm
Prevention of gingivitis
Mechanical control of plaque is the most effective way of controlling
plaque, and hence gingivitis
TOOOOOTHH BRUSSHH.
Effectiveness of oral home care procedures
1. Limited effectiveness even after receiving oral hygiene instructions in
children with low socioeconomic and schooling levels
2. After 6 months of oral hygiene instruction, 32% of subjects still had dental
plaque accumulation
3. At the end of the study 50% of children who received oral hygiene
instructions, still showed dental plaque accumulation
4. Patients between 55-80 years demonstrated limited dexterity even after
receiving toothbrushing instructions, both for manual and electric
toothbrushes
Mechanical plaque control (van der Weijden and Hioe, J Clin Perio, 2005)
Systematic review of effectiveness of self performed mechanical plaque
removal in adults with gingivitis using a manual toothbrush.
consistantly effective brushing is uncommon
in adults with gingivitis, the quality of self performed mechanical plaque
control is not sufficiently effective
Interdental cleaning
Dental floss is efficient in removing plaque
Very technique sensitive
Dependant on motivation and dexterity of patient
Only 10-40% of patients use floss on a daily basis
Motivation for and effectiveness of flossing are lost over time
Chemical plaque control
Brushing/flossing compliance and effectiveness studies suggest that a
chemotherapeutic approach to plaque control could be beneficial as an
adjunct to daily self-performed oral hygiene.
What is available on the market?
Enzymes
Fluoride (Stannous/Amine)
Metal Ions

Oxygenating Agents
Natural Products
Quaternary Ammonium
Compounds
Essential Oils
Povidone-iodine
NonIonic Detergents
Bisbiguanides

IDEAL PROPERTIES FOR ANTIBACTERIALS

Selective elimination of bugs
Absence of resistance
SUBSTANTIVITY
Safe (hard and soft tissues)
Reduces Plaque and Gingivitis
No staining
No taste alteration
No adverse effects on teeth or tooth substitutes
Easy to use
CHEAP
Biocides
Large group of diverse chemical agents that inactivate a variety of
microorganisms
Antiseptics and disinfectants
Inhibit a variety of microbial cellular processes
Multiple sites of action on target cell
The typical in-use concentrations of biocides are substantially higher than
is required to inhibit microorganisms in the planktonic state
Alternate
HERBAL
EECHINACEA

ECHINACEA PURPUREA
ECHINACEA ANGUSTIFOLIA
ECHINACEA PALLIDA
ECHINACEA PARADOXA
Echinacea is an herb native to North America Liquid extracts of the leaves
and above ground parts of Echinacea augustifolia and Echinacea purpura
in water/alcohol or glycerin are the products most commonly
encountered.
E. pallida may be encountered in Europe.

TAKE HOME MESSAGE

An ideal study should:
Published in a large refereed journal
Performed in Pts like yours
Double Blind
Real Placebo Controlled
Relate to the clinical procedures you do
Correct handling of statistics
Clinically significant result
One of many with similar results
Manufacturers

Mouthwashes which have been evaluated in trials of minimum 6 month duration

Six month randomized clinical trials
Chlorhexidine
Essential oils
Cetylpyridinium chloride (CPC)
Triclosan (toothpaste)
Stannous fluride (toothpaste)
Gel-Kam - Stannous Fluoride
0.4% w/v Stannous Fluoride, providing 1000 ppm fluoride ion and 3000
ppm active Stannous ion
Anti-bacterial effect
Long shelf life - 3 years
122gm tube, Mint and Fruit & Berry flavours

Stennous Fluride
Small antiplaque, antigingivitis effect
Possible qualitative effects on plaque rather than quantitative
Possible staining problems
2,4,4-trichloro-2- hydroxydiphenyl ether
Triclosan to its friends!

TRICLOSAN
Antibacterial
Acts on the cytoplasmic membranes of bacterial cells
At low (Bacteriostatic) [ ] it stops the up take of essential amino acids
At higher (Bactericidal) [ ] it disrupts the cell membrane allowing leakage
of the cytoplasmic contents
Triclosan
Phenolic compound
o Nonionicantibacterial
Somewhat effective against preexisting plaque
o poor substantivity
Unilever ~ with ZnCitrate
Colgate ~ Copolymer Gantrez Only formulation with co-polymer has antiplaque and anti-gingivitis effect
Triclosan
1. 0.3% Triclosan
2. 0.75% Zn Citrate
3. Unilever
0.3% Triclosan
2.0% Gantrez
o 0.3% Triclosan
o 5.0% Pyrophosphate
o Procter & Gamble (Crest Ultra Protection)
0.3% Triclosan
Macleans Complete Care
Sensodyne Dual protection
Colgate (Colgate Total)
Gunsolley systematic review
17 studies support the antigingivitis and antiplaque effect of 0.3%
triclosan + 2% Gantrez copolymer toothpaste.
Effect is modest clinically significant?
MOUTHRINSES
Mouthwashes which have been evaluated in trials of minimum 6 month
duration
o Six month randomized clinical trials
Chlorhexidine
Essential oils

Cetylpyridinium chloride (CPC)

Triclosan (toothpaste)
Stannous fluride (toothpaste)

Chlorhexidine
Used as the stable digluconate salt
At pH 7 dissociates +ve charge
0.2% CHX
o SAVACOL
o Rx 10ml from 1 min
0.12% CHX
o DIFFLAM Dental SolutF
o Savacol Freshmint
o Rx 15ml for 1 min
CHX Actions
Bactericidal
o Cationic-binds extra microbial complexes and ve charged
microbial cell walls and changes the osmotic equilibrium
Antiplaque
o Binds anionic acid groups of salivary glycoproteins thus
decreasing pellicle formation and plaque colonization
o Binds to salivary bacteria and prevents adsorption to the tooth
CHLORHEXIDINE Adsorption
Ability to adsorb (adhere) to anionic substances eg. HA, pellicle, salivary
glycoproteins, mucus membranes, polysaccharide coats of bacteria
Slow release gives prolonged bactericidal effect = substantivity
CHLORHEXIDINE Does it work??
Gunsolley (2006)
7 studies of 6 months duration
Very effective as an anti-plaque and anti-gingivitis
Substantive mode of action
Gold standard
X reactions
Saccharin Probably X reacts
Chlorhexidine (CHX) rinses and stannous fluoride dentifrices have each
been shown to possess antimicrobial activity and to clinically reduce
gingivitis. However, it has been reported that sequential use of SnF2 and
CHX solutions produced an antagonistic antiplaque effect which could
potentially limit the antigingivitis efficacy of these agents when used in
combination
Competes with other cations (eg Zn2+) for binding sites
SLS and CHX
Sodium Lauryl Sulphate (SLS) is a an anionic detergent

 Has the potential to interact with CHX and make the CHX unavailable
Barkvoll (1991) suggests the interval between the use of CHX and
toothpaste should be more than 30 min., probably nearer 2 hours.
Chlorhexidine -Side effects
Staining Yellow brown Gingival 1/3 and
interproximal sites
Dulling of Taste
Bitter Taste
Calculus formation
Desquamation
Quaternary Ammonium Compounds

Increase cell wall permeability

Decrease cell metabolism
Decrease binding sites for bugs
Usually 14% - 18% Alcohol base
pH 5.5. - 6.5
Can cause staining and burning sensations

Antibacterials Quaternary Ammonium Compounds

CPC (cetylpyridinium chloride)
Benzalconium chloride
o Greater initial oral retention than CHX (70% vs 30%)
o Equal antibacterial effect to CHX
o Long term studies ~ 20% Gingivitis
Actions:
Similar in vitro antibac action to CHX
Good adsorption but quick desorption
Ulceration/ burning of tongue
Other chemical agents (Gunsolley et al, 2005)
CPC (7 studies)
Inconsistent results
Concentration vary from 4.5% to 7% +/- alcohol
7% non-alcohol formulation is promising (Only

 available in US)
Few studies
Listerine
Essential oils(20studies)
o Significant antiplaque and antiginigivitis effect
Over the counter mouthwash containing two phenol- related essential oils,
thymol 0.064% and eucalyptol 0.092%, mixed with menthol 0.042% and
methyl salicylate 0.060% in a 22% hydroalcoholic vehicle.
At high concentrations, it disrupts the bacterial cell wall and results in
precipitation of cell proteins, whereas at lower concentrations, there is
inactivation of essential enzymes
No substantivity
Original formula
Dr Joseph J Lawrence, physician, St Louis, 1879
Thymol + eucalyptol + menthol in 1 27% ethanol base
Named Listerine after a lecture he attended in 1876 by surgeon Dr Joseph
Lister
Released for dental purposes 1896

Methodology
11 papers included in study
Baseline prophylaxis
Twice daily rinsing for 30s for 6 months or more
Control was 5% hydroalcohol or vehicle without active reagents
Antiplaque effect of EO mouthrinse

Anti-gingivitis effect
Statistically significant decrease in gingivitis
For interproximal sites, EO resulted in significantly more gingivitis
reduction compared to control mouthrinse, but there is no difference
compared to dental floss.
Effective as interdental anti-plaque/anti-gingivitis agent, as an adjunct to
flossing
Comparison of CHX with EO

 Four studies compared CHX and EO

CHX has greater antiplaque effect than EO
No significant difference between EO and CHX in terms of anti-gingivitis
effect
Conclusions
Plaque control is important for the primary prevention of gingivitis.
Although mechanical plaque removal is the most effective way to control
plaque, consistently effective mechanical cleaning is not carried out by
many patients.
When used as adjuncts to unsupervised oral hygiene, CHX and EO
containing mouthwashes provide an additional benefit with regard to
plaque
and gingivitis reduction as compared to a placebo or control.
Confounding issues in studies assessing antiplaque/antigingivitis products
Hawthorne effect
Effect on established plaque
Types of indices used
Safety
Role in periodontitis
o Subgingival penetration
o Pocket irrigation
o Anti-inflammatory effect
o Clinical significance
Hawthorne Effect
Attention increases productivity and compliance

Effectiveness against established vs developed plaque

CHX and EO containing mouthrinses are effective in decreasing the
formation of de novo plaque following professional prophylaxis
Antibacterials 17th Century style

Plaque mixed with vinegar in vitro was quickly killed

BUT

Prolonged rinsing with strong wine-vinegar failed to kill plaque bacteria

Effectiveness against established vs developed plaque
CHX and EO containing mouthrinses are effective in decreasing the
formation of de novo plaque following professional prophylaxis
Ineffective against developed plaque
Regular professional intervention is essential
30% of Plaque and Gingivitis Disappears

Further confounded by use of ordinal rather than continuous variables

Possible concerns with regular use
Allergy
IrritationCh
anges to flora
Dental Erosion
Alcohol
Irritation
Oral cancer
Listerine
1. thymol (0.063%)
2. menthol (0.042%)
3. eucalyptol (0.091%)
4. methyl salicylate

5. Synthetic, no impurities; pure ethanol (no congeners)

6. No turpentines, thus eliminating risk of allergy.
Allergy
Not reported with
o Essential oil mouthrinses
Extremely rare with
o Chlorhexidine
o Triclosan
These agents can exert mild irritant effects which are not immunological in
nature.
Irritation
Alcohol concentrations in mouthrinses can potentially cause irritation,
particularly in patients with major oral ulcerations, where the normal
mucin protection of the oral tissues is reduced.
Oral and GIT flora
The long term use of EO, chlorhexidine, and Triclosan oral care products
has been shown to be microbiologically safe.
Erosion risk
Low pH softdrinks (2.5-3.5) may contribute to dental erosion.
pH of Listerine EO rinses is 3.8-4.5 Low titratable acidity, rapidly cleared
and neutralized by saliva
In normal individuals the salivary pH remains above 5.5 following rinsing
and for 15 minutes following rinsing. [Claffey, 2003]
Erosion risk
Direct examination of mineral changes in human enamel in vitro shows that 14
hours of continuous exposure to Listerine is required before significant erosion
can be detected using QLF or micro-radiography
Ingestion of ethanol from mouthrinses
Ethanol is commonly included as a solvent for the active ingredients and
flavouring agents.
Most CHX-based and all EO mouthrinses contain ethanol.
7-12% for chlorhexidine products, and
22-27% for essential oil products.
But only some of this ethanol is bioavailable
This compares to:
o 5-7%ethanolcontentinbeer,and
o 12-14%ethanolcontentinwine.
Ingestion of ethanol
All mouthwashes containing ethanol should be stored out of reach of
children, because of the possible risks of toxicity if ingested.
Mouthrinses should not be deliberately ingested by children or adults as a

source of alcohol for recreational purposes.

Alcohol and oral cancer risk
Recent reports have discounted any link between alcohol in mouthrinses
and increased risk of oral cancer.
Detailed analysis of nine epidemiologic studies did not indicate any
association between oral cancer and mouthrinse use.
Low exposure time (30 secs twice daily) vs. recreational alcohol
Lack of impurities
Less salivary bacteria and plaque bacteria thus less acetaldehyde
production

Safety (from Stoeken et al; 2007)

Concern has been raised about association of the long term use of highpercentage alcohol- containing mouthwashes with oral cancer
It has not been established if these concerns are scientifically valid
Studies evaluating mouthwashes as a risk factor for oral cancer have been
inconsistent and sometimes contradictory
It has not been possible to establish a causative relation between
mouthwash use and the development of oral cancer
Safety
For chlorhexidine, Triclosan and a mixture of phenolic essential oils
(Listerine), there is a large body of supporting data from 6-month (or
longer) clinical trials, which supports their safe use as an adjunct to
conventional mechanical oral hygiene.
Advice to patients
CHX rinse may cause a bitter after taste or a temporary dulling of taste
perception
Frequent or long term use may cause surface staining of teeth, restorations
and the tongue, more so when the lifestyle includes tannins and red wine
PERIODONTAL DISEASES
Concept: only a small proportion of the population is susceptible to
severe
Periodontal disease (less than 15% of the population)
Multifactorial disease: involving a susceptible host, pathogenic
bacteria and environment (acquired/inherited).
Difficult to identify at risk population

Fundamentals of periodontitis management

1. Risk assessment
2. Good oral hygiene
< Biocides?
3. Adequate professional debridement
4. Regular maintenance tailored to the patients risk profile
Role of biocides in management of periodontitis
? Role as an oral hygiene adjunct in the active treatment of periodontitis
? Role in maintenance of periodontal health
Difficult to determine level of antiplaque/antigingivitis effect that would be
sufficient to produce clinically significant outcomes - patient specific
? Full mouth disinfection
? Anti-inflammatory effect
Full mouth disinfection
Teeth represent only about 25% of your total surface area of the mouth.

Periodontium
o Mucosal surfaces
o Oral soft tissues
Full mouth disinfection
The concept that a full mouth disinfection including full mouth debidement
in one visit, followed by twice daily mouthwash use, is superior to
quadrant debridement is yet to be proven.
Due to side-effects (increased temperature, fever) of this treatment, it
should be limited to selected cases
SUBGINGIVAL PENETRATION
Teeth for extraction Rinsed with Disclosing Solution OR Direct
Irrigation with Disclosing Solution
Pocket
Pathologically deepened sulcus
Lined by ulcerated epithelium
Anaphylactic reaction
IgE mediated hypersensitivity
Up in minutes, usually peaked 10-20min gone after 1 hour if survive

Triclosan Anti inflammatory properties

Inhibits Lipoxygenase 5 and 15 Inhibits Cyclooxygenase 1 and 2
o Phospholipid
o Arachidonic Acid
o HETEs & Leukotrienes
Prostaglandins and
thromboxanes Also interferes with cellular Ca release
Anti-inflammatory effects
Many phenolic compounds have an anti-inflammatory effect, in addition to
anti-bacterial- and anti-plaque effects.
o Triclosan,EssentialOils
This may be one aspect of the reduced degree of gingivitis observed in
patients using EO or Triclosan containing oral care products.
Triclosan and Gantrez
Effects on Periodontitis EllwoodetalJCP1998
o 3 year study of 641 11-13 yo pats
o 25% had Mean Attachment Loss
o 2.92-4.19mm
o Averageloss0.07mmvs
0.13mm in control
Colgate Total demonstrated a reduction in attachment loss of 50% when
compared with a control dentifrice (p<0.05)
Triclosan and Gantrez
Effects on Periodontitis
o 60 Perio Pts
o 3 years, reexamined every 3 months
At 36 months..statistically significant reductions in probing pocket depth.
o (-0.14mm Colgate Total vs +0.19mm control p < 0.01)

TAKE HOME MESSAGE

Question the manufacturers Plaque is a biofilm
The only way to truly remove a biofilm is mechanically.
That means:
Good OHI
Good Home care
Good Sc/Rp
o CHXIn My hands:
o Post Surg (Approx 10 days)
o ANUG
o Super Grot
o short term
o Toothpaste
o Total (Triclosan/Gantrez)
o Mouthwash
o No clinically proven role in treatment of
o periodontitis
Learning objectives
What is the relative importance of mechanical and chemical plaque control
in the management of gingivitis?
What is the rationale for chemical plaque control?
What is are the ideal characteristics of a chemical plaque control agent?
What level of evidence is required to support a products use in clinical
practise?
Which chemical plaque agents have sufficient evidence to support their
use?
How do chlorhexidine, triclosan and essential oils work and how effective
are they in the management of gingivitis?
What are the safety issues that need to be considered in relation to the use
of chemical plaque control?
What are the confounding issues associated with the use of chemical plaque
control?
What are the issues related to the use of chemical plaque control in the
management of periodontitis?
Is chemical plaque control useful in themanagement of periodontitis?

Furcation Involvement & Management 7

Periodontology Semester 2, 2012
Furcation:
Root complex: root trunk & cone
Degree of separation
Degree of divergence
Root anatomy:
Mandibular Vs Maxillary Molars
Fused/ narrow
Furcation Involvment:
Clinically detected by use of Nabors Probe
Radiographically detectable (limited e.g. root morphology)
Hamp Classification:
I.

Grade I:

II.

Grade II:

III.

Grade III

Epidemiology:
Molars were the most frequently missing teeth
Results for missing teeth = not specified
Prevalence % of furcation:
o Involvement in patients referred for periodontal treatment
o Maxilla > Mandible
o Distal site of the maxillary 1st molar (53%)
Tooth morphology: may contribute to the variability in prevalence of
molar furcation involvements.
o Score I: Class I
o Score 2 & 3: Class II & Class III

Prevalence % of furcation involvement in patients referred for

periodontal treatment:

Implication of furcation involvement:

Plaque retention-due to anatomy
Anatomic anomalies:
o Enamel pearl
o Gooves
o Pulpal openings
Inaccessibility to professional & self-performed plaque control
Less favorable treatment outcomes- compared to single rooted teeth.
Strategies of furcation therapy:
Make function accessible to OH
o Non-surgical debridement
o Access flap surgery (with/without) furcation plasty
o Tunnel preparation
Elimination of furcation:
o Root resection/separtation
o Hemi-section (mandibular molars
Regeneration therapy:
o Guided tissue regeneration (GTR)
o Enamel Matrix protein (Emdogain)
Treatment options according to the severity of furcation involvement
Severity
Class I
Class II

Class III

Tx options
Non-surgical therapy (ARP)
Furcation plasty
SRP
Furcation plasty
Regeneration (Mandibular molars)
Resectve surgeries (root
resection/hemi-section)
Tunnel preparation
Extraction
SRP
Resective surgeries
Tunnel preparation
extraction

Non-surgical approach:
Class I, II, III
Aim to remove supra & subgingival deposits, resulting in the resolution of
the inflammation.
Recession epected (especially- thin gingival biotype)- dentine & root
sensitivity.

Surgical Approaches:Access flap Surgery

+/- furcation plasty
+/- osseous recontouring
Aim: periodontal pocket elimination & reconstruct the positive alveolar
bone architecture
Recess, sensitivity & increased mobility (post operative).
Tunnel Preparation:
Deep Class II & Class III
Factors to consider
o Adequate separation angle of the roots
o Short root trunk
o Mesial & distal alveolar bone height
Root sensitivity & mobility
Increased risk of caries (daily use of fluoride is recommended).
Root Resection/Separation:
Factors to consider
o A short root trunk
o Divergence of the root cones
o No fusion between the root cone
o Amount of remaining periodontal support
o Adequate access for OH
Endodontic Tx
Comprehensive prosthodontics treatment planning required.
Regeneration Treatment:
1. Guided tissue regeneration (GTR)
2. Regeneration with use of enamel matrix proteins (emdogain)
Aiming to regenerate lost periodontium (alveolar bone, cementum
with inserting fibres)
Predictability & selection
The concept of GTR:
1. Occlusion of neighbouring soft tissue cells
2. Space creation & maintence
Enamel matrix Protein:
Primarily amelogenin (procine origin) +
prophylebe Glycol Alginate (PGA- carrier)
Promotion of PDL fibroblasts
(undifferentiated mesenchymal cells)
proliferation & inhibition of epithelial cell
proliferation & growth.
Osteoprotegerin (OPG) up-regulation: bone
remodelling by inhibiting osteoclastogenesis
Anti-microbial action (PGA action)

Predictability of the furcation therapies

Non-surgical furcation therapy
Class I
Number of multi-rooted
teeth
32

N
100
600
100
211
63
24

Observation period

Survival rate

5 years

100%

Non-surgical & conventional surgical therapy of molars with Furcation

involvement (class II & Class III)
Range of follow
up

Loss of molar with

Loss of molars
furcation
without furcation
involvement
involvement
5-24
12%
Na
15-53
32%
6%
15-29
57%
8%
15-34
43%
17%
10-34
23%
14%
8
23%
13%
Periodontal susceptibility of patients (rapid, moderate, no progression
groups

Predictability of the fucation therapy:

FLAP SURGERY fircation therapy:
Periodontal Tx decision for molars: An analysis of influencing factors &
long term outcomes
o Retrospective study
o Long-term observational period (mean 9.5 years)
o Tx 1313 moars with furcation involvement
o Mechanical debridement & access flap surgery
Results:
o 28% extracted during follow-up
o 4% treated with root resection/separation
o 68: maintained with conservation treatment
Conclusion:
o A conservative approach to tx of molars with even deep furcation
invasion may show a high long-term success rate, provided
maintence care (offered).

Predictability TUNNEL PREPARATIONS:

Success & failure
Emphasis on caries assessment & preventative management
Mean observational
period (year)
5
3.4
5.8
2

Caries incidents (%)

Survival rate (%)

57.1
23.5
16.7
Not reported

42.9
89.2
88.9
92.9

Root Resection/separation
Mean observational
Caries incidents (%)
period (year)
5
87
10
100
10
28
488
98.4
93.1
9.5
89.4
GUIDED TISSUE REGENERATION (GTR)
% of furcation closure
Mandibular
Class II
0-90%
Class III
0-38%

Survival rate (%)

100
62
67.97-11
10175
47

Maxillary
0-20%
0%

Complete closure of furcation defects: unpredictable

GTR vs OFD:
Randomized control trial (RCTs)
>6mths durations
patients with chronic periodontitis
interventions:
o GTR ve OFD
Primary outcome measurement
o Change in horizontal furcation depth
14 publications with classII defects

Reduction in furcation depth in surgical re-entry

Furcation Involvemrnt
Mandibular class II
Maxillary class II

Weight mean difference

(MM)
1.51
1.05

95% CL
0.39-2.63
0.46-1.64

Emdogain vs guided tissue regeneration:

A randomized clinical trial comparing enamel matric derivative &
membrane treatment of buccal class II furcation.
Involvement in mandible molars
GTR: 67%
Part I: study design & results for primary outcomes
improvement
Greater reduction of the furcation depth
EMD: 78%
improvement
Smaller incidence of post-operative pain/swelling

Clinical outcomes of regenerative procedures:

Furcation class II (buccal)
GTR ve OFD
MD & MX
EMD ve GTR
Mandibular buccal

Reduction in furcation depth

+1.5mm
+1.0mm
+0.75mm

Long-term prognosis:
Periodontal susceptibility
Endodontics & prosthetic considerations
o Prognosis of endodontic tx
o Remaining tooth structure (restorability)
Access to OH
Susecptibility to root caries
Conclusion
Furcation involvement is a common complication of periodontal disease that
should be seriously considered in the treatment planning
Non-surgical debridement should be the initial approach for furcation
management
Further treatment strategies should be considered:
o 1. Open Flap debridement (OFD)
o 2. Tunnel preparation (caries risk assessment is crucial)
o 3. Resective options
o 4. Regeneration therapy
Specific to class II buccal/ lingual mandibular first molars
Less predictable: Maxillary molar with class II buccal defect
Objectives
What is the degrees of furcation involvement and how do we measure it?
What is the prevalence of furcation involvement in patients with periodontal
diseases?
Why is furcation involvement a risk for the progression of periodontal disease and
what makes the management complicated?
What are the main treatment approaches for various degrees of furcation
involvement?
How predictable are those treatment options?
What is the prognosis of teeth with furcation involvement?

The Association Between

Periodontal and Systemic Disease
Periodontology: Semester 2, 2012
Focal Infection Theory
During 19th and early 20th century, foci of sepsis
were thought to be responsible for a variety of
inflammatory diseases such as arthritis, peptic
ulcers and appendicitis
Therapeutic edentulation
Theory was discredited when no improvement
resulted
Mechanisms of periodontal systemic health
interaction
Direct spread of bacteria
Release of inflammatory mediators
Immunological injury caused by oral bacteria

Specific Systemic Conditions Associated with Periodontal Disease

Cardiovascular Disease
Pulmonary Disease
Preterm Low Birth Weight
Diabetes
Cardiovascular disease
Atherosclorosis
Myocardial infarction
Stroke
Cardiovascular disease
41%ofAll Deaths in1997(52641)
CHD Largest single cause of death in Australia (80/day)
Most costly disease in the system
o ($3.7 Billion(93-94), 12% of the Total
1996-7 421 516 Hospitalisations
o Males over 64 are 12% of the population but 60% of the
hospitalisations
Cardiovascular disease

Stroke is second largest single cause of death in Australia (12 133 in

1997)
Stroke is the leading cause of long term disability
Indigenous Australians Die of CVD at twice the rate of others.

Arteriosclerosis atherosclerosis atheroma

Atherosclerosis
large elastic arteries
Causes:
o CHD (Angina)
o Myocardial infarction (Heart attack)
o Cerebral infarction (Stroke)
Cardiovascular disease: Risk factors
Genetic Factors
o Lipid metabolism
o Obesity
o Hypertension
o Diabetes
o Increased fibrinogen
Environmental factors
o Smoking
o Socioeconomic status
o Stress
o Diet
o Chronic disease levels
Cardiovasular disease
Classic risk factors such as hypertension, hypercholesterolemia and
cigarette smoking can account for one half to two thirds for the variation
in the incidence of cardiovascular disease

Periodontitis may account for a portion of the remaining unknown risk

factors

Proposed mechanisms
Direct in vasion o fbacteria and/or bacterial products(eg LPS) into the
endothelium
Systemic effect of periodontal infection exacerbates atheroma formation
Common hyperinflammatory phenotype
Cross reactivityantibodies directed against bacterial products can cause
collateral damage to the endothelial tissue
? Nutritionimpaired tooth function can result in poor nutrition and
subsequent increased susceptibility to cardiovascular disease
Mattila et al. BMJ 1989
2 Case Control Studies
100 pts with acute MI
Social Class controlled according to
occupation
Controlled for:
Age
Social Class
Hypertension
Serum lipid and lipoprotein concentrations
Smoking
Diabetes
Serum C Peptide
Dental Health still Significantly Associated

Evidence

Multiple studies show an increasedrisk of cardiovascular disease in

periodontitis patients of 1.2 to 3.5

Problems:
Few prospectives studies
Is it covariance?
A non-Casual markr is not likely to need treatment

Association is NOT Causality

Which came first?
Consistency of association ++
Strength of Association
+
Time sequence correct
+
Specificity of Associations +/Dose-response Effect
+
Biological Plausibility
++
Experimental Support
?
Intervention studies
The effect of periodontal treatment has
been investigated in relation to:
Markers of systemic inflammation
Incidence of cardiac events
Intervention studies
Systematic review (18 papers) shows:
Strong evidence that plasma CRP is elevated in periodontitis cases
Modest evidence that periodontal treatment can lower levels of CRP
Intervention studies
Pilot studies have shown that periodontal
treatment can improve measures of endothelial dysfunction and carotid
artherosclerosis.
Multicenter Periodontitis and Vascular Events
(PAVE) study examined effect of periodontal treatment on secondary
cardiovascular events.
o Positive trend but no significant effect
o BUT periodontal treatment was not effective (ie periodontal
parameters were not improved compared to control)
Cardiovascular disease and periodontitis
Conclusions:
An association between cardiovascular disease and periodontitis has
been demonstrated
However, the critical issue of causality has not been resolved, ie we dont
know if periodontitis has a role in the pathogenesis of cardiovascular
disease

Implications
Pts maybe more motivated towards treatment and OH
Pts may request clearance stored ucerisk
Failure to screen for Perio may havegreater consequences in terms of
litigation

Pulmonary disease
1. Bacterial Pneumonia
2. Chronic Obstructive Pulmonary Disease
Proposed mechanisms
1. Aspiration of oropharangeal contents, including plaque, especially in
infirm and elderly
2. Bacteria of oral/periodontal origin can be found in lungs of patients with
COPD
3. Reducing oral bacterial levels reduces risk of developing and exacerbating
pulmonary disease
Proposed mechanisms
Once in the lung, periodontal bacteria:
o Bind to lung epithelium
o Allow colonization by pulmonary pathogens
o Activate epithelial cells to produce inflammation, leading to fluid
accumulation
o Activate production of enzymes which breaks down lung
connective tissues
2 major studies
Scannapieco et al examined crosssectional NHANES I and NHANES III
data
Evidence
Hayes examened longitudinal VA Normative Aging Study
Both studies reported odds ratios of 1.8 to 4.5 (95% CI)
Periodontitis and pulmonary disease
Conclusion
An association may exist but it remains to be firmly established
The strength of the association is small
The causative mechanism remains unproven
ONLY RELAVENT IN COMPROMISED PATIENTS
Adverse pregnancy outcomes
Preterm Low Birth Weight
6%
Spontaneous preterm birth
Low birth weight infants
Low birth weight (<2.5kg)
Very low birth weight (<1.5kg)
Mechanism
70% of PTB is spontaneous with no
identifiable causes
Interuterine infection by periodontal pathogens
Increase in proinflammatory mediators can mimic events that lead to the
induction of labor
Multivariate the Logistic Regression Model for all cases and controls

5 year Prospective Study of 1200 Pts Data Based on 814

Perio At Baseline Sig Assoc with Increased incidence of prematurity
Dose Response

1313 Mumstobe assessed at 2124 weeks

If severe or generalised periodontitis adjusted odds of delivering before
37 weeks = 4.45 (95% CI 2.169.18)
Before 35 weeks 5.28 (95% CI 2.05 13.60)
Before 32 weeks 7.07 (95% CI 1.70 27.4)

Lopez et al 2002

Lopez et al 2002

Adverse pregnancy outcomes

Studies support notion that untreated moderate to severe generalized
periodontitis can lead to adverse pregnancy outcomes
This is support by some intervention studies whereby treatment of
periodontitis has been shown to decrease adverse pregnancy outcomes
Relationship between periodontitis and adverse pregnancy outcomes
appears to be stronger in developing countries and low socioeconomic
groups.
Results
Diabetes
Clinical syndrome characterized by hyperglycemia due to an absolute or
relative deficiency in of insulin
Type I early onset, insulin dependant
Type II late onset, noninsulin dependant
Modifying factors:

IDDM (type 1)
263 Pts compared to 59 non diabetic relatives and 149 unrelated non
diabetics
<12yearsNilPerio
1318years13.6%Perio
1932years39%Perio
o NO Perio in the related controls
o 2.5% Perio in unrelated controls
Longer the duration of diabetesthe more severe
NIDDM (type II)
Pima Indians
NIDDM 2.8 X risk for clinical attachment loss
3.4 X more radiographic bone loss
4.2 X more progressive bone loss
o 11.4 X in poor control
o X in good control
Diabetes
Is there a bidirectional relationship?

Uncontrolled diabetics are more susceptible to periodontitis

Does uncontrolled periodontitis influence glyceamic control, ie. Does the
presence of infection make it more difficult to control diabetes? AND
Does periodontal treatment improve

INTERVENTION STUDIES

Conclusion
Strength of association between periodontitis and systemic disease
Cardiovascular disease- possibly
Pulmonary disease- possibly
Adverse pregnancy outcome- possibly
Diabetes- possibly
What do I tell my patients today?
There is currently insufficient data to recommend treatment of
periodontal disease in a effort to reduce the risk of cardiovascular disease
or other systemic diseases, with the possible exception of adverse
pregnancy outcomes and diabetes.
Which systemic diseases have been associated with periodontal disease?
What are the main biological mechanisms proposed for this association?

Is there are a proven causative effect of periodontitis on systemic

diseases?
Does periodontal treatment improve systemic health?

Biologic width and recession

Periodontology, Semester 2, 2012

Outline
Biologic width
Crown lengthening
Recession
Sensitivity
Biologic Width: Present in 3D- three dimensional

BIOLOGICALWIDTH
(Av = 2.04mm)

Results of Violating the Biologic Width (eg. Subgingival Margin)

a) Increased pocket depth with an inflamed bleeding marginal gingiva.
Thick BIOTYPE
b) Recession with exposure of the sub gingival margin Thin BIOTYPE
Violation of Biologic Width

Crown lengthening
1) Re-establishment of biologic width
2) The apical repositioning of the entire periodontal attachment
apparatus.
3) Requires both soft (gingival) AND hard (bone) tissue removal
4) Required for predictable gingival margin
5) Simply removal of soft tissue by any technique (scalpel,
electrosurgery, laser) will lead to violation of biologic width.

Recession
Gingival Recession is associated with:
1) Anatomical variations
2) Prominent Roots of the Teeth
a) Muscle Attachments
3) Associated with Orthodontic Treatment
4) Trauma (physical damage) to the Gums
5) Plaque induced lesions
a. Gingivitis

b. Periodontitis
Anatomical - Prominent roots
1) When a tooth erupts into the mouth, it should be surrounded by bone. If
the bone is of a normal thickness, then it causes the developing gingiva
(which will cover the bone) to develop as a thick, tough layer of tissue.
This tissue needs to be tough in order to withstand the forces of chewing
food hitting the gums.
2) If the alveolar bone is thin or absent on one side of the tooth (usually
buccal) the gingiva that develops will be thin and fragile and not be able
to withstand the normal forces that are applied to it from chewing and
brushing.
Prominent roots

Anatomical Muscle attachment (frenum)

Especially when associated with tooth prominence
Interferes with oral hygiene
Anatomical Muscle attachment (frenum)

Orthodontic treatment
The primary problem with recession that is associated with orthodontic
treatment is that many times the patients do not have heavy, thick layers
of bone over the roots of the teeth which are to be moved.
Orthodontic treatment
If the teeth are very crowded before orthodontic treatment, the only way
to put the teeth into a good alignment may be if the roots of the teeth are
made more prominent.
The finest of orthodontic treatment can not overcome the lack of enough
space in the jaw where the teeth could be moved without making the
roots of the teeth more prominent.

This is especially true when you consider how many parents do not wish
for the orthodontist to extract teeth as part of the orthodontic treatment
plan!
There are also circumstances where recession will still occur even after
some extractions were done.

Orthodontic treatment
Perfect orthodontic treatment can not overcome what nature did not
adequately provide!!
Trauma
Brushing
Iatrogenic
o partial denture
o subgingival margins
Partial denture
In virtually all cases,
INFLAMMATION is the
CAUSE OF RECESSION

INFLAMMATION: the major

underlying cause of recession

Epithelium and
Recession

Epithelium and
Recession

RECESSION
1) RECESSION IS NOT A DISEASE ENTITY, BUT A PHYSIOLOGICAL
RESPONSE INVOLVING THE RE- ESTABLISHMENT OF BIOLOGIC WIDTH
2) TREATMENT INVOLVES THE DIAGNOSIS AND MANAGEMENT OF
UNDERLYING PROBLEM
3) SURGICAL INTERVENTION (GINGIVAL GRAFTING) IS UNPREDICTABLE
AND CAN ONLY BE USED AFTER UNDERLYING PROBLEM IS IDENTIFIED
AND ADDRESSED

Learning objectives
What is the biologic width and what are its dimensions?
What are the consequences of violating biologic width?
What is crown lengthening surgery and when is it indicated?
How does recession occur?
What factors predispose to recession?

Week 11 Perio notes

From Evernote:

WEEK 11 PERIO - IMPLANTOLOGY

Definition - What is a dental implant? A biocompatible alloplastic device,
usually made of titanium, placed within the bone to provide retention and
support for a fixed or removable prosthesis, thereby restoring function and
occlusion. (It is to replace already missing teeth!)
Types of implant systems:
Subperiosteal implants - implant with removable structure (Cr/Co casting),
poor long term prognosis - no longer used
Transosseous implants - invasive, goes below mandible and up through
from below, made of titanium - not common practice due to higher failure rate
and highly invasive. Should be aware of in case you have a patient with it.
Endosseous implant (root form) = most common = within the bone, high
success rate, screw/cylinder/blade type.
Common terms:
Tissue vs bone level - Tissue level implant has tissue collar, and it sticks up
into oral cavity, bone level is entirely within the bone.
One-piece vs. two piece - Sometimes the tissue collar comes separately
and needs to be added.
Internal hex vs. external hex connection - disadvantage of external hex is a
small micro gap may allow for microleakage of bacteria which may lead to
bone loss, advantage is versatile and can do any type of resto above even if
implant is not precisely placed
Patient suitability pre-assessment is very important. Then surgical phase
followed by restorative phase.
Screw retained implants are preferred because they can be removed if
necessary at any time, cement retained ones cannot. Also cement debris can
lead to perioimplantitis. However because of angulation and other reasons
sometimes cement retained are unavoidable.
Osteointegration (biological principle)
Many definitions - A direct functional and structural connection between
living bone and surface of a load carrying implant. Sometimes referred to as
'functional ankylosis'
Implant installation -> blood clot formation -> granulation tissue formation
(fibroplasia, angiogenesis) -> woven bone formation -> bone remodeling
(KNOW THIS SLIDE - not all the other little histopathology details)
Described as a cascade of biological events involved in bone formation and
osseointegration. 2 hours after installation, primary stability is crucial, blood
coagulum. Day 4, osteoclasts especially work in the pitch area to resorb bone,
granulation tissue. 1 week, woven bone and provisional matrix formation
'primary spongiosa'. 6, 8, 12 weeks it is hard to tell between native bone and
new bone that has formed.
Factors influencing osteointegration

 Patient factors (smoking, systemic health)

Site factors (bone volume and quality)
Implant designs (surface characteristics) - 1st/2nd/3rd generation, distance
vs. contact osteogenesis (different for generations?) - quality of
osteointegration much more improved in 2nd and 3rd generation because of
contact? osteogenesis (I think??)
Primary stability - mechanical stability of an inserted implant at the time of
placement (micro movement leads to disruption of blood clot formation,
angiogenesis and migration of osteogenic mesenchymal cells -> repair by
fibrous tissue not osteointegration = failed implant). Also, the initial hole that is
drilled is slightly smaller than the implant to ensure good primary stability
Operators skill level - very technique sensitive
Predictability: >95% will osteointegrate (esp. rough surface implant), 95% in
function after 5 years, 89% function after 10 years.
SEE OBJECTIVES!!