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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)
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
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
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
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?
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
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
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?
50 teeth
with
Class II
and III
furc and
>=
5mmPD
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
Sites: >7mm
Review 3mths
Similar results for both tx
Data >5yrs no major difference
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
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?
PERIODONTITIS
Conventional periodontal treatment
Before Treatment
After Treatment
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
i.
ii.
iii.
iv.
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.
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?
Plaque control
Oxygenating Agents
Natural Products
Quaternary Ammonium
Compounds
Essential Oils
Povidone-iodine
NonIonic Detergents
Bisbiguanides
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.
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
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
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
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
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
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.
N
100
600
100
211
63
24
Observation period
Survival rate
5 years
100%
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%
Maxillary
0-20%
0%
Furcation Involvemrnt
Mandibular class II
Maxillary class II
95% CL
0.39-2.63
0.46-1.64
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?
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
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
Problems:
Few prospectives studies
Is it covariance?
A non-Casual markr is not likely to need treatment
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
Lopez et al 2002
Lopez et al 2002
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?
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?
Outline
Biologic width
Crown lengthening
Recession
Sensitivity
Biologic Width: Present in 3D- three dimensional
BIOLOGICALWIDTH
(Av = 2.04mm)
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
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
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?