Periodontics and orthodontics for orthodontists by Almuzian

UNIVERSITY OF GLASGOW
Orthodontics and periodontics
Mohammed Almuzian
2013

Mohammed Almuzian, University of Glasgow, 2013 Page 1
Contents
Introduction................................................................................................... 3
Abbreviated version of the 1999 classification of periodontal diseases and
conditions:..................................................................................................... 3
Etiology of periodontal diseases ..................................................................... 4
Risk factors in periodontitis............................................................................ 5
1. Bacterial risk factors .......................................................................... 5
2. Race.................................................................................................. 6
3. Gender............................................................................................... 6
4. Age ................................................................................................... 6
5. Socio-economic status........................................................................ 6
6. Smoking ............................................................................................ 6
7. Systemic disease................................................................................ 6
8. Genetics............................................................................................. 7
9. Orthodontic treatment and appliances ................................................. 7
Diagnosis of periodontal diseases ................................................................... 7
1. CPITN............................................................................................... 7
Code.............................................................................................................. 8
2. Radiographs....................................................................................... 8
Treatment of periodontal diseases................................................................... 8
A) Initial periodontal therapy /non-surgical therapy /Cause Related Therapy
(CRT) includes .............................................................................................. 8
B) Monitoring response to therapy.................................................................. 9
Other periodontal surgery............................................................................. 10

The relationship of orthodontics and periodontics.......................................... 10
1. Does malocclusion cause periodontal disease?................................... 10
A. Crowding......................................................................................... 10
B. Increased Overjet ............................................................................. 11
C. Deep Overbite.................................................................................. 11
D. Other occlusal considerations ........................................................... 11
2. Does periodontal disease cause malocclusion?................................... 11
3. Periodontally compromised patient having an orthodontic treatment .. 11
4. Iatrogenic influence of orthodontic treatment on periodontium........... 13
Types.......................................................................................................... 13
Incidence..................................................................................................... 13
Gingival recession ....................................................................................... 14
5. Periodontal surgery as an adjunctive procedures to orthodontic
treatment ..................................................................................................... 17
6. Role of orthodontics in treatment of periodontal problems ................. 19

Orthodontics and periodontics
Introduction
 Periodontitis is a common disease affecting up to 40% of the adult population
over the age of 40 in the UK.
 Gingivitis precedes periodontitis but not all gingivitis progresses to periodontitis
Abbreviated version of the 1999 classificationofperiodontal diseases and
conditions:
I. Gingival Diseases
A. Dental plaque-induced gingival diseases
B. Non-plaque-induced gingival lesions (Viral, bacterial, fungal)
II. Chronic Periodontitis
 Slight: 1-2 mm;
 Moderate: 3-4 mm;
 Severe: > 5 mm
A. Localized
B. B. Generalized (> 30% of sites are involved)
III. Aggressive Periodontitis
 Slight: 1-2 mm CAL;
 Moderate: 3-4 mm CAL;
 Severe: > 5 mm CAL
A. Localized
B. Generalized (> 30% of sites are involved)
IV. Periodontitis as a Manifestationof Systemic Diseases

A. Associated with genetic disorders
B. Associated with hematological disorders
C. Associated with endocrine disorders
D. Not otherwise specified
V. Necrotizing PeriodontalDiseases
A. Necrotizing ulcerative gingivitis
B. Necrotizing ulcerative periodontitis
VI. Abscessesofthe Periodontium
A. Gingival abscess
B. Periodontal abscess
VII. Periodontitis AssociatedWith Endodontic Lesions
Combined periodontic-endodontic lesions
VIII. Developmentalor Acquired Deformities and Conditions
A. Localized tooth-related factors that modify or predisposeto plaque-
induced gingival diseases/periodontitis
B. Mucogingival deformities and conditions around teeth or edentulous
ridges
C. Occlusal trauma
Etiologyof periodontal diseases
1. Plaque is the principal aetiology
2. The main bacteria involved are:
o For gingivitis: gram-negative anaerobic bacilli, cocciand spirochetes.

o For deep destructive periodontal lesions: P. gingivalis, P. intermedia and
Actinobacillus actinomycetemcomitans.
3. Tissue destruction in periodontal disease is mainly due to the host's
responseto the presence of bacteria by complement activation. So that,
Antigenic substances released by plaque organisms elicit both cell-mediated and
humoral responses, while designed to be protective, also cause localized tissue
damage.
4. The damage is caused by one or all of the major endogenous mediators of
inflammation: histamine, protease, prostaglandins and leukotrienes, lysosomal
acid hydrolases, free radicals, complement and cytokines.
Risk factors in periodontitis
A. Bacterial risk factors
B. Race
C. Gender
D. Age
E. Socio-economic status
F. Smoking
G. Systemic disease
H. Genetics
I. Orthodontic treatment and appliances
1. Bacterialrisk factors
 Although specific bacteria have been considered potential periodontal
pathogens, it has becomeapparent that they are necessary but not sufficient for
disease activity to occur.

 The progression of the disease is related to hostbased risk factors
2. Race
 It was more prevalent in individuals of Afro-Caribbean origin.
3. Gender
 It has also indicated that destructive periodontitis was consistently more
prevalent in males than females
4. Age
 Periodontal disease prevalence increases with age.
5. Socio-economic status
 Data has indicated that periodontal disease is more severe in individuals
of lower socio-economic status.
6. Smoking
 Smokers are 5-7 times more likely to developed destructive disease than
non-smokers.
 They suffer more severe disease than non-smokers with deeper pockets
and greater clinical attachment loss.
 They also respond less well to all types of therapy and are more likely to
suffer recurrent disease.
7. Systemic disease
 There is positive evidence linking diabetes mellitus to increased risk for
the inflammatory periodontal diseases.

 Conditions with depressed neutrophil numbers and function, such as
neutropenia, Down's syndromes and Papillon-Lefèvre syndrome have been
reported with severe periodontitis.
8. Genetics
 Recently much attention has focused on genetic polymorphisms
associated with genes involved in cytokine productionthat have been linked to
an increased risk of adult periodontitis
9. Orthodontic treatment and appliances
 Band ledges
 Elastomeric modules
 Excessive proclination/expansion of teeth
 Bracket placement changes subgingival flora
Diagnosis ofperiodontal diseases
1. CPITN
 The Basic Periodontal Examination BPE, requires that the periodontal
tissues should be examined with a standardised periodontal probeusing light
pressure (15gm) to examine the tissues for plaque, bleeding, retentive factors
and pocketdepths.
 The dentition is divided into sextants and each tooth is probed
circumferentially.
 Only the highest scoreis recorded in each sextant. The scorecodes are as
follows;

Code
0 No bleeding or pocketing detected
1 Bleeding on probing - no pockets greaterthan 3.5mm
2 Plaque retentive factors present - no pockets greaterthan 3.5mm
3 Pocketsgreaterthan 3.5mm but less than 5.5mm in depth
4 Pocketsgreaterthan 5.5mm in depth
 When a BPE scoreof 3 or 4 is recorded then the orthodontist should refer
the patient back to their GDP or to a periodontologist for appropriate care
 Only when the GDP or periodontologist has deemed that periodontal
disease is not active should orthodontic treatment be undertaken but 6 months
later on.
2. Radiographs
Panoramic radiographs are often taken as a baseline record for orthodontic
screening. The Royal college of England in 2004 recommended:
 Horizontal bitewings for lesser pockets
 Vertical bitewings or periapicals for deeper pockets.
Treatment of periodontal diseases
A) Initial periodontal therapy /non-surgicaltherapy /Cause Related
Therapy (CRT) includes
1. Patient motivation through:
 Explanation of the causes and the risks.

 Demonstration of oral hygiene techniques
 Monitor compliance by plaque index.
2. Supragingival scaling.
3. Removal of plaque retention factors.
4. Subgingival scaling with root surface debridement.
5. Chemotherapeutic adjuncts may be appropriate - chlorhexidine gluconate
0.2 per cent
6. Occlusal adjustment if appropriate.
7. Smoking cessation advice
B) Monitoring response to therapy
Responseto therapy should be monitored through:
 Patient compliance (plaque and calculus index)
 Bleeding
 Pocketdepth (Following subgingival instrumentation a period of six to
eight weeks should elapse before any probing is performed. Indeed healing is
not complete for six months).
 Mobility.
Three scenarios might be identified:
1. Patients demonstrating good responsetreatment with adequate OH and
absence of evidence of pocket activity will require a maintenance regime to
conserve the improvement achieved.
2. Patients with inadequate responserelated to poorcompliance will not
benefit from surgical intervention but may show health gain from regular
professional dental prophylaxis.

3. Patients with adequate levels of oral hygiene but with residual active
periodontal pockets may benefit from more complex therapy including
periodontal surgery or the use of local antimicrobial therapy as an adjunct to
further non-surgical debridement.
Other periodontal surgery
1. Fibreotomy / circumferential supracrestal fibreotomy technique (CSF)
2. Fraenotomy: attachment of the fraenum is severed from the gingiva and
periosteum and is resited apically
3. Removal of gingival invaginations (clefts): Spaceclosure=piling of soft tissue
with deep vertical cleft running apically. If persisting> 5 years excise the cleft
with deep vertical incisions on either side of the cleft, leaving an open wound
and healing by secondaryintention
4. Gingivectomy
The relationship of orthodontics and periodontics
1. Does malocclusioncause periodontaldisease?
A. Crowding
Ainamo 1972,
 Concluded that irregularity of the teeth does not periodontal breakdown
 Irregularity does OH ability
 Association between irregularity & periodontal disease does become
significant when tooth brushing is average.
Bollen 2008 in her systematic review showed a positive correlation
Addy et al 1988
 Conclusion  periodontal breakdown not associated with crowding

B. IncreasedOverjet
Bjornas et al 1994
 Helm & Peterson 89  periodontal pocketing & gingivitis + OH is
poorerwith OJ
C. DeepOverbite
 Class II/2  gingival recession on labial surface of lowers, palatal uppers
D. Other occlusalconsiderations
 Rootapproximation  thin interdental bone
 Traumatic occlusion  giggling forces
 Incompetant lips  plaque more difficult to remove
2. Does periodontal disease cause malocclusion?
Profit 1978 equilibrium theory:
1. intrinsic forces by the tongue and lips
2. extrinsic forces:habits ( thumb sucking),orthodontic appliances
3. Forces from dental occlusion
4. Forces from the periodontal membrane
Loss of PD support  less able to withstand soft tissues + occlusal forces 
tooth movement
3. Periodontally compromisedpatient having an orthodontic treatment
A. There is no evidence that orthodontic treatment will worsen the PD
condition if the OH and PD condition is stabilized.
B. No treatment should be started unless these features are available
 Pockets less than 5mm
 Bleeding scores less than 15%

 Plaque scores less than 15%
 Cleanable teeth and prosthesis
 No root caries.
 Badersten 1984 says at least 6 months after stabilizing periodontal
treatment
C. Appliance: Orthodontic treatment might act as a retentive factor for
plaque and certain preventive measurement might be indicated:
 High standard of oral hygiene
 Keep the appliances and mechanics simple.
 Avoid hooks, elastics and excessive bonding resin outside the bracket
bases.
 Wire ligatures accumulate less plaque
 Bonds are preferable to bands.
D. Biomechanics:
 Light forced indicated during treatment since there is a change in the
center of resistance
 Reinforce anchorage
E. Adjunct to treatment
1. Physical
 Oral Hygiene Motivation Method (OHMM)
 electric toothbrush
 professional prophylactic programmes
2. Chemical
 0.12% chlorhexidine gluconate
 0.2% chlorhexidine gluconate usually recommended
F. Screening

• BPE probing 3 monthly. Boyd (1989) 3 monthly intervals
• full chart if greater than score3 in more than one sextant
G. Progress of treatment and PD status monitoring: Warning signs during
treatment need strict action, these includes:
 Inadequate OH
 Bleeding on probing
 Sub-gingival calculus
 Radiographic signs of bone loss
 Probing depths of greater than 4mm
It is preferable to terminate orthodontic treatment in patients who fail to respond
to instructions for oral hygiene procedures
H. Retention: in PD compromised dentition, the use of semireigid fixed
retainer to allow some functioning of the pd tissue during fixation.
4. Iatrogenic influence of orthodontic treatment on periodontium
Types
• Gingivitis
• Gingival recession
• Gingival hyperplasia
• ANUG
• Periodontitis
• Burns
• Bone loss
Incidence
A. Nearly all FA patients will get gingivitis but with no difference in
periodontal status between postorthodontic and non-orthodontic patients

B. rarely progresses to attachment loss
C. MH: Patients with certain medical conditions are more at risk of
periodontal problems for example poorly controlled diabetics or epileptics
whose anticonvulsants cause gingival hyperplasia
D. Mechanics: Certain treatment mechanics e.g. proclination of lower
incisors in a Class III case prior to surgery can result in gingival defects.
Management in these cases should be coordinated with a periodontologist, who
may recommend improved plaque control alone or a free gingival graft.
Gingival recession
Miller classification

Etiology
1. Plaque,
2. Position of the tooth,
3. Vigorous tooth brushing,
4. Traumatic occlusion,
5. Prominent fraenum
6. Thin marginal gingivae.
7. Alveolar plate is thin.
8. Orthodontic movement to position the tooth labially
Benefits of orthodontic treatment in relation to gingival recession, Johal
2013
1. Self-maintaining oral hygiene

2. Crown alignment within the dento-alveolar envelope
3. Removal of occlusal trauma
4. Rootalignment within the bone
Risk factors, Johal2013
One could consider the acronym ABEF to help take into account the risk factors:
A: Anatomy of the alveolar bone and proximity of the rootto the cortical plates
B: Biotype
E: Environment (oral hygiene, habits, poorbrushing,poor orthodontic
mechanics, active lingual retainers)
F: Functional matrix (smoking)
The mechanics or treatment modalities that could be employed to minimize
the risk of recession
1. Maintain good oral hygiene throughout orthodontic treatment
2. Eliminate potential causes of recession (piercing, smoking, traumatic tooth
brushing)
3. Avoid uncontrolled dento-alveolar expansion and maintain arch form by
extraction or IDS.
4. Customise bonding and mechanics
5. Modify tooth anatomy whenever indicated
6. in lower incisor crowding, consider segment arch mechanics and create space
before using it and use it wisely
7. Consider atypical extractions of severly involved tooth
8. Avoid jiggling because it may cause periodontal problems

9. Treat early (interceptive procedures and treatment in mixed dentition)
10.Gingival grafting before orthodontic treatment
Treatment of gingival recession,Johal 2013
1. Thorough instructions on plaque control should be provided.
2. Free gingival graft
3. EMD
4. Modified coronally advanced tunnel flap approach
5. envelope technique with connective tissue graft
6. The laterally positioned flap with or without connective tissue graft.
7. A frenectomy can also be considered
8. The gingiva is attached to the supracrestal portion of the root so that lingual
movement of the incisor will result in a labial increase in gingival height.
5. Periodontalsurgery as an adjunctive procedures to orthodontic
treatment
Fibreotomy (CSF).
Procedure
 Developed by Edward 1988
 Littlewood 2006 supportits advantages
 Basically this involves insertion of a scalpel into the gingival sulcus and
incising the circum-gingival fibers surrounding the tooth to a depth of about 3m
below the level of the alveolar crest.
 The blade also transects the transseptal fibres by entering the periodontal
ligament space.

Indicated
Improve retention after de-rotation
Contraindication
 Poororal hygiene,
 Gingivitis or active periodontal disease.
 In cases of treated periodontitis because the crevicular incision may
damage the long junctional epithelium
 Thin gingivae
Fraenotomy
Indication
 Unaesthetic fraenum
 When the fraenum with a fan-like attachment may obstructclosure
Removalof gingival invaginations (clefts)
Indication
 During orthodontic closure of extraction sites, the teeth tend to pushthe
gingivae ahead to create a pile of soft tissue.
 The excess gingiva has the appearance of an enlarged papilla with a deep
vertical cleft running apically.
 There is some resolution of these defects with time but many persist for 5
years after completion of orthodontic therapy.
Procedure
 Excise the cleft with deep vertical incisions on either side of the cleft,
leaving an open wound and healing by secondaryintention

Gingivectomy
Indication
 Improving aesthetic.
 This is particularly so in cases with missing lateral incisors, after
premolar auto transplantation and 'gummy' smiles.
 Increase the clinical crown length
Contraindication
 Gingivectomy should not be carried if there is a risk of exposing the root
surface.
6. Role of orthodontics in treatment of periodontal problems
Bollen 2008 showed that ortho treatment will not improve perio condition
Some authors prefer to perform orthodontic treatment before stabilizing the pd
condition based on the believe that orthodontic treatment would eliminate bony
defect as teeth moved ad thus reducing pocket depth.
However, Kokich (1996) mentioned that:
A. Gingival margin discrepancies
Gingival margin discrepancies can be addressed by surgical or orthodontic
means. Decision depends on:
1. Level of smile line: if low smile line and the gingivae can not be shown,
then the correction is unnecessary.
2. The depth of the gingival sulci over the teeth in question: If the sulcular
depth is unequal, coronal-lengthening surgery may alleviate the problem. If the
sulci are of equal depth, then orthodontic is indicated by extruding it to move its
gingival margin coronally allowing for correction of the gingival margin
discrepancy and then subsequent reduction to correct the resulting incisal edge
discrepancy.

3. Coronal tooth structure:. The overerupted tooth due to attristion or
abrasion should be slowly intruded to allow apical migration of the gingival
margin and then restored back up to the properheight.
B. ‘‘the missing papilla’’
Aetiologies (Zachirsson2004):
 Posttreatment interdental contactpoints that are located too far incisally,
Tarnow et al 1992 analyzed the correlation between the presenceof
interdental papillae and the vertical distance between the contact point
and the interproximal bone crest. When the vertical distance from the
contact point to the crest of bone was 5 mm or less, the papilla was
present almost 100% of the time. If the distance was 6 mm, most
commonly only partial papilla fill of the embrasure between the teeth was
found. the distance was 7 mm or more, the papilla was missing most of
the time. These findings indicate that the papilla will extend only a
limited distance from the alveolar bone crest to the interproximal contact.
Since the supracrestalconnective tissue attachment zone is normally
approximately 1 mm, the biologic height of the interdental papilla may be
limited to about 4 mm.
 Triangular-shaped or divergent crown shape
 Loss of periodontal supportdue to plaque-associated lesions.
 Improper (divergent) root angulations,
 Contours of prosthetic restorations,
 Traumatic oral hygiene procedures may also negatively influence the
outline of the interdental softtissues
Prevelances

 A recent study by Kurth and Kokich 2001 demonstrated that open
gingival embrasures is a common posttreatment finding in adult
orthodontic patients. In their sample of 337 patients with a mean age of
about 32 years, 38% had open spaces between the maxillary central
incisors.
 In another study, Burke et al 1994 found a 42% prevalence in adolescent
orthodontic patients with crowded central incisors.
 Treatment
1. Accept: Kokich Jr et al 1999 found that orthodontists identified a 2-mm
open spacebetween the maxillary central incisors as unattractive. However,
general dentists and lay people apparently were unable to detect an open
gingival embrasure unless it was 3 mm long. These results indicate that small
open spaces may not be noticeable enough by the average patient to necessitate
their correction.
2. IPS but with consideration to the TSD
3. Toothmovement with simple repositioning of the orthodontic brackets or
by judicious wire bending,
4. Selective cosmetic bonding
C. The ‘‘gummy smile’’
Causes
1. Vertical maxillary excess:it can be treated by orthognathic surgery
2. Gingival hyperplasia or coronalpositionedgingivae due to delayed
apical gingival migration in the adolescent. In this situation, gingival surgery
should be performed
3. Short lip: treated by plastic surgery
4. Over eruption of the teeth which treated by absolute incisor intrusion.
However, intrusion of teeth can shift supragingival positioned plaque
subgingivally. Professional subgingival scaling is particularly important during

the phase of active intrusion. Intrusion should generally be undertaken in
patients with an excellent standard of oral hygiene.
5. Combinations
D. Horizontal or AP bone regeneration
1. It has been shown that a tooth with a healthy periodontium maintains this
when it is moved into an area of reduced bone height.
2. It is important to emphasise that the periodontal condition must be
stabilised prior to treatment.
E. Vertical bone regeneration
During the orthodontic extrusion the relationship of the CEJ to the bonecrest is
maintained so that the bone follows the tooth. This means that the extrusive
tooth movement repositions the intact connective tissue and the vertical bone
defect is either eliminated or shallowed out.
Indicated
1. Used to shallow out infrabony defects
2. To increase the clinical crown length of a single crown.
F. Managementof drifting incisors
Migration and spacing of the upper anterior incisors is often the first indication
to the patient that there may a problem with their teeth.
G. Managementof tilted molar teeth (This invariably is the second
molar tooth).
Indications

1. Presence of a functionally disturbed occlusion.
2. Paralleling of abutment prior to prosthetic preparation.
Treatments options
1. Acceptance and monitoring its position
2. Orthodontic uprighting
3. Uprighting followed by spaceclosure.
Advantages
1. Easier abutment preparation enhancing parallelism.
2. Elimination or reduction of mesial periodontal lesions.
Factors must be considered
1. Assess the position of the 3rd molar. If the planned upright position is
impeded by the 3rd molar then it should be removed.
2. The most appropriate tooth movement should be considered. Distal crown
tipping increases the pontic space, while mesial root tipping reduces it.
3. Spaceclosure following uprighting by is complicated if there is a mesial
periodontal defect. When an infrabony defect is present, it is essential to ensure
that that the periodontal condition is stabilised prior to any uprighting.

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Periodontics and orthodontics for orthodontists by Almuzian