Iatrogenic effect of orthodontic by almuzian

Iatrogenic Effects of Orthodontic TreatmentMohammed ALMUZIAN

13University of Glasgow

Table of ContentsDefinition..............................................................................................................................................4

The potential hazards of orthodontic treatment are four area of interest: Elis and Benson 2002...........4

Tissue damage.......................................................................................................................................6

Intra-oral................................................................................................................................................6

Hard tissue damages..............................................................................................................................6

Enamel demineralisation.......................................................................................................................6

Definition..............................................................................................................................................6

Aetiology...............................................................................................................................................6

Classification.........................................................................................................................................6

Incidences..............................................................................................................................................7

Predictors for the development of white spot lesions.............................................................................7

Zone of demineralization.......................................................................................................................7

Complications........................................................................................................................................7

Enamel demineralisation is important to the orthodontist in three ways:...............................................8

Prevention of demineralization..............................................................................................................8

Treatment of enamel decalcification, Welbury & Carter, 1993...........................................................10

Enamel Fractures.................................................................................................................................11

Aetiology.............................................................................................................................................11

Prevalence...........................................................................................................................................12

Prevention............................................................................................................................................12

Interproximally stripped enamel..........................................................................................................12

Peridodontium problems......................................................................................................................13

Types...................................................................................................................................................13

Periodontal problems are important to the orthodontist.......................................................................13

Incidence.............................................................................................................................................13

Prevention............................................................................................................................................14

Gingival recession...............................................................................................................................15

Etiology...............................................................................................................................................15

Treatment............................................................................................................................................15

ANUG.................................................................................................................................................16

Sign and symptoms..............................................................................................................................16

Treatment............................................................................................................................................16

Alveolar bone loss...............................................................................................................................16

Incidence.............................................................................................................................................16

Mohammed Almuzian, University of Glasgow, 2013 1

Root Damage OIIRR...........................................................................................................................17

History.................................................................................................................................................17

Definition............................................................................................................................................17

Location of OIIRR.................................................................................................................................17

Mineral content & physical properties of cementum...........................................................................17

1. Mineral content........................................................................................................................18

2. Elastic modulus........................................................................................................................18

Prevalence...........................................................................................................................................18

OIIRR tends to occur commonly in the apical region because............................................................19

Patho-physiology of OIIRR.................................................................................................................19

Diagnosis of OIIRR.............................................................................................................................19

Classification of root resorption..........................................................................................................20

Important to the orthodontist in three ways.........................................................................................21

Factors that influence the severity of orthodontically induced inflammatory root resorption (OIIRR) 21

Repair and clinical consequences of OIIRR........................................................................................26

Prevention and management of OIIRR................................................................................................26

A. Before treatment..................................................................................................................26

B. Treatment of choice.............................................................................................................27

C. During treatment..................................................................................................................27

D. After treatment.....................................................................................................................27

Pulp damage........................................................................................................................................28

Incidence.............................................................................................................................................28

Aetiology.............................................................................................................................................28

Prevention and managements..............................................................................................................28

Soft-tissue damage...............................................................................................................................29

1. Direct damage by removable or fixed components..................................................................29

Aetiology.............................................................................................................................................29

Prevention............................................................................................................................................29

Prevention............................................................................................................................................30

2. Indirect damage by allergic reactions to nickel and latex.........................................................31

Allergies..............................................................................................................................................31

Hypersensitivity reactions:..................................................................................................................31

Latex Allergy.......................................................................................................................................31

Prevalence...........................................................................................................................................31

Individuals susceptible to allergic reactions include............................................................................31

How Should Potential Orthodontic Patients with Suspected Latex Allergy Be Managed?..................32


Nickel hypersensitivity........................................................................................................................32

Introduction.........................................................................................................................................32

Sign and symptom...............................................................................................................................33

Prevalence...........................................................................................................................................33

Treatment............................................................................................................................................33

Cytotoxicity.........................................................................................................................................34

Treatment failure.................................................................................................................................34

Increasing predisposition to other disorders........................................................................................35

Systemic effects...................................................................................................................................35

Pain......................................................................................................................................................35

Why there is a pain associated with orthodontic treatment..................................................................35

Pain control in orthodontic patients.....................................................................................................36

Bacterial endocarditis..........................................................................................................................36

Cross infection.....................................................................................................................................37

Prevention............................................................................................................................................37

Reuse of orthodontic materials from BOS.............................................................................................37

Radiation................................................................................................................................................38

The causes of excessive exposure to radiation in orthodontics.............................................................38

BOS guidelines for the management of inhaled or ingested foreign bodies.........................................39

Summary of the Royal College of Radiologists Guidelines on recommended radiographic views 2007...............................................................................................................................................................41


Iatrogenic Effects of Orthodontic Treatment

Definition

Deleterious damage to the individual patient as a result of orthodontic

treatment

The potential hazards of orthodontic treatment are four area of interest:

Elis and Benson 2002.

1. Tissue damage;

a. Intraoral effects

Teeth

• Crowns: decalcification, enamel trauma, Interporoximal stripping

• Roots resorption

• Pulp

Periodontium

• Bone - crestal bone resorption

• Gingivitis

• Periodontitis

Soft tissues

• Direct trauma - mucosal ulceration due to appliances

• Trauma from HG inner bow

• Clumsy instrumentation

• Burns

• Allergy/sensitivity

• Cytotoxicity

b. Extraoral effects

TMJ

TMD


Soft tissues

HG trauma to skin, eye or even the neck

Burns, Chemical from etchant/SEP or Thermal from overheating handpiece

Allergy, Nickel induced sensitivity associated with HG or Latex

Cytotoxicity

2. Treatment failure;

Incomplete treatment

Relapse

3. Greater predisposition to dental disorders.

Caries

Periodontal

4. Systemic effects

Psychological

Effect on the profile

Risk to airway

Pain

Bacterial endocarditis

Cross-infection

Radiation risks

Inhalation of foreign materials


Tissue damage

Intra-oral

Hard tissue damages

1. Enamel Damage

Enamel demineralisation

Definition

Enamel demineralisation is the loss of calcified tooth substances due to the

attack by acidic by-products of plaque metabolism that remove the mineral

and give the opaque white appearance. This is ranging from early lesions of

opaque white spots to marked cavitation. Mitchelle 2007. The acid is lactic

acid.

Aetiology

1. The reason is a change in the micro-flora (specially Strepcoccus mutans and

lactobacilli) after fitting the FA

2. The increase in food stagnation by FA with difficulty in maintaining good

OH.

3. O’Reilly and Featherstone (1987) noting that decalcification can occur within

1 month due to prolonged accumulation of plaque next to the bracket base.

Classification

WSL Index of Gorelick et al (1982).

1. Stage 0 (none),

2. Stage 1 is a slight rim,

3. Stage 2 a broad rim


4. Stage 3 cavitation.

Incidences

1. In one cross-sectional study, 50% of individuals undergoing orthodontics had

a non-developmental enamel opacity, compared with 25% of controls.

Gorelick 1982

2. Banks (2000) showing figures as high as 73%

3. Most commonly occur in lower canine and premolars as well as upper canine

and laterals

4. Fixed – labially, URA - palatally

5. May be influenced by dominant hand brushing i.e. in right handed patient, the

decalcification occurs on right side through less effective cleaning of that site.

Predictors for the development of white spot lesions

1. Interproximal caries,

2. Poor oral hygiene,

3. Diet issue.

4. Long treatment times and poor compliance but there is conflicting evidence

for this with Gorelick et al (1982) finding no relationship between length of

treatment and the number of lesions.

5. Negative correlation with age.

Zone of demineralization

1. Outer surface zone

2. Body lesion

3. Dark zone

4. Translucent zone

Complications

1. Aesthetic problems


2. It has been demonstrated that there is no overall increase in caries incidence

after fitting the fixed appliances, but a shift in distribution. This is seen from

the posterior to anterior teeth and interproximal to smooth surfaces

(Zachrisson & Zachrisson, 1971).

Enamel demineralisation is important to the orthodontist in three ways:

1. Before treatment: Its presence before treatment is a warning sign to the

orthodontist that diet and plaque control need attention or that the patient may

not be suitable for treatment.

2. During treatment: Its occurrence during treatment may necessitate a

shortened treatment plan or immediate discontinuation of treatment.

3. After treatment: Its detection after treatment may necessitate measures to

remineralise the lesion or improve its appearance.

Prevention of demineralization

A. Patient selection and education is essential. Patients with poor oral hygiene

should be excluded.

B. Dietary advice to reduce carbohydrates

C. Oral hygiene - Appropriate oral hygiene instruction and monitoring of

patients (Zachrisson 1974).

Conventional tooth brushing - Mechanical removal of plaque can be carried

out manually by conventional tooth brushing or by the use of electric brushes.

A paper published by Robinson et al 2005, as part of the Cochrane Group,

concluded that only powered toothbrushes with a rotation oscillation action

achieved a reduction in plaque and gingivitis compared to manual tooth

brushing and that this reduction was modest.

Interdental cleaning to ensure optimal dental health (Zachrisson 1974,

Casey 1988). Systematic review has looked at whether using an interspace

toothbrush in addition to a standard toothbrush improves plaque removal.

Unfortunately there were no evidences found (Goh, 2007, Cochrane review)


D. Periodic referral to hygienist were available to reinforce OH measures. Labial

surfaces of teeth should be inspected each visit and appropriate advice given.

Persistent poor oral hygiene; strongly consider early removal of appliances.

E. Adjunctive procedure including:

1. Xylotol chewing gum help to increase plaque control with no effect on

bonding strength (Isotupa 1995)

2. Chlorhexidine is a highly effective non-specific antimicrobial agent and

remains the most widely used agent in the chemical removal of plaque

(Grossman et al 1989). The disadvantage of chlorhexidine is its taste and

staining.

3. Fluoride mouthrinses

Daily rinsing with a 0.05% sodium fluoride daily mouth rinse or weekly

fluoride rinse of 0.2% has shown to be effective in reduction of white spot

formation.

However it had been noted that patient compliance was very low at 13%

(Geiger et al 1992). The patients most in need of fluoride rinses tend to be the

worst compliers. Cochrane review by Benson in 2013 show the effectiveness

of daily use of 0.05% fluoride but in non-orthodontic patient.

4. Tooth Mousse is a water based creme containing (CPP-ACP: Casein

Phosphopeptide – Amorphous Calcium Phosphate). Bailey 2009 RCT

showed its effectiveness.

5. Fluoride gels & varnishes: other topical applications, such as gels and

varnishes have been used but require patient compliance to be effective.

Professionally applied fluoride gels during treatment can be of benefit, but

are costly and time consuming (O’Rielly & Featherstone 1985). The latest

updated Cochrane review by Benson 2013 confirm the mildest effect of sixth

month application of fluoridated varnish.

6. Fluoride glass bead attached to the AW, but this has not been confirmed

by Benson 2013


7. Fluoride releasing devices – devices have been developed to release small

amounts of fluoride over a sustained period of time. Marini et al 1999,

designed intra-oral fluoride release devices placed in the upper molar bands

and showed no development of white spots. but this has not been

confirmed by Benson 2013

F. Attachment & appliance design

I. Brackets:

The selection of small brackets aids in reducing the areas of stagnation

Removing excess flash from around the brackets (Artun & Brobakken 1986).

II. Bands:

Placement of bands should ensure complete coverage of the enamel with

cement to prevent the formation of a void and plaque accumulation

(McGuinness 1992).

Periodic checking of the bands

III. Wires:

Minimal use of looped archwires will help to reduce plaque accumulation and

demineralisation (Mitchell 1992).

IV. Cements & adhesives

The use of fluoride containing glass ionomer cements has reduced the

incidence of demineralisation beneath molar bands (Mizrahi 1988, During

1989, Folet et al 2002). Glass ionomer containing fluoride have been shown

to have weaker bond strengths than composite (Cook & Youngson 1988) and

cause a higher number of bracket failures (Norevall et al 1996).

Composite resins containing Fluoride as bonding adhesives have not been

found to effective at reducing white spot formation (Mitchell 1992, Banks et

al 1997).

V. Elastic modules

The evidence demonstrates that fluoride releasing elastomeric modules may

reduce the prevalence of demineralisation (Banks et al 2000).


However the addition of fluoride to elastics may affect their physical

properties so that they deteriorate rapidly in the mouth. Docherty et al 2002

showed that there was no difference between normal ligatures and fluoride

ligatures.

Treatment of enamel decalcification,

Welbury & Carter, 1993

1. If the decalcification developed while the patient is wearing the

appliance, it is recommended to:

A. Reinforce OHI

B. Fluoride mouth wash

C. Removal of archwires for a visit to allow remineralisation

D. Remove appliance as last resort.

2. After removing the appliance

E. The WSL can resolve to certain extent spontaneously. Artun 1986 found that

50% will resolve spontaneously within six month after debonding.

F. Topical fluoride in the form of gels, varnishes, toothpaste and mouthwashes

are effective in the treatment of demineralisation. Ogaard, 1989 suggests that

this will remineralise the outer layers of the lesion too early, leaving the deep

layers hypomineralised and hence the lesion remains white. Instead a no

fluoride or a low fluoride mouthrinse is recommended to allow

remineralisations from the base of the lesion (Linton, 1996)

G. Tooth Mousse is a water based creme containing (CPP-ACP: Casein

Phosphopeptide – Amorphous Calcium Phosphate). Bailey 2009 RCT

showed its effectiveness.

H. Microabrasion, a technique developed by Croll & Cavanaugh 1986,

involves the use of 18% hydrochloric acid mixed as slurry with pumice, is

rubbed over the affected lesion and removes the surface layer of enamel.

This results in an overall improvement of the lesion (Welbury & Carter

1993).Mohammed Almuzian, University of Glasgow, 2013 11

I. Restorative intervention if frank cavitation

Enamel Fractures

McGuinnes 1992, Zachrisson et al 1980

Aetiology

1. Abrasion by ceramic bracket

2. Abrasion of the upper canine during retraction of lower canine when OB is

not complete reduced.

3. During debonding: small cracks in the enamel surface are seen following

removal of orthodontic brackets by bur or due to mini-fracture of the enamel

or the tooth restoration. There were appreciably more cracks with chemically

bonded ceramic brackets.

Prevalence

2% more than control

Prevention

1. Careful bracket positioning

2. Do not place ceramic brackets on lower incisors in cases with

increased/normal OB

3. Removal of lower canine brackets during canine retraction if necessary

4. Careful debonding, particularly when working on 'risk' teeth e.g. heavily

restored teeth, hypoplastic teeth.

5. Use tungsten carbide burs in slow handpiece to remove composite

6. Care when debonding ceramic brackets Bishara et al., 1990

Use of the modern ceramic bracket that has a feature of bond failure in

debonding.

Remove composite around bases before debonding to allow full seating of the

debonding pliers


Use specially designed debonding pliers

Co2 lasers for debonding

Electrothermal debonders can be used

Ultrasonic devices

Interproximally stripped enamel

1. Some claim that it will be carious later but the six years follow up study by

Jarjoura 2006 disagree with this.

2. Some claim it cause reduction in the interseptal bone and deepening in the

PD pocket. (Artun, 1987)

Peridodontium problems

Bollen 2008 systematic review show that there is a negative statistic effect

but not clinical from orthodontic treatment on alveolar bone loss, pocket and

gingival recession

Types

1. Gingivitis

2. Gingival recession

3. Gingival hyperplasia

4. ANUG

5. Periodontitis

6. Burns

7. Alveolar bone loss

Periodontal problems are important to the orthodontist

1. Poor gingival health before treatment means that the patient is unsuitable for

treatment unless they can improve and maintain good plaque control.


2. Special consideration needs to be given to the mechanics when periodontal

support is reduced

3. Its occurrence during treatment may necessitate a shortened treatment plan or

immediate discontinuation of treatment.

4. Sometimes orthodontic intervention is indicated because of periodontal

problems e.g. a lower incisor in crossbite may have attachment loss or

treatment because of periodontal drift

Incidence

1. Nearly all FA patients will get gingivitis.

2. Rarely progresses to attachment loss

3. No difference in periodontal status between post orthodontic and non-

orthodontic patients

4. 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

Prevention

A. Patient selection — good OH and motivated

B. Ensure no active periodontal disease prior to treatment

C. Mechanics

Bonds are better than bands

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.

D. Adjunct to treatment

Physical

1. Oral Hygiene Motivation Method (OHMM)


2. Electric toothbrush

3. Professional prophylactic programmes

Chemical

1. 0.12% chlorhexidine gluconate

2. 0.2% chlorhexidine gluconate usually recommended

Screening

1. No Pre-existing periodontal disease needs

BPE probing 3 monthly

Full chart if greater than score 3 in more than one sextant

2. Pre-existing periodontal disease , Orthodontic treatment is not

contraindicated in this group, but certain precaution should be followed:

• The patient is sufficiently motivated

• Disease is controlled

• Three-monthly periodontal checks and routine scaling and polishing

• Keeping the forces light

• Bone loss alters position of centre of resistance of teeth and force required to

achieve movement

• Permanent retention

Gingival recession

Etiology, Johal 2013

1. Plaque,

2. Thin marginal gingivae.

3. Alveolar plate is thin.

4. Position of the tooth,


5. Vigorous tooth brushing,

6. Traumatic occlusion,

7. Prominent fraenum

8. Orthodontic movement to position the tooth labially

Treatment

1. Thorough instructions on plaque control should be provided.

2. Correct method of brushing

3. Correct cross bite

4. Correct tooth position AP: 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. Frenectomy

6. Surgical intervention with the aim is to increase the thickness of the covering

gingiva by using for example a free gingival graft, and not the apical-coronal

width.

ANUG

Sign and symptoms

Pain

Halitosis

Bleeding

Loss of papillae

Ulceration

Lymphadenitis


Malaise

Treatment

1. OHI

2. Chlorhexidine mouthwash

3. Local debridement

4. Metronidazole tds 200 mg 3 days

5. Review 1 week

6. At review, if the lesion has failed to resolve then advise the use of

miconazole nitrate 2% gel applied topically four times a day for 2 weeks;

7. If the lesion still fails to resolve then request haematological and

sensitivity test. Alternatively the patient could be referred to a local oral

surgery or oral medicine consultant;

8. Finally, if the lesions are recalcitrant, painful and causing distress then

removal of fixed orthodontic appliances may be necessary.

Alveolar bone loss

Incidence

1. Uncommon Kennedy et al., 1983;

2. 10% of orthodontic patients had significant attachment loss (1- 2mm)

compared with controls, but 50% had no loss, mean loss of attachment

0.1mm compared with controls , Zachrisson, 1976

3. Bone loss during treatment unrelated to previous bone loss.

4. Long term bonded retainer as that teeth at high risk of relapse (Shapira 1994,

BOS 2013)

Root Damage OIIRR

History

First discussed by Bates, 1856


Definition

It is an inflammatory process that results in a loss of substance from

mineralized cementum and dentine and it considered as a transient

external inflammatory root resorption.

It can be occur in 3-4 week and take 6week to be identifiable

radiographically.

Location of OIIRR

1. Apical or Lateral - difficult to detect lateral resorption on R/G's which

subdivided into:

A. Cemental or surface resorption with remodelling.

B. Deep dentinal resorption with repair. The resorbed cementum and the outer

layers of the dentine are repaired with cementum material which may or may

not restore the root to its original size and shape.

2. Circumferential apical root resorption. Significant resorption of the root

apex results in root shortening with no evidence of regeneration.

Mineral content & physical properties of cementum

Rex et al (2005)


1. Mineral

content

There was no difference in calcium (Ca), phosphorus (P)

and fluoride (F) concentrations between the buccal and

lingual surfaces of the root

There was a decreasing concentration gradient for Ca, P

and F from cervical to apical third

There is an increasing concentration gradient for Ca and

P from the outer to the inner layer of the root at the

cervical and middle thirds of the root

2. Elastic

modulus

Cementum has a lower elastic modulus than dentine to

cope with movement of the root during function.

The hardness and elastic modulus of cementum decreases

steadily from cervical to apical third.

The average hardness of cementum in the middle third of

the root

Prevalence

Usually apical rather than lateral (unless using RME), Kenndey 1983

The teeth susceptible to root resorption include the upper and lower incisors

and the lower first molars (Kennedy et al 1983), this is because of their

morphology and because most of the movement involved these teeth.

Minimal OIIRR

1. Very WIDE Variation. !!!! (Why do the figures for reported incidence vary

so much? Some report number of patients with resorption, whilst others

report number of teeth. Some methods of detecting resorption are more

sensitive than others i.e. CT v periapical radiographs

Mild: 90% of patient Weltman 2010.

Moderate: 2-4mm 6-13% (Linge and Linge 1983)

Severe more than 4mm: 5% in adult and 2% in adolescent (Linge

and Linge 1983)


OIIRR tends to occur commonly in the apical region because

1. The fulcrum of most tooth movement is usually at the apical half of the

root, so the force is concentrated at this area.

2. The orientation of the periodontal fibres at the apical end is different,

which increases the stress in the region ,

3. The apical third of the root is covered by cellular cementum

4. The apical third of the root has different mineral contents with different

physical properties than other parts of the root.

Patho-physiology of OIIRR

Three mechanisms or theories.

1. Usually when the force applied to the tooth, the bone and the cementum will

resorb. But the cementum will be repaired again during recovery period

between activation visits. If the cementoblastic activity is low, the cementum

will not be repaired (Berezniak 2002)

2. Mechanical damage to the natural barriers of resorption (the cementoid layer

and the more mature periodontal collagen fibres). Once this have been lost

this leaves the cementum exposed to osteoclast , Once resorption of the

cementum has occurred then the underlying dentine can be destroyed which

is irreversible. Kindealn 2008.

3. Possible increase in the osteoclastic and cementoclastic activity.

Diagnosis of OIIRR

1. History

2. Clinical examination

3. Radiographical examinations:

DPT (overestimate resorption by 20% compared to PA one,

Sameshima and Sinclair 2001) this is because the apices being outside

the focal trough and thus seemingly resorbed. Also DPT not clear

because of the narrow focal trough at the anterior area. Another


problem: The shape of the curved focal trough is pre-determined and

patients have to be positioned carefully within the machine to ensure

that their teeth and the supporting structures appear in focus on the

resultant film. Incorrect positioning results in a distorted image with

teeth appearing foreshortened, magnified and/or out of focus

depending on the positioning error. In addition, normal anatomical

structures can appear as radiolucent or radiopaque shadows

superimposed over the teeth as either real or actual shadows or as

ghost or artefactual shadows all of which can degrade the quality of

the final image.In orthodontic patients, another common problem is

one of skeletal base discrepancy. In markedly class II or class III

cases, it may not be possible to position both the upper and lower

labial segment teeth within the focal trough of the machine

simultaneously (Leach and Ireland 2001)

PA (the paralleling technique and the bisected angle technique. The first is

better Ireland 2001). PA is not accurate in quantifying the amount of

resorption (Katona 2006) Ferguson 1992

Occlusal radiographs may be needed to supplement the DPT. Issacson 2008.

the upper standard occlusal radiograph is in effect a large bisected angle

technique periapical and so it is less reproducible

Lateral ceph can be used for upper incisor but it carries 5-12% magnification

(Chan and Darenedliler 2004) and superimposition is problematic (Leach and

Ireland 2001)

CT or CBCT

Digital radiography is a relatively recent development in dentistry enabling

the film packet to be replaced with a digital image receptor. Two types of

receptors have been developed – CCD (charge coupled device) sensors and

photo-stimulable phosphor imaging plates. Both systems have intraoral

receptors suitable for periapical radiography but only photo-stimulable

phosphor plates have been produced for occlusal radiography. Digital


radiography has been shown to demonstrate a similar degree of sensitivity to

film-based radiography in the detection of resorption, but with a lower

radiation dose (Borg 1998)

Classification of root resorption

Types of resorptionBrezniak & Wasserstein, 1993

1. Physiological - resorption of deciduous teeth

2. Inflammatory due to orthodontic treatment

3. Replacement - Ankylosis

4. Idiopathic - no identifiable cause

Classification according to the degree of resorption.Levander and Malmgren (1988) classification

It is a commonly used contemporary classification which divides apical

root resorption into five categories.

1. grade 0 no resorption

2. grade 1 indicates an irregular root outline (blunting)

3. grade 2, 0-2 mm root resorption (minor)

4. grade 3, > 2-4 mm (moderate)

5. grade 4, resorption > one third of root length or more than 4mm (extreme)


Important to the orthodontist in three ways

1. It can be detected prior to treatment and therefore affect the treatment plan.

The most commonly resorbed tooth detected prior to treatment is the upper

lateral incisor, which may have been resorbed by an impacted canine tooth in

48% of cases as detected by medical CT scan (Ericson & Kurol 2001). A

study about the influence of detecting OIIRR on TP: In 2006, Bjerklin

and Ericson analysed the treatment outcome and treatment planning before

and after a computerized tomography investigation of children with retained

and ectopically positioned maxillary canines and some degree of root

resorption. The diagnosis and a treatment plan were originally based on

extraoral and intraoral photographs, study models, the patient’s history,

conventional radiography, and, if available, lateral head films. Approximately

one year later, the same examiner drew up a new treatment plan based on the

same records but with a supplemental CT examination. The treatment plans

of 35 (43.7%) of the 80 children were modified to reflect this new

information. Of those patients with root resorption on the incisors adjacent to

retained canines, more than half of the treatment plans were altered. A CT

investigation of root resorption can therefore be an important source of

information for treatment planning for children with retained or ectopically

erupting maxillary canines.

2. It can be detected during treatment and therefore alters the treatment

mechanics.

3. It can be detected after treatment and worries the orthodontist about what

they have done.

Factors that influence the severity of orthodontically induced

inflammatory root resorption (OIIRR)

Brinzniazk 1991, 2002

There are biological and mechanical factors that influence the severity of

orthodontically induced inflammatory root resorption (OIIRR).


1. Biological factors

a. Race

b. Gender

c. Age factors

Chronological age

Dental age

d. Genetic factors

e. Medical and social factors

Asthma and allergy

Endocrine and hormone imbalance

Nutrition

Drugs

Alcohol consumption

f. Local factors

Types of malocclusion

Hypodontia

Habits

Occlusal trauma

Traumatised teeth

Pre-existing root resorption

Endodontically treated teeth

Transplanted teeth

Hypo-functional periodontium

Specific tooth vulnerability

Abnormal root morphology

2. Mechanical factors

Duration of treatment

Distance of movement

Magnitude of forceMohammed Almuzian, University of Glasgow, 2013 24

Duration of force

Direction of force

Treatment mechanics

In details

1. Biological factors

a. Genetic factors

b. Race - Hispanic>White>Asian

b. Medical and social factors

Asthma and allergy: This could be attributed to the close proximity of the

roots to the inflamed maxillary sinus and or the presence of inflammatory

mediators in these patients

Nutrition: deficiency of dietary calcium and vitamin D

Endocrine and hormone imbalance: hyperparathyroidism , Paget’s disease

and hypophosphatemia are hypothesized to be related to OIIRR . An excess

of thyroid hormones which increased bone turnover were found to reduce

root resorption during orthodontic tooth displacement in a rat model.

Drugs: Inhibiting cyclo-oxygenase and the subsequent inhibition of the

production of prostaglandins with (NSAIDs) can be useful in decreasing bone

and root resorption. Bisphosphonates directly or indirectly induce apoptosis

in osteoclasts which play a role in the inhibition of bone resorption.

Alcohol consumption: The presence of ethanol in the circulation inhibits

the hydroxylation of vitamin D3 in the liver, thus hindering calcium

homeostasis and resulting in a rise in parathyroid hormone (PTH). PTH in

turn enhances the resorption of mineralized tissues including tooth roots.

c. Genetic

There is a responsabile gene called IL-1A & IL-1B (Al-Qawasimi 2003)

d. GenderMohammed Almuzian, University of Glasgow, 2013 25

Some studies have suggested that orthodontically treated females had a

greater incidence of OIIRR than males. (3.7:1)

Few studies have shown the opposite

However, most of the studies have found no correlation between gender

and the extent.

d. Age factors

Chronological age: The periodontal membrane becomes aplastic, narrow and

less vascular with age causing more OIIRR.

Dental age: Partially formed roots have been found to develop normally

during orthodontic treatment and it has been suggested that teeth with open

apices may be less susceptible to OIIRR. (Harris and Baker 1990).

e. Local factors

Habits: bruxism, nail-biting associated with more OIIRR

History of trauma: associated with more OIIRR.

Hypofunctional periodontium: associated with more OIIRR.

Teeth with pre-existing root resorption: these teeth are very much more

susceptible to root resorption as indicated by Massler and Malone (1952),

Goldson and Henrikson (1975) and Linge and Linge (1983). As a rough

guide, the rate of root resorption seems to double on teeth with pre-existing

root resorption.

Transplanted teeth: Transplanted teeth are no more susceptible to OIIRR

than normal teeth provided the transplant is without complication and the

orthodontist waits three months before attempting tooth movement (Paulsen

et al 1995).

Traumatised teeth may undergo EARR as a consequence of their trauma

even if they do not undergo orthodontic treatment; if this is the case, then

these teeth behave in the same way as teeth with pre-existing root resorption.

Traumatised teeth that do not exhibit root resorption prior to orthodontic

treatment behave normally.


Endodontically treated teeth : In general, it is felt that endodontically

treated teeth are less susceptible to root resorption than normal teeth and this

is substantiated by Remington et al (1989), Owman-Moll et al (1995) and

Costopoulos and Nanda (1996).

Occlusal trauma: due to jiggling effects associated with more OIIRR.

Specific tooth vulnerability to root resorption: The teeth most frequently

affected by OIIRR according to severity are the maxillary lateral incisors,

maxillary central incisors, mandibular incisors, distal root of mandibular first

molar, mandibular second premolars and maxillary second premolars .

Abnormal root morphology: (Kindelan 2008)

i. Blunt

ii. Pipette-shaped roots

iii. Single rooted teeth

iv. Narrow and thin roots.

v. diminutive laterals are not more susceptible,

However, Lee et al 1999 showed that there is no correlation. The latest study by

Mirabella and Artun 1995 showed that long teeth suffer more resorption and

this because they require more force to be moved than shorter.

Types of malocclusion:

i. treatment of ectopic canines, may get more resorption of 2 and 4, this may be

due to

• Pre-existing resorption not detected before treatment

• Due to the increased treatment times associated with these cases

• Due to intrusive force when the canine is extruded.

ii. hypodontia — teeth moved more distances and have small or narrow pipette

roots

iii. no risk factors related to increased OJ and OB

Mechanical factors (Weltman 2010)Mohammed Almuzian, University of Glasgow, 2013 27

1. Duration of orthodontic treatment: more OIIRR in longer duration

2. Magnitude of applied force: more OIIRR with high force

3. Direction of force: more OIIRR in intrusive force

4. Amount of apical tooth movement : more OIIRR in long movement

5. Treatment mechanics: more OIIRR with:

• FA type (Begg more the SWA)

• Superelastic archwires

• Rectangular AWs

• Intermaxillary traction appliance due to jiggling force.

• Cortical bone contact with root apices

• HG and J hook

• Orthognathic decompensation

Repair and clinical consequences of OIIRR

1. Repair of root resorption begins when the applied orthodontic force is

discontinued or reduced below a certain level and within a week (20–26

g/cm) Schwarz

2. Many studies have demonstrated that the resorptive defects were repaired by

deposition of new cementum and establishment of new PDL.

3. However, the original root contours and lengths were never re-established.

4. Severely resorbed teeth were found to be functioning in a reasonable manner.

5. The worst outcome was hypermobility

Prevention and management of OIIRR

Ghafari 1994 and Brezniak, 2002 recommendations include

A. Before treatment

All the risk factors should be considered:

1. General considerations. The patient/parents must be informed about the risk

of OIIRR as a consequence of orthodontic treatment.


2. Thorough assessment of familial tendency and medical history.

3. Habit control

4. Consideration of the Age. Treatment of moderate to severe malocclusions is

commenced when most of the incisors had open apices, which is before the

age of 9 years.

5. Consideration of the malocclusion associated risk.

6. Root-filled teeth are not necessarily at greater risk of root resorption and may

safely be moved using orthodontic appliances, providing:

Teeth are clinically symptomless and radiographically satisfactory;

It is 6 months after a new root filling;

A radiograph is taken 6 months after the start of active treatment.

B. Treatment of choice

There is no specific appliance that makes resorption less

C. During treatment

If resorption occurs during treatment, then follow these

recommendations:

1. The force levels should be modified or a 2–3 months’ pause in treatment with

passive archwires should be implemented (Levander 1994).

2. Then take a radiograph,

A. if the resorption continue then try to modify the treatment,

B. if the resorption stopped then continue but the mechanical risk factors:

Levander 1999, Brezniak 2002)

Decreased treatment duration,

Longer intervals between activations

Limiting tooth movement for OIIRR-prone teeth, e.g. Intrusion and torque ,

The use of light intermittent forces and avoidance of sustained jiggling

intermaxillary elastics ,

Consider IDS instead of extraction

Consider early fixation


D. After treatment

Final records including radiographs are recommended and are even

mandatory. If OIIRR is present on the final radiographs, then

1. the patient/parents should be informed

2. For teeth with severe resorption, follow-up radiographic examinations are

recommended until OIIRR is no longer progressive and repaired.

3. Flexible bonded retainer that allow physiological functional of the

periodontium is recommended as that teeth at high risk of relapse (Shapira

1994, BOS 2013)

4. The use of teeth with severe resorption as abutment teeth should be

reconsidered. Each 3mm of root resorption is equivalent to 1mm of alveolar

bone loss regarding the tooth support (Kalkwarf 1986).

5. In cases of extreme resorption, endodontic treatment may be considered as

well using CaOH

6. Occlusal trauma might lead to further OIIRR, this should be considered and

the occlusion might be relieved.

7. Long term prognosis even in sever resorption is quite good (Levander and

Malmgren 2000).

NB: Ahangari 2010 Cochrne review (they talked about root resorption in

general not specifically in orthodontic) Our explicit search revealed that despite

the relatively high prevalence of this defect, treatment options are generally

case-dependant and there is no high level evidence in this respect. It appears

that the clinician's experience in conjunction with patient's preference would

make up the most suitable therapeutic approach.

Pulp damage

Incidence

1. Pulpitis - 90% get transient pain in the first month

2. Rarely leads to loss of vitalityMohammed Almuzian, University of Glasgow, 2013 30

Aetiology

1. In previously traumatised teeth because trauma causes degenerative change in

the pulp making it unable to sustain orthodontic forces

2. Composite polishing burs/stones

3. Electrothermal debonders - significant hyperaemia

Prevention and managements

Prevention includes:

1. Care when treating previously traumatised/RCT teeth

2. Care needed not to overheat teeth when removing composite at debond

3. Care when using electrothermal debonders,

If loss of vitality developed then:

1. Analgesic like ibuprofen or paracetamol to relief pain.

2. Monitor baseline vitality and repeat 3 mthly. Atack (1999)

3. Use light forces

4. If the tooth develops pulpitis, a pause of treatment for 3 weeks is indicated.

(Bergius, 2002)

Soft-tissue damage

They can be damaged in two ways:

1. Direct damage by removable or fixed components

A. Intra-oral tissues:

Aetiology

1. Mechanical ulceration from

Brackets,

Distal ends,

Long spans,

Displacement of HG whisker


Clumsy instrumentation

2. Chemical bum from etch/SEP

3. Thermal burn — hot instrument, electrothermal debonder

4. Inflammation under the Nance with loss of bone attachment has been

recorded (Singh 2009)

Prevention

1. Turn in hooks

2. Trim or turn in long ends

3. Careful operating

4. Use stopper to prevent wire sliding

5. Bumper sleeving on long spans of archwires, lacebacks

6. Safety straps on HG to keep whisker within HG tube

7. Use of wax as necessary with addition of benzocaine to relive pain

8. Chlorohexidine to reliefe pain of ulceration

B. extra-oral soft tissues:

1. HG induced

A. Eyes: ulcer or opthalmitis

B. Skin

Injuries associated with displacement of HG whisker Samuel & Jones, 1994

Bruising associated from neck strap

Prevention

1. Safety eyeglass during fitting and adjustments

2. Careful adjustments of HG to maintain good fit - not too tight/loose

3. Safety products e.g. NiTom locking facebow, straps,blunt-ended

whiskers, snap release HG

4. Clear instructions given to patient/parents regarding wear and care of HG

(written and verbal)

5. Advise not to play in HG

6. Any problems to discontinue wear and contact orthodontistMohammed Almuzian, University of Glasgow, 2013 32

7. Advice to seek ophthalmic opinion if trauma occurs involving the eye,

however small

2. extra oral burns

Chemical - etchant/SEP

• Physical

3. Infections like

A. Angular cheilitis (Short and Cross 2008)

Angular cheilitis is a multi-factorial disease of infectious origin. Clinically it

is characterized as an eroded and erythematous non-vesicular lesion radiating

from the angle of the mouth which may be unilateral or bilateral in

presentation.

It caused by Candida, Streptococci and Staphylococci,

Predisposing factors

I. Microbiological changes,

II. Haematological deficiencies

III. Loss of vertical dimension in the elderly

IV. Immunocompromised individuals

V. Healthy patients undergoing orthodontic treatment

B. Other record a case of parotitis associated with trauma of the Stenson

duct by FA (Mccarthy 2012)

2. Indirect damage by allergic reactions to nickel and latex

Latex Allergy

Prevalence

1% of population

Individuals susceptible to allergic reactions include

1. Healthcare professional

2. Latex industry worker


3. Patient with multiple previous operation

4. Patient hypersensitive to certain food

5. Individuals with allergic rhinitis, Asthma and eczema;

6. Atopic patient

7. Patients with atypical spina bifida.

How Should Potential Orthodontic Patients with Suspected Latex Allergy

Be Managed?

1. Definitive diagnosis:

Latex allergy can be diagnosed with either

Patch testing

Pin prick testing,

Blood test

2. Appointment and surgery management:

Appointments should be scheduled for the early morning with use of a latex-

screened area to segregate latex-free products to avoid contamination.

3. Appliance design and handling

Latex-free gloves including vinyl.

The use of elastomeric ties could be avoided with use of self-ligating

brackets.

Space closure should be undertaken with nickel– titanium coils.

Where inter-maxillary elastics are required, latex-free elastics can be used,

although they are subject to greater force degradation.

4. Staff training

Staff should be aware of emergency protocols for dealing with anaphylactic

reactions and auxiliary staff should be aware of the diagnosis.


Nickel hypersensitivity

Introduction

Nickel is found in arch wires, bands, brackets and headgear, with

stainless steel containing nickel in the ratio of 18:8, with 8 referring to the

level of nickel.

Delayed (Type IV those related to nickel or latex are typically Type IV

reactions.

It mainly released in the first week after bonding.

Sign and symptom

1. For the gingivae:

Gingivitis in the absence of plaque

Gingival hyperplasia

2. For the tongue:

Burning sensation in the mouth

Metallic taste

Numbness/tingling sensation

Soreness of the side of the tongue

3. For the lip:

Labial swelling

Angular cheilitis

Labial desquamation

4. Extra-oral signs and symptoms can include localised dermatitis in sites of

prolonged skin contact with nickel-containing objects, for example, headgear

studs. This can present as a maculopapular skin rash or vasculitis-like skin

lesions.


Prevalence

1. Nickel hypersensitivity affects around 30% of the population (Nickel

allergy is more common in girls (30%) than in boys (3%) and in

adolescents with pierced ears (31%) than those without ear piercing (2%)

(Bass et al., 1993) . 10 % in female and 3% in male (Nelsen and Menn

1993).

2. It has been suggested that a threshold concentration of approximately 30

ppm of nickel may be sufficient to elicit a cytotoxic response.(O’Rahilly

2003)

3. More serious if contact the skin than mucosa, 5 - 12 times the

concentration of nickel required to provoke mucosal lesions compared

with skin lesions

Treatment

1. Definitive diagnosis:

Patch testing by using a cutaneous sensitivity (patch) test of 5% nickel

sulphate in a petroleum jelly substrate

Pin prick testing,

Blood test (immunoassay)

2. Appliance design and handling

Consideration could be given to use of nickel-free brackets, e.g. ceramic,

gold, titanium or polycarbonate brackets.

The use of nickel– titanium archwires should be avoided where intra-oral

signs of a reaction are noted. These wires may be replaced by fibre-reinforced

composite wires, stainless steel wires with reduced nickel content, titanium

molybdenum alloy or titanium niobium wires.

Rarely, in severe cases, consideration could be given to the use of clear

plastic aligners.

Remove appliance

3. Staff training


Staff should be aware of emergency protocols for dealing with anaphylactic

reactions and auxiliary staff should be aware of the diagnosis.

Cytotoxicity

1. Allergic reactions are composite and acrylic.

2. No-mix adhesives are more toxic than two-paste adhesives.

Treatment failure

It includes:

1. Failure to complete a course of orthodontic treatment

Common (4–23%)

Treatment may fail through:

A. Patient non-complianceIncorrect diagnosis

B. Incorrect management.

2. Relapse

Increasing predisposition to other disorders

1. Temporomandibular : it is better to Record signs and symptoms before

treatment; advise patients seeking joint disorder treatment for such

disorder that there may not be an improvement with orthodontics

2. Periodontal problem: no evidence

3. Psychological – teasing if the treatment was not appropriate

4. Risk to airway: like mandibular set back in short throat cases,

5. Effect on the profile:

The effect of extractions on the facial profile has remained a controversial

issue.

Paquette 1992, 4 extraction has an effect but not significant,

Johnston 93 showed that 4 extractions don’t flatten the face).


However the above evidences are applied on an average patient and are

should be taken in flat or retrusive profile.

Systemic effects

Pain

Why there is a pain associated with orthodontic treatment

1. Orthodontic pain arises from ischemia, inflammation, and edema in the

compressed periodontal ligament.

2. In an inflamed and ischemic periodontal ligament, mediators such as

histamine, bradykinin, prostaglandins, serotonin, and substance P are

released.

3. These mediators irritate the nerve ends of the pain receptors, thus causing

pain.

4. Orthodontic pain usually begins at 2 hours after force application and reaches

its maximum intensity at bed-time or at 24 hours,

5. It lasts approximately 5 to 7 days.

Pain control in orthodontic patients

1. Paracetamol

2. Non-steroidal anti-inflammatory drugs (NSAIDs). Ashley 2012 in a

Cochrane review could not determine whether or not painkillers before

treatment are of benefit in pediatric and orthodontic separator placement

3. Low-level laser therapy,

4. Transcutaneous electrical nerve stimulation,

5. Vibratory stimulation of the periodontal ligament,

6. Chewing gum or biting on a wafer. The mechanism of these methods that

the chewing on the teeth help in restoring the normal vascular and

lymphatic circulation of the periodontal ligament, thus preventing or Mohammed Almuzian, University of Glasgow, 2013 38

relieving inflammation and oedema, and finally relieving pain and

discomfort. Farzanegan 2012.

Bacterial endocarditis

A. Chorhexidine CHX mouthwash should not be given as this has not been

proved to be effective

B. New guidelines advise that antibiotic prophylaxis (ABC) should not be

given to children and adults with structural cardiac defects undergoing

dental intervention procedures. Reasons for changes

1. Regular tooth brushing presents greater risk of IE than a single dental

procedure

2. No consistent association between having dental procedures and Infective

Endocarditis (1E)

3. Clinical effectiveness of antibiotic cover (ABC) not proven

4. Antibiotic cover may cause more deaths through fatal anaphylaxis than

no ABC

5. ABC is not cost effective

C. Advice to patients

Patients should be given clear and consistent information including:

1. Why ABC no longer used

2. Benefits and risks of ABC

3. The importance of maintaining good oral health

4. Information about symptoms of IE and when to seek help

Cross infection

Types

1. Patient to patient

2. Patient to operator


3. Operator to patient

4. Any source to 3rd party

Prevention

1. Medical history

2. Use cross-infection control measures, e.g. safety spectacles, gloves, face-

masks

3. Proper sterilisation/disinfection procedures

4. Hepatitis B vaccination

5. Ultrasonic cleaning of tried-in bands reduces but does not completely

eliminate salivary proteins, there is a need to investigate a more effective

method of cleaning, Benson & Douglas,2007

Reuse of orthodontic materials from BOS

The reuse of orthodontic materials involves several possible problems:

1. Patient’s attitude

Patients and parents may be unhappy at the thought that the appliance in

question is “second-hand”

2. Device performance

It is conceivable that the performance of a particular component may be

affected by reuse. For instance, the mechanical behaviour of a superelastic

archwire could be different

3. Cross-infection control

in the case of bands that have been tried in for size but not actually used, it

was thought that the lumen of any attached tubes might not be adequately

sterilised by autoclaving. Recent evidence suggests that this concern is

unfounded and that previously tried in bands can be adequately sterilised

using a bench top autoclave1.


Radiation

X-ray radiation can damages tissue either directly (stochastic) or to the

genetic tissues.

While the risks are low, with Ireland and McDonald (2003) quoting

figures of 1.8 deaths for every 1 million OPT radiographs taken, it is

essential that this risk is taken into account when taking such films.

The causes of excessive exposure to radiation in orthodontics

Isaacson & Thom, 2001

1. Wrong diagnosis

2. Inappropriate justification

3. Inappropriate radiographs choice.

4. Faulty x-ray set.

5. Wrong speed film.

6. Lack of beam collimation.

7. Problem with processing

BOS guidelines for the management of inhaled or ingested foreign bodies

The operator should obviously take all necessary precautions to prevent

such accidents from occurring.

However, the following guidelines are written to help formulate an action

plan when a patient presents with an inhalation/ingestion episode.

1. Is the object still visible in the mouth or entrance to the oropharynx? If it

is, attempts should be made to remove it by appropriate means, with the

patient reclined. Failing this, the patient should be encouraged to cough

up the object.

2. What has been inhaled or ingested? Is it a bracket, band, archwire or

auxiliary? It is important to know its size, shape, likely flexibility and


radio-opacity. This will not only aid localisation of the object but will

help predict the likely outcome of the incident.

3. How long ago did the episode take place? Was it minutes, hours, days, or

weeks ago? In the absence of any signs or symptoms, then the longer it

has been since the incident the less likely it is the patient will need to be

referred for advice and an x-ray. Late presentation can cause a persistent

cough.

4. If the object is not visible, does the patient have any signs or symptoms

indicating where it is?

A. Inhalation

This may lead to respiratory obstruction and present as coughing, choking

or inspiratory stridor.

It is important to maintain or re-establish the airway.

The patient should remain in the reclined position, and be encouraged to

cough up the object.

If this is not successful and the symptoms persist, immediately summon

help and call for an ambulance.

Fortunately most fixed appliance components are sufficiently small that

upper respiratory tract obstruction is unlikely.

However, an aspirated component, if not coughed up, may pass through

the trachea and into a bronchus.

In such instances it is important the patient is immediately sent to the

local hospital for advice, where they will probably have a chest x-ray in

order to confirm the presence and location of the object.

It will then need to be removed using bronchoscopy. If the object is likely

to be radiolucent, this information must also be provided to the hospital.

B. Ingestion

Following ingestion of an object, the patient may not present with any

immediate signs or symptoms.


However, if it becomes lodged in the oesophagus, it may cause pain or

vomiting and its presence will need to be confirmed.

The patient should be sent to the local hospital for advice and a chest x-

ray.

The object will then need to be removed using fibre-optic endoscopy as a

matter of urgency.

If a foreign body reaches the stomach, it is likely that it will eventually

pass through the gastrointestinal tract.

Management of an ingested foreign body, which is asymptomatic and has

reached the stomach, entails informing the patient of the event, as well as

explaining the likely signs and symptoms should the object not

subsequently pass through the gut. The signs and symptoms include pain

and vomiting.

The risk of perforation or obstruction from the stomach onwards is

related to the size, shape and likely flexibility of the foreign body. If

greater than 5cm in length, it is unlikely to pass through the duodenum.

If it passes the duodenum, the next most likely site of obstruction is the

ileocaecal valve. In any case, obstruction can lead to perforation and

subsequent infection.

Ideally, the stools should be checked by the patient to see if the object has

been passed.

The patient should be referred to the local hospital for advice if the object

is not noted to pass the gut after 6 days.

However, some objects such as orthodontic brackets are very small and

relatively smooth and may well pass through the gut unnoticed, even if

the stools are checked.

If it is certain that the object was ingested and not inhaled, then a follow-

up referral and x-ray is not always required.

5. When should I send the patient to the local hospital?


Referral to the local hospital in each and every case would not only be

impractical, but would lead to patients being exposed to unnecessary radiation

with its associated risks.

However, if you suspect an object may have been inhaled, or it is larger than

5cm in length and has been swallowed, then you should refer the patient to the

Radiology or Accident and Emergency Department of your local hospital for

advice.

Summary of the Royal College of Radiologists Guidelines on recommended

radiographic views 2007

1. Suspected inhalation then chest x-ray.

2. Suspected to be in the pharynx or upper oesophagus then chest x-ray

indicated.

3. If the foreign body is not passed within 6 days then an abdominal x-ray

maybe indicated.

4. Ingested foreign body is sharp or large - abdominal x-ray is indicated for

localisation. Most swallowed foreign bodies that pass the oesophagus will

pass the remainder of the gastrointestinal tract. A chest x-ray will only be

indicated if the abdominal x-ray is negative.


Iatrogenic effect of orthodontic by almuzian

Health & Medicine

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