April, 2011

Orthodontic Scars

Dr. Deepa Verma⁺

Dr. Stutee Bali Grewal⁺⁺

Dr. Priyanka Sethi Kumar⁺⁺⁺

Dr. Bhavna Singh⁺⁺⁺⁺

+  BDS, MDS, Professor
Department of Orthodontics & Dentofacial Orthopedics
Santosh Dental College & Hospital
1 Santosh Naga, Pratap Vihar
Ghaziabad – 201009
U.P, India                                      

++  BDS, MDS, DNB, Professor
Department of Orthodontics & Dentofacial Orthopedics
Santosh Dental College & Hospital
1 Santosh Nagar, Pratap Vihar
Ghaziabad – 201009
U.P, India                                        

+++  BDS, MDS, Senior Lecturer
Department of Orthodontics & Dentofacial Orthopedics
Santosh Dental College & Hospital
1 Santosh Nagar, Pratap Vihar
Ghaziabad – 201009
U.P, India                                                                                                                            

++++  BDS, (MDS), Post graduate student – (Corresponding author)
Department of Orthodontics & Dentofacial Orthopedics
Santosh Dental College & Hospital
1 Santosh Nagar, Pratap Vihar
Ghaziabad – 201009
U.P, India                                        

 

Address for Correspondence:

Bhavna Singh BDS (MDS)
Post graduate student                                                                                                                                                                                                   Department of Orthodontics & Dentofacial Orthopedics
Santosh Dental College & Hospital
1 Santosh Nagar, Pratap Vihar
Ghaziabad – 201009
U.P, India                                                                                                                             E-mail: sweet.bhavnasingh@gmail.com

Phone: +919415140478

ABSTRACT

All forms of treatment, medical and dental (including orthodontics), have potential risks and limitations. Fortunately, in orthodontics, risks are infrequent and when they do occur, they are usually of minor consequence. Nevertheless, all potential risks and limitations should be considered when making the decision to undergo orthodontic treatment. Orthodontic treatment could carry with it the risk of various types of tissue damage (e.g.: decalcification, lacerations etc), an increased predisposition to dental disorders (e.g.: temporomandibular joint disorders and periodontal diseases) and treatment failure. If correcting a malocclusion is to be of benefit, the advantages offered should outweigh any possible damage. It is important to implement risk control procedures during and after orthodontic treatment. Clinicians should be vigilant in assessing and monitoring every aspect and stage of the patient’s orthodontic treatment to achieve an uneventful, secure, and successful final result.

INTRODUCTION

Crowded, irregular and protruding teeth have been a problem for some individuals since antiquity. Although orthodontic treatment has recognized benefits of significantly improving mastication, speech, appearance, overall dental health, comfort and self-esteem of the patient yet, sometimes orthodontic appliances can cause harm. Like many other medical/dental interventions, it is not free of certain inherent risks.¹ Some patients may be more at risk than others; they need to be identified early and managed appropriately to avoid adverse sequelae.

Orthodontics has the potential to cause significant damage to hard and soft tissues. Treatment can be associated with considerable discomfort, particularly immediately after appliance adjustment. This discomfort tends to be poorly perceived by clinicians, at times, as it takes place at a distance from the clinical setting. Orthodontic scars which may present during and after treatment, however, are seldom severe or frequent enough to offset the advantages of treatment. Nevertheless, they should be considered and addressed in order to achieve successful results.²

Orthodontic scars can be broadly classified as:

Sl no.	Orthodontic Scar
1.	Lesions of Enamel	a)     Enamel decalcification / White spot lesions  b)     Physical damages on enamel (Enamel Wear / Enamel Fractures)
2.	Periodontal tissues	a)     Gingivitis / Gingival enlargement  b)     Gingival recession c)      Dark Triangles
3.	Soft tissue damage	a)     Direct damage by removable/fixed appliances and their component parts:  i.            Impingements (E.g.:- Lingual arch, TPA, Loops, Archwires, brackets, bands etc) ii.            Lacerations (E.g.:- brackets, molar tubes, ligature ties etc) iii.            Ulcerations (E.g.:- brackets, molar tubes, ligature ties etc) iv.            Injury to eyes (E.g.: Headgears, Face-bow injury) b)     Indirect damage by allergic reactions to either:- i.            Nickel or ii.            Latex c)      Soft tissue complications related to Implants i.            Primary mobility ii.            Ulceration of overlying soft tissue iii.            Periimplantitis iv.            Delayed mobility and Failure v.            Fracture during removal

1. Enamel Decalcification / White Opaque Lesions

White opaque lesions around orthodontic attachments (Figure 1) are a common problem during and following fixed orthodontic treatment.³ Plaque accumulation promoted by appliance components and bonding materials results in subsequent acid production by the bacterial plaque.^1-3 This causes demineralization and an alteration in the appearance of the enamel surface. Early lesions appear as opaque, white spots⁴ which may progress to a frank caries if mineral loss continues.^5,6 Clinically, they can be detected as early as 4 weeks into treatment⁷ and their prevalence among orthodontic patients ranges from 2-96%.^7-9 The labio-gingival area of the lateral incisors is the most common site and the maxillary posterior segments are the least common site for their formation.¹⁰ Their incidence is usually more among male patients due to poorer oral hygiene standards than females.^8,11

 

The most important means of preventing demineralization is to ensure that the patient’s oral hygiene is of a high standard throughout treatment. Fluoride is a well established anti-cariogenic agent. It works by calcium fluoride formation which inhibits or limits the size of the lesion and enhances enamel remineralization following treatment. Several methods of applying fluoride have been used during orthodontic treatment to minimize the risk of demineralization. Topical fluoride applications like 0.05% sodium fluoride¹², 1.2% acidulated phosphate fluoride mouthrinse (weekly)¹³, 0.4% stannous fluoride gel¹⁴ and fluoride varnish¹⁵ can be used. However, each requires adequate compliance from the patient to work. For non-compliant patients, fluoride containing cements/bonding agents^16-19 and fluoride releasing elastomeric ligatures^20,21 can be used.

2. Physical damages on enamel (Enamel Wear / Enamel Fractures)

Enamel damage most commonly results from occlusal/incisal contact with orthodontic brackets; being worst with ceramic, metal, and composite brackets (in that order). The frequently affected areas are – incisal edge of the upper anterior teeth²², buccal cusps of upper posterior teeth and upper canine tips during retraction. Careless use of an orthodontic band seater or band remover can also result in enamel fracture. Care is required especially when large restorations are present, since these can result in fracture of unsupported cusps²³. Debonding can also result in enamel fracture, both with metal and ceramic brackets.^24,25 Such cracks provide stagnation areas for the development of caries, can cause partial tooth fracture, or may discolour.²⁶ Zachrisson et al.²⁶ found that the prevalence of pronounced cracks in relation to the total number of cracks was 6% for debonded/banded teeth and 4% for untreated teeth. There were appreciably more cracks with chemically bonded ceramic brackets.²⁷

In order to avoid all forms of enamel damage, all carious lesions are dealt with before active orthodontic treatment starts. Extreme care is needed when placing appliances, to avoid direct contact between the orthodontic brackets and the opposing teeth. When contact between orthodontic bracket and the tooth is unavoidable, then adjacent teeth should properly share the occlusal loading.²² A night guard is sometimes required for patients who grind their teeth at night. Care must always be taken while removing brackets and residual bonding agents so as to minimize the risk of enamel fracture²⁴. Appropriate dietary advice should be given to minimize tooth substance loss. It was believed that since carbonated drinks and pure juices are the most common causes of erosion, they should be avoided in patients with fixed appliances.²⁸ However, recent research has not supported the same.

3. Periodontal tissues

a) Gingivitis / Gingival enlargement

Following placement of a fixed appliance there is gingival inflammation in almost all orthodontic patients (Figure 2). Usually it is transient and does not lead to attachment loss.^29-31 The interproximal areas are usually more affected than the facial areas, and posterior teeth more than anterior teeth. Gingival hyperplasia can be a problem around orthodontic bands, leading to pseudo-pocketing and giving the illusion of attachment loss; however, this usually resolves within weeks of debanding.³² Adult patients may be at higher risk of periodontal problems, particularly those who seek orthodontic treatment because of pre-existing periodontal disease.

 

Three-monthly periodontal checks and routine scaling and polishing are advisable.³¹ Treatment mechanics should be modified for these patients by keeping the forces light in view of the shortened root support. Patients who require particular attention are those with systemic diseases such as diabetes or epilepsy, particularly poorly controlled diabetics and the epileptics whose seizures are controlled by phenytoin based drugs, which can cause gingival hyperplasia.

b) Gingival recession

Studies have shown that alveolar bone loss and gingival recession occurs more often in orthodontic patients than in normal subjects, the difference being small but significant.^33,34 Bands induce more gingival inflammation than bonds, since they are more plaque retentive and their margins are often placed subgingivally. Gingival recession and loss of alveolar bone have been reported as a result of teeth moving in the presence of inflammation.³⁵ Labial movement of mandibular incisors may also result in gingival recession (Figure 3).

 

c) Dark Triangles

Dark triangles may be seen as an unaesthetic open gingival embrasure during the course of orthodontic treatment due to the following two reasons³⁷:-

(i)     Loss of attachment due to periodontal disease which has an increased probability on account of difficulty with oral hygiene maintenance owing to the various orthodontic attachments.

(ii)   When crowded and rotated anterior teeth are corrected orthodontically, (especially in adults) the connector moves incisally leading to the appearance of black triangles.

Thus, adequate oral hygiene maintenance should be advised and monitored throughout the treatment to avoid any attachment loss. If such unaesthetic areas do appear, they can be treated most readily by removing enamel at the contact point so that the teeth can be moved closer together. Moving the connector point apically eliminates most if not all of the space. However, care should be taken not to distort the proportional relationships of the teeth to each other and, if possible, the progression of connector heights should be maintained. Both, actual and potential black triangles should be noted during examination and the patient should be prepared for reshaping the teeth later to minimize the esthetic problem.

4. Soft-tissue damage

Intra-oral and extra-oral soft tissues can be damaged in the following ways:

• Direct damage by removable or fixed components
• Indirect damage by allergic reactions to nickel and latex
• Soft tissue complications due to implants

 

A) Direct damage by removable or fixed components

(i) Removable appliances

Removable appliances are used mainly in the form of retainers at the end of fixed orthodontic treatment or for the management of minor orthodontic problems which require a simple tipping type of tooth movement. They carry with them the risk of allergy to acrylic component and tissue impingement by sharp edges and wire components (retentive clasps, springs, canine retractors etc.). Allergy and toxicity may occur due to the unpolymerized material of acrylic resin and is the greatest immediately following polymerization, although cytotoxicity may still be seen 2 years after polymerization.^35,38

Undercuts should be blocked out prior to acrylisation and sharp edges of the appliance should be carefully rounded-off to avoid trauma during insertion and removal of the appliance. Patients should be recalled a few days after appliance delivery to check for any tissue impingement.

(ii) Fixed appliance and its components parts

Archwire, Brackets, Bands etc.

Lacerations/Ulcerations to the gingiva and oral mucosa may often occur in the initial phase of treatment as the patient gets accustomed to fixed appliances, during treatment or between sessions due to rubbing of the lips and cheeks on the archwire, brackets (Figure 4), bands and cleats, especially where long unsupported stretches of wire rest against the lips.¹ Excessive muscular activities of the cheek or tongue act as triggers. Loose or broken appliances or blows to the mouth may also be a potential cause of injury.

Though the oral tissues quickly keratinize and “toughen up” to a new appliance, the use of dental wax over the bracket and rubber tubing on the unsupported archwire may reduce trauma and discomfort.²

Trans-Palatal Arch / Lingual Arch

Occasionally the trans-palatal arch or a lingual arch may cause trauma to the palate, lingual mucosa or tongue if adequate soft tissue clearance is not provided during their fabrication and placement.

Headgear

Headgear can cause injury if it is displaced either during sleep or rough play. The inner arch of the facebow is not only sharp but also rich in oral microorganisms. A penetrating eye injury may not cause immediate pain, but the oral bacteria may invade and proliferate rapidly even through a small abrasion. There is a risk of damage and infection of the eye. These eye infections are usually very hard to manage and the eye can be lost due to an overwhelming infection.³⁹

Samuels and Jones⁴⁰ classified the types of headgear injuries as follows:

• Accidental disengagement when playing (27% of all headgear injuries);

• Incorrect handling (27% of all headgear injuries);

• Disengagement by another child (19% of all headgear injuries); and

• Disengagement while asleep (27% of all headgear injuries).

To minimize the risk of injury, headgears now have safety features which stop them from being accidentally displaced or recoiling back into the face or the eyes. The use of safety bows, rigid neck straps, and snap release products are mandatory to prevent the bow from disengaging from the molar tubes or acting as projectiles. They should not to be worn while playing and the headgear strap should always be removed before the face-bow is disengaged.⁴⁰ Patients should be given both verbal and written safety instructions after fitting the headgear.⁴⁰

Loops, Utility arches

These are often used during orthodontic treatment for space closure, space maintainance or intrusion. Utmost care must be taken during their fabrication as they extend into the vestibular area and are prone to tissue impingement.(Figure 5) Even minor amounts of continuous tissue impingement, if disregarded, may lead to more serious problems like ulceration or tissue hyperplasia around the loop. In extreme situations, the loop may become completely embedded in the hyperplastic tissue requiring surgical excision for removal. Thus, careful fabrication and regular monitoring are essential to avoid such unwanted complications. Long and unsupported horizontal segments of utility arches may be covered with rubber tubing (Figure 6) to avoid tissue impingement and patient discomfort.

B) Indirect damage by allergic reactions to either nickel or latex.

(i) Nickel allergy

Nickel hypersensitivity affects three in ten of the general population⁴¹. Nickel is found in orthodontic wires, bands, brackets and headgears. Patients become nickel sensitive due to previous contact with jewelery, glasses and watches⁴¹. Females are more susceptible, perhaps due to ear piercing. Intra-oral signs and symptoms of nickel hypersensitivity are rare because the concentrations of nickel necessary to provoke a reaction in the mouth are higher than those needed on the skin.⁴² Intra-oral signs are highly variable and difficult to diagnose. These include loss of taste or metallic taste, numbness, burning sensation, soreness at the side of the tongue, angular cheilitis (Figure 7) and erythematous areas or severe gingivitis in the absence of plaque.⁴³ Since such signs and symptoms are difficult to identify, nickel allergy in response to orthodontic appliances may be under-diagnosed.

For sensitive patients, exposed metalwork should be covered with tape or headgear use should be discontinued.

(ii) Latex allergy

Latex sensitivity may occur in response to contact with latex gloves, elastomeric ligatures or intra- and extra-oral elastics. The commonest sites affected are the gingivae and tongue, (Figure 8) but the perioral region can also be affected.⁴⁴ Natural rubber latex sensitivity is associated with atopy, reflecting a predisposition to producing IgE antibodies. The main types of reaction to natural rubber latex (NRL) are irritant contact dermatitis, allergic contact dermatitis and NRL allergy. The prevalence of NRL allergy has been reported as being less than 1% in the general population and 5–15% in health care workers.⁴⁵ A standard medical history usually identifies patients with confirmed NRL allergy. Hypersensitivity to certain foods such as avocados, potatoes, bananas, tomatoes, chestnuts, kiwi fruit and papaya are associated with NRL allergy.⁴⁶

In latex sensitive patients, steel ligatures or self-ligating brackets may be used. The treatment plan might need to be modified, avoiding Class II or Class III traction using elastics.²

C) SOFT TISSUE COMPLICATIONS RELATED TO IMPLANTS

The introduction of microimplants to orthodontics as an excellent source of skeletal anchorage, has led to their extensive use in various critical anchorage situations. Their simple design and ease in implantation makes them comfortable for the patients. However, they are not free from potential problems and soft tissue complications.

The following type of complications can occur with mini-screws:

a) Inadequate primary Stability

The primary stability of a mini-implant is poor in cases where the cortex is thinner than 0.5mm and the density of the trabecular bone is low. It can also occur due to an over-drilled hole (more than the diameter of the miniscrew) or excessive trauma during placement.

b) Ulceration / trauma to soft tissue overlying the implant

The implant head can be covered with a layer of composite (Figure 9) or the patient can be instructed to keep the implant surface covered with a piece of wet cotton to avoid trauma and subsequent ulceration.

 

c) Peri-implantitis

Inflammation of gingival tissue around the implant can occur if adequate oral hygiene is not maintained by the patient (Figure 10). Patients should be motivated and instructed to maintain high level of oral hygiene throughout treatment. 0.2% chlorhexidene mouthwash can also be prescribed.

d) Delayed mobility

The optimum force that a miniscrew can withstand is 50N – 450N.⁴⁷ Delayed mobility and failure can occur because of Implant overloading beyond 450N. Such screw should be removed and replaced

e) Screw fracture during removal

Lateral forces during removal can cause fracture. It is rare if taken out straight. If the microimplant is left for a very long time, this also could lead to fracture on removal as a result of partial or full osseointegration.

Implant failure (mobility / fracture) can occur due to screw, operator and/or patient related factors:

Ø      Screw-Related Problems⁴⁸

A screw can fracture if it is too narrow or the neck area is not strong enough to withstand the stress of removal. The solution is to choose a conical screw with a solid neck and a diameter appropriate to the quality of bone.

Ø      Operator-Related Problems⁴⁸

Application of excessive pressure during insertion of a self-drilling screw can fracture the tip of the screw. It is important not to wiggle the screwdriver when removing it from the screw head. The screwdriver will not stick if the long extension is removed before the part surrounding the screw touches the mucosa. Excessive heat generation during pre-insertion drilling can lead to local necrosis of bone and subsequent failure

Ø      Patient-Related Problems⁴⁸

In patients with thick mucosa, the distance between the point of force application and the centre of resistance of the screw will be greater than usual, thus generating a large moment when a force is applied. Loosening can occur, even after primary stability has been achieved, if considerable bone remodelling has occurred because of either the resorption of a deciduous tooth or post-extraction healing. Mini-implants are contraindicated in patients with systemic alterations in the bone metabolism due to disease, medication, or heavy smoking.

 

REFRENCES

1.      Paul Yun-Wah Lau, Ricky Wing-Kit Wong. Risks And Complications In Orthodontic Treatment. Hong Kong Dental Journal 2006;3:15-22.

2.      Pamela E. Ellis And Philip E. Benson. Potential Hazards Of Orthodontic Treatment – What Your Patient Should Know. Dental Update;December 2002:493-97.

3.      O’Reilly MM, Featherstone JD. Demineralization and remineralization around orthodontic appliances: An in vivo study. Am J Orthod Dentofac Orthop 1987; 92: 33-40.

4.      Øgaard B, Rolla G, Arends J. Orthodontic appliances and enamel demineralization. Part-1. Lesion development. Am J Orthod Dentofac Orthop 1988;94:68-73.

5.      Arends J, Christoffsen J. The nature of early caries lesions in enamel. J Dent Res 1986;65:2-11.

6.      Zachrisson BU, Zachrisson S. Caries incidence and orthodontic treatment with fixed appliances. Scand J Dent Res 1971;79:183-192.

7.      Mizrahi E. Enamel demineralization following orthodontic treatment. Am J Orthod 1982;82:62-67.

8.      Gorelick L, Geiger AM, Gwinnett AJ. Incidence of white spot formation after bonding and banding. Am J Orthod 1982;81:93-98.

9.      Mitchell L. Decalcification during orthodontic treatment with fixed appliances- an overview. Br J Orthod 1992;19:199-205.

10. O’Reilly MM, Featherstone JDB. Decalcification and remineralization around orthodontic appliances: an in vivo study. J Dent Res 1985;64:301.

11.  Zachrisson BU, Zachrisson S. Caries incidence and oral hygiene during orthodontic treatment. Scand J Dent Res 1971;79:394-401.

12. Geiger AM, Gorelick L, Gwinnett AJ, Benson BJ. Reducing white spot lesions in orthodontic populations with fluoride rinsing. Am J Orthod Dentofac Orthop 1992;101:403–407.

13.  Boyd RL. Comparison of three self-applied topical fluoride preparations for control of decalcification. Angle Orthod 1993;63:25–30.

14. Boyd RL. Long-term evaluation of a SnF2 gel for control of gingivitis and decalcification in adolescent orthodontic patients. Int Dent J 1994;44:119–130.

15. Buyukyilmaz T, Tangugsorn V, Ogaard B, Arends J, Ruben J, Rolla G. The effect of titanium tetrafluoride (TiF4) application around orthodontic brackets. Am J Orthod Dentofac Orthop 1994;105:293–296.

16. Statemann MW, Shannon IL. Control of decalcification in orthodontic patients by daily self-administered application of a water free 0.4% stannous fluoride gel. Am J Orthod 1974;66:273-279.

17. Shannon IL, West D. Prevention of decalcification in orthodontic patients by daily self-treatment with 0.4% gel. Ped Dent 1979;1:101-103.

18. Kaswiner LM. Hard and soft tissue damage accompanying orthodontic therapy. Clin Prev Dent 1981;3:9-13.

19. Adriaens ML, Dermaut LR, Verbeeck MH. The use of Fluor Protector, a fluoride vernish, as a caries prevention method under orthodontic molar bands. Eur J Orthod 1990;12:316-319.

20. Banks PA, Chadwick SM, Asher-McDade C, Wright JL. Fluoride-releasing elastomerics – a prospective controlled clinical trial. Eur J Orthod 2000;22:401–407.

21. Mattick CR, Mitchell L, Chadwick SM, Wright J. Fluoride-releasing elastomeric modules reduce decalcification: a randomized controlled trial. J Orthod 2001;28:217–219.

22. Swartz ML. Ceramic brackets. J Clin Orthod 1988;22:82-8.

23. McGuinness N. Prevention in orthodontics—a review. Dent Update 1992;19:168-70,172-75.

24.  Meister RE. Comparison of enamel detachments after debonding between Uniteck’s dynalok bracket and a foil mesh bracket: a scanning electron microscope study. Am J Orthod 1985;88:266-73.

25. Jones M. Enamel loss on bond removal. Br J Orthod 1980;7:39-44.

26. Zachrisson BU, Skogan O, Hoymyhr S. Enamel cracks in debonded, debanded, and orthodontically untreated teeth. Am J Orthod 1980;77:307–319.

27. Artun J. A post-treatment evaluation of multibonded ceramic brackets in orthodontics. Eur J Orthod 1997;19:219–228.

28. Travess H, Roberts-Harry D, Sandy J. Orthodontics. Part 6: Risks in orthodontic treatment. Br Dent J 2004;196:71-77.

29. Alstad S, Zachrisson BU. Longitudinal study of periodontal condition associated with orthodontic treatment in adolescents. Am J Orthod Dentofac Orthop 1979;76:277–286.

30. Sadowsky C, BeGole EA. Long-term effects of orthodontic treatment on periodontal health. Am J Orthod 1981;80:156–172.

31. Polson AM, Subtelny JD, Meitner SW, et al. Longterm periodontal status after orthodontic treatment. Am J Orthod Dentofac Orthop 1988;93:51–58.

32. Zachrisson BU. Cause and prevention of injuries to teeth and supporting structures during orthodontic treatment. Am J Orthod 1976;69:285–300.

33. Alstad S, Zachrisson BU. Longitudinal study of periodontal condition associated with orthodontic treatment in adolescents. Am J Orthod 1979;76:277-86.

34.  Zachrisson BU, Alnaes L. Periodontal condition in orthodontically treated and untreated individuals. II. Alveolar bone loss: radiographic findings. Angle Orthod 1974;44:48-55.

35. Vanarsdall RL. Complications of orthodontic treatment. Curr Opin Dent 1991;1:622-33.

36. McComb JL. Orthodontic treatment and isolated gingival recession: a review. Br J Orthod 1994;21:151–159.

37. W. R. Proffit, H. W. Fields, D. M. Sarver. Contemporary orthodontics. 4^th ed; Mosby.

38. Tell RT, Sydiskis RJ, Isaacs RD, Davidson WM. Long-term cytotoxicity of orthodontic direct bonding adhesives. Am J Orthod Dentofac Orthop 1988;93:419–422.

39. Booth-Mason S, Birnie D. Penetrating eye injury from orthodontic headgear – a case report. Eur J Orthod 1988;10:111–114.

40. Samuels RH, Jones ML. Orthodontic facebow injuries and safety equipment. Eur J Orthod 1994;16:385-94.

41. Bass JK, Fine H, Cisneros GJ. Nickel hypersensitivity in the orthodontic patient. Am J Orthod Dentofac Orthop 1993;103:280–285.

42. Magnusson B, Bergman M, Bergman B, Soremark R. Nickel allergy and nickel-containing dental alloys. Scand J Dent Res 1982;90:163–167.

43. Dunlap CL, Vincent SK, Barker BF. Allergic reaction to orthodontic wire: report of case. J Am Dent Assoc 1989;118:449–450.

44. Jacobsen N, Hensten-Pettersen A. Changes in occupational health problems and adverse patient reactions in orthodontics from 1987 to 2000. Eur J Orthod 2003; 25: 591–98.

45. Poley GE Jr, Slater JE. Latex allergy. J Allergy Clin Immunol 2000; 105(6): 1054–62.

46. Cullinan P, Brown R, Field A, et al. Latex allergy. A position paper of the British Society of Allergy and Clinical Immunology. Clin Exp Allergy 2003; 33: 1484–99.

47. Park HS, Bae SM, Kyung HM, Sungh JH. Micro-implant anchorage for treatment of skeletal Class I bialveolar protrusion. J Clin Orthod 2001;35:417-22.

48. Brite Melson. OVERVIEW Mini-Implants: Where Are We? JCO 2005;39,09:539–547.