Key topics

• White spot lesion
• Root resorption
• Gingivitis and loss of marginal bone support
• Bone dehiscence
• Allergic reactions
• Pain and injuries of appliance
• Risk of temporomandibular disorder (TMD)

Learning objectives

• To understand how to avoid white spot lesions
• To be able to describe risk factors in apical root resorption
• To understand and describe orthodontic tooth movements in labial/buccal direction as a risk factor to bone dehiscence
• To understand problems with orthodontics in Nickel-sensitive individuals
• To describe possible risk-factors for TMD in orthodontic patients

Introduction

Many studies have, despite insufficient scientific evidence, emphasised the need for orthodontic treatment due to unfavourable consequences of several malocclusions such as crowding (predisposition to gingivitis), functional crossbites (risk of developing of temporomandibular dysfunction), open bite (deficient chewing capacity), proclined maxillary incisors (risk of traumatic injuries), and impacted teeth (risk of root resorption). On the other hand, an orthodontic treatment may in some cases initiate some adverse effects, and clinical studies have from time to time reported that orthodontic treatment may cause damage to the teeth and their supporting tissues. This chapter aims to point out some possible adverse tissue reactions to avoid complications in the orthodontic clinic.

Damage to teeth

White spot lesions

It is generally regarded that treatment with fixed orthodontic appliances can cause enamel demineralization adjacent to the brackets, because of accumulation of aciduric and acidogenic bacteria (Chapman et al., 2010). This enamel demineralization, called white spot lesions (WSL), is an unwanted clinical problem with a reported prevalence of 15 to 85% (Chapman et al., 2010; Sonesson et al., 2014). The WSL have limited ability to improve after fixed appliance removal and therefore the final esthetical result may be jeopardized (Figure 11.1). There exists various strategies to prevent WSL during treatment and evidence is found that fluoride varnishes, gels and high-fluoride tooth paste or fluoride-containing bonding materials could be fluoride supplement alternatives to reduce the incidence and severity of WSL adjacent to bracket and bands (Derks et al., 2004; Sonesson et al., 2014).

Since food debris and plaque are risk factors for WSL and gingivitis, it is very important to apply a suitable hygiene programme with topical fluoride administration for every individual patient. To learn from this is: Do not start an orthodontic treatment until the patient can understand and practise plaque control.

Pulpal reaction

When removing the bond material left at the enamel surfaces after debonding, there is a risk that increased temperature will result in pulp damage (Vukovich et al., 1991). Thus, the use of water-cooling is especially important in this procedure. Orthodontic extrusion and intrusion have been associated with vascular changes and pulpal oedema in adult patients. Those rare disturbances seem to be more severe when greater forces are applied for a longer time.

Root resorption

Root resorption continuous to be one of the most frequent lesion, associated with orthodontic treatment (Kurol et al., 1996; Weltman et al., 2010; Lund et al., 2012). There are two types of root resorption: one appears as small superficial resorptions, associated with the hyaline zone, and undergoes repair, while the other is localised at the apex of the root and leads to shortening of the root.

Resorption at tooth surface

By electron microscopy, Kvam (1972) demonstrated resorption defects in the periphery of the hyalinised zone (Figure 11.2). A side effect of the cellular activity during removal of the necrotic hyalinised tissue is that the cementoid layer of the root is left with a raw unprotected surface, which is attacked by resorptive cells that resemble the osteoclast in structural and functional aspects (Brudvik and Rygh, 1994). Root resorption then occurs around this cell-free tissue, starting at the border of the hyalinised zone. The first sign of root resorption (initial phase) is a penetration of cells from the periphery of the necrotic tissue where mononucleated fibroblast-like cells, stained negatively by tartrate-resistant acid and phosphatase (TRAP), start to attack the precementum/cementum surface. Root resorption beneath the main hyalinised zone occurs in a later phase, during which multinucleated TRAP-positive cells are involved in removing the main mass of necrotic PDL tissue and in resorbing the outer layer of the root cementum, opposite to the TRAP-negative cells that are involved, even in the resorption of the bone surface. Those results support the statement by Tanaka et al. (1990), where separate clast cells are resorbing bone and tooth structures simultaneously.

When the orthodontic force has terminated, repair starts with a synthesis of collagen fibres by fibroblast/cementoblast-like cells, and new cementum is deposited on the root surface simultaneously with re-establishment of the new PDL. However, resorption continues in the area where hyalinised tissue persists, even after active force had terminated (Brudvik and Rygh, 1995). For the clinician, it is important to know that minor resorption lacunae can be repaired during periods of no force or possibly during periods of extremely low force application.

Resorption at tooth apex

Apical root resorption (Figure 11.3) is a multifactorial problem and a serious complication in orthodontic treatment. It is known that root resorption is the result of cell activity, and the osteoclast is the inevitable cell during tooth movement, but the biological factors triggering the process are not yet fully understood. However, the decisive factors for developing root resorption appear to be controlled primarily by the pulp status and the extent of injury to the innermost cells in the periodontal ligament (PDL). Teeth in a formative stage display less root resorption during orthodontic tooth movement.

Ketcham (1929) was first to report on apical root resorption in vital permanent teeth, and he found that the maxillary incisors are more frequently involved than other teeth, a statement verified by many later clinical studies. Tendency to resorption is greater in teeth with invagination and pipette-shaped roots (Levander and Malmgren, 1988) and in dentitions with agenesis (Kjaer, 1995). Trauma to maxillary incisors before orthodontic treatment is a factor strongly associated with resorption during treatment.

Most findings indicate that orthodontic forces in terms of magnitude, direction and duration are important for an understanding of the resorptive process; the duration of the force is more critical than the magnitude. Furthermore, correction of overjet and intrusion of teeth are significantly correlated to apical root resorption. The type of the orthodontic appliance thus appears to be of importance.

Although the cause and mechanism remain unknown, it is known that there are high-risk teeth and certain types of patients who are particularly susceptible. The degree of root resorption is usually less than 2 mm, but can be more extensive in some cases.

Although radiographs do not disclose root resorption at an early stage of the orthodontic treatment, X-ray inspection of orthodontic patients is recommended. The first inspection should take place during the treatment, as root resorption proceeds very rapidly in some patients, and continued controls thus are of importance.

Damage to tooth-supporting tissues

Gingival inflammation caused by bacterial plaque at the gingival margin (Figure 11.4) is characterised by great plaque index, bleeding tendency and pocket depth, and has been observed more frequently in molars with orthodontic bands than in bonded ones (Boyd and Baumrind, 1992). A highly probably explanation for these differences is the difficulty in plaque removal on the gingival margin of the bands. An alternative explanation for at least part of the attachment loss is the mechanical injury caused by the placement of the bands too deep into the gingival pocket.

Gingival recession, i.e. displacement of the soft tissue margin apical to the cement-enamel junction (CEJ) with exposure of the root surface can be observed in combination with orthodontic treatment, especially with alignment and proclination of crowded incisors (Figure 11.5). An experimental study in the monkey could demonstrate that the apical displacement of the gingival margin was a result of a reduced soft tissue thickness of the free gingiva (Wennström et al., 1987). The volume of the covering soft tissue should be considered as a factor that may develop gingival retraction during or after active orthodontic treatment. Thus, the tooth should be moved within the envelope of the alveolar process by a light force, and with bone, not through bone.