Background

The purpose of orthodontic treatment is to achieve an improvement in dental occlusion, while at the same time enhancing aesthetic appearance. During orthodontic treatment patients are at heightened risk of dental caries (decay) and gum disease, which if allowed to develop can both jeopardise the success of the treatment and cause permanent damage to the teeth and gums.

The formation of carious lesions and gum disease as a result of orthodontic treatment can be attributed to inadequate elimination of dental bio-film. The oral hygiene challenge associated with fixed appliances are well documented and mainly centre on reduced access to certain areas of the teeth, but less so in the case of aligners where it is the inhibition of saliva function which is as much a threat to good oral health.

To counter these adverse indications it is essential to have a comprehensive understanding of the various risk factors and implement preventive measures which can be undertaken prior to and during orthodontic treatment.

Introduction

As a provider of orthodontic treatment you want the best outcomes in occlusion and dental health for your patients. At Dent-O-Care we are committed to helping practices achieve the highest level of care in terms of prevention of caries and gum problems during treatment. To enhance awareness among members of the clinical team this Best Practice Guide contains an overview of key oral hygiene considerations, before proceeding to consider what constitutes best practice in terms of risk assessment and prevention; from the minimum care standards which should be employed through to the setting up of an advanced care pathway which will help to establish your practice as a centre of orthodontic excellence and help safeguard treatment success.

Caries

Dental caries is the result of bacteria-induced breakdown of the hard tissues of the tooth by progressive local demineralisation.

Etiological factors

Carious lesions are formed under the simultaneous action of several contributory factors; cariogenic bacteria in dental plaque, food, its morphology and a time scale sufficient for the carious lesion to grow.

Cariogenic bacteria

Dental biofilm contains a broad variety of bacteria. Streptococcus mutans is the main micro-organism responsible for human caries. This bacterium uses carbohydrates as a nutrient and energy source, metabolising them to form lactic acid, which lowers pH and thereby causes the demineralisation of tooth enamel. This infectious disorder develops with a prevalence which is related to the degree of oral pathogens present.

Diet

Food plays an essential part in the formation and spread of caries. Cariogenic bacteria can survive in the mouth and proliferate only if there are sufficient fermentable food sugars to meet metabolic requirements in situ. Sucrose is the commonest food carbohydrate. It is naturally present in most fruits and vegetables, but is also deliberately added to many food and beverage products.

Essential etiological food-related factors include the duration of the cariogenic conditions, oral retentiveness and the physical form of the food, the types and concentrations of carbohydrates present, and the patient’s eating habits.

Morphology

Dental anatomy can constitute a host-related risk factor. Deficient dental contact points favour the development of dental plaque and caries. Caries can also start in the pits and crevices of the back teeth, which form irregular areas which even the finest bristles of a toothbrush, cannot easily penetrate.

Saliva

Saliva also plays an important part in the cariogenic process. Its action is essentially cario-protective, through its mechanical “wash-out” action, responsible for eliminating food waste, and through some of its constituents which act on the remineralisation of the enamel, maintain and lubricate the oral tissues. As such any reduction in saliva flow will favour the development of caries.

Like any disease, caries evolves according to the unstable equilibrium between the intensity of the pathological factors cited above and the biological defense response. Caries appears when the balance between demineralisation and remineralisation at the tooth surface is disturbed. Dental caries is a dynamic process with periods of progression alternating with stationary phases. This cariogenic process is generally reversible in its initial stages in favourable conditions, but it is irreversible once it has reached an advanced stage (Charland & Salvail, 2003).

Orthodontic treatment and increased risk of caries

Alongside the usual risk factors for dental caries, orthodontic treatments are also a non-negligible risk factor (Gorton & Featherstone, 2003; Travess et al, 2004). Introducing a fixed appliance or aligner in the mouth favours the build-up of dental plaque, making oral hygiene very difficult, restricting salivary self-cleaning and so creating an environment which favours the onset of caries (Ahn & Kho, 2003; Derks et al, 2007).

An orthodontic appliance placed in an adult or child will alter the oral microsystem significantly. Multiple plaque retention factors will be created overnight, putting the patient in a high risk group for caries and for adult patients a high risk group for periodontal inflammation.

The teeth most vulnerable to demineralisation are the maxillary incisors and the first permanent molars. The three locations most at risk of demineralisation are: the cervical areas, the areas located under the bands and the enamel adjacent to cemented brackets (O’Reilly & Featherstone, 1987; Jordan & LeBlanc, 2002).

White spots or initial lesions of the enamel are present in 25–30% of patients who are following an orthodontic treatment plan (Jordan, 1998). White spot lesions can be reversed with care but are best avoided by taking preventive measures.

Prevention of caries & gum disease

Due to the heightened risks associated with orthodontic treatment we recommend that a preventive, prophylactic approach should be implemented before, during and after the orthodontic treatment.

References

  • Ahn, S.J. & Kho, H.S. Adhesion of oral streptococci to experimental bracket pellicules from glandular saliva. Am. J. Orthod. Dentofacial. Orthop.; 2003; Vol 124, n°2: 198-203.
  • Derks, A.; Katsaros, C.; Frencken, M.A. & Kuijpers-Jagtman, A.M. Caries-inhibiting effect of preventive measures during orthodontic treatment with fixed appliances; a systematic review. Caries Res. 2004; Vol 38, n°5: 413-420.
  • Gorton, J. & Featherstone, J.D.B.In vivo inhibition of demineralization around orthodontic brackets. Am. J. Orthod. Dentofacial Orthop. 2003; Vol 123, n°1: 10-14.
  • Jordan, C.N. Prevention of white spot enamel formation during orthodontic treatment. Gen. Dent. Sep-Oct 1998:498-502.
  • Jordan, C. & LeBlanc, D.J. Influences of orthodontic appliances on oral populations of mutans streptococci. Oral Microb. Immun. 2002; 17(2): 369-447.
  • O’Reilly, M.M. & Featherstone, J.D. Demineralization and remineralisation around orthodontic appliances: an in vivo study. Am. J. Orthod. Dentofacial Orthop.1987; Vol 92, n°1: 33-40.
  • Travess, H., Roberts-Harry, D. & Sandy J. Orthodontics. Part 6: Risks in orthodontic treatment. Br. Dent. J.2004; Jan 24; Vol 196, n°2: 71-77.