Dr. Cecil C. Steiner asked in the context of bone loss and tooth movement “Do we really want to know what we are doing to our patients or are we afraid to find out?” 1959. The premise of his question was the relationship between orthodontics and bony defects. In the previous blog we discussed the relation between extraction in orthodontic treatment and the associated effect to the facial profile, in this blog we will look the extraction decision and the effect on the alveolar housing, with a focus on bone loss and recession.
Orthodontic tooth movement in the cancellous or medullary bone is the favoured playground for tooth movement, with carousels of bone deposition and resorption occurring in a rich environment of blood supply and cellular / acellular ratio. However, when a tooth approaches the cortical plate, there is a darker twist . The relatively avascular cortical plate and unfavourable cellular / acellular ratio results in resorption without deposition, i.e. bone loss.
As the tooth moves towards the cortical plate a cascade of events take place to the periodontium: Thinning of the alveolar bone occurs first, the cortical plate is triangular when viewed laterally, the thinnest aspect (cervical bone) undergoes resorption and consequently there is vertical bone loss occurs. Due to the loss of vertical bony support the attached and free gingival fibres also head south and recede to maintain the distance with the new position of the cervical bone. The finale, the gingival fibres thin. The overall effect of thinning and vertical loss of both bone and soft tissue Dersot 2012.
There are 3 types of bony defects, of which dehiscence and fenestration have been associated with orthodontic tooth movement:
A series of papers have investigated the effects of non-extraction treatment on the soft and hard tissues. More recently CBCT studies have shed light on the topic. One study showed an average of 1.2mm vertical bone loss, which appears small, however 4% incisors and 13% of 1st molar mesiobuccal roots were completely exposed Garlock 2016. The same study showed lingual vertical bone loss of 1.33mm. This becomes difficult to explain as the dentition is moving away from the lingual plate, tipping maybe a factor, however patient factors may have played a part, as we will discuss later Garlock 2016.
Expansion in non-extraction cases has shown up to 20% buccal bone loss Cattaneo 2011, it was interesting to note, the canine and premolars displayed the greatest bony defects, not the anterior teeth.
If non-extraction sounds like the problem, it is worth considering the effects of extraction on the bone, as Cecil Steiner said “do we really want to know what we are doing”. A CBCT looking at extraction cases with premolars found 84% of the lingual surfaces of mandibular central incisors demonstrated bone height decrease of 2 mm. A similar, if not slightly higher amount than non-extraction treatment, albeit on a different tooth surface. There is something to note about upper incisor retraction following extractions, in maximum anchorage cases the upper incisors may approach the incisive canal, and there is a risk of severe root resorption if contact occurs. The incisive canal should be seen as the anatomical limit of upper incisor retraction Chung 2015.
There is a misnomer that the patient has no bony defects prior to orthodontic treatment, and the braces did it. Population studies have found that in untreated patients a prevalence of a dehiscence at 51.1% and a fenestration at 36.5% Evangelista 2010. There are a series of patient factors to be aware of, which can increase or reduce the chances of creating a bony or soft tissue defect.
Gingival phenotype: The soft tissues vary in their response to bony changes. The thicker the gingiva the more resilient it is to change, whereas thinner gingiva responds to any bony changes and ‘unzip’. The critical size is 0.5mm thickness of attached gingiva, less than this increases the risk of recession. Thicker gingiva on the other hand resists recession even if bone height and thickness reduce Yared 2006
Plaque and inflammation: A variable which is not to be ignored. Birte Melsen in her 2005 study showed patient inflammation and plaque was a greater factor in recession defects than orthodontic tooth movement variables, including inclination changes.
Position of teeth within the bone: Upper incisors typically don’t lie in the middle of the labial and palatal bone, they are positioned a third from the labial plate (2/3rds from the palatal cortical bone). Lower incisors are in the middle of the labial and lingual cortical plates. This is an important factor, as it indicates greater scope for upper incisor retraction than any other antero-posterior movement of the incisors Andrews 2022.
Thickness of bone: Bone thickness varies from tooth to tooth as well as its vertical position. The thinnest bone is the buccal cervical bone, and it is thinnest anteriorly within the arch. For context the thinnest bone is the labial and cervical aspect of the lower incisors at 0.75mm and labial and cervical aspect of the upper incisors 0.76mm Elnagar 2021, Garlock 2022. Facial types affect bone thickness, with hyperdivergent patients having thinner labial and lingual cortical bone, and therefore more susceptible to bone loss through tooth movement when compared to average or hypodivergent patients (likelihood of bony defect in orthodontic treatment 22%, 5% and 0 respectively) Hoang 2016.
CBCT studies have increased our understanding of the effects of tooth movement with and without extractions on the alveolar bone, revealing what we do better than plain radiographs have done previously. However a CBCT is limited in its sensitivity, and if bone is less than 0.6mm, it can appear as a bony defect, when in actual fact it is present, a false positive Redua 2020. The figure of 0.6mm sensitivity has been contested, as it depends on the voxel size of the scan, some machines are able to deliver 0.125mm. Jeffrey Miller had wonderful insight into the contested issue and said (paraphrased) it does not matter, as anything smaller than 0.6mm is an issue regardless for orthodontic planning.
Jeffrey Miller has coined the term recently of ‘Orthodontically induced Dehiscence’ (OID), and it an apt term to describe what can occur, however both extractions and non-extraction can be the cause, and therefore we reject the claim either side is right, and instead point to initial assessment of both hard and soft tissues, periodontal health, and planned tooth movement to be of greater value in choosing treatment plan.
Papers on this topic are keen to report the changes to the bone volume (which we have avoided in this blog). The challenge is interpreting the effects of this on the reduced bone thickness or height, as it is not clear if vertical bone or thinning of bone has occurred, or it may simply indicate the tooth is approaching the cortical plate but all is good with the cellular / acellular ratio, or it may imply the tooth has approached the cortical plate and a defect is looming. Research is still yet to answer, how close is too close to the cortical plate, and it is therefore still not possible to fully answer Cecil Steiner’s question of ‘what are we doing’.
On the next blog, we will discuss the effect of extraction on the airway.
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We hope you have enjoyed this blog, This blog started with a conversation between Kerolos AlHakeem, Farooq Ahmed and James Andrews, to follow more conversations, clinical tips and commentaries on orthodontics please check us out on Instagram / facebookBi
It is interesting how most only view recession buccally. But excessively proclining lower incisors most often is evidenced by seeing recession on the lingual of the incisors and deserves more academic attention. This can be mitigated in the lower arch with an MBT bracket Rx but not entirely.