Is dental crowding influenced by toothwear? A remarkable 13-year follow-up study.
One of the aims of this blog is to highlight publications and issues that are unusual and innovative. A significant debate in orthodontics centres on the aetiology of malocclusion, particularly crowding. This new paper discusses an unusual research project and provides insight into this perennial question.
Dental crowding is a common orthodontic problem. It has been suggested that this is a result of the consumption of processed food. Nevertheless, there are many other factors that we need to consider as aetiological agents. These include late mandibular growth, mesial tooth migration, reduction in interproximal wear, and potential deficiency in mandibular bone growth.
We know Beggs’s theory that tooth overcrowding is a modern disease partly caused by reduced tooth wear. Studies have reinforced this theory, suggesting that tooth wear is one environmental component of the aetiology of malocclusion.
As a result, contemporary orthodontic theory suggests that malocclusion has a genetic component, and environmental influences may modify its effects.
The authors of this paper examined the effects of tooth wear on the development of tertiary crowding. They defined this as crowding that occurs between late adolescence and adulthood.
A team from Belem, Brazil, did this study. Progress in Orthodontics published the paper.
Tooth wear and tertiary crowding: a 13 year cohort study in Amazon Indigenous populations
Renata Travassos da Rosa Moreira Bastos et al
Progress in Orthodontics: Advance access: https://doi.org/10.1186/s40510-024-00550-2
What did they ask?
They did this study to
“Examine the relation of tooth wear on tooth wear in Amazon’s Indigenous population”.
What did they do?
The team completed a 13-year longitudinal study of 40 Indigenous individuals. It is important to clarify that this population’s diets are traditional. They generally consist of forest products based on cassava, nuts, fish, wild game meat, sweet potatoes, and yams.
The initial data collection from this population occurred in 2009. The team assessed 66 participants from two remote villages (T0). They returned in November 2022 to gather data on the same individuals (T1).
Their main inclusion criteria included people under 50 with all their permanent teeth. At T1, they excluded anyone who had lost more than eight teeth or people who had lost anterior teeth.
One examiner collected study casts, photographs and did a clinical examination.
They measured dental crowding with Little’s Index. One member of the team recorded the following data.
- Little’s index for dental crowding.
- Intercanine width
- Arch perimeter
- Toothwear using the Mockers classification system.
Standard demographics of the participants were recorded.
They conducted a relevant statistical analysis, including exploratory univariate statistics. Then, they applied multivariate regression analysis to the dependent variable of dental crowding, where applicable.
What did they find?
At the beginning of the study, they collected data from 47 individuals. After 13 years, the sample size was reduced to 40, resulting in a response rate of 60.6%. This group comprised 24 females and 16 males. Initially, the mean age was 16.0 years (±5.83), while at the conclusion of the study, the mean age was 29.6 years (±5.91).
The authors provided a large amount of data on each of the two villages they studied. I do not have the space to go into this here. But you can access the paper. However, the authors did point out that from T0 to T1 there was:
- A slight increase in anterior crowding of less than 1mm.
- A decrease in arch perimeter of less than 1.5mm
- Tooth wear increased between 0.65 and 0.99 units.
Their regression analysis showed that the reduction in crowding was linked to tooth loss in the upper arch. In the lower arch, the decrease in crowding was related to the amount of tooth wear. It was also related to changes in the arch perimeter. The other variables did not show any associations.
Their conclusion was:
“After thirteen years dental crowding and tooth wear increased. The changes seem to have different aetiological components for each dental arch. In the mandible, the crowding of incisors was associated with increased tooth wear and decreased arch dimensions. In the maxilla, only tooth loss caused changes in alignment. The impact of increased tooth wear on the aetiology of tertiary crowding is minor and confined to the lower dental arch arch”.
What did I think?
This study was thoroughly conducted and highly ambitious. The authors noted that most studies examining the aetiology of crowding have been cross-sectional. Therefore, they offer a low level of evidence. This was an unprecedented 13-year study.
The method was sound, and the final response rate was good for a longitudinal study of this duration.
We must consider whether this study provides information that helps us understand the aetiology of malocclusion. This is a controversial area. I have always struggled with this problem. I am sure that we all remember trying to understand Moss’s functional matrix papers. They were a total mystery to me. I always wondered if those who said they understood them were trying to fool us all!
Final thoughts
The authors of this paper offer some guidance in their discussion. In simple terms, they point out that genetic factors dominate the aetiology of malocclusion. Nevertheless, environmental factors, such as tooth wear, are a secondary influence on crowding and malocclusion. I agree with this.
Finally, we must consider whether we can modify any of these factors with our treatment. Contrary to the views of the “myofunctional practitioners”. There is no evidence to suggest that we can.
Emeritus Professor of Orthodontics, University of Manchester, UK.
This is a fascinating study, Kevin – thanks for bringing it to our attention.
I agree that the etiology of (tertiary) crowding remains controversial. Prior to Begg, I believe the early stalwarts (such as Hunter and Black) reported on the anterior component of force to explain later lower crowding since it cannot be explained by Moss’ functional matrix hypothesis. I struggled with his concept and eventually formulated the Spatial Matrix Hypothesis (SMH). Regarding lower incisor crowding, the SMH posits that this clinical sign represents a dysfunctional spatial matrix. Moss and others believed that form follows functions, whereas the SMH posits that ‘deformity follows dysfunction’. The ‘deformity’ (in this case lower incisor crowding) is, in part, the outcome of temporo-spatial patterning (i.e. certain genes are expressed at certain times at certain locations). Using the SMH, with ageing the craniofacial sutures undergo slow, prolonged synostosis. Clinically, this is seen as vertical drift of the midface (‘getting long in the tooth’). This change encroaches onto the mandibular spatial matrix, which compensates by exhibiting lower incisor crowding, inter alia. Interproximal tooth wear (as noted by Begg) might be an environmental compensatory method but that has largely been superseded by our soft, processed, refined, modern diet.
It’s interesting that my Spatial Matrix Hypothesis is finally gaining some traction since it can be used to explain various craniofacial conditions, such as malocclusion, upper airway and sleep issues. In fact, a paper I submitted to a major Sleep journal prior to Christmas had the Reviewer saying ‘Additionally, what the authors describe as a reversal so-to-speak of Moss’ Functional Matrix Hypothesis (FMH), which posits that ‘deformity follows dysfunction’….I think this is brilliant; and using the FMH as a preamble to introducing one of the author’s recently proposed hypothesis of a Spatial Matrix Hypothesis was a good segue to an interesting, novel and clinically relevant idea”. Here’s some literature on the SMH in case anyone’s interested.
Singh GD. Comment on ‘Near-normalized maxillomandibular relationship and upper airway in infants with Robin sequence treated with Stanford orthodontic airway plate’. Cleft Palate Craniofac J 2025 doi.org/10.1177/10556656251313846. Epub ahead of print.
Singh GD. Pneumopedics and craniofacial epigenetics: Biomimetic oral appliance therapy for pediatric and adult sleep disordered breathing. World Scientific Press, 2021. ISBN 978-981-122-534-5.
Singh GD and Krumholtz JA. Epigenetic Orthodontics in Adults, Appliance Therapy Group, USA, 2009. ISBN: 9780984054701
Singh GD. Spatial matrix hypothesis. Brit. Dent. J. 202(5), 238-239, 2007.
Singh GD. On Growth and Treatment: The spatial matrix hypothesis. In: Growth and treatment: A meeting of the minds. McNamara JA Jr (ed.) Vol 41, Craniofacial Growth Series, Ann Arbor, USA, 2004, 197-239.
This takes me back to my MDSc Dissertation in 1985 where I studied the relationship of tooth size and arch dimensions related to crowding in a comparison of two ethnic groups during my Orthodontic training 40 years ago!