Download “To what extent might the dental impacts of having a cleft lip and/or

“To what extent might the dental impacts of having a cleft lip and/or palate
affect healthy gums and caries risk in Western European patients?”
Introduction and Background
Having a cleft lip and/or palate (CL/P) occurs once in every 700 births, and is a well-known
craniofacial anomaly in Western Europe today. There are numerous possible causes and several
responsible genes have been identified (Huynh-Ba G et al., 2009). CL/P is made during foetal
development; there is incomplete fusion of the bones in the face, subsequently creating a hole in
the palate, and/ or a cleft in the lip. Children in the UK have this repaired with surgery as a baby. This
report consists of the most significant factors affecting oral health and risk of tooth decay due to
dental abnormalities and other oral impacts created by a cleft. It is evident that dental abnormalities
are an issue for those with CL/P: approximately two thirds of cleft patients may have some sort of
dental anomaly (Deacon, 2012). Furthermore, the prevalence of these is higher than in the general,
unaffected population (Clark, 2012).
Having CL/P predisposes a child to numerous disadvantages, such as bullying, due to the asymmetry
of their face (Seehra et al., 2011). One of the most interesting but often overlooked types of impacts
are the dental abnormalities that can arise from having CL/P, which can impact on the health of the
teeth and gums. For caries (decay) to happen, there must be an adequate tooth surface, dental
plaque (volume is affected by oral hygiene), and food for the bacteria to use for reproduction. The
relationship between oral hygiene and decay is linked but not mutually exclusive (Clark, 2012).
Decay will occur and affect teeth when there is a greater net demineralisation than mineralisation of
the teeth (Yip, Smales, 2012). Demineralisation is where tooth minerals are lost from the teeth, such
as calcium in hydroxyapatite in the enamel. Remineralisation occurs as these minerals are restored,
and such as with fluoride from toothpaste during brushing.
Figure 1: Types of cleft
lip and/or palate
1
1. ORTHODONTIC TREATMENT
Most cleft palate patients need orthodontic treatment due to their “skeletal and dental
abnormalities.” These will include differences in tooth shape, hypodontia (missing teeth, creating
gaps which much be filled), and in some cases supernumerary (extra) teeth, which need to be
aligned. Furthermore, clefts which involve the alveolus – the gum – means that a patient will need
bone grafting, usually using hip bone. Others may have just an isolated cleft in their lip and would
just need the standard bracket orthodontic treatment (Enocson, 2012). The greater the severity of
the cleft, the greater the need for and duration of treatment.
It is generally accepted that most, if not all cleft patients need orthodontic treatment. The main
reason for this is because patients will have scarring from their cleft surgery, which affects the bite
as the face grows. This is supported by journal evidence by Dahllӧf et al. in 1989. It is difficult to
statistically determine how much orthodontic treatment is needed and how long for, but it is rarely
unnecessary. This is due to the fact that scarring varies in both extent and location. On average,
orthodontic treatment will take two to five years (Enocson, 2012).
i)
Diet
Having orthodontic treatment means that a patient will have to go on a ‘soft food’ diet. This
increases chances of caries due to the fact that the ‘soft food’ stays in the mouth for longer, as there
is less of a chance of swallowing caused by higher levels of saliva, as soft food is easier to consume.
This means that there is more food for ‘cariogenic’ (decay-causing) bacteria to thrive upon,
increasing the risk of caries (Cheng et al., 2007).
ii)
Physical Appliance
A person with CL/P with a brace will get food stuck between the appliance wires, and it is harder to
remove these and clean all tooth surfaces when brushing (Clark, 2012).
iii)
Mineralisation
Teeth in cleft patients when they first have orthodontic appliances fitted are newly-erupted, so the
mineralization process of the teeth may be incomplete (calcium is still needed to strengthen the
enamel). Cheng et al.’s 2007 article mentions that the “demineralisation process” can be
“counteracted” because of the increased salivary flow rate caused by having such an attachment in
the mouth. This is because saliva has a “higher buffering capacity and pH.” On the other hand,
different people can do this to different extents. It has been shown that children with CL/P have a
lower salivary flow rate than control groups, which is another factor predisposing a child to caries
(Dahllӧf, 1989).
iv)
Outcome
It is evident that having orthodontic treatment increases the chances of developing caries for those
with CL/P. Richter at al. from their 2011 article suggest that any preventive measures taken to avoid
developing caries was not effective.
This could be evidence that Cheng et al.’s argument on saliva being a buffer may be invalid, because
saliva, in the 2011 investigation, has not saved the oral hygiene of the patients. Furthermore, the
2
patients were randomly selected, and the outcome did not seem to be affected by gender, age and
other factors be strongly influential. It was mentioned that oral hygiene was associated with caries
risk, but not strongly. This indicates that the 2011 article is valid, especially as it is supported by
research undertaken by Parapanisiou et al. in 2009, where most patients with clefts had a high rate
of caries and most of them were having orthodontic treatment at this time. Although the Grecian
(2009) investigation was not to ascertain whether caries risk is heightened by undergoing
orthodontic treatment in those with CL/P, the results are supported by both Cheng et al. and Richter
et al.’s outcomes, so it is a useful source. A 2011 article by Enaia et al. supports Richter’s view that,
despite attempts to prevent caries, its increased prevalence is an inevitable side effect for the
populations of patients undergoing orthodontic treatment. These three studies, despite being from
three different countries, where treatment patterns – both dentally and orthodontically – are likely
to differ due to the difference in health systems and styles of dental treatment, all have the same
conclusion. Accepting the fact that they will also be peer-reviewed, it must be acknowledged that
having orthodontic appliances for people with CL/P will certainly have increased risk of caries.
Furthermore, those undergoing orthodontic treatment should brush for four minutes three-to-four
times a day, to retain good oral hygiene, which is unlikely to be followed by many teenagers of
today. However, those with CL/P may be more motivated to brush as they should be already aware
of their increased need to look after their teeth. After treatment, patients should be happy
aesthetically with the result, and therefore will be more likely to brush to retain the look (Enocson,
2012). The theme of oral hygiene will be explored further on to a greater extent. However, many
teenagers undergoing orthodontic treatment are unlikely to go on a soft-food diet apart from the
first day, which counteracts arguments about increased caries risk due to diet (Clark, 2012).
As for the gums, it was observed in Stec et al.’s 2007 article that those with CL/P undergoing
orthodontic treatment had worse periodontal health than those without.
2. MALOCCLUSION
Due to the previously mentioned fact that most children with CL/P will undergo orthodontic
treatment, they will certainly have irregularities in tooth arrangement on shape.
Figure 2: A (normal) B (Class 1 malocclusion) C (Class 2 Malocclusion) D (Class 3 Malocclusion)
Malocclusion is where teeth are not correctly arranged as the patient bites. Vettore and Campos
provided statistical evidence for this in their 2010 journal article: a fifth of patients had an open bite
(teeth do not close over each other), 60% had an anterior crossbite (front teeth cross over each
other), 40% had a posterior crossbite (back teeth cross over each other), and molar and canine
malocclusion was 82% and 74% respectively.
3
There was a 70% incidence of crowding in the front teeth and 66% in the incisal segments of the
mouth. This is very strong evidence to suggest that if one has CL/P, they will have some crowding or
malocclusion which requires orthodontic correction. 61% of the cases in the article used here
needed correction. Although fixation would then reduce dental impacts, the person with CL/P will
have this throughout childhood before the patient would be ready for treatment to take place
(Enocson, 2012).
Because the teeth around the cleft site will not be in ideal positions, brushing in this area can be
hard, especially as the bristles of the toothbrush will not be able to reach certain areas (Stec et al.,
2007). Cheng et al.’s 2007 article also supports this, where it is added that the tongue and saliva,
which take part in naturally cleaning the teeth, will not be able to do so: particularly in the cleft area.
Therefore, the risk of caries is increased. This is confirmed by Clark who states that maximum
cleaning efficiency may not be possible due to arrangement of the teeth. Like in Cheng et al.’s
article, she reports that the tongue runs around the tooth automatically after food consumption,
and this is called the clearance rate. She states that it is those with CL who are more affected (as the
cleft usually affects the gum as well, where teeth grow from – unlike in CP). There is a longer
clearance rate for those with CL, so the teeth suffer from sugary food attack for a greater period of
time. Therefore, more cariogenic bacteria can stick to plaque.
3. MORPHOLOGICAL ABNORMALITIES
Many journal articles acknowledge that tooth size is affected in children with clefts. The tooth size in
both jaws may be affected, the impacts being heaviest in children with CP (Walker, 2009). The
morphology (shape) of molars was similar to those without clefts, which supports the view that the
front teeth at the site of the cleft are the main areas where dental abnormalities arise. Furthermore,
the source is reliable as it states that the upper incisors wee the most commonly “abnormal in
morphology,” which is supported by Ranta et al.’s 1986 study, and Enocson validates this view. Vichi
and Franchi elaborate on this in their 1995 article, stating that as well as the lateral’s absence,
abnormalities in its morphology are the second most common abnormality noticed.
Having small teeth creates food traps that saliva cannot easily wash away. This would cause
cariogenic bacteria to lodge more easily in these areas, especially between the teeth – as with
braces – and feed off carbohydrates released by the food as it is broken down by saliva. However,
Clark confirmed that people undergoing orthodontic treatment should have a lower caries risk
Figure 3: Supernumerary tooth
Figure 4: Hypodontia (missing upper
laterals)
4
anyway due to the fact that they should be avoiding fizzy drinks and chewy sweets.
Clark stated that dilacerations, where the root of the tooth is split, supernumerary teeth, missing
teeth and taurodontism (where there is a larger pulp in the tooth) were all found in those with CL/P.
She stated that taurodontism doesn’t directly affect dental health. Dilaceration is more common if
one has “alveolar trauma,” where the gum has been injured in some way, such as from a sporting
accident. In an elective project by Vessey (2011), it was observed that, regarding those with isolated
cleft lip, supernumerary teeth were observed in around a quarter of patients, 21.4% had hypodontia,
and 7.4% had microdontia (small teeth). This is firm evidence that there is a higher than normal rate
of abnormalities in those with CL: Vessey reported, referencing other journal articles, that
supernumerary teeth occurred in 1.5-3% of the unaffected population, around 3.6% had hypodontia,
and just 1% had microdontia. Although this report focused on those with isolated CL and not CP, it is
evident from other literature that any sort of cleft has a higher than average chance of causing a
dental abnormality.
When there are supernumerary teeth, they may need to be extracted. If a missing tooth occurs,
usually the upper lateral on the cleft side (Clark, Enocson, 2012), there can be orthodontic
movement bringing the canine round. The tooth may be filed or a crown added to it to look more
like a lateral (flattened edge, less pointed). The crown would have to be replaced every ten-tofifteen years, but this is unlikely to have a great impact on dental health (Clark, 2012).
4. ENAMEL HYPOPLASIA
Enamel hypoplasia occurs when amelogenesis, the process of enamel formation, has failed. It is one
of the most significant abnormalities that can impact on a person with CL/P’s dental health (Clark,
2012, Dahllӧf et al., 1989). Hypoplasia has been identified as one of the most frequent abnormalities
by Vichi and Franchi in 1995, where maxillary incisors are concerned (and these are often the most
affected teeth). It develops when there is not enough secretion of calcium, so the enamel is weak.
There are local or general reasons for those with CL/P to having enamel hypoplasia. Locally, which
usually refers to the gum with a cleft, this will have “impeded on amelogenesis” on the nearby teeth.
Generally, if a child is ill – either from usual children’s infections (especially where the child suffers
from high temperatures) such as chicken pox, or additional syndromes that are commonly found
alongside CL/P such as Pierre-Robin, feeding issues causing chest infections as the windpipe isn’t
properly closed, means that a child will be unwell. Instead of providing adequate protein amounts
for amelogenesis, therefore, a lot of the energy and proteins of the baby are used to repair the body
rather than the teeth. Enamel hypoplasia is permanent, and determined in the first sixth months of
life: it will affect the adult teeth as well (Clark, 2012). Vichi and Franchi, furthermore, highlighted
that the most commonly hypoplastic tooth was the enamel on the cleft side.
5
Figure 5: Enamel hypoplasia
Hypoplastic teeth are rougher due to this lack of mineralisation. Therefore, adhesion of bacteria
onto the tooth surface is easier than on smooth enamel, so caries risk is increased. The teeth the
most likely to be affected are the back teeth (the 6s normally) and the front ones. With CP, incisors
are less likely to be hypoplastic because the cleft is not directly affecting the gum, but the back teeth
can still suffer from this (Clark, 2012). This is supported with journal evidence by Dahllӧf et al.
(1989), where children without an alveolar cleft (involving the gum) had fewer cases of hypoplasia
than those with. Franchi and Vichi’s 1995 article supports this, adding that the upper centrals are
most commonly affected if there is a CL. Maciel et al. (2005) have proven that the most frequent
cases of dental defects were in the incisors on the cleft side of the mouth. This indicates that clefts
definitely will affect mineral composition during tooth formation. Galante et al. in 2005 observed the
incidence of dental abnormalities in those with CL/P, and support the fact that enamel hypoplasia is
the most severe for people with CL and CP. They mention that milk tooth canines are not greatly
affected by this, but Clark has confirmed that enamel hypoplasia is something which affects both
decidious and adult teeth.
Cheng et al.’s 2007 article confirms the increased caries risk, especially the fact that teeth are
vulnerable: they can’t easily be remineralised. This indicates that knowledge about enamel
hypoplasia in this field of research is general knowledge for dentists, and could be another particular
area of study. It also mentions that there has been no significant evidence that adult hypoplastic
teeth in those with CL/P increases caries risk, but the permanent nature of hypoplasia which Clark
highlighted to me indicates that there would be increased caries risk despite the lack of journal
research into such a specific area.
Li et al.’s 1996 study of Chinese children proved that they had a higher prevalence of caries. Because
it was a rural Chinese population being studied, this may not be a realistic representation of CL/P
children in general, mainly due to strong differences in diet, oral healthcare implements and
education, to European children. Yet, if we take into account that rural Chinese children without
clefts are also at a higher caries risk than children from Western Europe, this would still be a valid
source proving that hypoplasia increases caries risk. Although the findings support previously
mentioned sources, I do not know whether those in rural China with CL/P will be treated differently
due to possible lack of understanding of the craniofacial anomaly, which may further affect their
dental health development. Additionally, this does not look at Western populations, which means
that outcomes could vary when reviewed in different countries.
5. PERIODONTAL HEALTH
Maintaining healthy gums is vital for good teeth and oral hygiene in general (Boloor, Thomas, 2010).
If oral hygiene is poor, which can happen from not brushing properly or for long enough, periodontal
(gum) disease can develop.
6
Inflamed gums – gingivitis
Plaque (yellow)
Figure 6: Gingivitis. Figure 7: Localised (L) and Generalised (R) Periodontitis
Gingivitis happens when the gums become inflamed, but this can be reduced with better cleaning.
Periodontitis is permanent. There is bone loss and subsequent gum recession due to a build-up of
plaque, which also comes from not brushing (Spindel, 2008).
In a 2010 journal article by Boloor and Thomas, they noticed that gingivitis is very prevalent amongst
those with CL/P, and for those with clefts including the alveolus, periodontitis was more common. A
European study by Dahllӧf et al. in 1989 saw that children with CL/P had more gingival inflammation,
particularly in the maxillary anterior region (cleft site). The reason given was difficulty in cleaning
around that area, and that the lip is “thin and taut” in many cases. This is supported by Clark, and is
used in reference by Cheng et al. in their 2007 article.
Huynh-Ba et al.’s 2009 study observes the periodontal health of those with CL/P over 25 years. It
states that there was gingivitis and loss of gum attachment in all of their subjects – its active stage at
that present moment in time. This long time period of this investigation is useful in determining the
long-term effects a cleft can cause in the mouth. Furthermore, for those with CL/P who had an
alveolar bone graft, there seems to be yet more bone loss. Unlike the findings of Thomas and Boloor,
it was noticed that there was greater PPD (pocket probing depth), meaning that levels of
periodontitis in those with CL/P were worse compared to those with a cleft in the alveolus.
Despite these highly indicative results, the conclusion to this Huynh-Ba’s article was that the
patients’ poor oral hygiene may have been due to a poor “dental health programme.” However,
Clark states that diet is a very strong factor in oral health, and that a short, fifteen-minute check-up
with a dentist cannot compensate for lack of tooth brushing at home and diet regulation. It has been
acknowledged that periodontal conditions did worsen over the twenty-five years, and that this was
not entirely due to the dentist, but also that the cleft causes an increased risk of periodontal disease
progression. On the other hand, it was suggested that this can be prevented by “supportive
periodontal therapy.”
Huynh-Ba et al.’s article has been supported by Stec et al.’s 2007 study comparing periodontal
health in two European populations. They found that plaque accumulation was not the most
significant cause for “periodontal destruction of the cleft area,” but other factors were not
suggested. Stec et al. did mention that high plaque levels in the cleft area were found in patients,
which supports Clark and Cheng et al. in that it is harder to brush in that area, increasing gum
disease and caries risk. More reasons for poor periodontal conditions were that clefts can cause the
7
slow development of teeth, orthodontic treatment, and “prosthetic restorations” – plates or
dentures to replace missing teeth. They state that other factors play a large role in the cleft area,
such as the type of surgical procedure.
The fact that Germany, Poland and the USA do not have a national health system, which could be
one of the causes of a poor dental care plan; cleft patients may not be able to afford the best
treatment and will therefore be put off going for checkups.
6. PATIENT INTEREST, UPBRINGING, AND CLEFT PATIENT’S OWN ORAL CARE
CL/P patients are more likely to suffer from poor oral hygiene as the lip which is repaired by the
surgery is less elastic, so people will be anxious about brushing in and around their cleft and that
region (Cheng et al., 2007).
Enocson reported that people should, after orthodontic treatment, have more self-esteem, as their
teeth have an improved aesthetic appearance. This is supported by Cheng et al.’s article where it is
mentioned that some sources suggest that children with clefts have 3.5 more times the number of
decayed surfaces, and that this is “more evident in the primary dentition.”
Because children will not usually undergo orthodontic treatment until all adult teeth have come
through, they will not yet be at the stage where they are motivated to clean them: consequently, the
milk teeth may suffer.
The same article suggests that one of the reasons that children with CL/P have poor oral hygiene is
that their parents have not been well educated on diet, which plays a very important role in
preventive dental care, and how to brush the teeth of toddlers with clefts. This could imply that
children in lower socioeconomic backgrounds are at greater risk, because the article suggests that
less stable social situations, where diets are not so regimented and more spontaneous, can cause
bad eating habits. This is especially due to the fact that poor oral hygiene is more common in
deprived areas, and Clark stated that worse living standards that come with lower socioeconomic
class is associated with dental caries, and has been proven in an article by Sarri and Marcenes (a
means of dental neglect).
The link to socioeconomic background and caries risk for those with CL/P is supported by a study
looking at Russian children with clefts (Williams et al., 1998), where access to toothbrushes was
greatly restricted. At the time that the research was being undertaken, Russia was still recovering
from the collapse of the USSR. Although having CL/P seems to make children more prone to caries
anyway, if there was no access to oral hygiene care, the extra attention needed for a child with CL/P
would mean that lack of implements would greatly impact on oral hygiene care. However, it can only
be suggested that the “unavailability of dental hygiene products,” their cost, and the poor level of
education of parents caused the 45% of children with decayed teeth – especially as any additional
socioeconomic conditions are not analysed here. Nevertheless, these impacts are supported by
Cheng et al.’s report. The fact that the Russian study makes an educated prediction matching a
future journal article proves the reliability and truth in both sources: parents play a large role in the
oral health of children with CL/P.
Another factor inducing caries in children is the parental tendency to be overindulgent due to the
altered physical appearance, or perceived “condition” of their child, being more tempted to treat
8
them with sweets and other sugary, cariogenic foods. This is suggested by Cheng et al. and Clark, but
due to the sensitive and subjective nature of this issue, it has not been researched thoroughly.
Furthermore, if a baby is bottle-fed at bedtime and/or sleeps with one, this increases incidences of
tooth decay. This is because less saliva is produced at night, so the lactose from milk cannot be
washed away. If parents give children drinks at bedtime, they are less likely to be motivated in
looking after the children’s teeth such as brushing at night (Cheng et al., 2007, Clark, 2012).
Parents may be very anxious to care for their child with CL/P, but oral health can often be
overlooked as a less obvious area of concern for the general population, and parents may be more
distracted with the surgery their children will be going under. Therefore, caries risks are higher from
the outset. Parents, particularly mothers, who kiss their children on the mouth and share “food and
utensils” are the most likely to transfer the cariogenic bacteria Streptococcus mutans (SM) (Cheng et
al., 2007). If SM is high in numbers before even the eruption of the first teeth at three months of
age, caries is inevitable from the start.
7. OTHER APPLIANCES IN THE MOUTH
Babies with cleft palates can have intraoral appliances for up to eighteen months which helps
feeding and speech. However, the two main cariogenic microorganisms, SM and Lactobacillus, are
able to colonise more in the mouth (Cheng et al., 2007). Caries risk is therefore increased by 7.6
times in a baby compared to a child with CP without this at the age of two-and-a-half years, although
because every cleft case is different, it is difficult to statistically devise whether this is common for
those with CP. Most often, these appliances are used when the baby is relatively young. This is one
of the main areas of concern orally for those with CP (Clark, 2012).
8. CLEFT IN THE PALATE AND/OR FISTULA (HOLE)
If there is a hole or cleft in the palate, it is possible that fluid from the nose can drain into the mouth.
As it is sticky, it makes plaque glue more easily to teeth, encouraging retention of cariogenic
bacteria. These reproduce more as they are in the mouth for a longer time period. However, this
proposed fact has not yet been researched properly and is still only under speculation (Cheng et al.,
2007). Conversely, a lot of children with CP are only diagnosed late, after a long time, which means
that the cleft is left unrepaired for longer, harbouring yet more cariogenic bacteria.
9. SLOW TOOTH DEVELOPMENT
It has been noted by two journal articles that tooth formation is slower in those with CL/P,
particularly if they are boys (Ranta, 1986, Borodkin et al., 2008). This is contrasted with a study on
Chinese children, where the delayed tooth formation was not found to be significant (Cheung Lai et
al., 2008). However, since this report focuses on the Western world, particularly Europe, it is Ranta’s
report, which is supported by the American Borodkin, that I look to as the most suitably valid for this
investigation. Slower tooth formation would imply that teeth take longer to become mineralised,
and are therefore more prone to caries. However, in the two main studies – by Dahhlӧf et al. and
Cheng et al., this has not been noticed as a great factor increasing likelihood of caries, apart from
when teeth undergo orthodontic treatment.
CASE STUDY REPORT
My case study is a female of seventeen years of age, with a cleft lip but not palate.
9
She has had lip repair operations in the past, including stitching and realignment. The nose has been
affected and was tucked under during operation to obtain as symmetrical a shape as possible.
She has all of her teeth apart from her upper left lateral (UL2). This seems to be the main dental
impact; there is no restorative dentition such as fillings or crowns apart from a plate with a false
tooth to replace the missing lateral.
There is not as much bone in the direct site of the cleft as the rest of the gums. This could increase
her risk of gum recession in old age.
At around thirteen, she underwent orthodontic treatment and had a fixed retainer for a year
afterwards. Despite the increased caries risk here, she has looked after her teeth and subsequently
the treatment has not significantly affected her oral health.
My case study’s dental anomaly seems to be minimal compared to literature findings, but the impact
on her oral health I believe to have been nevertheless increased; but her own motivation to look
after her teeth has prevented caries and/or poor periodontal health.
Despite her success in maintaining good oral hygiene and health, she has had to adopt a special
method of brushing, particularly because she has reported that the false tooth is at risk of coming
out, which can cause the gum to bleed. A common reaction to the bleeding risk is discouragement
from brushing, which would cause plaque levels on the teeth to rise, elevating caries and gum
disease risk. Therefore, it must be my case study’s own will that she has overcome this fear, and
others with the same dental anomaly may have responded differently to the issue. There is an
increased risk of the intraoral appliance increasing colony numbers of SM and Lactobacilli, but,
again, her own oral healthcare routine has prevented this from happening. Crowding of the teeth
before her orthodontic treatment would have made her more vulnerable to bacterial colonisation
due to food traps and so on, but this has evidently not affected her.
Conclusion
It is evident from my research that there is a high variety of dental anomalies amongst those with CL
and CP as well as prevalence. Most types of these increased caries risk in some way, but did not
directly cause it. Slow tooth development and cleft fistulas seemed to be the least prevalent
abnormalities affecting caries, as there has not been much research into them with relation to CL/P.
Periodontal health seems to be affected most by orthodontic treatment, followed by crowding of
the teeth. Caries prevalence is less in adult teeth than milk teeth mainly due to the greater ease of
brushing after orthodontic treatment and teeth being stronger due to maximal calcification. This
would mean that overall, seeing as adult teeth are the most permanent, caries risk and periodontal
health should not be dramatically higher.
The most severe abnormality was enamel hypoplasia, and is more likely for those with isolated CL.
As well as being the most severe, it is the anomaly which increases caries risk the most. However,
diet and lifestyle are hugely influential on the risk of caries, whether one has hypoplasia or not. For
children, home care and regulation of food and drink is the most common cause for caries. Looking
at which of these impacts are made worse by CL/P, enamel hypoplasia is more common, but, if the
socioeconomic conditions are at a poor standard, the social impacts will affect a child’s dental health
more. However, taking my case study into account, where the child with CL/P is in a moderate-tohigh income family, background does not increase risk of caries but enamel hypoplasia inevitably
10
would. Therefore, enamel hypoplasia is the most severe impact on caries risk for those with CL/P,
due to its permanence and severity, but diet and oral healthcare are nevertheless of paramount
importance.
APPENDIX
Case Study Analysis
Including a case study in my investigation is an opportunity to test the journal’s findings, and to
provide an example case of someone with CL, looking at particular impacts on an individual.
I found the fact that my case study had a cleft lip but not palate interesting as it enabled me to
investigate whether this may have supported or not differences in impacts on the teeth, or whether
the situation would be similar regardless. On the contrary, since every cleft case is different, I have
realised that it is not in my powers to determine whether having a cleft lip would have had lessened
impacts because there is no possible control I could compare her to - anyone with a cleft palate may
have had the same problems if they had a cleft lip as well. It is for these reasons that I did not delve
into details in the field of study of whether having a CL is much different than a CL/P or CP.
Her missing lateral is in accordance with the literature and the orthodontist Enocson, defined as
“hypodontia of the lateral incisor on the cleft side of the mouth.” The fact that she has undergone
orthodontic treatment supports the literature and the experience of Enocson, who is a practising
orthodontist. I have found that it would be an interesting alternative field of study the effects of
having a plate on oral health for those with CL/P where they need a replacement tooth.
I acknowledge that my case study is not necessarily an accurate representation of all young people
with CL/P. However, since this is a first-hand account and a primary source, I would say that using a
case study is a very reliable source.
Analysis of Sources
The majority of my sources have selective methods of choosing their subjects and acceptable sample
sizes, indicating that they are reliable. When they state that the results are in accordance with past
findings, I felt that this eliminated the need for me to look at older (and possibly less relevant)
articles. As research and advancements is constantly moving forwards, I felt it most appropriate to
look at more recent articles when selecting my sources.
When assessing enamel hypoplasia, a limitation with using Li et al.’s article is that there have been
no demographic studies of Chinese children with better access to dental care with enamel
hypoplasia (with/without CL/P) and without, so it is difficult to draw valid conclusions from the given
information with such a vague provenance.
An outside field of study I noticed was when reading Silva et al.’s 2008 study of a genetic link
between those with CP and hypodontia. I did not use this source directly for the report as it was not
strictly relevant and was background research.
Walker SC’s 2009 study was highly useful and relevant as incidence or morphological anomalies was
evaluated in the north of England, which is a good representative of Western Europe.
In the Periodontal Health part of the report, the fact that Huynh et al.’s 2009 article was used as a
point of reference by Boloor and Thomas does not prove that it itself is a valid source. On the other
hand, its results generally match the pattern amongst CL/P patients: most subjects had poor oral
11
hygiene, and the teeth were not looked after very well. Even though the conclusion was the same as
Huynh-Ba et al.’s, it does not increase the source’s reliability or usefulness due to the fact that I have
concentrated my works more on those in Western Europe. Furthermore, the usefulness of Boloor
and Thomas’s article is limited as the subjects had not had their lips or palates repaired due to the
lack of treatment available in India – many in the UK and Western Europe will have had repair
surgery and orthodontic treatment, which would eliminate all sorts of problems contributing to
plaque build-up, such as crowding of the teeth, and leaking of sticky mucus from the nose into the
mouth. The stated levels in the article of periodontitis and gingivitis may differ to that of the general
population, however, despite the fact that the clefts have not been repaired. Furthermore, the four
means of criteria as to assessing periodontal health and oral hygiene in Huynh-Ba et al.’s study,
compared to just two in Boloor and Thomas’s indicate that the former had a more reliable
methodology.
It must be acknowledged that periodontal disease is not always easy to assess, particularly as, like
caries, this multifactoral disease will not be caused by a cleft alone. Therefore, any literature findings
are only observations and not definitive truths. This applies to caries, too, as it is influenced by many
things. A possible flaw to my investigation could be that anomalies may not have been caused by the
cleft, but a genetic and/or independently caused factor.
In the periodontal health section where I have used papers looking at a variety of countries from the
Western world, the fact that similar conclusions could be drawn from this range of locations
indicates that these sources were reliable, even though the conclusions are most likely accountable
by the similar socioeconomic conditions of Germany and North America (especially taking into
account availability of cleft treatment and oral hygiene products). It would be interesting to assess
the impacts of the type of healthcare system on dental health between countries, but not being
directly important I have not elaborated on this topic.
My primary sources: Clark; Deacon; and Enocson, are useful as they witness a large number of
people with CL/P on a regular basis. However, their observations may be subjective as they are only
based on clinical experience in the hospitals they work for, so there is a risk that what they say is
limited to the demographics of their patients. On the other hand, what they have stated is in
accordance with the literature, and are first-hand accounts of the dental issues associated with
those with CL/P today, so I consider their evidence valid for this investigation.
Due to the difference in severity of cleft lip/palate of subjects, there are obvious limitations to my
sources. However, it is evident that most of the interlinking or supportive journal articles are all
reliable as they can be compared directly to each other.
Contradicting Articles
The work by Hasslӧf and Twetman from 2007 criticises four investigations into the prevalence of
caries in those with CL/P, stating that they were not the appropriate standard of investigation,
implying that this renders them invalid. Furthermore, Jindal et al. quote this in their 2011 study of
the prevalence of caries in those with CP. However, Twetman and Hasslӧf’s work only investigated
articles published before 2006, but there has been evidence since then that reliable, peer-reviewed
journals have proven that having CL/P can increase chances of caries. Jindal et al.’s article title –
“Women Are More Susceptible to Caries but Individuals Born with Clefts Are Not” – is also
suspicious, because they have already made the conclusion and therefore any work within must be
12
heavily biased. They refer in the article to the fact that controls are in essence hand-picked, but
evidence that controls are randomly selected is written in the articles. Therefore, Jindal et al.’s work,
despite being recent and counterbalancing a lot of the previously mentioned evidence, is clearly
biased and it is not correct to establish a conclusion based on their findings. The random link to
increased prevalence of caries in women is greater evidence for this – instead of this being a
separate investigation, it is oddly tied to CL/P patients, and assumes that all women will become
pregnant within their lifetimes, which is not true for a number of females in Western Europe. It is for
these reasons that these sources I decided against using for my investigation.
Bibliography – Reference List
BOLOOR V, THOMAS B (2010) Comparison of periodontal status among patients with cleft lip, cleft
palate, and cleft lip along with a cleft in palate and alveolus. Journal of Indian Society of
Periodontology, 14(3):168-172
BORODKIN ET AL. (2008) Permanent tooth development in children with cleft lip and palate.
Paediatric Dentistry, 30(5):408-13
CHENG LL ET AL. (2007) Predisposing Factors to Dental Caries in Children with Cleft Lip and Palate: A
Review and Strategies for Early Prevention. The Cleft Palate-Craniofacial Journal, 44(1):67-72
CHEUNG LAI ET AL. (2008) Dental Development of Chinese Children with Cleft Lip and Palate. The
Cleft Palate-Craniofacial Journal, 45(3):290-96
CLARK V (2012) Practising Paediatric Dentist; personal communication
DAHLLӦF G ET AL. (1989) Caries, gingivitis and dental abnormalities in preschool children with cleft
lip and/or palate. Cleft Palate Journal, 26(3): 233-38
DEACON S (2012) Practising Orthodontist; personal communication
ENAIA M ET AL. (2011) White-spot lesions during multibracket appliance treatment: A challenge for
clinical excellence. American Journal of Orthodontics and Dentifacial Orthopaedics, 140(1):e17-24
ENOCSON L (2012) Practising Orthodontist; personal communication.
GALANTE JM ET AL. (2005) Prevalence of enamel hypoplasia in deciduous canines of patients with
complete cleft lip and palate. The Cleft Palate Craniofacial-Journal, 42(6):675-8
HASSLӦF P, TWETMAN S (2007) Caries prevalence in children with cleft lip and palate—a systematic
review of case-control studies. International Journal of Paediatric Dentistry, 17(5):313-9
HUYNH-BA G ET AL (2009) Periodontal disease progression in subjects with orofacial clefts over a 25year follow-up period. Journal of Clinical Periodontology, 36(10):836-42
JINDAL A ET AL. (2011) Women Are More Susceptible to Caries but Individuals Born with Clefts Are
Not. International Journal of Dentistry
LI Y ET AL. (1996) Caries experience in deciduous dentitions of rural Chinese children 3-5 years old in
relation to the presence or absence of enamel hypoplasia. Caries Research 30(1):8-15
13
MACIEL SP ET AL. (2005) Difference in the prevalence of enamel alterations affecting central incisors
of children with complete unilateral cleft lip and palate. ASDC Journal of Dentistry for Children,
62(6):412-7
PARAPANISIOU V ET AL. (2009) Oral health status and behaviour of Greek patients with cleft lip and
palate. European Archives of Paediatric Dentistry 10(2):85-9
RANTA R (1986) A review of tooth formation in children with cleft lip/palate. American Journal
Orthodontics Dentofacial Orthopaedics, 90(1):11-8
RICHTER AE ET AL. (2011) Incidence of caries lesions among patients treated with comprehensive
orthodontics. American Journal of Orthodontics and Dentofacial Orthopaedics, 139(5):657-64
SEEHRA J (2011) Bullying in schoolchildren – its relationship to dental appearance and psychological
implications: an update for GDPs. British Dental Journal, 210(8):411-5
SARRI G, MARCENES W. (2012) Child dental neglect: is it a neglected area in the UK? British Dental
Journal, 213(3): 103-104
STEC M ET AL. (2007) Periodontal status and oral hygiene in two populations of cleft palates. The
Cleft Palate-Craniofacial Journal, 44(1):73-8
SPINDEL (2008) Ask Dr Spindel: What is the difference between Gingivitis and Periodontitis? Available
at:
http://lspindelnycdds.blogspot.co.uk/2008/02/what-is-difference-between-gingivitis.html
(Accessed: 15/08/2012)
SILVA AP ET AL. (2010) Dental anomalies of number in the permanent dentition of patients with
bilateral cleft lip: radiographic study. Cleft Palate Craniofacial Journal, 45(4):473-6
VESSEY J (2011) The incidence and type of dental anomalies in patients with isolated cleft lip
University of Bristol, Elective Project
VETTORE M, CAMPOS A (2010) Malocclusion characteristics of patients with cleft lip and/or palate.
European Journal of Orthodontics, 33(3):311-7
VICHI M, FRANCHI L (1995) Abnormalities of the maxillary incisors in children with cleft lip and
palate. The Cleft Palate-Craniofacial Journal, 42(4):392-5
WALKER SC ET AL. (2009) Abnormal tooth size and morphology in subjects with cleft lip and/or
palate in the north of England. European Journal of Orthodontics, 31(1):68-75
WILLIAMS, W. N. ET AL (1998) Oral Health Status of Russian Children with Unilateral Cleft Lip and
Palate. Cleft Palate Craniofacial Journal, 35(6):489-94
YIP K, SMALES R (2012) Oral diagnosis and treatment planning: part 2. Dental caries and assessment
of risk. British Dental Journal, 213(2):59-66
Figure 1 Available at: http://walterdgraciamd.files.wordpress.com/2012/05/cleft5251.jpg (Access
date: 14/09/2012)
14
Figure 2 Available at: http://medical-dictionary.thefreedictionary.com/malocclusion (Access date:
20/09/2012)
Figure 3 Available at: http://supernumeraryteeth.com/ (Access date: 19/09/2012)
Figure 4 available at: http://www.braces4oxford.co.uk/MissingTeeth.htm (Access date: 19/09/2012)
Figure 5 available at: http://www.pbs.org/wgbh/nova/education/activities/3409_inca_07.html
(Access date: 19/ 09/2012)
Figure 6 available at: from http://www.cdhb.govt.nz/dentalcare/youth/tooth-decay.htm (Access
date: 18/09/2012)
Figure 7 available at: http://www.macleans.co.nz/lookingafter/periodontitis.aspx (Access date:
17/09/2012)
Other general dental knowledge expressed I have developed from doing work experience in
Dentistry during 2011 and 2012.
GLOSSARY
Amelogenesis – the process of enamel formation
Alveolar Bone Graft – an operation involving grafting of hip bone being used to restore the cleft in
the gum
Alveolus – the gum (including the underlying bone)
Bacteria – a type of microorganism which can live in the mouth
Bite – the arrangement of the teeth upon biting
Bracket orthodontic treatment – more colloquially known as ‘train tracks,’ where brackets are
attached to the teeth, linked together by wires which pull them into a straight arrangement
Caries – tooth decay
Cariogenic – causing caries. For example, cariogenic bacteria may be Streptococcus mutans or
Lactobacilli which thrive in the mouth and cause tooth decay
Central – any one of the central teeth in the mouth. There are two upper and two lower centrals,
and are in the middle of the row of teeth
CL – shortening of the term Cleft lip
Cleft lip – a cleft in the lip
CL/P – shortening of the term Cleft lip and palate
CP – shortening of the term Cleft palate
Cleft palate – a cleft in the palate, often looking like a hole
15
Crossbite – the teeth suffer malocclusion upon biting, where they do not cross over each other
correctly
Demineralised – the state where the minerals (especially calcium) have been removed from the
teeth, leaving them more vulnerable due to increased porosity
Dilaceration – where the shape of the tooth’s root is damaged, usually by a physically traumatic
incident
Enamel – the outer layer of the tooth (the visible part)
Enamel hypoplasia – condition where the enamel is severely weakened and vulnerable
Gingivitis – where the gums are inflamed, usually due to plaque build-up, and is reversible
Hydroxyapatite – one of the main mineral structural components of the enamel, which is calcified
Hypodontia – where there is a tooth (or teeth) missing
Incisal segment – the part of the mouth concerning the incisors (at the front of the mouth)
Lateral – the teeth next to the centrals and canines. There are usually two on the upper row and two
on the bottom row
Malocclusion – where the teeth do not align properly
Microdontia – where teeth are smaller than would be considered normal
Open bite – where the teeth do not close over each other upon biting, leaving a visible gap between
the bottom and top rows
Orthodontic treatment – treatment involving the rearrangement of teeth from abnormal positions
and angles into straight rows, to obtain a normal bite
Periodontal health – the health of the gums
Periodontitis – permanent inflammation of the gums, involving loss of bone and attachment of the
gum to the teeth, symptomatic of gum disease and irreversible.
Pocket probing depth – the depth of pockets between the tooth enamel and the gum, caused by
plaque and a sign of poor periodontal health. The deeper the pocket, the worse the health of the
gums
Remineralised – the state where the teeth have been fully restored with minerals (usually calcium)
and are stronger
Taurodontism – where the pulp (root) of the tooth is abnormally large
16