Printer Friendly

Oral health of children with intractable epilepsy attending the UK National Centre for Young People with Epilepsy.


Epilepsy is the most common neurological disorder in children [Office for National Statistics UK, 2003]. It has been estimated that in Europe, approximately 6 per 1,000 of the population have active epilepsy [Forsgren et al., 2005], 40% of cases occurring in children. Some 30% of cases of epilepsy are difficult to manage and are associated with moderate to severe learning difficulties. It has been reported that children with epilepsy have a high level of dental caries DMFS [Storhaug and Host, 1987]. This may be attributed to a number of factors including long term use of sugar-based medication, for example sodium valporate [Roberts and Roberts, 1979; Maguire et al., 1996]. Reduced salivary secretion and lowered buffering capacity associated with diphenylhydantoin may also contribute to an increase in dental caries [Lundstrom et al., 1982].

Patients with epilepsy have greater plaque scores compared with healthy controls [Seymour et al., 1985]. Plaque accumulation and gingival inflammation were associated with phenytoin induced gingival hyperplasia [Modeer et al., 1986]. The plaque score was similar or significantly greater in patients treated with carbamazepine compared with those treated with phenytoin [Lundstrom et al., 1982] and gingival inflammation and bleeding were also reported to be more prevalent in phenytoin treated individuals [Hassell et al., 1994]. Gingival hyperplasia is a well-recognised side effect of phenytoin [Modeer et al., 1986] and the incidence and severity is much greater in the gingival tissues associated with the maxillary and mandibular incisor teeth [Eeg-Olofsson et al., 1983]. A significantly lower salivary IgA has been reported to be associated with treatment with phenytoin that may increase the susceptibility of the gingival tissues to inflammatory stimuli [Brown et al., 1991].

There is little data for developmental dental defects in children with epilepsy although teeth that are small, late erupting, and root abnormalities have been observed [Girgis et al., 1980; Scully, 1998].

An important oro-dental finding is trauma to both the hard and soft tissues sustained during a seizure [Lynch et al., 1998] and the extent of these injuries is often determined by the severity and duration of the seizure. In a Nigerian community 46% patients with epilepsy have injured anterior teeth [Ogunbodede et al., 1998]. Generalised tonic-clonic seizures in association with other seizure types appear to be most frequently associated with dental trauma. In addition, higher levels of dental trauma are associated with at least three drug related adverse effects [Buck et al., 1997]. The purpose of this investigation was, therefore, to estimate the prevalence of oro-dental disease and anterior tooth trauma in children with intractable epilepsy.

Materials and Methods

Subjects. Children and adolescents, aged between 4 and 16 years, with intractable epilepsy, defined as resistant to at least two anti-epileptic drugs (AEDs), were recruited from the residential centre for children and teenagers with epilepsy, NCYPE, Lingfield, England. Control subjects were children without epilepsy matched for age; gender and ethnicity recruited from local schools (St. Stephen's Church of England School, South Godstone; Oxted Secondary School, Oxted, Surrey). All parents were given an information sheet and asked for written consent. Children aged 12 years and above were also given the information sheet and asked to sign an assent form where appropriate and children under 12 years were asked for verbal consent.

Clinical procedures. Studies were completed to assess the reproducibility of recording indices for caries and the Kappa value calculated [Altman, 1991]. Full arch toothblocks (10) were examined by the main examiner (TP) and another dental surgeon (GJR) using the WHO criteria for caries diagnosis to assess inter-rater agreement [World Health Oral Surveys, 1987]. The same toothblocks were examined again after one week by the main examiner to assess intra-rater agreement [Cleaton-Jones et al., 1989]. Indices for bacterial dental plaque and gingivitis were recorded for 8 children by both examiners.

Dental caries. All teeth were examined using WHO criteria [1987] and recorded as the dmfs / dmft and the DMFS / DMFT indices.

Bacterial dental plaque. Four gingivally related quadrisections of each tooth (mesiobuccal, distobuccal, mesiolingual, distolingual) were visually examined for plaque deposits using a modification of the index of O'Leary [Franco et al., 1996]. The proportion of tooth quadrisections that had discernible deposits of bacterial dental plaque was calculated as a percentage of the total number of primary and permanent tooth quadrisections present to give the plaque index.

Gingivitis. The gingivae were visually examined for inflammation using the same simplified gingival index based on the number of tooth quadrisections associated with gingival inflammation to give the gingivitis score. The proportion of tooth quadrisections with associated gingival inflammation was calculated as a percentage of the total number of primary and permanent tooth quadrisections present to give the gingivitis index.

Developmental enamel defects. Developmental enamel defects were recorded using the FDI notation [Ainamo, 1982].

Incisor tooth trauma. The maxillary and mandibular incisor teeth were examined for trauma [International Association of Dental Traumatology, 2008] as follows:

* Uncomplicated Crown Fracture--Enamel only,

* Enamel and dentine fractures,

* Avulsions,

* Discolouration.

Statistical analysis. All data was tested for normality using the Shapiro-Wilk test [Altman, 1991] and found to be non-normal in distribution. Categorical data were subjected to analysis using either the McNemar or Chi square test. Continuous variables between the subjects and controls were compared using the Mann Whitney U test. Comparisons between the groups of subjects with learning difficulties were made using the Kruskal Wallis Test. The statistical package used was SPSS version 10.


From a total of 70 subjects who fulfilled the inclusion criteria, 39 children with epilepsy were included. Parents of 20 children refused consent and a further 11 children were excluded because they were unable to cooperate sufficiently to complete the clinical examination. The mean age was 12.9 years (SD[+ or -]2.3) and there were 30 males and 9 females. Of these, 21 children had symptomatic focal epilepsy, a further 17 symptomatic generalised epilepsy and one other child had epilepsy undefined as focal or generalised (Table 1). There was no significant difference in the dental caries or plaque gingivitis score and index between the different groups of educational disability.

All subjects had been assessed for cognitive ability as part of routine clinical management; 2 children had cognitive ability within the normal range. Learning disability was mild (n = 3), moderate (n = 15) and severe (n = 19) (Table 1). There were 20 children who had behavioural problems defined as requiring a behaviour management program and 6 were receiving additional psychotropic medication at the time of the study.

The Anti-Epileptic Drugs (AEDs) prescribed for this group of subjects are shown in Table 2; most of them receiving at least two AEDs. One child was receiving oral prednisolone for seizure control and 14 subjects had previously been treated with phenytoin. Other medical disorders in addition to epilepsy occurred in 15 children (Table 3).

The control children were fit and healthy, not receiving medication and within the average range of academic ability. Of the control children 8 were recruited from St. Stephen's Church of England School and a further 29 from Oxted Secondary School. It was not possible to match 2 of the children with epilepsy from the schools and data from 2 historical controls were included from a related investigation using identical methodology. The mean age was 13.1 years (SD[+ or -]2.1) which was not significantly different from the subjects.

Reproducibility. For dental caries, the Kappa value for inter-examiner agreement was 0.64 and 0.89 for intra-examiner agreement. For bacterial dental plaque the Kappa value was 0.86 and for gingivitis, 0.88. This was good agreement for inter-examiner dental caries and substantial agreement for intra-examiner dental caries, bacterial dental plaque and gingivitis [WHO Oral Health Surveys, 1987].

Dental caries. The proportion of children with epilepsy who were caries free was 25.6%, which was not significantly different from the 33.3% of the matched controls. There was no significant difference in the dmfs/dmft or the DMFS / DMFT between the children with epilepsy and control children (Table 4).

Bacterial dental plaque and gingivitis. The mean plaque score and index were significantly greater for the permanent teeth only, for the children with epilepsy, 68 (SD [+ or -] 31.5) and 78.1 (SD [+ or -] 25.1) compared with the controls, 42.9 (SD [+ or -] 32.2) and 48.9 (SD [+ or -] 24.1) (p = 0.0001 and p = 0.0001, respectively) (Table 5).

The mean gingivitis score and index were significantly greater for the permanent teeth only, for the children with epilepsy, 27.9 (SD [+ or -] 33.8) and 52.9 (SD [+ or -] 33.4) compared with the controls, 15.9 (SD [+ or -] 21.8) and 16.9 (SD [+ or -] 21.5) (p = 0.0001 and p = 0.0001, respectively) (Table 5). Of the 14 children who had been treated with phenytoin in the past, evidence of gingival hyperplasia was observed in 3 of them. Gingival hyperplasia was not apparent in any subjects on other AEDs.

Developmental enamel defects. These were mainly white/ cream opacities. There was no significant difference in the number of children with epilepsy, n = 15 (38.5%) and the controls, n = 11 (28.2%) with developmental enamel defects.

Incisor trauma. A significantly greater number of children with epilepsy had experienced trauma to their anterior teeth, n = 21 (54%) compared with the controls, n = 5 (12.5%) (Chi square 14.679, df 1, p = 0.0001). There was a significantly greater number of children in the epilepsy group with fractured maxillary left, n = 16 and fractured maxillary right, n = 10 central incisors compared with the control children, n = 1 and n = 1, respectively (chi square 17.355, df 3, p = 0.001 and Chi square 9.009, df 3, p = 0.03, respectively) (Table 6). Two of the children with epilepsy and 1 control child had avulsed a maxillary central incisor; 2 with epilepsy only, had a discoloured central incisor tooth.


There were no significant differences in the dental caries score for either the primary or permanent teeth in the children with intractable epilepsy compared with the controls, which is in contrast with some earlier reports [Storhaug and Holst, 1987]. More recently, other workers reported that factors related to epilepsy, particularly antiepileptic medication may increase the risk of caries in girls [Rajavaara et al., 2003]. The DMFT of the children with epilepsy, 2.5 was similar to a group for children with unilateral cleft lip and palate, 1.9 [Lucas et al., 2000]. The DMFT was greater than that recorded for some other groups of chronically sick children, for example children undergoing liver transplantation, 1.2 [Sheehy et al., 2000], 0.9 for children with craniosynostosis [Mustafa et al., 2001] and 0.7 for children with haemophilia [Sonbol et al., 2001]. It is possible that the reason for this is that the children with craniosynostosis and haemophilia were cared for at a multidisciplinary centre with an integral program of preventive dental care.

The diet at NCYPE is carefully monitored with very few sweets consumed between meals. The increased use of sugar free medication in the treatment of epilepsy helps to minimise the risk of dental caries. For many of the children, both the physical and intellectual difficulties associated with severe epilepsy can make spitting and rinsing difficult. This in turn can enhance the topical effect of the fluoride containing toothpaste used by the children [Ashley, 2001]. Children and adolescents at NCYPE are helped with oral hygiene by professional carers as appropriate including brushing twice daily with fluoride toothpaste. This enhanced dental prevention is probably the reason for the lower levels of dental caries compared with other studies [Storhaug and Holst, 1987], [Rajavaara et al., 2003]

The higher mean plaque and gingivitis score and index for the permanent teeth in the children with epilepsy were not unexpected as 7 of the children had a motor disorder, which may have affected their ability to brush effectively. Behavioural problems, requiring a behaviour management program, occurred in 20 children (51%) of which 6 (15%) were receiving psychotropic medication. Behaviour may have affected compliance with oral hygiene. There were 37 (95%) of the children who had learning disabilities with this being in the severe range for 19 (49%). The latter required support for activities of daily living and were a group in whom behaviour problems were more prevalent.

This finding was similar to other groups of sick children with limited manual dexterity. For example, the plaque and gingivitis scores of children with dystrophic epidermolyis bullosa were significantly greater than for the matched controls [Harris et al., 2001]. Many children with craniosynostosis have hand deformities and also experience difficulty with toothbrushing [Mustafa et al., 2001]. In addition, toothbrushing and other oral hygiene practices were difficult for the carers because of the behavioral problems associated with epilepsy and learning disability. This indicates that children with learning difficulties, even with the help of carers, have relatively poor oral cleanliness. It might also be anticipated that children with mild learning difficulties would have better dental health than children with severe learning difficulties. This was not demonstrated in the statistical analysis because there were significantly more subjects with moderate to severe learning difficulties compared with those within the normal range or with mild learning difficulties.

It has been reported that 10% of a group of individuals with epilepsy suffered a dental injury for which a key predictor was seizure severity [Buck et al., 1997]. Most of the subjects included at NYCPE in this study experienced a variety of seizure types including tonic-clonic and drop attacks. The relationship between the seizure type and adverse effects of AEDs and incisor trauma needs to be further explored.

The proportion of children with incisor tooth trauma was greater than for 15 year old adolescents without epilepsy, 13% [Ashley, 2001] but similar to a group of Nigerian epileptic children [Lynch et al. 1998]. The Nigerian investigators believed that the placement of hard objects between the teeth to prevent tongue biting during seizures contributed to the high prevalence of damage to teeth in their study. This is not recommended practice within Great Britain. The children in the current study sustained more fractured maxillary left central incisors than right central incisors and although this was not significantly different, it was not possible to explain this difference. The large amount of dental trauma in these children reflects the severity of epilepsy. Although protective headgear is often worn, this does not protect against trauma to the jaws and teeth unless an ice hockey type face shield is worn.


There was no significant difference in the proportion of children with epilepsy with dental caries compared with the control group. Children with intractable epilepsy had a higher mean plaque score and index and a higher mean gingivitis score for the permanent teeth. A significantly greater number of children with epilepsy had experienced trauma to the anterior teeth, compared with the controls. These represent a significant burden of treatment for health care providers and distress for the subjects and their parents/carers. These findings have implications for the service provided for children with intractable epilepsy in relation to prevention of gum inflammation and management of tooth trauma.


Ethical approval was granted by the Eastern Surrey Local Research Ethics Committee associated with the NCYPE in Surrey, the Eastman Dental Institute & Hospital Joint Research and Ethics Committee, and the Institute of Child Health and Great Ormond Street Hospital For Children NHS Trust. Part of this work was undertaken by Great Ormond Street Hospital for Children National Health Service Trust which received a proportion of its funding from the NHS Executive; the views expressed in this publication are those of the authors and are not necessarily those of the NHS Executive.


Ainamo J A. Epidemiological index of developmental defects of dental enamel (DDE Index). Int J Dent 1982;32:159-167.

Altman, D. G., Practical Statistics For Medical Research. 1st ed., Chapman & Hall. London, 1991.

Ashley P. Toothbrushing: why when and how? Dent Update 2001;28:36-40.

Brown R.S, Weaver, W T, Bottomley W. On the mechanism of drug--induced gingival hyperplasia. J Oral Pathol Med 1991;20:201-209.

Buck D, Baker GA, Jacoby A,Chadwick DW. Patients' experience as a result of epilepsy. Epilepsia 1997:38:439-445.

Cleaton-Jones P, Hargreaves J A, Fatti J P, Chandler HD, Grossman ES. Dental caries diagnosis calibration for clinical field studies. Caries Res 1989;23:195-199.

Eeg-Olofsson O, Lundstrom, Hamp, S. E. Oral state of children with epilepsy on treatment with sodium valproate. Scand J Dent Res 1983;91:219-23.

Forsgren L, Beghi E, Oun A, Sillanpaa M. The epidemiology of epilepsy in Europe--a systematic review. Eur J Neurol 2005;12:245-253.

Franco E, Saunders C P, Roberts G J, Suwanprasit A. Dental disease, caries related microflora and salivary Iga of children with severe congenital cardiac disease: an epidemiological and oral microbial survey. Pediat Dent 1996; 18: 228-235.[20]

Girgis S S, Staple H, Miller W A, Sedrank, N, Thompson D. Dental root abnormalities and gingival overgrowth in epileptic patients receiving anticonvulsant therapy. J Periodontol 1980; 5: 474-482.

Harris J C, Bryan R A, Lucas V S, Roberts GJ. Disease and caries-related microflora in children with dystrophic epidermolysis bullosa. Pediatr Dent 2001;11:66-70.

Hassell TM, Burtner AP, McNeal D, Smith RG. Oral problems and genetic aspects of individuals with epilepsy. Periodontol 2000 1994; 6: 68-78.

International Association of Dental Traumatology. 2008. www.iadt-dentaltrauma. org 2008 (electronic citation) [google search International Association of Dental Traumatology].

Lucas V S, Gupta R, Olubenga O O, Gelbier M, Roberts GJ. Dental health indices and caries associated microflora in children with unilateral cleft lip and palate. Cleft Palate Craniofac J 2000; 37: 447-452.

Lundstrom A, Eeg-Olofsson O, Hamp S E. Effects of anti--epileptic drug treatment with carbamazepine or phenytoin on the oral state of children and adolescents. J Clin Periodontol 1982; 9: 482-488.

Lynch M, Brightman V J. Greenberg, M. S. Neuromuscular Diseases. Burket's Oral Medicine, Diagnosis and Treatment. 9th ed., JB Lippincott & Company, Philadelphia, 1998.

Maguire R., Rugg Gunn A J, Butler TJ. Dental health of children taking antimicrobial and non-antimicrobial liquid medication long-term. Caries Res 1996; 30: 16-21.

Modeer T, Dahllof G, Theorell K. Oral health of non--institutionalized epileptic children with special reference to phenytoin medication. Community Dent Oral Epidemiol 1986; 14:165-8.

Mustafa D. Lucas, V S, Junod P, et al.. The dental health and caries--related microflora in children with craniosynostosis. Cleft Palate Craniofac J 2001;38:629-635.

Office For National Statistics, London, UK. Childrens' Dental Health Survey, 2003.

Ogunbodede E O, Adamolekun B, Akintomide A O. Oral health and dental treatment needs in Nigerian patients with epilepsy. Epilepsia 1998; 39: 590-4.

Rajavaara P, Vainionpaa L, Rattya J,et al. Tooth by tooth survival analysis of dental health in girls with epilepsy. Eur J Paediatr Dent 2003;4:72-77

Roberts I F, Roberts G J. Relation between medicines sweetened with sucrose and dental disease. Br Med J 1979;2:14-16.

Scully C. Neurological Disorders. Medical Problems in Dentistry. Butterworth Heineman, UK, 1998.

Seymour R A, Smith D G, Turnbull D N. The effects of phenytoin and sodium valproate on the periodontal health of adult epileptic patients. J Clin Periodontol 1985;12:413-9.

Sheehy E C, Roberts G J, Beighton D, O'Brian G. Oral health in children undergoing liver transplantation. Int J Paediatr Dent 2000; 10: 109-111.

Sonbol H, Pelargidou M, Lucas V S, et al. Dental health indices and caries related microflora in children with severe haemophilia. Haemophilia 2001; 7: 468-474.

Storhaug K, Holst D. Caries experience of disabled school--age children. Community Dent Oral Epidemiol 1987;15:144-9.

WHO Oral health Surveys. Basic Methods. Geneva, 1987.

T. Percival *, S. E. Aylett **, F. Pool ***, A. Bloch-Zupan ****, G. J. Roberts *****, V. S. Lucas *****.

* Dept. Paediatric Dentistry, University of the West Indies; ** Dept. of Neurology, Integrated Neurosciences Unit, Great Ormond Street Hospital for Children, and *** The National Centre for Young People With Epilepsy, **** Dept. Paediatric Dentistry, Eastman Dental Institute For Oral Health Care Sciences, University College London, ***** Dept Dental Paediatrics, Kings College London Dental Institute, London, England.

Postal address: Dr. V.S. Lucas. Dept. Dental Paediatrics, Kings College London Dental Institute, Bessemer Road, London, SE5 9RW, England.

Table 1. Distribution and types of epilepsy occurring in
a group of British children and assessment of their
learning ability.

Epilepsy syndrome No. of Children

Symptomatic partial 21
Symptomatic generalised 17
Undefined focal or generalised 1

Total 39

Cognitive ability

Within normal range 2
Mild learning ability 3
Moderate learning ability 15
Severe learning ability 19

Table 2. Anti--Epileptic Drugs used in a group of 39 British
children with epilepsy.

Anti--Epileptic Drugs No. of Children

Clozapan 3
Carbamazepine 11
Felbamate 1
Ethosuxamide 5
Gabapentin 2
Lamotrigine 24
Levetiracetam 3
Methsuxamide 1
Nitrazepam 2
Oxcarbazepine 4
Phenytoin 2
Ramecamide 12
Topiramate 19
Sodium valproate 2

Table 3. Co--existing Medical Problems occurring in a group
of 39 British children with epilepsy.

Medical Diagnosis No. of Children

Hemiplegia 5
Four limb cerebral palsy 2
Ring chromosome 22 1
47 XYY 1
Kleinfelters syndrome 1
Asthma 1
Eczema 2
Diabetes mellitus 1
Juvenile chronic arthritis 1
Hypothyroidism 1
No co--existing medical
problems 23
Total 39

Table 4. Decayed, Missing, Filled Surfaces and Teeth in both Primary
and Permanent Dentition in a group of British children with epilepsy

Epilepsy group (n = 39)

 Mean SD Median Min-Max

dmfs 3.3 7.7 0 0-19
dmft 1.0 2.0 0 0-5.0
DMFS 3.7 4.4 2 0-20
DMFT 2.5 2.7 2 0-13

Control group (n = 39)

 Mean SD Median Min-Max P-value

dmfs 3.3 5.1 0.5 0-12 ns
dmft 2.0 2.9 0.5 0-7.0 ns
DMFS 4.4 6.7 1.0 0-21 ns
DMFT 1.9 1.9 1.0 0-6.0 ns

ns = not significant

Table 5. Plaque and Gingivitis Score and Index in a group of
children with epilepsy compared with a control group of children.

Epilepsy group (n = 39)

 Mean SD Median Min-Max

Primary teeth
Plaque score 26.2 21.1 26.0 0-48
Plaque index 54.8 41.4 52.8 0-100
Gingivitis score 21.0 16.6 16.5 4-48
Gingivitis index 43.5 34.4 32.9 10-100

Permanent Teeth
Plaque score 68.0 31.5 82.1 8-112
Plaque index 78.1 25.1 88.5 23.9-100
Gingivitis score 47.9 33.8 44.0 0-112
Gingivitis index 52.9 33.4 58.3 0-112

Control group (n = 39)

 Mean SD Median Min-Max P- value

Primary teeth
Plaque score 14.3 17.7 6.5 0-41 ns
Plaque index 29.5 34.8 17.2 0-85.4 ns
Gingivitis score 8.7 ) 11.2 3.0 0-24 ns
Gingivitis index 17.7 21.3 8.7 0-45.8 ns

Permanent Teeth
Plaque score 42.9 23.2 42.0 0-88 p = 0.0001
Plaque index 48.9 24.1 46.9 0-92.4 p = 0.0001
Gingivitis score 15.8 21.8 11.0 0-83 p = 0.0001
Gingivitis index 16.9 21.5 13.1 0-88 p = 0.0001

ns = not significant

Table 6. Prevalence of anterior tooth trauma in a group
of 39 epileptic children compared with a control group of
39 children.

 maxillary left

 Epilepsy Group Control Group

Central incisor 16 1
Lateral incisor 1 0
Canine 1 0

Chi square 17.355, df 3, p = 0.001

 maxillary Right

Central incisor 10 1
Lateral incisor 5 1
Canine 2 0

Chi square 9.009, df 3, p = 0.03

 mandibular left

Central incisor 1 1
Lateral incisor 3 0
Canine 1 0

No fractured mandibuar right anterior teeth in either the
epilepsy or control groups
COPYRIGHT 2009 European Academy of Paediatric Dentistry
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2009 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Percival, T.; Aylett, S.E.; Pool, F.; Bloch-Zupan, A.; Roberts, G.J.; Lucas, V.S.
Publication:European Archives of Paediatric Dentistry
Article Type:Report
Geographic Code:4EUUK
Date:Mar 1, 2009
Previous Article:Use of mobile telephone short message service (SMS) as a reminder: the effect on patient attendance.
Next Article:A study of the management of 55 traumatically intruded permanent incisor teeth in children.

Related Articles
Quality of life in children with well-controlled epilepsy.
Social and Psychological Aspects of Epilepsy.
Health Zone: How Sam recruited Charles to childhood epilepsy campaign.
Surgery for epilepsy outshines medication.
EPILEPSY TOLL `MUST BE CUT' P r o f esso r says hund r eds o f dea t hs avo i dab l e.
Mood, anxiety disorders common in epileptics: quality of life impairment.
In association with the NHS: Duo training to curb taboo over epilepsy; Medics in the region have been training nurses in the developing world about...
City's care for epilepsy is slammed; HEALTH: Seizure sufferers are receiving sub-standard treatment, says damning new report.

Terms of use | Privacy policy | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters