DOI: 10.1111/ipd.12136
Enamel defects on permanent successors following luxation injuries to primary teeth and carers’ experiences ANNE B. SKAARE, ANNE-LISE MASENG AAS & NINA J. WANG Department of Paediatric Dentistry and Behavioural Science, Institute of Clinical Dentistry, University of Oslo, Oslo, Norway
International Journal of Paediatric Dentistry 2015; 25: 221–228 Background. Trauma to primary teeth may have
consequences. Aim. To study frequency of enamel defects in per-
manent successors after luxation injuries, and to report carers’ experiences. Methods. Children 8–15 years (n = 170) suffering luxation injury to primary dentition in 2003 were reexamined in 2010. Permanent successors (n = 300) were clinically examined and photographed. Data from dental records, registration form and a questionnaire were analysed by crosstabulation and tested by chi-square and t-test. Results. Enamel defects were registered in 130 successor teeth, 22% due to trauma, 21% due to other aetiological factors (MIH, dental fluorosis,
Introduction
Traumatic injuries to primary teeth are common1–6. Most epidemiological studies are retrospective reporting on prevalence which includes new and old injuries3. Prospective incidence studies, on the other hand, may also register injuries not remembered by the patient and/or carer or not visible in retrospective studies. The Public Dental Service system in Scandinavia offers free, regular dental care for all children from birth to 18 years of age and thus all, or almost all dental injuries are registered and followedup4. The risk of sequelae in the permanent dentition is well documented, and the more severely affected the primary tooth, the higher the frequency of developmental disturCorrespondence to: Prof. Anne B. Skaare, Department of Paediatric Dentistry and Behavioural Science, Institute of Clinical Dentistry, University of Oslo, P.O. Box 1109 Blindern, 0317 Oslo, Norway. E-mail: [email protected]
idiopathic). Successors with enamel defects were after concussion 8%, subluxation 18%, lateral luxation 41%, intrusion 38% and avulsion 47%. Enamel defects were associated with the child’s age and severity of the injury (P < 0.05). Six children had enamel defects in successors of noninjured primary teeth. Anxiety recorded by carers was associated with severity and number of injured teeth (P < 0.05). According to carers eight children developed dental fear, seven were younger than 3.5 years and had had their injured teeth removed. Conclusion. Minor luxation injuries and indirect trauma may cause enamel defects in permanent successors. Lower age at injury, severity and number of injured teeth affect carer and child negatively.
bance in the permanent successor7–15. The most common sequela is discolouration of enamel7,8,11. Intrusion injuries followed by avulsions are most often reported to cause mineralization disturbances, 41–77% and 30– 52%, respectively10–12,14,15. According to the literature lateral luxation and subluxation cause defects less frequently, in the range 10– 30%7–11. Due to design and presentation of results, however, the studies are difficult to compare. When anterior teeth are involved, aesthetics is an issue, and in particular, this is critical for the permanent incisors. It is of importance to minimize sequelae in the permanent successor, and immediate care and follow-up are important to minimize the risk of negative outcome in both dentitions16. In addition to the physical impact of the trauma, necrosis and periapical inflammation may injure the developing tooth17,18. A child’s ability to cooperate may be limited after physical trauma. Every clinician experiences children who do not cooperate and display behaviours that interfere with clinical procedures. The
© 2014 BSPD, IAPD and John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
221
222
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situation is distressing both for the child and the parents, and the clinician must manage the behavioural challenges and the trauma19,20. Painful experience early in life is shown to be associated with later avoidance and dental fear21,22. The aim of the present investigation was to study the frequency of enamel defects in permanent teeth after luxation injuries to primary predecessors and to report the carers’ experiences. Material and methods
All children with primary tooth injuries (n = 266, age 1–8 years) registered in the Public Dental Service (PDS) in a county of Norway in 20034 were invited to a follow-up examination of permanent successors by the principal investigator in 201023. Seventythree children (with 94 primary luxated teeth, 79% non-severe) had either moved out of the county (n = 21), did not want to participate (n = 13), did not attend for the scheduled appointment (n = 27) or had received orthodontic treatment with unreadable enamel surfaces (n = 12), leaving 193 children aged 8–15 years, with 338 successor teeth available for evaluation. Excluding also dental hard tissue injuries and injuries only to soft tissue, 170 children with 300 permanent successors to luxated primary teeth, were analysed. The severity of the luxation injuries was classified as severe; displacement (extrusion, lateral luxation, intrusion and avulsion) and non-severe; no displacement (concussion, subluxation). If combination injuries (hard tissue/luxation), only the luxation injury was registered. This study was based on all available information, the clinical examination, clinical close-up photographs, radiographs, dental records, pre-designed follow-up registration form from the year of trauma (2003) and a questionnaire to the carers (2010) to assess possible consequences of the trauma. The pre-designed follow-up registration form was developed for the clinicians to record clinical findings (tooth colour, fistula/abscess) and radiological findings (apical periodontitis, root resorption), and whether extraction
had been performed during the follow-up period. An intraoral examination accompanied by clinical photographs was undertaken by the principal investigator in the public clinics as described previously23. The clinical photos were evaluated by three calibrated paediatric dentists for mineralization disturbances based on a modified DDE (Developmental Defects of Enamel) index24. Enamel disturbances were classified as defects due to trauma or due to other causes. Enamel defects not caused by trauma included Molar-IncisorHypomineralization (MIH), dental fluorosis or idiopathic defects. First permanent molars were examined clinically and photographed when MIH was diagnosed. Radiographs were taken when developmental disturbances, beyond those clinically observed, were suspected in successor teeth. Concurrently with the follow-up examination, accompanying carers of the participant completed the questionnaire, to assess possible distress related to the trauma; this was categorised as not at all stressful, somewhat stressful, very stressful or do not know/ remember. When distress was recorded, the type of distress was grouped as: (i) time-consuming; (ii) concern about consequences for teeth; or (iii) the child’s emotions (pain or dental anxiety). Written informed consent was obtained from the parents of all participants, and ethical approval was obtained from the Regional Committee for Medical Research Ethics and the Norwegian Social Science Data Services. Data were analysed by cross-tabulations and tested by chi-square and t-test using the Statistical Package for the Social Sciences (version 20; SPSS, Inc. Chicago, IL, USA). Cohen’s unweighted kappa and proportional agreement were used to calculate interobserver agreement. The level of statistical significance was set at P < 0.05. Results
Mineralization disturbances Enamel defects were registered in 130 successor teeth. Table 1 shows that out of the 300
© 2014 BSPD, IAPD and John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
© 2014 BSPD, IAPD and John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
1.0 21.3
223
4.6 0.7 2.7 22.0
3.0
5.7 7.6
3.0 1.0 12.0 2.0
0 4.2 4.2 37.5 22.7
8.3
15.4
7.7
11.4 4.5 6.8 40.9
4.5
2.3 11.4
15.8 47.3
5.2 4.2
15.8 10.5 20.8 4.2 4.5 15.9 2.3 7.7
0.7 17.5 3.2 25.5 7.9
4.4 3.6 1.6
14.3
1.6
5.1 11.7
7.7
7.7 2.9 0.7 11.7 1.5 3.2 3.2
Demarcated opacity ≤3 mm >3 mm Diffuse opacity ≤3 mm >3 mm Hypoplasia ≤3 mm >3 mm Combination Total
6.3
0.7 25.5
O T T
O
T
O
T
O
T
O
Total n = 300
Aetiology
O
teeth which sustained trauma, 22% of the successors had enamel defects most probable due to trauma whereas other aetiological factors were recorded in an equal proportion (21%). Interexaminer agreement measured by kappa was in the range 0.63–0.84 and proportional agreement 92–96%23. The proportions of permanent teeth with enamel defects caused by a luxation injury were after concussion 8%, subluxation 18%, extrusion 8%, lateral luxation 41%, intrusion 38% and avulsion 47% (Table 1). Table 2 shows the proportion of permanent teeth with enamel defects classified according to the modified DDE index and according to aetiology (trauma or other causes). Other causes were Molar-IncisorHypomineralization (MIH), dental fluorosis or defined as idiopathic. Fig. 1 shows an example of an enamel disturbance classified as idiopathic. When trauma was assessed the aetiological factor, minor demarcated opacities (≤3 mm) were most frequent (12%), Fig. 2. An example of a small opacity after a severe trauma is shown in Fig. 3. Hypoplasia was observed in 5% of the successors when trauma was the cause of the defect, whereas diffuse opacities were most frequent in teeth when the defects were due to other causes (13%). Statistically significant associations were found between enamel defects in the permanent successors and the child’s age at the time of injury (P < 0.05) and between enamel defects and the severity of the injury, dis-
T
25.5 25.5 15.4 22.7 4.2 0 21.3
O
16 35 2 10 1 0 64
T
7.9 17.5 7.7 40.9 37.5 47.3 22.0
Aetiology
5 24 1 18 9 9 66
Aetiology
63 137 13 44 24 19 300
Aetiology
Concussion Subluxation Extrusion Lateral luxation Intrusion Avulsion Total
Aetiology
%
Aetiology
n
Aetiology
%
Enamel defect (Modified DDE index)
n
Avulsion n = 19
Injured teeth n
Intrusion n = 24
Diagnosis
Lateral Luxation n = 44
Other causes
Extrusion n = 13
Due to trauma
Subluxation n = 137
Enamel defects
Concussion n = 63
Table 1. Numbers and proportions of permanent teeth with enamel defects (due to trauma and other causes) by type of luxation injury to primary predecessor (n = 300).
Table 2. Proportions% of permanent teeth with enamel defects classified according to the modified DDE index and according to aetiology (T = trauma, O = other causes) after a luxation injury to the primary predecessor (n = 300).
Consequences of injuries to primary incisors
224
A. B. Skaare, A.-L. M. Aas & N. J. Wang
Fig. 1. The photo shows teeth 11 and 21 with demarcated opacities >3 mm. Diagnosis: 51 subluxation at 3.5 years. No enamel defects on 6 years molars rule out Molar-Incisor Hypomineralization and the symmetry indicates an idiopathic aetiology according to three independent examiners.
placement (37.0%) or no displacement (14.5%), (P < 0.001). More severe defects were observed after displacement injuries at a lower age. Half of the teeth with lateral luxation that caused a defect in the permanent successor (9 of 18) were displaced in a buccal direction; an example is shown in Fig. 4. In six of 170 children (3.5%), a successor to a non-injured primary tooth adjacent to a severe luxation injury had enamel defects due to the trauma (indirect trauma). These six children had sustained a severe injury before the age of 4 years; avulsion (n = 1), intrusion (n = 3) and lateral luxation (n = 2). The defects were hypoplasia (n = 3), demarcated opacity (n = 2) and a combination (n = 1). An example of a permanent successor to a non-injured primary tooth is shown in Fig. 5a–c, the only permanent tooth in the study with a malformation of the crown. Of the 170 children, 62% had more than one injured tooth. Delayed eruption or other eruption problems were registered in 6.5% of the children and malposition of the permanent successor in 4% of the children. Follow-up
Fig. 2. The photo shows tooth 11 with a demarcated opacity < 3 mm. Diagnosis: 51 subluxation at 3 years of age.
Fig. 3. The photo shows tooth 21 with a demarcated opacity
Enamel defects on permanent successors following luxation injuries to primary teeth and carers’ experiences ANNE B. SKAARE, ANNE-LISE MASENG AAS & NINA J. WANG Department of Paediatric Dentistry and Behavioural Science, Institute of Clinical Dentistry, University of Oslo, Oslo, Norway
International Journal of Paediatric Dentistry 2015; 25: 221–228 Background. Trauma to primary teeth may have
consequences. Aim. To study frequency of enamel defects in per-
manent successors after luxation injuries, and to report carers’ experiences. Methods. Children 8–15 years (n = 170) suffering luxation injury to primary dentition in 2003 were reexamined in 2010. Permanent successors (n = 300) were clinically examined and photographed. Data from dental records, registration form and a questionnaire were analysed by crosstabulation and tested by chi-square and t-test. Results. Enamel defects were registered in 130 successor teeth, 22% due to trauma, 21% due to other aetiological factors (MIH, dental fluorosis,
Introduction
Traumatic injuries to primary teeth are common1–6. Most epidemiological studies are retrospective reporting on prevalence which includes new and old injuries3. Prospective incidence studies, on the other hand, may also register injuries not remembered by the patient and/or carer or not visible in retrospective studies. The Public Dental Service system in Scandinavia offers free, regular dental care for all children from birth to 18 years of age and thus all, or almost all dental injuries are registered and followedup4. The risk of sequelae in the permanent dentition is well documented, and the more severely affected the primary tooth, the higher the frequency of developmental disturCorrespondence to: Prof. Anne B. Skaare, Department of Paediatric Dentistry and Behavioural Science, Institute of Clinical Dentistry, University of Oslo, P.O. Box 1109 Blindern, 0317 Oslo, Norway. E-mail: [email protected]
idiopathic). Successors with enamel defects were after concussion 8%, subluxation 18%, lateral luxation 41%, intrusion 38% and avulsion 47%. Enamel defects were associated with the child’s age and severity of the injury (P < 0.05). Six children had enamel defects in successors of noninjured primary teeth. Anxiety recorded by carers was associated with severity and number of injured teeth (P < 0.05). According to carers eight children developed dental fear, seven were younger than 3.5 years and had had their injured teeth removed. Conclusion. Minor luxation injuries and indirect trauma may cause enamel defects in permanent successors. Lower age at injury, severity and number of injured teeth affect carer and child negatively.
bance in the permanent successor7–15. The most common sequela is discolouration of enamel7,8,11. Intrusion injuries followed by avulsions are most often reported to cause mineralization disturbances, 41–77% and 30– 52%, respectively10–12,14,15. According to the literature lateral luxation and subluxation cause defects less frequently, in the range 10– 30%7–11. Due to design and presentation of results, however, the studies are difficult to compare. When anterior teeth are involved, aesthetics is an issue, and in particular, this is critical for the permanent incisors. It is of importance to minimize sequelae in the permanent successor, and immediate care and follow-up are important to minimize the risk of negative outcome in both dentitions16. In addition to the physical impact of the trauma, necrosis and periapical inflammation may injure the developing tooth17,18. A child’s ability to cooperate may be limited after physical trauma. Every clinician experiences children who do not cooperate and display behaviours that interfere with clinical procedures. The
© 2014 BSPD, IAPD and John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
221
222
A. B. Skaare, A.-L. M. Aas & N. J. Wang
situation is distressing both for the child and the parents, and the clinician must manage the behavioural challenges and the trauma19,20. Painful experience early in life is shown to be associated with later avoidance and dental fear21,22. The aim of the present investigation was to study the frequency of enamel defects in permanent teeth after luxation injuries to primary predecessors and to report the carers’ experiences. Material and methods
All children with primary tooth injuries (n = 266, age 1–8 years) registered in the Public Dental Service (PDS) in a county of Norway in 20034 were invited to a follow-up examination of permanent successors by the principal investigator in 201023. Seventythree children (with 94 primary luxated teeth, 79% non-severe) had either moved out of the county (n = 21), did not want to participate (n = 13), did not attend for the scheduled appointment (n = 27) or had received orthodontic treatment with unreadable enamel surfaces (n = 12), leaving 193 children aged 8–15 years, with 338 successor teeth available for evaluation. Excluding also dental hard tissue injuries and injuries only to soft tissue, 170 children with 300 permanent successors to luxated primary teeth, were analysed. The severity of the luxation injuries was classified as severe; displacement (extrusion, lateral luxation, intrusion and avulsion) and non-severe; no displacement (concussion, subluxation). If combination injuries (hard tissue/luxation), only the luxation injury was registered. This study was based on all available information, the clinical examination, clinical close-up photographs, radiographs, dental records, pre-designed follow-up registration form from the year of trauma (2003) and a questionnaire to the carers (2010) to assess possible consequences of the trauma. The pre-designed follow-up registration form was developed for the clinicians to record clinical findings (tooth colour, fistula/abscess) and radiological findings (apical periodontitis, root resorption), and whether extraction
had been performed during the follow-up period. An intraoral examination accompanied by clinical photographs was undertaken by the principal investigator in the public clinics as described previously23. The clinical photos were evaluated by three calibrated paediatric dentists for mineralization disturbances based on a modified DDE (Developmental Defects of Enamel) index24. Enamel disturbances were classified as defects due to trauma or due to other causes. Enamel defects not caused by trauma included Molar-IncisorHypomineralization (MIH), dental fluorosis or idiopathic defects. First permanent molars were examined clinically and photographed when MIH was diagnosed. Radiographs were taken when developmental disturbances, beyond those clinically observed, were suspected in successor teeth. Concurrently with the follow-up examination, accompanying carers of the participant completed the questionnaire, to assess possible distress related to the trauma; this was categorised as not at all stressful, somewhat stressful, very stressful or do not know/ remember. When distress was recorded, the type of distress was grouped as: (i) time-consuming; (ii) concern about consequences for teeth; or (iii) the child’s emotions (pain or dental anxiety). Written informed consent was obtained from the parents of all participants, and ethical approval was obtained from the Regional Committee for Medical Research Ethics and the Norwegian Social Science Data Services. Data were analysed by cross-tabulations and tested by chi-square and t-test using the Statistical Package for the Social Sciences (version 20; SPSS, Inc. Chicago, IL, USA). Cohen’s unweighted kappa and proportional agreement were used to calculate interobserver agreement. The level of statistical significance was set at P < 0.05. Results
Mineralization disturbances Enamel defects were registered in 130 successor teeth. Table 1 shows that out of the 300
© 2014 BSPD, IAPD and John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
© 2014 BSPD, IAPD and John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
1.0 21.3
223
4.6 0.7 2.7 22.0
3.0
5.7 7.6
3.0 1.0 12.0 2.0
0 4.2 4.2 37.5 22.7
8.3
15.4
7.7
11.4 4.5 6.8 40.9
4.5
2.3 11.4
15.8 47.3
5.2 4.2
15.8 10.5 20.8 4.2 4.5 15.9 2.3 7.7
0.7 17.5 3.2 25.5 7.9
4.4 3.6 1.6
14.3
1.6
5.1 11.7
7.7
7.7 2.9 0.7 11.7 1.5 3.2 3.2
Demarcated opacity ≤3 mm >3 mm Diffuse opacity ≤3 mm >3 mm Hypoplasia ≤3 mm >3 mm Combination Total
6.3
0.7 25.5
O T T
O
T
O
T
O
T
O
Total n = 300
Aetiology
O
teeth which sustained trauma, 22% of the successors had enamel defects most probable due to trauma whereas other aetiological factors were recorded in an equal proportion (21%). Interexaminer agreement measured by kappa was in the range 0.63–0.84 and proportional agreement 92–96%23. The proportions of permanent teeth with enamel defects caused by a luxation injury were after concussion 8%, subluxation 18%, extrusion 8%, lateral luxation 41%, intrusion 38% and avulsion 47% (Table 1). Table 2 shows the proportion of permanent teeth with enamel defects classified according to the modified DDE index and according to aetiology (trauma or other causes). Other causes were Molar-IncisorHypomineralization (MIH), dental fluorosis or defined as idiopathic. Fig. 1 shows an example of an enamel disturbance classified as idiopathic. When trauma was assessed the aetiological factor, minor demarcated opacities (≤3 mm) were most frequent (12%), Fig. 2. An example of a small opacity after a severe trauma is shown in Fig. 3. Hypoplasia was observed in 5% of the successors when trauma was the cause of the defect, whereas diffuse opacities were most frequent in teeth when the defects were due to other causes (13%). Statistically significant associations were found between enamel defects in the permanent successors and the child’s age at the time of injury (P < 0.05) and between enamel defects and the severity of the injury, dis-
T
25.5 25.5 15.4 22.7 4.2 0 21.3
O
16 35 2 10 1 0 64
T
7.9 17.5 7.7 40.9 37.5 47.3 22.0
Aetiology
5 24 1 18 9 9 66
Aetiology
63 137 13 44 24 19 300
Aetiology
Concussion Subluxation Extrusion Lateral luxation Intrusion Avulsion Total
Aetiology
%
Aetiology
n
Aetiology
%
Enamel defect (Modified DDE index)
n
Avulsion n = 19
Injured teeth n
Intrusion n = 24
Diagnosis
Lateral Luxation n = 44
Other causes
Extrusion n = 13
Due to trauma
Subluxation n = 137
Enamel defects
Concussion n = 63
Table 1. Numbers and proportions of permanent teeth with enamel defects (due to trauma and other causes) by type of luxation injury to primary predecessor (n = 300).
Table 2. Proportions% of permanent teeth with enamel defects classified according to the modified DDE index and according to aetiology (T = trauma, O = other causes) after a luxation injury to the primary predecessor (n = 300).
Consequences of injuries to primary incisors
224
A. B. Skaare, A.-L. M. Aas & N. J. Wang
Fig. 1. The photo shows teeth 11 and 21 with demarcated opacities >3 mm. Diagnosis: 51 subluxation at 3.5 years. No enamel defects on 6 years molars rule out Molar-Incisor Hypomineralization and the symmetry indicates an idiopathic aetiology according to three independent examiners.
placement (37.0%) or no displacement (14.5%), (P < 0.001). More severe defects were observed after displacement injuries at a lower age. Half of the teeth with lateral luxation that caused a defect in the permanent successor (9 of 18) were displaced in a buccal direction; an example is shown in Fig. 4. In six of 170 children (3.5%), a successor to a non-injured primary tooth adjacent to a severe luxation injury had enamel defects due to the trauma (indirect trauma). These six children had sustained a severe injury before the age of 4 years; avulsion (n = 1), intrusion (n = 3) and lateral luxation (n = 2). The defects were hypoplasia (n = 3), demarcated opacity (n = 2) and a combination (n = 1). An example of a permanent successor to a non-injured primary tooth is shown in Fig. 5a–c, the only permanent tooth in the study with a malformation of the crown. Of the 170 children, 62% had more than one injured tooth. Delayed eruption or other eruption problems were registered in 6.5% of the children and malposition of the permanent successor in 4% of the children. Follow-up
Fig. 2. The photo shows tooth 11 with a demarcated opacity < 3 mm. Diagnosis: 51 subluxation at 3 years of age.
Fig. 3. The photo shows tooth 21 with a demarcated opacity
