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  1. 1. PAEDIATRIC DENTISTRY TRAUMATIC INJURIES IN THE CHILD Updated April 2007 1. INTRODUCTION AND OVERALL ASSESSMENT 1.1 Prevalence and Aetiology 1.1.1 Primary Dentition 1.1.2 Permanent Dentition 1.2 History 1.2.1 Medical History 1.2.2 Non-Accidental Injuries 1.3 Classification 1.3.1 Injuries to Hard Tissues 1.3.2 Injuries to Periodontal Tissues 1.3.3 Injuries to Supporting Bone 1.3.4 Injuries to Gingiva and Oral Mucosa 2. EXAMINATION 2.1 Extra-oral 2.2 Intra-oral 2.3 Additional Investigations 2.3.1 Sensibility Tests 2.3.2 Radiographs 3. TREATMENT PLANNING 3.1 Primary Dentition 3.1.1 Effects on developing permanent teeth 3.2 Permanent Dentition 3.2.1 Crown fractures 3.2.2 Root fractures 3.2.3 Immature Apices Technique for Vital Pulpotomy Technique for Induction of Apical Barrier 3.2.4 Intrusions, Subluxations, Luxations 3.2.5 Replantation 3.2.6. Preventive measures C:lectrau_inj 1
  2. 2. 1. INTRODUCTION AND OVERALL ASSESSMENT 1.1 Prevalence. 1.1.1 Primary Dentition Trauma to the primary dentition is a common occurrence, but many accidents are never seen by a dentist as they are of a very minor nature. It has been reported that 24% - 35% of five year old children showed evidence of some kind of dental injury. The most usual age at which injuries occur is between 2 and 4 years. Children at this age have incompletely developed co-ordination and judgement and injure themselves usually whilst playing or exploring their surroundings. Injuries often comprise of tooth luxations as the bone surrounding the teeth is very resilient. 1.1.2 Permanent Dentition The prevalence of trauma in published literature varies widely and largely depends on the population sampled, gender and age. The Child Dental Health Survey of 2003 in the United Kingdom showed that almost 11% of 12 year olds had experienced some trauma with a ratio of almost 2:1 of boys to girls. When children reach school age accidents in the playground are common. The peak age in the U.K is 7-10 years of age with the peak time of year in the summer months. Other common aetiological factors are bicycle injuries, contact sports, road traffic accidents and assaults. Although horse-riding is a minority sport it is a significant source of injury. People with learning disabilities and epilepsy also have been shown to have a high prevalence of trauma and are at special risk. 1.2 History of Trauma Vital information to obtain is:- How the accident happened. May give an indication of other injuries. Consider non-accidental injury (see below). When the accident happened. Time interval between injury and treatment may significantly affect prognosis. Where it happened. Consider tetanus protection. Medico-legal implications. Check if there are any symptoms. 1.2.1 Medical History Bleeding disorders Cardiac disease Epilepsy Allergies - specifically to Penicillin Anti-tetanus protection - date of booster Did trauma cause loss of consciousness, amnesia, drowsiness, vomiting or headache? C:lectrau_inj 2
  3. 3. 1.2.2 Non Accidental Injuries, Child Abuse. (N.A.I) A child is considered to be abused if he or she is treated in a way that is unacceptable in a given culture at a given time. Since Kempe et al (1962) published their paper on the “Battered Child Syndrome” this has now been recognised as an International issue with widespread prevalence. In the U.K. there are more than 20 times the number of reported cases than 10 years ago with at least 1 child per 1,000 per year suffering from physical abuse. In the U.S.A more than 95% of serious intra-cranial injuries during the first year of life are the result of abuse. It has been estimated that at least 80 children per week in U.S.A and 2-3 children per week in Britain will die as a result of abuse or neglect. These figures are much lower in Scandinavia. Contributory factors:- Poorer socio-economic groups Social deprivation Single parent families Young parents of low intelligence Parents themselves abused as children Psychiatric illness Alcohol and other drug abuse Poverty Unemployment Marital problems Disabilities Diagnosis:- Delay in seeking medical help Inconsistent history History not compatible with observed trauma Parents mood and behaviour abnormal Child’s appearance and interaction with parents is abnormal. “Frozen awareness”. Child’s and parent’s accounts differ. Physical signs:- Bruising of different ages Bruises on ears and neck Fraenum tear on non-ambulatory child Human hand marks Abrasions and lacerations caused by a variety of objects Burns, cigarette etc. Bite marks. C:lectrau_inj 3
  4. 4. Dentist’s Role: GDP may be first professional to see or suspect N.A.I. Primary aim is to ensure safety of the child. Secondary aim - provide help and counselling for parents or carers so that the abuse stops. • Severe injuries - refer immediately to hospital based Paediatrician. • Suspicion - contact G.M.P./Social Services/Local Child Welfare dept. Ensure that clinical records are complete and comprehensive with photographs if possible. 1.3 Classification Textbook and Colour Atlas of Traumatic Injuries to the Teeth. J O Andreasen and F M Andreasen. Blackwell Publishing. 2005. 4th Edition. 1.3.1. Injuries to Hard Tissues a. Enamel Infraction. Incomplete fracture/crack, no loss of tooth substance b. Enamel Fracture Loss of tooth substance confined to enamel c. Enamel - Dentine Fracture. d. Coronal fracture with exposure of pulp Root fracture - Apical third - Middle third - Coronal third - Comminution 1.3.2 Injuries to Periodontal Tissues a. Concussion trauma to supporting structures giving marked reaction to percussion but no mobility or displacement of tooth. b. Subluxation loosening but no displacement. c. Extrusive Luxation partial displacement of tooth out of socket. d. Lateral Luxation displacement of tooth laterally, accompanied by comminution or fracture of alveolar socket. e. Intrusive Luxation displacement of tooth into alveolar bone, accompanied by comminution or fracture of alveolar socket. f. Avulsion complete displacement of tooth out of socket. C:lectrau_inj 4
  5. 5. 1.3.3 Injuries to Supporting Bone a. Comminution of alveolar socket found in intrusive and lateral luxations. b. Fracture of alveolar socket wall c. Fracture of alveolar process d. Fracture of mandible or maxilla/Nasal complex 1.3.4 Injuries to Gingiva or Oral Mucosa a. Laceration b. Contusion c. Abrasion 2. EXAMINATION The use of a standardised examination sheet can be very helpful: - See departmental Trauma Form. 2.1 Extra-Oral Asymmetry? Palpate facial skeleton Record any extra-oral wounds/bruising Paraesthesia 2.2 Intra-Oral Record any injuries to oral mucosa or gingiva - is suturing necessary? General Condition of Mouth - Caries, O.H, Rapid Orthodontic Assessment Examine tooth crowns for - presence and extent of fractures, pulp exposures, changes of colour Record displacement of teeth Abnormalities in occlusion? Abnormal mobility of teeth or alveolar segments? Percussion. 2.3 Additional Investigations 2.3.1 Sensibility tests Mechanical stimulation Ethyl chloride (ice, carbon dioxide snow, etc.) Electric Pulp testing Laser Doppler Flowmetry C:lectrau_inj 5
  6. 6. 2.3.2 Radiographs Extra-oral views - to exclude facial fractures Intra-oral. Use standard paralleling devices. It is important that radiographs are taken to assess:- Root fracture State of apex - dental age may not coincide with chronological age. Size of pulp Periapical rarefaction Baseline for comparison with future radiographs For soft tissue damage, consider soft tissue radiographs - pieces of tooth may be embedded in the lips. If part of the tooth remains unaccounted for arrange for chest x-ray. 3. TREATMENT PLANNING 3.1 Primary Dentition Much of the trauma in infants and young children results in soft tissue damage and/or tooth displacements rather than fracture of the teeth. Treatment options are much simpler than the permanent dentition. a. Enamel Fractures Smooth edges, apply Duraphat fluoride varnish b. Enamel and dentine fractures Hardsetting calcium hydroxide preparation over exposed dentine with glass ionomer or composite restoration c. Pulp involvement. Usually requires extraction. Extirpation of pulp and root filling with a resorbable paste e.g., Kri paste, non setting Zinc Oxide-Eugenol, or Calcium Hydroxide has been shown to lead to a higher incidence of hypoplastic defects in permanent successors. d. Discoloured and/or non vital teeth, even if symptomless, require radiographic and clinical follow-up. If there is evidence of periapical involvement pulpectomy or extraction should be considered, as there is risk of damage to permanent successors. e. Luxations: Intrusion - allow to re-erupt and monitor Extrusive and lateral - if minimal displacement leave (or CAREFULLY reposition - only for suitable cases). If interfering with occlusion - then extract. f. Avulsion: Replantation is contra-indicated due to possible damage to successor. C:lectrau_inj 6
  7. 7. 3.1.1 Effects on developing permanent teeth. Traumatic injuries to the primary teeth may indirectly affect the developing permanent teeth resulting in :- a. Hypoplasia due to - Direct trauma - Infection b. Dilaceration of crown or root. c. Arrested development, failure of eruption of the successor It is essential that the parents of a child who has suffered trauma to the primary dentition should be warned of the possibility of damage to the permanent teeth. 3.2 Permanent Dentition There are two questions that must be asked for any dental injuries - It is possible to save the tooth? The main factors that reduce the prognosis are:- Severe mobility A root fracture in the coronal third of the root A coronal fracture extending subgingivally A non-vital tooth with an open apex. Even if the long term prognosis seems poor it may be desirable to keep the tooth as a maintainer of space and alveolar bone. If it is possible to save the tooth, is it desirable? General condition of the mouth and attitude of the patient and parent to treatment. Orthodontic consideration, e.g. Increased overjet, Gross incisor crowding. Any serious medical conditions, mental or physical handicap. 3.2.1 Crown Fractures. a. Enamel fractures Smooth edges, apply Duraphat fluoride varnish. Follow up with sensibility tests, etc. b. Enamel and Dentine fractures. Hard setting calcium hydroxide preparation (e.g. Dycal, Life) should be placed over all exposed dentine as soon as possible. A composite or glass ionomer bandage (dressing) can be used initially followed by a definitive composite restoration. The sensibility should be monitored regularly post trauma. Early treatment improves the chance of maintaining pulp vitality. Follow up after 3 months and thereafter at 6 monthly intervals. c. Pulp involvement. C:lectrau_inj 7
  8. 8. Closed Apex: - extirpate pulp, conventional endodontic treatment. Consider Ca(OH2) therapy for 6/12 prior to definitive root filling. Open Apex - see later. 3.2.2 Root Fractures These are relatively uncommon - comprising less than 5% of injuries affecting the permanent dentition, and usually affecting maxillary central incisors in the 11-18 years old age group. Clinical examination usually reveals a slightly extruded tooth often displaced lingually. Radiographs will only show a root fracture if the central beam is directed within a maximum range of 15 to 20 degrees of the fracture plane. Therefore take 2 views. The principles of treatment are reduction of displaced coronal fragments and immobilisation to optimise the possibility of the fractured segments uniting with a calcified material. This is usually a combination of dentine and cementum. It is mainly middle third root fractures which require splinting. Recent information suggests this time should be approximately 2-3 weeks and that splinting should not be rigid (Andreasen, 2001). Apical third root fractures are not often mobile enough to need splinting. Coronal third root fractures usually have insufficient root length on the crown for adequate function. It is sometimes impossible to conserve teeth with coronal third fractures but occasionally extrusion of the root portion by Orthodontic means is used followed by endodontic treatment and the provision of a post retained crown with a diaphragm. The pulp is more likely to survive after root fracture than after luxation, but pulp canal obliteration and external/internal resorption are common. 3.2.3 Immature Apices If a crown fracture involving the pulp occurs in an immature tooth with an open apex then it is important to attempt to maintain a vital radicular pulp so that continued root growth and normal apexogenesis can occur. If the pulp exposure is small and the child seen immediately, pulp capping with hard setting calcium hydroxide or MTA can be attempted. If the child is seen soon after the trauma has occurred and the pulp exposure is greater than 1mm then a vital pulpotomy should be carried out. Technique for Vital Pulpotomy:- a. Local anaesthesia b. Isolate - rubber dam c. Swab tooth with chlorhexidine C:lectrau_inj 8
  9. 9. d. The amount of pulp removed depends on the condition of the underlying pulp. Initially remove 2mm of the pulp and surrounding dentine using a diamond bur in a conventional handpiece. Cool area with sterile saline/water. Once healthy pulp is reached the bleeding stops quickly. (note: Cvek pulpotomy = partial removal of coronal pulp). If profuse haemorrhage occurs the pulp is hyperaemic and further tissue must be removed. If necessary, remove tissue as far as cervical constriction to be sure that necrotic debris has been removed. e. Clean and wash out all pulpal remnants with saline and allow haemorrhage to stop. f. Apply non setting Ca(OH)2 or MTA over amputated pulp stump. g. Seal with hard setting Ca(OH)2 and glass ionomer or composite without applying any pressure. h. Restore to ensure good seal. i. Follow up, 3 months then 6 monthly and take radiographs and sensibility tests. If pulp becomes necrotic, then prepare canal for root filling and attempt to induce an apical barrier with non-setting Ca(OH)2 or apexify with MTA. Technique for Induction of Apical Barrier:- First Visit Anaesthesia is not usually required. However, occasionally there is some vital tissue in the apical region. a. Isolate tooth, using rubber dam. b. Swab tooth and surrounding tissues with chlorhexidine. c. Open root canal via cingulum - good access is essential. d. Remove pulp remnants. e. Take a diagnostic radiograph, full working length 1 to 2mm from apex. If there is a purulent discharge, leave the tooth on open drainage for 24 hours. If no discharge proceed to ‘f’. f. Use progressive technique to mechanically prepare the root canal with files and copious irrigation. Do not use instruments within 2mm of apex, to avoid damaging granulation tissue. This tissue is responsible for apical closure. g. Irrigate freely with sterile water. h. Dry canal with paperpoints. i. Place non setting Ca (OH)2 paste in dry root canal to completely fill it to the apex. Use cotton wool pledget to compress the paste to the apex j. Seal access cavity with cotton wool pledget, then a zinc oxide - eugenol or glass ionomer cement. C:lectrau_inj 9
  10. 10. ( note: Other root canal medicaments which have been recommended to control infection in the root canal include poly-antibiotic pastes, corticosteroid pastes, Ledermix, and paramonochlorphenol. However, the scientific literature supports the simple use of Ca(OH)2). k. Replace Ca(OH)2 usually at 3 monthly intervals. Interim Visits a. Remove dressing, file and irrigate with water or saline to remove Ca(OH)2 paste. Dry with paper points. b. Check for apical barrier formation using a paper point. If no barrier is detected then redress with Ca (OH)2 paste - as above. c. If complete barrier found - place G.P. root filling. d. If the tooth has a large periapical radiolucencency it is better to wait until there is clear evidence that bony healing is occurring before the final G.P. root filling is placed. 3.2.4 Intrusions, Subluxations, Luxations Intrusions Although these injuries may be severe, they occur relatively rarely and this factor contributes to the difficulties in defining the correct treatment. Mildly intruded (less than 3mm) incisor teeth with incomplete root development - usually re-erupt. Intruded teeth with complete apices. if mild may re-erupt if moderate to severe, may require repositioning manually or orthodontically severely intruded teeth have a poor prognosis Subluxations and Luxations Subluxated teeth retain their normal position in the dental arch but the tooth is mobile in a horizontal direction and there is usually haemorrhage from the gingival crevice. Laterally luxated teeth usually have their crowns displaced lingually. Most Luxations represent a combined injury to the pulp and periodontium. Fixation is not needed following minor injuries but follow up of the vitality of the teeth is essential. More severe injuries require repositioning of teeth under a local anaesthetic then compression of labial and palatal bone plates to ensure complete repositioning and good healing. Then splint with acid-etch retained material for 3 weeks. Follow-up vitality. C:lectrau_inj 10
  11. 11. 3.2.5 Replantation If a child is seen within a few hours of avulsion of teeth then replantation should be considered. Studies have shown a 90% success rate if teeth are replanted within 1 hour. A natural tooth is a valuable space-maintainer during the growth period even though it may subsequently be lost. a. Management at site of accident:- • If telephone advice is sought and re-implantation is appropriate then advise immediate replantation. • If this is not possible then store in cold fresh milk (alternatives would be normal saline or saliva). • Advise patient to attend dental surgeon immediately. b. Initial Management:- History - How, When, Where etc. See Section 1.2. General Medical History See Section 1.2.1. General State of Mouth See Section 2.2. Replantation:- • Local Anaesthesia - may not be required if presentation to G.D.P. is immediate. • Wash out blood clot in socket with saline if necessary. • Do not handle root surface of tooth - if dirty rinse with milk, normal saline or water. • Reimplant and reposition. • Splint to adjacent teeth for 7 to 10 days at splint removal visit - use of acid etch retained materials with or without arch wire. Do not splint rigidly. • Arrange antibiotic analgesia and anti-tetanus protection. • Home care advice - O. H. with Corsodyl mouthwash - Soft diet. • Review within 48 hours. c. Follow-up Management Endodontic Treatment:- • Open apex + short extra-oral time – delay endodontic treatment as tooth may re-vascularize. Review at 3 - 4 week intervals, take radiographs. If becomes non-vital treat as in 3.2.3. - induction of apical barrier (or apexify with MTA). • Closed apices - commence endodontic treatment at 7 to 10 days. Thorough mechanical cleansing etc. Insert Calcium Hydroxide, seal access. Re-dress with Ca(OH)2 for 6 to 12 months. Replace after 3 to 6 months. If no evidence of root resorption then obturate canal with G.P. The main reason for failure of replanted teeth is inflammatory and replacement resorption of the root. This is much more likely to occur in teeth that have been C:lectrau_inj 11
  12. 12. allowed to dry out of the mouth and/or those that have had prolonged periods of extra-oral time. 3.2.6 Preventive Measures a. Provision of sports mouth guard for at risk groups e.g. sports patient with Class II Division I. b. Educating parents/school e.g. Colgate leaflets, posters etc. Further Reading:- Essentials of Traumatic Injuries to the Teeth. J O Andreasen and F Andreasen. Blackwell Munksgaard. 2000. 2nd Edition. Textbook and Colour Atlas of Traumatic Injuries to the Teeth. J O Andreasen and F M Andreasen. Blackwell Publishing. 2005. 4th Edition. Practical Treatment Planning for the Paedodontic Patient. A S Blinkhorn, I C Mackie and S Anthony. Quintessence. 1992. Paediatric Dentistry. R R Welbury, M S Duggal and M-T Hosey. Oxford Medical. 2005. National Clinical Guidelines 1997. Faculty of Dental Surgery. The Royal College of Surgeons of England. RCS (Eng.) & DoH. 1997. Treatment of the Avulsed Permanent Incisor Teeth in Children. T A Gregg & D Boyd. International Journal of Paediatric Dentistry. 1998; 8: 75-81. Treatment of Traumatically Intruded Permanent Incisor Teeth in Children. M J Kinirons. International Journal of Paediatric Dentistry. 1998;8:165-168. Rev: Oct 06 C:lectrau_inj 12