Oral Health Group
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Acute Facial Swelling and the Importance of a Dental Consultation – A Case Report

January 1, 2005
by Keith Titley, BDS, MScD, FRCD(C), Karen Campbell, DDS


In general most facial infections are of odontogenic origin and they do not normally occur without a predisposing condition.1 These infections can be caused by dental caries or deep restorations that approximate the pulp, infected pulps leading to a periapical abscess, periodontal abcess and pericoronitis. Failure to institute early treatment may result in the development of osteoperiostitis of the jaw, osteomyelitis and deep fascial space infection.1

Children are particularly susceptible to rapid systemic involvement so that early recognition and management of an emergent facial swelling is critical for successful resolution. The principles of management are common to both children and adults. These include establishment of drainage by surgical incision, removal of the source of the infection by extraction of the offending tooth or by instituting endodontic treatment. In some cases, identification of an appropriate antibiotic by culture and sensitivity testing for pathogenic bacteria may be required. Medical supportive treatment for fever, pain, dehydration and assessment of airway compromise may also be indicated.2

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There are instances however, when a patient may present with acute facial swelling for which there appears to be no obvious odontologic origin. A cursory intra oral examination may reveal oral mucosa that appears to be within the limits of normal, teeth that are morphologically normal and no clinical evidence of caries. The following case is illustrative of this specific situation and underscores the importance of appropriate and timely dental consultation for the patient that presents with acute facial swelling to the hospital emergency department setting.

CASE REPORT

Patient: Female aged 10 years.

Chief complaint: Patient presented for a ‘check-up’ at the University of Toronto Pediatric Dental Clinic in January, 2004.

Medical history: Her medical history was non-contributory, no medications or known drug allergies.

Previous dental history: The patient had received regular dental care at a private practitioner’s office and reported that she had a check-up in July, 2003 where she had been declared caries free and had a cleaning. In November of 2003, she had an infected loose (presumed exfoliating) maxillary left primary canine tooth (63) extracted because of pain and associated swelling. The dentist prescribed oral amoxycillin (dose unknown) in a ‘three times daily’ dosing schedule. Two days later the patient presented in a hospital emergency room with a left- sided facial cellulitis extending to the periorbital area.

The emergency room staff did not request an examination by dentistry because their oral examination revealed an apparently caries free dentition with no abcesses. The patient was placed on intravenously administered clindamycin and transferred to a hospital closer to her home where she was admitted and treated for a “sinus infection” for 17 days. After this amount of time the swelling had resolved so the patient was discharged but reported that there was still some discomfort associated with the area.

EXTRA-ORAL EXAMINATION

The patient was a healthy, well-developed pre-adolescent female exhibiting no extra-oral swelling, asymmetry, indurations, erythema or trismus. The patient exhibited a degree of anxiety related distress.

INTRA-ORAL EXAMINATION

The patient was in the “ugly duckling” stage of mixed dentition development with an Angles Class 1 molar relationship, 50 percent overbite and 5mm overjet. There was no clinical evidence of caries, oral hygiene was rated as fair and there was a midline palatal torus. All erupted teeth were within normal morphological limits with the exception of the maxillary left permanent lateral incisor (22). This tooth was peg shaped with a small pit at its cusp tip, detectable by careful inspection and probing. Tooth 22 was also tender to percussion and appeared dark on transillumination. An associated area of erythema was noted in the labial vestibule apical to tooth 22.

RADIOGRAPHIC EXAMINATION

Since the patient had presented for a check up bitewing radiographs were taken in addition to periapical radiographs of the maxillary anterior teeth (Fig. 1). No proximal carious lesions were found on the bitewing radiographs confirming the clinical impression that the patient was caries free. The periapical radiograph of tooth 22 revealed a type III dens invaginatus3 with an area of apical rarefaction continuous with the follicular space of the unerupted maxillary left permanent canine (23).

DIAGNOSIS

Chronic dentoalveolar infection associated with non-vital 22, secondary to a Type III dens invaginatus.

PROGNOSIS

The prognosis for tooth 22 was deemed hopeless because of the complicated root anatomy, poor crown morphology, unfavourable crown:root ratio and the previous history of severe infection involving a period of prolonged hospitalization.

TREATMENT PLAN

The initial treatment plan was to extract tooth 22 in order to both effectively eliminate the potential for re-infection and recurrence of the facial cellulitis and to allow tooth 23 to passively erupt. Future treatment considerations for this patient will include assessment of the morphology of tooth 23 for suitability for cosmetic reshaping in combination with orthodontic closure of the residual arch space. Alternatively, ditalization of tooth 23 using fixed orthodontic appliances could also be considered to create space for either a dental implant or fixed or removable prosthetic replacement for tooth 22.

TREATMENT

Due to the patient’s extreme anxiety, tooth 22 was extracted using local anaesthesia supplemented with nitrous oxide sedation. The surgery was completed without complications and the patient was dismissed in good condition with appropriate verbal and written post-operative instructions. Arrangements were made for follow-up and included six monthly recall appointments to monitor caries status, oral hygiene and the developing dentition.

DISCUSSION

Dens invaginatus was first described by Ploquet in the tooth of a whale in 17943 and by Salter in a human tooth in 1855 where he named it a ‘warty tooth’.4 The prevalence has been reported to range from 0.04 to 10 percent in subjects surveyed.5 Synonyms for this malformation include: dens in dente, invaginated odontome, dilated gestant odontome, dilated composite odontome, tooth inclusion and dentoid in dente. The most commonly affected teeth are maxillary permanent lateral incisors with bilateral occurrences not being uncommon.3 The anomaly has also been found in maxillary central incisors, canines, premolars and molars and in mandibular incisors and premolars.3,6 It has also been reported to occur in primary teeth although this is rare.3

In the majority of cases a dens invaginatus is detected by chance but teeth that present clinically with unusual crown morphologies such as barrel-shaped, conical or peg-shaped, dilated or with deep cingulum pits may be important indicators of the anomaly. On the other hand affected teeth may show no clinical signs of the malformation.3 Frequently, a definitive diagnosis can only be made with the use of a periapical radiograph. If one tooth demonstrates the anomaly, it is prudent to inspect the contralateral tooth because of the frequency of bilateral occurrence.3

Dens invaginatus is an anomaly of morphodifferentiation during which part of the enamel organ becomes invaginated so that part of it protrudes into the dental papilla.7 This invagination forms a space or cavity that allows for early bacterial colonization and stagnation producing conditions that are conducive for the initiation of early caries.

Since the dentin between the floor of the invagination cavity is often very poorly formed or incomplete these bacteria and their products can gain access to the dental pulp resulting in pulp necrosis sometimes even before the completion of root development.7,8 The anomaly has been described as occurring in three forms:9

Type I: The invagination is a minor enamel lined form, confined within the cro
wn of the tooth and does not extend beyond the external amelocemental junction.

Type II: An enamel lined form that invades the root but remains confined within it as a blind sac. The invagination may communicate with the pulp, may or may not be grossly dilated and when dilated may cause a corresponding dilation of the root or crown.

Type III: The invagination extends all the way from the crown to the apex creating a second foramen either in the apical or periodontal area. There is usually no communication with the pulp and the invagination may appear completely lined with enamel but more often part of it is lined with cementum.

The treatment of dens invaginatus can present a challenge to the clinician particularly if the affected tooth has a complicated morphology and complex system of root canals.10

The recommended treatment for Type I cases is one of prevention and control in which the defect is sealed with a fissure sealant or restoration.

For Type II cases treatment may vary from restoration of the defect, endodontic therapy or a combination of endodontic treatment and root end surgery.

Treatment recommendations for the more complex Type III cases may include endodontic therapy, surgical therapy, a combination of endodontic and surgical therapy, intentional replantation where combined endodontic-surgical treatment fails and apical access can only be attained by extracting the tooth, and finally extraction when the invaginated tooth causes an aesthetic or functional disturbance.10,11

It is recommended that in the planning of treatment, consideration must be given to accessibility and complexity of the root canal system, apical morphology, patient cooperation and most particularly the skill of the operator.8

This case underscores the importance of seeking a dental consultation when a patient with an acute facial infection presents in a hospital emergency room particularly since the majority of cases of dens invaginatus are detected by chance and affected teeth may show no clinical signs of malformation.3 A clinical examination by emergency room staff revealed an apparently caries free dentition and normal oral mucosa and resulted in the patient being treated for a maxillary sinus infection. Failure to seek a dental consultation in this case also resulted in a prolonged period of hospitalization with its accumulative costs to the health care system. Despite resolution of the facial swelling and discharge from hospital, the patient continued to report discomfort on the area because the underlying cause was never identified and definitively treated.

An examination by a dentist at the time of the initial presentation to the emergency department would have prompted a more detailed investigation including the appropriate intra oral radiographs. Appraisal of these radiographs would have resulted in the diagnosis of the dens invaginatus as the causative factor. Definitive treatment could then have been instituted without delay to resolve the acute alveolar infection that had arisen because of this anomaly.

Hospital emergency room staff should be encouraged to seek a dental consultation for any patient presenting with an acute facial swelling. Dentists should be encouraged to liaise with their local professionals in this regard and offer assistance to confirm or rule out dental causes in cases of acute facial swelling.

Keith Titley is Professor, Department of Pediatric Dentistry, University of Toronto, and Editorial Board Member for Pediatric Dentistry, Oral Health.

Karen Campbell is Master of Science candidate, Department of Pediatric Dentistry, University of Toronto.

Oral Health welcomes this original article.

REFERENCES

1.Sandor GKB, Low DE, Judd PL, Davidson RJ. Antimicrobial treatment options in the management of odontogenic infections. J Can Dent Assoc. 1998; 64: 508-514.

2.Kilgore TB. Minor oral surgery in pediatric dentistry. In Braham RL, Morris ME. Textbook of pediatric dentistry. 2nd ed., 1985; pp407-430. Williams and Wilkins, Baltimore, MD 21202, USA.

3.Hlsman M. Dens invaginatus: Aetiology, classification, prevalence, diagnosis, and treatment considerations. Int Endod J. 1997; 30: 79-90.

4.Ruprecht A, Sastry KARH, Batniji S, Lambourne A. The clinical significance of dental invagination. J Pedod. 1987; 11: 176-181.

5.Hovland EJ, Block RM. Nonrecognition and subsequent endodontic treatment of dens invaginatus. J Endod. 1977; 3: 360-361.

6.Froner IC, da Costa Rocha LF, da Costa WF, da Rocha Barros VM, Morello D. Complex treatment of dens invaginatus type III in maxillary lateral incisor. Endod Dent Traumatol. 1999; 15: 88-90.

7.Rushton MA, Cooke BED. Oral histopathology: A manual for students and practitioners of dentistry. 1963; pp20-22. E and S Livingstone Ltd., Edinburgh and London.

8.Rotstein I, Stabholz A, Heling I, Friedman S. Clinical considerations in the treatment of dens invaginatus. Endod Dent Traumatol. 1987; 3: 249-254.

9.Oehlers FAC. Dens invaginatus (dilated composite odontome) 1. Variations of the invagination process and associated anterior crown forms. O.S., O. M., and O.P. 1957; 10: 1204-1218.

10.Sousa SMG, Bramante CM. Dens invaginatus: treatment choices. Endod Dent Traumatol. 1998; 14: 152-158.

11.Linder C, Messer HH, Tyas MJ. A complex treatment of dens invaginatus. Endod Dent Traumatol. 1995; 11: 153-155.


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