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Article ID: WMC002531 ISSN 2046-1690 Aggressive Hyperplastic Dental Follicle: Report of a Bilateral Case. Corresponding Author: Prof. Sergio E Cury, DDS PhD, Oral Pathology - UniFOA - University of Volta Redonda, 27.310-060 - Brazil Submitting Author: Prof. Sergio E Cury, DDS PhD, Oral Pathology - UniFOA - University of Volta Redonda, 27.310-060 - Brazil Article ID: WMC002531 Article Type: Case Report Submitted on:29-Nov-2011, 06:30:11 AM GMT Published on: 29-Nov-2011, 04:53:29 PM GMT Article URL: http://www.webmedcentral.com/article_view/2531 Subject Categories:ORAL MEDICINE Keywords:Dental follicle, Unerupted teeth, Hyperplasia How to cite the article:Cury S E, Cury M P, Cury S N, Luderer L A, Carvalho M , Molina O T. Aggressive Hyperplastic Dental Follicle: Report of a Bilateral Case. . WebmedCentral ORAL MEDICINE 2011;2(11):WMC002531 Source(s) of Funding: None Competing Interests: None WebmedCentral > Case Report Page 1 of 6

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Page 1: Aggressive Hyperplastic Dental Follicle: Report of a ...Aggressive Hyperplastic Dental Follicle: Report of a Bilateral Case. Corresponding Author: Prof. Sergio E Cury, DDS PhD, Oral

Article ID: WMC002531 ISSN 2046-1690

Aggressive Hyperplastic Dental Follicle: Report of aBilateral Case.Corresponding Author:Prof. Sergio E Cury,DDS PhD, Oral Pathology - UniFOA - University of Volta Redonda, 27.310-060 - Brazil

Submitting Author:Prof. Sergio E Cury,DDS PhD, Oral Pathology - UniFOA - University of Volta Redonda, 27.310-060 - Brazil

Article ID: WMC002531

Article Type: Case Report

Submitted on:29-Nov-2011, 06:30:11 AM GMT Published on: 29-Nov-2011, 04:53:29 PM GMT

Article URL: http://www.webmedcentral.com/article_view/2531

Subject Categories:ORAL MEDICINE

Keywords:Dental follicle, Unerupted teeth, Hyperplasia

How to cite the article:Cury S E, Cury M P, Cury S N, Luderer L A, Carvalho M , Molina O T. AggressiveHyperplastic Dental Follicle: Report of a Bilateral Case. . WebmedCentral ORAL MEDICINE2011;2(11):WMC002531

Source(s) of Funding:

None

Competing Interests:

None

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Aggressive Hyperplastic Dental Follicle: Report of aBilateral Case.Author(s): Cury S E, Cury M P, Cury S N, Luderer L A, Carvalho M , Molina O T

Abstract

This paper reports the case of an 11-year old boyexhibiting a unique form of aggressive bilateralhyperplastic dental follicle of his unerupted maxillarycanines. He was asymptomatic and unaware of thisoccurrence. Biopsy of the overlying tissue associatedwith the impacted canines revealed no significantpathological process other than focal inflammation andsome hyperplasia within the dental follicle.

Introduction

Pericoronal radiolucencies are common radiographicfindings observed in dental practice, especially in theorthodontic clinic. They usually represent a normal orenlarged dental follicle that requires no intervention;alternatively, they may represent a pathological entitythat requires appropriate management andhistopathological interpretation. A pericoronal spacegreater than 2.5 mmon an intraoral radiograph andgreater than 3 mmon a panoramic radiograph shouldbe regarded as suspicious (1).Two structures form the pericoronal follicle: thereduced enamel organ and the ectomesenchyme.Both can be the origin of several types of diseasesduring or after odontogenesis. Hamartomas, cysts andothers changes like hyperplasia have been reported(2,3).

Case Report(s)

An 11-year old white boy was referred to the privateOrthodontic Clinic, Volta Redonda, Brazil, with clinicalabsence of the maxillary canines and no history ofthose teeth ever being present. The patient’s medicalhistory was noncontributory. Panoramic and periapicalradiographs were obtained, which revealed expansive,well-circumscribed radiolucent lesions associated withunerupted maxillary canines. The width of thepericoronal space was18.3 mmon the panoramicradiograph and 13.3 mmon the periapical radiograph.The radiographs also revealed severe root resorptionof the central and lateral incisors (Figure1 A, B, C andD).

The patient was admitted on Department of OralSurgery,DentalSchool, University Center of VoltaRedonda, Brazil for surgical management under localanesthesia and the lesion was removed performedthrough an intraoral approach. The central incisorssurrounded by the lesion were maintained, but thelateral incisors were lost. The specimen consisted of ahard and well-demarcated capsule about12 mmindiameter each one.Hematoxylin and eosin-stained sections revealed ahyperplastic dental follicle similar to the tissue aroundthe developing tooth, with proliferation of odontogenicepithelium with superficial cuboidal cells andstratification of the underlying layers, resemblingtypical or reduced ameloblasts, besides a larger denseconnective tissue with a mononuclear inflammatorycomponent (lymphocytes and plasma cells) (Figure 1E and F). No tumor characteristics such asodontogenic fibroma, odontogenic myxoma orameloblastoma were evident in the lesionsAt two months after surgery, the patient interrupted thetreatment because of change of residence to anotherstate and was thus lost to follow-up.

Discussion

There are many etiologic factors associated with thisphenomenon, but the exact cause is often difficult todiagnose. These lesions may enlarge considerably ifallowed to develop unchecked, and have the potentialfor pathological transformation (1).Differential diagnosis should include principally withthe dentigerous cyst. Recent reports have supportedthis conclusion, emphasizing the fact that themicroscopic features of hyperplastic dental folliclesand dentigerous cysts are similar, with difficult ofdifferentiation (4,5). The dentigerous cyst is a lesionfrequently associated with unerupted teeth. In the past,however, many cysts considered to be dentigerousturned out to be inflammatory paradental cysts (6) ornormal follicular variations like hyperplasia erroneouslydiagnosed as cysts (3). Reported bilateral or multipleDC are extremely rare usually associated withd e v e l o p m e n t a l s y n d r o m e s s u c h a smucopolysaccharidosis, basal cell nevus syndromeand cleidocranial dysplasia (7).Tooth eruption is a complex and tightly regulated

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process that involves cells of the tooth organ and thesurrounding alveolus. Mononuclear cells (osteoclastprecursors) must be recruited into the dental follicleprior to the onset of eruption (8,9). In mechanicalstress condition like the eruption pressure, it releasesubstances like a aracdonic acid, prostraglandins andcitokins (Interleucin 1 and Tumor Necrose Factor). Thepresence of the high levels of this mediadors in thedental follicle have been describe on the literature, andplay a important role in bone remodeling, boneresorption, and new bone deposition (10,11). In ourcase, is it possible that the eruption physical power ofthe permanents canines with tissue hyperplasiacaused by chronic inflammation, and osteoclastrecruitment associate with the substances above willbe responsible for the aggressive external rootresorptions of the adjacent teeth.New researches will be achieved to elucidate theetiology of this lesion.

References

1. Farah CS, Savage NW. Pericoronal radiolucenciesand the significance of early detection. Aust Dent J.2002; 47(3):262-5.2. Damante JH, Fleury RN. A contribution to thediagnosis of the small dentigerous cyst or theparadental cyst. Pesqui Odontol Bras, 2001;15(3):238-46.3. Fukuta Y, Totsuka M, Takeda Y, Yamamoto H.Pathological study of the hyperplastic dental follicle. JNihon Univ Sch Dent, 1991; 33:166-73.4. Daley TD, Wysocki GP. The small dentigerous cyst:a diagnostic dilemma. Oral Surg Oral Med Oral PatholOral Radiol Endod, 1995; 79:77-81.5. Glosser JW, Campbell JH. Pathologic change insoft tissues associated with radiographically “normal”third molar impactions. Br J Oral Maxillofac Surg,1999; 37:259-60.6. Bohay RN, Weinberg S, Thorner PS. Theparadental cyst of the mandibular permanent firstmolar: report of a bilateral case. ASDC J Dent Child,1992; 59:361-65.7. Ustuner E, Fitoz S, Atasoy C, Erden I, Akyar S.Bilateral maxillary dentigerous cysts: A case report.Oral Surg Oral Med Oral Pathol Oral Radiol Endod,2003;95:632-5.8. Wise GE, Frazier-Bowers S, D'Souza RN. Cellular,molecular and genetic determinants of tooth eruption.Crit Rev Oral Biol Med, 2002; 13(4):323-334.9. Cahill DR, Marks SC Jr. Tooth eruption: evidencefor the central role of the dental follicle. J Oral PatholMed, 1980; 9:189-200.

10. Consolaro A. Reabsorções Dentárias nasespecialidades clínicas. 2ª Ed. Dental Press Editora,Maringá. 2005. 181p.11. Alhashimi N, Frithiof L, Brudvik P, Bakhiet M.Orthodontic tooth movement and de novo synthesis ofproinflammatory cytokines. Am J Orthod DentofacialOrthop. 2001;119(3):307-12.

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Illustrations

Illustration 1

Figure 1: Panoramic radiograph (A); Periapical radiograph of the right side (B); Central periapical radiograph (C); Periapicalradiograph of the left side (D); Larger dense connective tissue with a mononuclear inflammatory component lined by nonkeratinisedepithelium- Microscopy low magnification (E and F); Proliferation of nonkeratinised epithelium with superficial cuboidal cells-Microscopy high magnification (G and H).

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