Case Report

By Prof. Sergio E Cury , Prof. Maria Dorotea P Cury , Prof. Sergio Elias N Cury , Prof. Loreley A Luderer , Prof. Marcus Vinicius Carvalho , Prof. Omar T Molina
Corresponding Author Prof. Sergio E Cury
Oral Pathology - UniFOA - University of Volta Redonda, - Brazil 27.310-060
Submitting Author Prof. Sergio E Cury
Other Authors Prof. Maria Dorotea P Cury
Oral Pathology - UniFOA - University of Volta Redonda, - Brazil

Prof. Sergio Elias N Cury
Oral Pathology - UniFOA - University of Volta Redonda, - Brazil

Prof. Loreley A Luderer
Oral Pathology - UniFOA - University of Volta Redonda, - Brazil

Prof. Marcus Vinicius Carvalho
Oral Pathology - UniFOA - University of Volta Redonda, - Brazil

Prof. Omar T Molina
Oclusion and Stomatology, Dental School, UNIRG Fundation, - Brazil


Dental follicle, Unerupted teeth, Hyperplasia

Cury SE, Cury MP, Cury SN, Luderer LA, Carvalho M, Molina OT. Aggressive Hyperplastic Dental Follicle: Report of a Bilateral Case.. WebmedCentral ORAL MEDICINE 2011;2(11):WMC002531
doi: 10.9754/journal.wmc.2011.002531
Submitted on: 29 Nov 2011 06:30:11 AM GMT
Published on: 29 Nov 2011 04:53:29 PM GMT


This paper reports the case of an 11-year old boy exhibiting a unique form of aggressive bilateral hyperplastic dental follicle of his unerupted maxillary canines. He was asymptomatic and unaware of this occurrence. Biopsy of the overlying tissue associated with the impacted canines revealed no significant pathological process other than focal inflammation and some hyperplasia within the dental follicle.


Pericoronal radiolucencies are common radiographic findings observed in dental practice, especially in the orthodontic clinic. They usually represent a normal or enlarged dental follicle that requires no intervention; alternatively, they may represent a pathological entity that requires appropriate management and histopathological interpretation. A pericoronal space greater than 2.5 mmon an intraoral radiograph and greater than 3 mmon a panoramic radiograph should be regarded as suspicious (1).
Two structures form the pericoronal follicle: the reduced enamel organ and the ectomesenchyme. Both can be the origin of several types of diseases during or after odontogenesis. Hamartomas, cysts and others changes like hyperplasia have been reported (2,3).

Case Report(s)

An 11-year old white boy was referred to the private Orthodontic Clinic, Volta Redonda, Brazil, with clinical absence of the maxillary canines and no history of those teeth ever being present. The patient’s medical history was noncontributory. Panoramic and periapical radiographs were obtained, which revealed expansive, well-circumscribed radiolucent lesions associated with unerupted maxillary canines. The width of the pericoronal space was18.3 mmon the panoramic radiograph and 13.3 mmon the periapical radiograph. The radiographs also revealed severe root resorption of the central and lateral incisors (Figure1 A, B, C and D).
The patient was admitted on Department of Oral Surgery,DentalSchool, University Center of Volta Redonda, Brazil for surgical management under local anesthesia and the lesion was removed performed through an intraoral approach. The central incisors surrounded by the lesion were maintained, but the lateral incisors were lost. The specimen consisted of a hard and well-demarcated capsule about12 mmin diameter each one.
Hematoxylin and eosin-stained sections revealed a hyperplastic dental follicle similar to the tissue around the developing tooth, with proliferation of odontogenic epithelium with superficial cuboidal cells and stratification of the underlying layers, resembling typical or reduced ameloblasts, besides a larger dense connective tissue with a mononuclear inflammatory component (lymphocytes and plasma cells) (Figure 1 E and F). No tumor characteristics such as odontogenic fibroma, odontogenic myxoma or ameloblastoma were evident in the lesions
At two months after surgery, the patient interrupted the treatment because of change of residence to another state and was thus lost to follow-up.


There are many etiologic factors associated with this phenomenon, but the exact cause is often difficult to diagnose. These lesions may enlarge considerably if allowed to develop unchecked, and have the potential for pathological transformation (1).
Differential diagnosis should include principally with the dentigerous cyst. Recent reports have supported this conclusion, emphasizing the fact that the microscopic features of hyperplastic dental follicles and dentigerous cysts are similar, with difficult of differentiation (4,5). The dentigerous cyst is a lesion frequently associated with unerupted teeth. In the past, however, many cysts considered to be dentigerous turned out to be inflammatory paradental cysts (6) or normal follicular variations like hyperplasia erroneously diagnosed as cysts (3). Reported bilateral or multiple DC are extremely rare usually associated with developmental syndromes such as mucopolysaccharidosis, basal cell nevus syndrome and cleidocranial dysplasia (7).
Tooth eruption is a complex and tightly regulated process that involves cells of the tooth organ and the surrounding alveolus. Mononuclear cells (osteoclast precursors) must be recruited into the dental follicle prior to the onset of eruption (8,9). In mechanical stress condition like the eruption pressure, it release substances like a aracdonic acid, prostraglandins and citokins (Interleucin 1 and Tumor Necrose Factor). The presence of the high levels of this mediadors in the dental follicle have been describe on the literature, and play a important role in bone remodeling, bone resorption, and new bone deposition (10,11). In our case, is it possible that the eruption physical power of the permanents canines with tissue hyperplasia caused by chronic inflammation, and osteoclast recruitment associate with the substances above will be responsible for the aggressive external root resorptions of the adjacent teeth.
New researches will be achieved to elucidate the etiology of this lesion.


1. Farah CS, Savage NW. Pericoronal radiolucencies and the significance of early detection. Aust Dent J. 2002; 47(3):262-5.
2. Damante JH, Fleury RN. A contribution to the diagnosis of the small dentigerous cyst or the paradental 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. J Nihon Univ Sch Dent, 1991; 33:166-73.
4. Daley TD, Wysocki GP. The small dentigerous cyst: a diagnostic dilemma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 1995; 79:77-81.
5. Glosser JW, Campbell JH. Pathologic change in soft tissues associated with radiographically “normal” third molar impactions. Br J Oral Maxillofac Surg, 1999;  37:259-60.
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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: evidence for the central role of the dental follicle. J Oral Pathol Med, 1980; 9:189-200.
10. Consolaro A. Reabsorções Dentárias nas especialidades 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 of proinflammatory cytokines. Am J Orthod Dentofacial Orthop. 2001;119(3):307-12.

Source(s) of Funding


Competing Interests



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