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Case Report

Follicular with plexiform ameloblastoma in anterior

mandible: Report of case and literature review

Rahul Srivastava a,*, Parvathi Devi b, Bhuvan Jyoti c, Shobhit Pradhan d, Ashutosh Shukla e

a Senior Lecturer, Department of Oral Medicine and Radiology, Rama Dental College, Hospital and Research Centre, Kanpur, Uttar Pradesh,

Indiab

Professor and Head of the Department, Department of Oral Medicine and Radiology, Rama Dental College, Hospital and Research Centre,Kanpur, Uttar Pradesh, IndiacDental Surgeon and Consultant, Oral Medicine and Radiology, Ranchi Institute of Neuro-Psychiatry and Allied Sciences, IndiadSenior Lecturer, Department of Oral Pathology, HIDS, Paonta Sahib, Himachal Pradesh, Indiae Student, Department of Oral and Maxillofacial Surgery, Rama Dental College, Hospital and Research Centre, Kanpur, Uttar Pradesh, India

a r t i c l e i n f o

Article history:

Received 10 November 2011

Accepted 9 July 2012

Keywords:

Ameloblastoma

Plexiform

Follicular

a b s t r a c t

Ameloblastoma is a benign tumor of odontogenic epithelium which is more commonly

seen in the posterior region of mandible and the maxilla. About 66% of ameloblastomas

occur in mandible most often in the molar ascending ramus area, while only 10% is seen in

mandibular anterior area. Ameloblastomas are slow growing, locally invasive, rarely ma-

lignant and in most cases can cause severe abnormalities of the face and jaw. These are

seen usually between 40 and 60 years of age. Radiographically it appears as radiolucent

lesion usually with well circumscribed borders. Early lesions usually appear unilocular

while established ones are generally multilocular. This is a case report of a 40 year old male

patient with follicular as well as plexiform type of ameloblastoma who presented with a

swelling in lower anterior teeth region, slow growing and crossing the midline which was

associated with no pain.

2012 Indian Journal of Dentistry. All rights reserved.

1. Introduction

Benign mandibular swellings can be due to a wide variety oflesions and can be divided into odontogenic and non-

odontogenic origin. Among these are ameloblastoma, radic-

ular cyst, dentigerous cyst, keratocystic odontogenic tumor,

central giant cell granuloma, fibroosseous lesions and oste-

omas.1 The ameloblastoma is a benign odontogenic tumor of

epithelial origin that exhibits a locally aggressive behavior

with a high level of recurrence, being believed to theoretically

come from dental lamina remains, the enamel organ in

development, epithelial cover of odontogenic cysts or from

the cells of the basal layer of the oral mucosa.2

The ameloblastoma is a relatively rare dental tumordescribed for the first time by Broca in 1868, and so denomi-

nated by Churchill in 1934. According to Larsonn and Alme-

ren, its incidence is 0.6 cases per million, while Shear and

Singh found an incidence of 0.31 cases per million in a white

population of Witwatersrand in South Africa.3 The etiology of

ameloblastoma is still unknown but has been linked to faulty

regulation of the genes involved in tooth development.4

Several causative factors have been proposed, including

* Corresponding author. 783/4 W-1, Saket Nagar, Juhi-2, Kanpur, Uttar Pradesh-208014, India. Tel.:91 9450326179.E-mail address: [email protected] (R. Srivastava).

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nonspecific irritating factors such as extraction, caries,

trauma, infection, inflammation, or tooth eruption; nutri-

tional deficit disorders; and viral pathogenesis.5 It generally

occurs in bone, and it has been postulated that the epithelium

of origin is derived from one ofthe following sources: cell rests

of the enamel organ, epithelium of odontogenic cysts, dis-

turbances of the developing enamel organ, basal cells of the

surface epitheliumor heterotropic epithelium in other parts ofthe body. The theory of an odontogenic origin for the amelo-

blastoma is supported clinically by the tumors common

occurrence in the tooth bearing area and is further reinforced

by the finding of Spouge that one in every three such tumors

are mural proliferations in intimate association with the

reduced enamel forming epithelium of dentigerous cysts.6

Ameloblastomas can occur at any location in the mandible

or maxilla, but the regions of the inferior molars and

mandibular ramus are the most prevalent anatomical loca-

tions (80%). When the tumor occurs in the maxilla, the pos-

terior region is the most affected, and the evolution and

invasion of the tumor may compromise the maxillary sinus

and the orbit.7 Ameloblastomas of the mandible occur 12years earlier than those of the maxilla. Ameloblastomas occur

most frequently in the molar region of the mandible. In

Blacks, ameloblastomas occur more frequently in the anterior

region of the jaws.8 The lesion presents prevalence between

the third and the fourth decade of life, equally affecting both

genders and having no predilection for race. Radiographically,

the neoplasia can be presented as a unilocular or multilocular

radiolucent image in the shape of soap bubbles or honey-

comb. The absorption of the adjacent teeth roots is not found

to be uncommon and the presence of a tooth inside, usually

the inferior third molar can be associated to the tumoral

mass.2 The chief histopathological variants of ameloblastoma

are the follicular and plexiform types, followed by the acan-thomatous and granular cell types. Uncommon variants

include desmoplastic, basal cell, clear cell ameloblastoma,

keratoameloblastoma and papilliferous ameloblastoma.9

2. Case report

A 40 years old male patient reported to the department of oral

medicine and radiology with chief complaint of swelling in the

lower front teeth region since 6 months. Patient gave the

history of swelling in the anterior mandibular region which

gradually increased in size to attain the present size which

was asymptomatic. On examination patient was moderatelybuilt and nourished and his vital signs were within normal

limit. Extraoral examination revealed a diffuse swelling pre-

sent over the chin region measuring approximately 5 7 cms

in size, extending superioinferiorly from lower lip up to infe-

rior border of the mandible andanteroposteriorly from right to

left corner of the mouth. Overlying skin of the swelling was

normal (Fig. 1).

Intraorally, solitary well defined swelling in anterior part of

mandible extending from 35 to 45, crossing the midline with

vestibular obliteration. Overlying mucosa was normal in color,

smooth and shiny. There was generalized edema of gingival

with bleeding on probing and deposits of stains and calculus

(Fig. 2). Grade I mobility was present in 31,32,41,42 and teeth

from 35 to 45 were found to be nonvital. Swelling was firm in

consistency and non tender on palpation. Based on history

and clinical examination, a provisional diagnosis of amelo-

blastoma was given. Fine needle aspiration of fluid was done

and sendfor biochemical examination which revealed protein

content 6.7 gm% (Fig. 3). Cross sectional mandibular occlusal

projection revealed expansion of buccal and lingual cortical

plate along with multilocular radiolucency extending from 35

to 46 separated by thick septae (Fig. 4). Panoramic radiograph

showed a large well defined multilocular radiolucency in the

mandible extending from 36 to 46. The radiolucency was

corticated and separated by thick septae with scalloped bor-

ders. Root resorption in relation to 34, 35 was seen and there

was widening of periodontal ligament space and loss of lam-

ina dura (Fig. 5). Axial CT images demonstrated well defined

multilocular expansile lesion with destructive changes and

cortical thinning (Fig. 6). Incisional biopsy of the lesion was

performed and microscopic examination revealed long

Fig. 1 e Patient showing extraoral swelling in chin region.

Fig. 2 e Intraoral examination showing swelling in anterior

part of mandible.

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anastomosing cords or larger sheets of epithelium which were

bounded by columnar or cuboidal ameloblast like cells sur-

rounding more loosely arranged epithelial cells. Supporting

stroma tends to be loosely arranged and vascular. It was alsocomposed of many small discrete island of tumor composed

of peripheral layer of cuboidal or columnar cells whose nuclei

were generally well polarized. This closely resembles amelo-

blasts or preameloblasts. Central parts of follicles were

showing stellate reticulum like cells. Cyst formation is rela-

tively common in this type (Figs. 7 and 8). Histopathological

findings were suggestive of both plexiform and follicular

ameloblastoma. A final diagnosis of plexiform and follicular

ameloblastoma was made with respect to the above findings.

3. Differential diagnosis

The first in the clinical differential diagnosis was Odontogenic

Keratocyst (OKC) commonly occurs in mandibular posterior

region, develop during 2nd and 3rd decade of life, it has ten-

dency to grow in anterior posterior direction with in medul-

lary cavity without causing obvious bone expansion,

aspiration may reveal thick, yellow and cheesy material. The

next entity was considered central giant cell granuloma typi-

cally occurs anterior to mandibular first molar and often cross

the midline affects mostly adolescents and young adults. The

next entity that was considered was Calcifying epithelial

odontogenic tumor (CEOT) as this too has a predilection for

the age range of 8e92 years with average age of 42 years and

for the posterior areas of the mandible (premolar molar area).

(Table 1) As radiological differential diagnosis, first entity was

considered Odontogenic keratocyst (OKC), contains curved

septa but usually grow with in medullary cavity withoutcausing obvious bone expansion and rarely causing root

resorption. Next, Central giant cell granuloma (CGCG) was

considered that presents with multilocular radiolucency and

often shows the resorption of the root surfaces of the adjacent

teeth having more granular and ill defined septa. The next

entity was considered Odontogenic Myxoma. In the early

stage it has an osteoporotic appearance, consisting of multi-

locular radiolucency with well-developed locules. In the sec-

ond stage of break-out or in the destructive phase, it is

characterized by loss of locules with significant expansion.

These lesions may cross the midline and may cause root

resorption and tooth displacement.10e13 (Table 2)

The microscopic differential diagnosis may include ame-loblastic fibroma and squamous odontogenic tumor. Micro-

scopic appearance ameloblastic fibroma shows cords and thin

strands of odontogenic epithelium resembling the dental

lamina, cap and bell stages of early odontogenesis. Fibroblasts

and embryonic connective tissue form the background.

Squamous Odontogenic tumor consists of elongated and

round islands of normal looking stratified squamous epithe-

lium against a cellular fibrous connective tissue background.

Epithelial islands may vary in size which has a basal cell layer

of inactive appearing cuboidal cells. Some islands are

composed of matured intermediate cells with prominent

desmosomal bridges. Many epithelial islands have central

areas of microcyst formation.14,15

4. Discussion

Ameloblastoma is a tumor originated from the epithelium

involved with the formation of teeth. It has aggressive

behavior and recurrent course, but it is rarely metastatic.

Ameloblastoma represents 1% of all tumors and cysts that

involve maxillomandibular area and about 10% of odonto-

genic tumors. Ameloblastoma can be classified in three types,

considering clinical and radiographic features: solid or mul-

ticystic (86% of cases), unicystic (13% of cases) and periph-

erical (1% of cases).16 Based mainly on the clinical behavior

Fig. 3 e Aspirated fluid.

Fig. 4e

Mandibular occlusal projection.

Fig. 5 e Panoramic radiograph.

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and prognosis, three types of ameloblastoma can presently be

distinguished: the conventional or classical, intraosseous,

solid or multicystic ameloblastoma, the unicystic amelo-

blastoma, and the peripheral ameloblastoma.5

Ackerman et al, in their study of unicystic amelo-

blastomas, defined three subgroups. Group I (42%) consisted of

a unilocular cyst with a nondescript but variable epithelial

lining. Inactive odontogenic cell rests might be present in the

fibrous wall, but there was no infiltration by neoplastic

epithelium. Group II lesions (9%) featured intraluminal plexi-

form proliferation but no infiltration of the cyst wall. In Group

III lesions (49%), plexiformor follicular d type ameloblastoma,

sometimes in continuity with the cyst lining, infiltrated the

wall. Group III lesions need to be treated more aggressively

similar to solid/multicystic Ameloblastoma.17 Sirichitra V and

Dhiravarangkura P in 1984 studied 147 cases of intrabony

ameloblastomaand found that there was no direct correlation

between the histologic patterns and the radiographic ap-

pearances of the tumors but there is a slight indication that

both monocystic and polycystic types tend to have the plexi-

form pattern, while the soap-bubble type tends to have the follicular

pattern.18 Ameloblastoma in the mandible can progress to

great size and cause facial asymmetry, displacement of teeth,

loose teeth, malocclusion, and pathologic fractures. Tumor

size may ranges from 1 to 16 cm at presentation which result

from expansion of bone and invasion into soft tissue. Typi-

cally ameloblastoma present as painless slow growing mass.1

The tumor is usually asymptomatic, grows slowly and small

lesions can be detected only by routine radiographic exami-

nations. Recently, the World Health Organization (WHO)

considered the desmoplasic ameloblastoma not only a histo-

logical variant, but a clinic variant of this tumor itself.2

There are a lot of histological subtypes of ameloblastoma:

plexiform, follicular, unicystic, basal cells, granulous cells,

clear cells, acantomatous, vascular and desmoplastic. The

most common histological patterns are plexiform and follic-

ular. There are no data that prove the relation of the subtypes

with clinical course.16 On histology, the follicular variant ex-

hibits islands and sheets of stellate-shaped cells with central

cyst formation. The plexiform subtype consists of anasto-

mozing cords of stellate-shaped tumor cells with two to three

layers of ameloblast-like cells peripherally. Various less

frequent histologic subtypes are also described but these (as

well as the follicular and plexiform subtypes) have little clin-

ical significance.4 The majority of patients with amelo-

blastoma are asymptomatic and the symptoms appear with

the tumoral expansion.16 Follicular ameloblastoma presents

as a painless swelling or slow expansion of the jaws, and it is

described as multilocular expansile radiolucency that occurs

Fig. 6 e Axial CT images demonstrated well defined multilocular expansile lesion with destructive changes.

Fig. 7e

Follicular type. Fig. 8e

Plexiform type.


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most frequently in mandibular molar/ramus area.5 Several

extensive surveys and reviews of ameloblastoma have been

published, the most notable being those of Robinson in 1937

and Small and Waldron in 1955. Analysis of more than 1000

cases by the latter authors revealed that the ameloblastoma

most commonly occurs in the 20e

49 years age, with averageage at first diagnosis being about 39 years.17

Kim S.G et al compared the clinical, radiologic, and histo-

pathologic features of 71 intraosseous ameloblastomas. Data

with respect to the patients ages, sex, tumor locations, and

surgical treatment history, as well as the radiographic findings

and number of recurrences, were analyzed. They found 39

(54.9%) of the 71 subjects were males, and 32 (45.1%) were

females. 62 (87.3%) of the 71 ameloblastomas were located in

the mandible. Swelling was the most common symptom and

was experienced by 27 (38.0%) patients. Radiographically, 42

(59.2%) of the 71 tumors were unilocular with a well-

demarcated border. Of the remaining 29 cases, 14 were mul-

tilocular, 2 were of soapbubble shape, and 13 were unknownin appearance. The most common histologic pattern was

plexiform, rather than follicular or acanthomatous.19

In the case reported here, the patient was male and was in

fourth decade of his life. Clinically, it manifests in anterior

part of mandible initially as a painless small swelling which

gradually increased in size. Histopathological features

revealed both follicular as well as plexiform ameloblastoma

which adds to the unique case till reported in literature.

Ameloblastoma was known for its high recurrence rate if

excision was incomplete. Therefore the treatment of choice is

surgical excision with wide free margins.1

Bachmann and Linfesty (2009) reported a solid/multicystic

type ameloblatoma that showed a variety of histologic types,

with plexiform and follicular predominating and was treated

with a partial resection of the mandible.20 The traditional

approach for a mandibulectomy is through a lipsplitting

incision and though it has the disadvantage of postoperativemorbidity; it gives a better exposure for complete tumour

removal. Shirani et al (2007)in a series of 7 patients introduced

a new technique of removal of large ameloblastoma with

immediate reconstruction by using only an intraoral incision.

It has the advantages of removing and repositioning of the

mandible intraorally and therefore allows removal of the

lesion and reconstruction procedure to be done simulta-

neously. Facial scar and damage to the marginal mandibular

nerve that innervate the lips can also be avoided via this

technique. Eppley (2002) in his review of 60 mandibular

ameloblastoma cases have shown that there was no recur-

rence of those cases treated via en bloc resection as compared

to enucleation and curettage in which the recurrence rate wasas high as 25%e50%. Reconstruction of large mandibular de-

fects represents a challenge to head and neck reconstructive

surgeons. There are different methods of mandibular recon-

struction for large defect. Among all, microvascular surgery

has become the preferred option. Four donor sites i.e., fibula,

iliac crest, radial forearm, and scapula have become the pri-

mary sources of vascularized bone and soft tissue for the oral

reconstruction. Among all these, fibula has multiple advan-

tages including bone length and thickness, donor site location

permitting flap harvest simultaneously with tumor resection

because both teams are at different end of the table, and

Table 1 e Clinical differential diagnosis.

Features Ameloblastoma OKC CGCG CEOT

Incidence 11% of odontogenic tumors 7e11% of odontogenic cysts F

1.7:1

F > M M > F

6:5

Sign and

symptoms

Painless swelling and

slow growth

Painless swelling Aggressive: pain, swelling,

rapid growth.

Painless swelling and slow

growth

Site Mandible posterior ramus Mandible molar ramus Mand > Max.

Anterior to 1st molar

May cross midline

Mandible: Maxilla

2:1

Premolar molar region

Table 2 e Radiological differential diagnosis.

Features Ameloblastoma OKC CGCG Odontogenic myxoma

Periphery and shape Smooth, oval Smooth, round or oval Irregular/double boundary Irregular

Borders/margins Well define and often

curved

Well corticated unless sec.

infected, scalloped

Well defined smooth and

scalloped

Mand: well corticated

Max: poorly defined

Cortical expansion Both buccal and lingual Minimal expansion, rare Uneven expansion both buccal

and lingual perforation

Both buccal and lingual

Internal structure Multilocular/unilocular

Honeycomb/soap-bubble

Radiolucent: common,

Multilocular: curved

internal septa

Multilocular, thin more granular

and ill define septae

Multilocular well develop

locules

Tennis racket, step ladder

Associated with

impacted tooth

38% e e

Root resorption Extensive Rare Profound, irregular outline Rare

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minimal donor site morbidity and therefore should be

considered as a choice in reconstruction. Another method of

reconstruction is internal distraction osteogenesis as has been

popularized by McCarthy et al (1992).1 Clokie and Sandor

(2008) described latest technique using bioimplant containing

BMP-7, they included 10 patients with major mandibular de-

fects following resection of biopsy-proven ameloblastoma le-

sions or osteomyelitis of the mandibular body or ramus. Theresection defects were spanned with rigid reconstruction

plates to hold the remaining mandibular segments in the

correct position. The defects were filled with a bioimplant

containing bone morphogenetic protein-7 (BMP-7) in a dem-

ineralized bone matrix (DBM) suspended in a reverse-phase

medium to effect sustained BMP delivery. Radiographic evi-

dence of mandibular bone formation was found in all cases

and at the end of 1 year, functional and esthetic reconstruc-

tion of the mandible was complete.21

However, ameloblastomas that appear as unilocular le-

sions radiographically may be treated conservatively (i.e.,

with enucleation or curettage or both) whenever all areas of

the cystic lumen can be controlled intraoperatively. Supra-periosteal resection of the bone is necessary when extensive

thinning or perforation of the cortical plates is noted.

Chemotherapy and radiation seem to be contraindicated.

Postoperative follow-up is important in the management of

ameloblastoma.19 Present case was treated with En bloc

resection followed by reconstruction of deformity with allo-

graft under general anesthesia.

5. Conclusion

Ameloblastomas are an enigmatic group of oral tumors.

Ameloblastomas not only occur in the posterior region, butcan also occur in anterior region of the jaw. Since variants of

ameloblastoma differ in biologic behavior, the histopatho-

logical examination is essential along with instrumental ex-

amination which is of significance to the clinician for effective

treatment plan as well as to prevent recurrence.

Conflicts of interest

All authors have none to declare.

r e f e r e n c e s

1. Kahairi A, Ahmad RL, Islah Wan L, Norra H. Management oflarge mandibular ameloblastoma e a case report andliterature reviews. Arch Orofacial Sci. 2008;3:52e55.

2. Alves PM, Pereira KMA, Vasconcelos MG, Souza LB,Queiroz LMG, Medeiros AMC. Desmoplasic ameloblastoma inmaxilla e report of case and review of the literature. Int JMorphol. 2008;26:263e268.

3. Di Cosola M, Turco M, Bizzoca G, et al. Ameloblastoma of thejaw and maxillary bone: clinical study and report of ourexperience. Av Odontoestomatol. 2007;23:367e373.

4. Nicholson RM, Teague D, White B, Ramalingam P,

Abdelsayed R. Fine needle aspiration findings in malignantameloblastoma: a case report and differential diagnosis.Diagn Cytopathol. 2009;37:586e591.

5. Sanjay CJ, David MC, Kaul R, Ramnarayan BK,Ramachandra P. Intraosseous ameloblastoma masqueradingas exophytic growth: a case report. Imaging Sci Dent.2011;41:89e93.

6. Adebiyi EK, Ugboko IV, Esan OOG, et al. Clinicopathologicalanalysis of histological variants of ameloblastoma in asuburban Nigerian population. Head Face Med. 2006;42:1e8.

7. Oliveira LR, Matos BHF, Dominguete PR, et al. Ameloblastoma:report of two cases and a brief literature review. Int JOdontostomat. 2011;5(3):293e299.

8. Reichart PA, Philipsen HP, Sonner S. Ameloblastoma:biological profile of 3677 cases. Eur J Cancer B Oral Oncol.

1995;31:86e99.9. Varkhede A, Tupkari JV, Mandale MS, Sardar M. Plexiform

ameloblastoma of mandible e case report. Clin Exp Dent.2010;2:146e148.

10. White SC, Pharaoh MJ. Oral radiology: principles andinterpretation. 5th ed. Missouri: CVMosby; 2004: 409.410-57.

11. Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 4thed. Philadelphia: WB Saunders; 1993: 258e317.

12. Langlais RP, Langland OE, Nortje CJ. Multilocularradiolucencies. In: Langlais RP, Langland OE, Nortje CJ, eds.Diagnostic imaging of jaws. Malvern: Williams and Wilkins;1995:327e384.

13. Rajendran R, Sivapathasundharam B. Shafers text book of oralpathology. 5th ed. New Delhi: Elsevier; 2006: 381e391.

14. Barnes L, Eveson JW, Teichart P, Sindranky D. Pathology &

geneticse

head and neck tumours (WHO). Lyon: IARC Press;2005: 296e300.

15. Reichart PA, Philipsen HP. Odontogenic tumors and allied lesions.London: Quintessence Publishing; 2004: 41e77.

16. Formiga CNM, Kohayagawa HM, Teixeira HM, et al.Ameloblastoma: a case report. Appl Cancer Res.2007;27:165e168.

17. Rao G, Kumar BV, Shyamala K. Plexiform unicysticameloblastoma in a four year old Child. Ind J Dent Adv.2010;2:391e394.

18. Sirichitra V, Dhiravarangkura P. Intrabony ameloblastoma ofthe jaws. An analysis of 147 Thai patients. Int J Oral Surg. 1984

Jun;13(3):187e193.19. Kim SG, Jang HS, Ju K. Ameloblastoma: a clinical,

radiographic, and histopathologic analysis of 71 cases. OralSurg Oral Med Oral Pathol Oral Radiol Endod. 2001;91:649e653.

20. Bachmann AM, Linfesty RL. Ameloblastoma, solid/multicystictype. Head Neck Pathol. 2009 Dec;3(4):307e309.

21. Clokie CM, Sandor GK. Reconstruction of 10 majormandibular defects using bioimplants containing BMP-7.

J Can Dent Assoc. 2008;74(1):67e72.

http://refhub.elsevier.com/S0975-962X(12)00068-8/sref1http://refhub.elsevier.com/S0975-962X(12)00068-8/sref1http://refhub.elsevier.com/S0975-962X(12)00068-8/sref1http://refhub.elsevier.com/S0975-962X(12)00068-8/sref1http://refhub.elsevier.com/S0975-962X(12)00068-8/sref1http://refhub.elsevier.com/S0975-962X(12)00068-8/sref1http://refhub.elsevier.com/S0975-962X(12)00068-8/sref1http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref2http://refhub.elsevier.com/S0975-962X(12)00068-8/sref3http://refhub.elsevier.com/S0975-962X(12)00068-8/sref3http://refhub.elsevier.com/S0975-962X(12)00068-8/sref3http://refhub.elsevier.com/S0975-962X(12)00068-8/sref3http://refhub.elsevier.com/S0975-962X(12)00068-8/sref3http://refhub.elsevier.com/S0975-962X(12)00068-8/sref3http://refhub.elsevier.com/S0975-962X(12)00068-8/sref4http://refhub.elsevier.com/S0975-962X(12)00068-8/sref4http://refhub.elsevier.com/S0975-962X(12)00068-8/sref4http://refhub.elsevier.com/S0975-962X(12)00068-8/sref4http://refhub.elsevier.com/S0975-962X(12)00068-8/sref4http://refhub.elsevier.com/S0975-962X(12)00068-8/sref4http://refhub.elsevier.com/S0975-962X(12)00068-8/sref5http://refhub.elsevier.com/S0975-962X(12)00068-8/sref5http://refhub.elsevier.com/S0975-962X(12)00068-8/sref5http://refhub.elsevier.com/S0975-962X(12)00068-8/sref5http://refhub.elsevier.com/S0975-962X(12)00068-8/sref5http://refhub.elsevier.com/S0975-962X(12)00068-8/sref5http://refhub.elsevier.com/S0975-962X(12)00068-8/sref5http://refhub.elsevier.com/S0975-962X(12)00068-8/sref6http://refhub.elsevier.com/S0975-962X(12)00068-8/sref6http://refhub.elsevier.com/S0975-962X(12)00068-8/sref6http://refhub.elsevier.com/S0975-962X(12)00068-8/sref6http://refhub.elsevier.com/S0975-962X(12)00068-8/sref6http://refhub.elsevier.com/S0975-962X(12)00068-8/sref6http://refhub.elsevier.com/S0975-962X(12)00068-8/sref7http://refhub.elsevier.com/S0975-962X(12)00068-8/sref7http://refhub.elsevier.com/S0975-962X(12)00068-8/sref7http://refhub.elsevier.com/S0975-962X(12)00068-8/sref7http://refhub.elsevier.com/S0975-962X(12)00068-8/sref7http://refhub.elsevier.com/S0975-962X(12)00068-8/sref7http://refhub.elsevier.com/S0975-962X(12)00068-8/sref8http://refhub.elsevier.com/S0975-962X(12)00068-8/sref8http://refhub.elsevier.com/S0975-962X(12)00068-8/sref8http://refhub.elsevier.com/S0975-962X(12)00068-8/sref8http://refhub.elsevier.com/S0975-962X(12)00068-8/sref8http://refhub.elsevier.com/S0975-962X(12)00068-8/sref8http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref10http://refhub.elsevier.com/S0975-962X(12)00068-8/sref10http://refhub.elsevier.com/S0975-962X(12)00068-8/sref10http://refhub.elsevier.com/S0975-962X(12)00068-8/sref10http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://dx.doi.org/10.1016/j.ijd.2012.07.001http://dx.doi.org/10.1016/j.ijd.2012.07.001http://dx.doi.org/10.1016/j.ijd.2012.07.001http://dx.doi.org/10.1016/j.ijd.2012.07.001http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref21http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref20http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref19http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref18http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref17http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref16http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref15http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref14http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref13http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref12http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref11http://refhub.elsevier.com/S0975-962X(12)00068-8/sref10http://refhub.elsevier.com/S0975-962X(12)00068-8/sref10http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-8/sref9http://refhub.elsevier.com/S0975-962X(12)00068-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