**1. Introduction**

[15] Caylakli F, Yavuz H, Cagici AC, Ozluoglu LN. Endoscopic sinus surgery for maxil‐

[16] Buyukkurt MC, Omezli MM, Miloglu O. Dentigerous cyst associated with an ectopic tooth in the maxillary sinus: a report of 3 cases and review of the literature. Oral Surg

[17] Scott A. Martin. Conventional Endodontic Therapy of Upper Central Incisor Com‐

[18] Pogrel M A. Treatment of Keratocysts: The Case for Decompression and Marsupiali‐

[19] Miloro M. Peterson's Principle of Oral and Maxillofacial Surgery. Second Edition.. In Miloro M., Ghali G. E., Larsen P. E., Waite P. Editors. BC Decker Inc. 2004 p.575-596 [20] Bello SA, Oketade IO, Osunde OD. Ectopic 3rd molar tooth in the maxillary antrum.

[21] Varol A, Türker N, Göker K, Basa S. Endoscopic retrieval of dental implants from the

[22] Kim JW, Lee CH, Kwon TK, Kim DK. Endoscopic removal of a dental implant through a middle meatal antrostomy. Br J Oral Maxillofac Surg. 2007, 45(5):408-9. [23] Chen CT, Chen YR. Endoscopically assisted repair of orbital floor fractures. Plast Re‐

[24] Nour YA. Variable extent of nasoantral window for resection of antrochoanal polyp: selection of the optimum endoscopic approach. Eur Arch Otorhinolaryngol. 2014 Jul

[25] Dhingra PL, Dhingra S. Diseases of Ear, Nose and Throat. Chapter 82 5th edition,

[26] Garip H, Garip Y, Oruçoğlu H, Hatipoğlu S. Effect of the angle of apical resection on apical leakage, measured with a computerized fluid filtration device. Oral Surg Oral

[27] Lin LM, Pascon EA, Skribner J, Langleland K. Clinical, radiographic, and histologic study of endodontic treatment failures. Oral Surg Oral Med Oral Pathol

[28] Torabinejad M, Watson TF, Pitt FTR. Sealing ability of a mineral trioxide aggregate

[29] Torabinejad M, Higa RK, McKendry DJ, Pitt FTR. Dye leakage of four root end filling

bined with Cyst Decompression: A Case Report. JOE 33(6), 2007, 753-757

lary sinus mucoceles. Head Face Med. 2006 Sep 6;2:29.

zation. J Oral Maxillofac Surg 63:1667-1673, 2005

Case Rep Dent. 2014;2014:620741.

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materials: effects of blood contamination.J Endod 1994;20:159-63.

A tumor is defined, in brief, as abnormal growth of tissue; tumoral formations are classified under two main headings, benign and malignant. The oro-facial region including the jaw bones, maxilla and mandible, is a site for a multitude of neoplastic conditions. Odontogenic tumors (OTs) constitute a wide range and diverse kind of lesions derived from tooth forming apparatus and its remnants. OTs originate from epithelium or ectomesenchyme or from both, showing varying degrees of inductive interaction between these embryonic components of the developing tooth germ. [1]. The majority of these tumors occur intraosseously within the maxillofacial skeleton, while extraosseous odontogenic tumors occur nearly always in the tooth-bearing mucosa. Due to their specific structure and location they have been identified and classified by pathologists into a separate group, differing in histogenesis, biology, clinical findings and radiological signs from other tumors developing in the oral cavity and facial bones (Figure 1).

The aim of the chapter is to review multidisciplinary treatment approaches to pediatric patients with benign jaw tumors from a radiological and clinical point of view and assess advantages and disadvantages of the current treatment techniques, possible complications and their prevention in the light of the recent literature.

#### **1.1. Etiology of odontogenic tumors**

According to current literatures, it is known that the potential sources for development of an odontogenic tumor are varied, and these include:


**Figure 1.** Odontogenic tumors arising from odontogenic tissues

From a biological point of view, some of these lesions represent hamartomas with varying degrees of differentiation, while the rest are benign or malignant neoplasms with variable aggressiveness and potential to develop metastases. These tumors constitute a heterogeneous group of diseases with diverse clinical and histopathological features [3]. The relative fre‐ quency of OTs obtained from studies from different parts of the world, have varied widely. Some authors have reported that OTs are rare with a relative frequency of 1%, while others have reported OTs constitute up to 32% of jaw lesions [4-6]. These disparities have been suggested to be due to the differences in terminology and classification and also, possibly due to racial and or genetic differences in the occurrence of the various types of OTs. OTs comprise a large heterogeneous group of lesions originating from the epithelium and/or odontogenic ectomesenchyme and remnants. OTs include entities of a hamartomatous nature, such as odontoma, benign neoplasms, some of which are aggressive as is the case of ameloblastoma and myxoma and malignant neoplasms capable of metastasis [2, 7].

Primary jaw tumors are broadly classified into odontogenic and nonodontogenic groups. The World Health Organization (WHO) classified this group of lesions in 1971 and 1992. In 2005, the WHO published the latest updated edition of the classification of OTs. There were 6 major changes in this schema from the previous versions namely:


The latest WHO classification has been used as a global standard for the last 10 years but our knowledge of odontogenic tumors continues to evolve.

#### **The latest WHO classification of odontogenic tumors**

**1. The pre-functional dental lamina** (odontogenic epithelium with ability to produce a

**2. The post-functional dental lamina**, a concept that covers those epithelial remnants such as Serre´s epithelial rests, located within the fibrous gingival tissue; the epithelial cell rests of Malassez in the periodontal ligament and the reduced enamel organ epithelium, which

**3. The basal cell layer of the gingival epithelium**, which originally gave rise to the dental

**4. The dental papilla**, origin of the dental pulp, which has the potential to be induced to

**6. The periodontal ligament**, which has the potential to induce the production of fibrous

From a biological point of view, some of these lesions represent hamartomas with varying degrees of differentiation, while the rest are benign or malignant neoplasms with variable aggressiveness and potential to develop metastases. These tumors constitute a heterogeneous group of diseases with diverse clinical and histopathological features [3]. The relative fre‐

produce odontoblasts and synthesize dentin and/or dentinoid material.

tooth), which is more abundant distal to the lower third molars.

covers the enamel surface until tooth eruption.

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and cemento-osseous mineralized material [2].

**Figure 1.** Odontogenic tumors arising from odontogenic tissues

lamina.

**5. The dental follicle.**

**1. Malignant odontogenic tumors Odontogenic carcinomas** Metastasizing (malignant) ameloblastoma Ameloblastic carcinoma - primary type Ameloblastic carcinoma - secondary type (dedifferentiated), intraosseous Ameloblastic carcinoma - secondary type (dedifferentiated), peripheral Primary intraosseous squamous cell carcinoma solid type Primary intraosseous squamous cell carcinoma derived from keratocystic odontogenic tumor Primary intraosseous squamous cell carcinoma derived from odontogenic cysts

Clear cell odontogenic carcinoma

Ghost cell odontogenic carcinoma

#### **Odontogenic sarcomas**

Ameloblastoma fibrosarcoma

Ameloblastic fibrodentino-and fibro-odontosarcoma

**2. Benign odontogenic tumors**

#### **Odontogenic epithelium with mature, fibrous stroma without odontogenic ectomesenchyme**

Ameloblastoma, solid/multicystic type

Ameloblastoma, extraosseous/peripheral type

Ameloblastoma, desmoplastic type

Ameloblastoma, unicystic type

Squamous odontogenic tumor

Calcifying epithelial odontogenic tumor

Adenomatoid odontogenic tumor and Keratocystic odontogenic tumor

#### **Odontogenic epithelium with odontogenic ectomesenchyme, with or without hard tissue formation**

Ameloblastic fibroma

Ameloblastic fibrodentinoma

Ameloblastic fibro-odontoma

Odontoma



Odontoameloblastoma

Calcifying cystic odontogenic tumor

Dentinogenic ghost cell tumor

#### **Mesenchyme and/or odontogenic ectomesenchyme with or without odontogenic epithelium**

Odontogenic fibroma

Odontogenic myxoma and myxofibroma

Cementoblastoma

#### **Bone-related (Fibro-osseous) lesions**

Ossifying fibroma

Fibrous dysplasia

Osseous dysplasia

Periapical Osseous Dysplasia

Focal Osseous Dysplasia

Florid Osseous Dysplasia Central giant cell granuloma Cherubism Aneurysmal bone cyst Solitary (Simple) bone cyst **Other tumors** Melanotic neuroectodermal tumor of infancy

#### **Classification of the Latest Benign Fibro-Osseous Lesions of the Craniofacial Complex**: [8]

#### **1. Bone dysplasias**

Clear cell odontogenic carcinoma Ghost cell odontogenic carcinoma

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**2. Benign odontogenic tumors**

Ameloblastoma, solid/multicystic type

Ameloblastoma, desmoplastic type Ameloblastoma, unicystic type Squamous odontogenic tumor

Calcifying epithelial odontogenic tumor

**formation**

Odontoma

Ameloblastic fibroma

Ameloblastic fibrodentinoma Ameloblastic fibro-odontoma


Odontogenic fibroma

Cementoblastoma

Ossifying fibroma Fibrous dysplasia Osseous dysplasia

Calcifying cystic odontogenic tumor Dentinogenic ghost cell tumor

Odontogenic myxoma and myxofibroma

**Bone-related (Fibro-osseous) lesions**

Periapical Osseous Dysplasia Focal Osseous Dysplasia

Adenomatoid odontogenic tumor and Keratocystic odontogenic tumor

Ameloblastoma, extraosseous/peripheral type

Ameloblastic fibrodentino-and fibro-odontosarcoma

**Odontogenic epithelium with mature, fibrous stroma without odontogenic ectomesenchyme**

**Odontogenic epithelium with odontogenic ectomesenchyme, with or without hard tissue**

**Mesenchyme and/or odontogenic ectomesenchyme with or without odontogenic epithelium**

**Odontogenic sarcomas** Ameloblastoma fibrosarcoma

#### a. Fibrous dyspla


#### **2. Cemento-osseous dysplasia**


#### **3. Inflammatory/reactive processes**


#### **5. Neoplastic lesions (Ossifying fibromas)**

	- i. Trabecular type
	- ii. Psammomatoid type

In pace with new findings of new genetic and molecular changes, classification of odontogen‐ ic tumors will necessitate further modification and subsequent changes in the classification system. Hence a new and revised version of the classification will always be dynamic. Charac‐ teristics andepidemiology ofjaw tumors have beendescribed mostly in adults. Compared with their adult counterparts, jaw tumors in childhood show considerable differences. Tumors of the head and neck represent only 2% to 5% of all pediatric tumors. OTs in children constitute approximately 3% of all tumor like growths in the oral cavity, jaws and salivary glands in all age groups [9]. In general, OTs in the pediatric population are rare and considerably more so than in the adultpopulation.There aredifferences in the spectrum ofdiseases seen in this group and in adults. When the diseases are similar, there are sometimes differences in their clinical behavior. There are additional management concerns when working with children. Treat‐ ment burden is given relatively greater consideration in children since they are growing and developing and treatment may exert untoward influences therein. It is important for the clinicians involved in the diagnosis and treatment of pediatric head and neck tumors to understand certain patterns that follow the development of these lesions, so that misdiagno‐ sis and delays in treatment can be avoided. Because of their relative rarity, this broad spec‐ trum oflesions require careful attention and close collaboration between pediatricians, medical oncologists, radiotherapists, pathologists and surgeons working in the head and neck area. Pathology is uncommon among the pediatric age group, its incidence and prevalence has been increasing in recent years, and it remains a significant cause of morbidity and mortality in this population. Recently, Jones and Franklin performed a retrospective investigation of oral and maxillofacial pathologies within a 30-year period. Those authors verified that biopsies in patients aged between 10 and 16 years represented 8.2% of all cases reported.[10]

#### **Classification of pediatric jaw tumors**

The various classifications systems proposed by authors are enumerated as below:

#### **1. Jaw Tumors in Children (11)**

**1.Classification of non-odontogenic jaw tumors in children** I. Benign mesenchymal tumors a) Giant cell lesions b) Fibro-osseous lesions c) Myxoma II. Hematopoietic and reticuloendothelial tumors a) Langerhans cell histiocytosis b) Burkitt's lymphoma c)Lymphoma III. Neurogenic tumors a) Neurofibroma b) Neurilemmoma c) Neuroma d)Ganglioneuroma e) Neuroblastoma


In pace with new findings of new genetic and molecular changes, classification of odontogen‐ ic tumors will necessitate further modification and subsequent changes in the classification system. Hence a new and revised version of the classification will always be dynamic. Charac‐ teristics andepidemiology ofjaw tumors have beendescribed mostly in adults. Compared with their adult counterparts, jaw tumors in childhood show considerable differences. Tumors of the head and neck represent only 2% to 5% of all pediatric tumors. OTs in children constitute approximately 3% of all tumor like growths in the oral cavity, jaws and salivary glands in all age groups [9]. In general, OTs in the pediatric population are rare and considerably more so than in the adultpopulation.There aredifferences in the spectrum ofdiseases seen in this group and in adults. When the diseases are similar, there are sometimes differences in their clinical behavior. There are additional management concerns when working with children. Treat‐ ment burden is given relatively greater consideration in children since they are growing and developing and treatment may exert untoward influences therein. It is important for the clinicians involved in the diagnosis and treatment of pediatric head and neck tumors to understand certain patterns that follow the development of these lesions, so that misdiagno‐ sis and delays in treatment can be avoided. Because of their relative rarity, this broad spec‐ trum oflesions require careful attention and close collaboration between pediatricians, medical oncologists, radiotherapists, pathologists and surgeons working in the head and neck area. Pathology is uncommon among the pediatric age group, its incidence and prevalence has been increasing in recent years, and it remains a significant cause of morbidity and mortality in this population. Recently, Jones and Franklin performed a retrospective investigation of oral and maxillofacial pathologies within a 30-year period. Those authors verified that biopsies in

patients aged between 10 and 16 years represented 8.2% of all cases reported.[10]

The various classifications systems proposed by authors are enumerated as below:

**Classification of pediatric jaw tumors**

278 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

I. Benign mesenchymal tumors a) Giant cell lesions b) Fibro-osseous lesions

c) Myxoma

c)Lymphoma III. Neurogenic tumors a) Neurofibroma b) Neurilemmoma c) Neuroma d)Ganglioneuroma e) Neuroblastoma

**1.Classification of non-odontogenic jaw tumors in children**

II. Hematopoietic and reticuloendothelial tumors a) Langerhans cell histiocytosis b) Burkitt's lymphoma

**1. Jaw Tumors in Children (11)**


#### V. Malignant mesenchymal tumors

	- a)Squamous cell carcinoma
	- b)Mucoepidermoid carcinoma
	- c)Adenoid cystic carcinoma
	- d)Adenocarcinoma

#### 2. **Classification of odontogenic jaw tumors in children**

	- a) Ameloblastoma (Peripheral, Unicystic, Solid, Multicystic)
	- b) Adenomatoid odontogenic tumor
	- c) Calcifying epithelial odontogenic tumor
	- a)Cementoma
	- b)Periapical cemental dysplasia
	- c)Cementifying fibroma
	- d)Cementoblastoma
	- e)Odontogenic fibroma
	- a)Ameloblastic fibroma
	- b) Odontoma

#### **3. Classification of Small Round Cell Tumors in children**

	- Askin's tumor
	- Neuroepithelioma

#### 4. **International classification of childhood cancer (12)**

#### **Malignant Bone tumors**


#### **Soft tissue and other extraosseous sarcomas**


### **2. Clinical sign and symptoms of pediatric jaw tumors**

Pediatric patients encompass a very interesting study group, as several long term physiological changes take place in the maxillofacial area. During the mixed dentition period, children can refer with a complaint of swelling in the maxillofacial area, which may or may not be associated with pain. These mostly include both hard and soft tissue pathologies. When involving bone, only odontogenic cysts or odontogenic tumors as a category have been considered. Intraosseous pediatric jaw lesions can present in diverse clinical patterns and their diagnoses can vary from odontogenic to non-odontogenic pathogeneses, which can rarely include connective tissue pathology. The great majority of pediatric jaw tumors are non-odontogenic [13,14].

OTs can be observed casually or after the appearance of nonspecific symptoms. Because of their slow-growth tendency, usually they do not cause pain. The odontogenic tumors grow in the jaw, through the haversian system, without metastases but with a high probability of relapse. In the majority of cases, tumors of the head and neck in children are first seen by general practitioners or pediatricians with subsequent delays in investigations and diagnosis. Some of these tumors may disappear spontaneously without any treatment. During the mixed dentition period, children can report with complaint of swelling in the maxillofacial area, which may or may not be associated with pain. A history of trauma also needs to be elicited, because they are prone to falling down during playing, which can affect the jaws. Because of the complex anatomy and development of the head and neck, neoplasms during infancy and childhood arising at this site represent the most difficult challenges in clinical practice. [15]

#### **3. Diagnosis of pediatric jaw tumors**

The odontogenic cysts and tumors are a diverse group of lesions that represent deviation from normal odontogenesis. The physical signs and symptoms of odontogenic cysts and tumors

will depend to a certain extent on the dimensions of the lesion. A small lesion is unlikely to be diagnosed on a routine examination of the mouth because signs will not be demonstrable. Such lesions are only likely to be detected at an early stage as the result of routine radiographic examination. Exceptions are some early lesions that may present in conjunction with a devitalized tooth, which is detectable on clinical examination. Some cystic lesions may become secondarily infected, leading to their diagnosis. Clinical absence of one or more teeth without the history of extraction may also be a clinical indicator of an undiagnosed odontogenic cyst or tumor because many of these lesions are associated with impacted or congenitally missing teeth. As the lesion grows, other indirect changes may occur. An enlarging lesion between two teeth can cause the crowns to converge and the roots to diverge. Growth that is nearly undetectable visually may lead to difficulty with denture retention. As the lesion enlarges even further, expansion of the bone may be seen directly. This is usually toward the buccal surface of the alveolar bone because this is the thinnest area and expansion occurs here most easily. Clinically evident expansion is often a late finding, especially in lesions developing within the ramus or angle of the mandible or within the maxillary sinus. Lesions in these areas may become extremely large before expansion is observed clinically. Masses in the neck confront the pediatrician with greater opportunities for evaluation before a decision regarding biopsy or excision is reached. Signs of systemic involvement must also be determined.

#### **3.1. Radiographic and imaging studies**


A tissue diagnosis becomes necessary in order to diagnose and initiate proper therapy.

#### **3.2. Biopsy**

4. **International classification of childhood cancer (12)**

280 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

c) Ewing tumor and related sarcomas of bone d) Other specified malignant bone tumors e) Unspecified malignant bone tumors **Soft tissue and other extraosseous sarcomas** a) Rhabdomyosarcomas

> d) Other specified soft tissue sarcomas e) Unspecified soft tissue sarcomas

**3. Diagnosis of pediatric jaw tumors**

**2. Clinical sign and symptoms of pediatric jaw tumors**

b) Fibrosarcomas, peripheral nerve sheath tumors and other fibrous neoplasms

Pediatric patients encompass a very interesting study group, as several long term physiological changes take place in the maxillofacial area. During the mixed dentition period, children can refer with a complaint of swelling in the maxillofacial area, which may or may not be associated with pain. These mostly include both hard and soft tissue pathologies. When involving bone, only odontogenic cysts or odontogenic tumors as a category have been considered. Intraosseous pediatric jaw lesions can present in diverse clinical patterns and their diagnoses can vary from odontogenic to non-odontogenic pathogeneses, which can rarely include connective tissue pathology. The great majority of pediatric jaw tumors are non-odontogenic [13,14].

OTs can be observed casually or after the appearance of nonspecific symptoms. Because of their slow-growth tendency, usually they do not cause pain. The odontogenic tumors grow in the jaw, through the haversian system, without metastases but with a high probability of relapse. In the majority of cases, tumors of the head and neck in children are first seen by general practitioners or pediatricians with subsequent delays in investigations and diagnosis. Some of these tumors may disappear spontaneously without any treatment. During the mixed dentition period, children can report with complaint of swelling in the maxillofacial area, which may or may not be associated with pain. A history of trauma also needs to be elicited, because they are prone to falling down during playing, which can affect the jaws. Because of the complex anatomy and development of the head and neck, neoplasms during infancy and childhood arising at this site represent the most difficult challenges in clinical practice. [15]

The odontogenic cysts and tumors are a diverse group of lesions that represent deviation from normal odontogenesis. The physical signs and symptoms of odontogenic cysts and tumors

**Malignant Bone tumors** a) Osteosarcomas b) Chondrosarcomas

c) Kaposi's sarcoma


OTs have a specific histological structure reflecting various stages of odontogenesis and are located mainly in the jaws, rarely in other parts of the skeletal system. Due to their specific structure and location they have been identified and classified by pathologists into a separate group of neoplasms differing from other lesions developing in the oral cavity and facial bones [17]. Odontogenic tissue is programmed to produce dentin and enamel due to active interac‐ tions between odontogenic mesenchyme and epithelium. Tooth formation is achieved via odontogenic mesenchyme and epithelium stage- and spatial-specific differentiation from early tooth development to late maturation [18]. Therefore, when odontogenic tissue becomes undifferentiated and undergoes tumoral changes, it has the potential to produce abnormal calcifications with enameloid, dentinoid, and cementum-like material histologic features. For this reason, these odontogenic calcifications are important odontogenic tumor characteristics and occasionally are accompanied by odontogenic epithelium ghost cell change and amor‐ phous odontogenic mesenchyme hyalinization [19].

Aspiration cytology, a well established diagnostic tool in adult oncology, is recently gaining acceptance in pediatric population, as clinicians add this technique to their diagnostic arma‐ mentarium. Fine-needle aspiration cytology is a useful and reliable tool in the diagnosis of head and neck OTs with no contraindications and minimal complications even in children [20].

More than 95% of all OT reported in large series are benign and around 75% are represented by odontomas, ameloblastomas and myxomas (which could be considered as "relatively frequent OT"). Due to the inclusion of the odontogenic keratocyst as a tumor, these figures will be modified significantly, as this lesion is more frequently diagnosed than the other three entities. Some studies have shown epidemiological data that demonstrate that there is a second group of OT, which, although rare in terms of general pathology, are of "intermediate frequency" with respect to other OT, which have to be considered in the differential diagnosis of tumors of the oral and maxillofacial regions; therefore they have to be included within the contents of pathology of the graduate and post-graduate courses of oral and general pathology. The lack of specific markers to confirm the odontogenic origin of all the lesions included in the current WHO classification makes diagnoses mainly on anatomic considerations, or on the histomorphological similarities among some tumors with the above mentioned odontogenic structures. However, as most OT contain variable amounts of epithelium, and the fact that such tissue may express several of the more than 20 cytokeratin markers (intermediate filaments of the epithelial cells) known to date, there are some studies that have demonstrated that cytokeratins 14 and 19 are the more frequently expressed by OT, and that these are also expressed in the different epithelial structures of the developing tooth [21, 22], leading to promote their use as a diagnostic tool to support the odontogenic nature of these entities. Additionally, the expression of amelogenin, a representative protein of the enamel matrix, which is produced by secretory ameloblasts and that seem to actively participate in the process of production and mineralization of enamel, has been consistently demonstrated within the enamel matrix and the cytoplasm of the cells of the reduced enamel epithelium, stratum intermedium and stellate reticulum of the enamel organ, as well as in some epithelial OT, particularly at the basal endings of the cuboidal or columnar cells of ameloblastomas and in cells of calcifying epithelial odontogenic tumor, malignant ameloblastoma and ameloblastic carcinoma [22]. Therefore, the use of these markers is a valuable tool to discard other types of epithelial lesions that may develop within the oral and maxillofacial regions. More recently, calretinin, a 29-kDa calcium-binding protein has been shown to be expressed in both unicystic and solid ameloblastomas but not in other types of odontogenic cysts, and this finding led some authors to propose it may be considered a specific immunohistochemical marker for neoplasitic ameloblastic epithelium [23] and an important diagnostic aid in the differential diagnosis of cystic odontogenic lesions, particularly the keratocystic odontogenic tumor [24]. In the same way, the expression of cytodifferentiation of neoplastic epithelium via epithelialmesenchymal interactions and mineralization markers, such as bone morphogenetic protein (BMP) is of great value to study those lesions that are characterized by the production of hard dental tissues [25, 26].
