SURGICAL MANAGEMENT OF BENIGN ODONTOGENIC TUMOURS

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SURGICAL MANAGEMENT OF BENIGN ODONTOGENIC TUMOURS J T AROTIBA Department of of Oral &Maxillofacial Surgery Faculty of Dentistry College of Medicine/ University College Hospital, University of Ibadan, Ibadan.

Objectives To be able to Define and classify odontogenic tumours. Describe the common clinical features of odontogenic tumours . Describe how to examine, evaluate and diagnose a patient presenting with odontogenic tumour. Discuss the surgical treatment of these tumours

INTRODUCTION Tumour – general term for swelling of tissues Tumour = Neoplasia - New growth An abnormal mass of new tissue the growth of which exceeds, and is uncoordinated with that of the normal tissue and which persists after cessation of the stimuli that provoked or evoked it(Willis 1957).

INTRODUCTION In the oral cavity, both neoplastic and non-neoplastic tumefactions (swellings) arise from tissues concerned with tooth formation (dental hard tissue) as well as from non-dental tissues. These are called odontogenic and non-odontogenic tumours respectively.  Odontogenic tumours are tumours arising from dental tissues or their progenitor (embryonic)cells. They are usually located in the jawbones- central- but occasionally may be located in the surrounding oral soft tissues- peripheral.

INTRODUCTION They are mostly slowly growing lesions, which are benign ( about 95%) although a few are malignant or have malignant variants. They may be locally aggressive (infiltrative) and, with the exception of a few (e.g AOT), are more commonly seen in the mandible than the maxilla.   They may be purely epithelial, purely mesenchymal or mixed.

PREVALENCE There is geographic variation in the incidence of odontogenic tumours especially ameloblastoma.  Odontogenic tumours constitute 19% to 30% of jaw tumours in Asian and African Countries where as in North/ South America and Canada they are 1% to 9%.  They can occur at any age but more common around second to fifth decades with peak in 2nd and 3rd decades of life.  Equal sex incidence or a slightly higher female incidence.

CLASSIFICATION Past efforts: Broca (1869) suggested a classification of odontogenic tumours. He used the term ‘odontome’ for all tumours arising from dental formative tissues and divided them into different types according to the stage of development of the tooth at the inception of the tumour  Bland –Sutton (1888) modified this by basing classification on the tissue from which the tumour arose. Gabell, James and Payne (1914) modified Bland–Sutton‘s work but still included non-neoplastic cysts of dental origin

CLASSIFICATION 1. Epithelial Odontomes—arising from dental epithelium eg Amelo, epithelial cysts etc 2. Composite odontomes---arising from both dental epithelium and dental mesenchyme   3. Connective tissue odontomes--- arising from dental mesenchyme only Thoma and Goldman (1946) classified Odontogenic tumours based on tissue of origin into those from ectodermal (Epithelium), mesenchymal and mixed dental tissues discarding the use of the general term ‘odontome ‘. They omitted the non-neoplastic cysts

CLASSIFICATION American Academy of oral Pathology (Robinson 1952) went further to amplify Thoma’s classification; EPITHELIAL TUMOURS Adamantinoblastoma Enameloma MESENCHYMAL TUMOURS Odontogenic fibroma Dentinoma Cementoma

CLASSIFICATION ODONTOGENIC MIXED TUMOURS (ODONTOMES) Soft odontoma – epithelium and mesoderm Soft and calcified odontome—adamantinoma arising with forming or completely formed odontome. Completely formed odontome with enamel, dentine, pulp, p.d.l, Compound Complex.

CLASSIFICATION Pindborg and Clausen (1958) Classified OTs based on embryonic principle- the inductive changes exerted by dental tissues on each other during embryonic development which they also thought could have some influence on the pathogenesis of these tumours. WHO established a Collaborating centre for Histological Typing of Odontogenic Tumours and Allied Lesions in 1966 headed by Pindborg J.J and in 1971, Pindborg and Kramer (1971) published the first authoritative WHO guide to the classification of OTs. This was revised in 1992 by Kramer, Pindborg and Shear (1992) basing classification on type of odontogenic tissues involved and behaviour of tumour. The more recent revisions, however are in 2002 by Philpsen and Reichart and 2005 (WHO histological classification). ASSIGNMENT: Describe the Classification of OTs  based on the most recent WHO Classification

Modified WHO Recommended classification ( 2002, 2005) TUMOURS OF ODONTOGENIC EPITHELIUM: Ameloblastoma –solid multicystic, extraosseus(peripheral), desmoplastic, unicystic. Adenomatoid Odontogenic Tumour. Calcifying epithelial odontogenic Tumour. Squamous Odontogenic Tumour. Keratocystic Odontogenic Tumour. Ameloblastic carcinoma & Malignant ameloblastoma Clear cell odontogenic carcinoma

Classification MIXED TUMOURS. Ameloblastic fibroma Ameloblastic Fibro-odontoma Ameloblaastic fibro - dentinoma Odonto-ameloblastoma. Compound Odontoma Complex Odontoma Calcifying cystic odontogenic tumour Dentinogenic Ghost cell tumour Ameloblastic Fibrosarcoma

Classification TUMOURS OF ODONTOGENIC ECTOMESENCHYME. Odontogenic Fibroma Granular cell odontogenic Tumour Odontogenic myxoma Cementoblastoma.

PRINCIPLES OF DIAGNOSIS &MANAGEMENT HISTORY : Ask patient about; Duration: long /short/prolonged with(out) pain?. Mode of onset: spontaneous/ following trauma or infection? Progress of tumour: slow/stationary or rapid/fast? Site, Shape of swelling? Surface characteristics smooth, normal overlying skin/mucosa, engorged, ulcerated ?etc. Consistency: hard, firm, soft fluctuant. Associated symptoms: pain, abnormal sensations, anaesthesia/parasthesia, discharge, tenderness, lymphadenopathy, trismus, nasal obstruction etc. Any similar swelling somewhere else?

Associated loss of weight, recurrence, Drug history Family history: hereditary? Social History: Habit

PRINCIPLES OF DIAGNOSIS &MANAGEMENT CLINICAL EXAMINATION Thorough and detailed systematic examination from extra-oral to intra- oral. Inspection No, Size, Shape, Colour, Site(anatomical location). Surface: smooth, lobulated , irregular, ulcerated, fungating growth. Attachments: Pedunculated /sessile Integrity of overlying skin or mucosa. Temperature of overlying skin Palpation for: Consistency- soft , firm, hard/ indurated, bony hard, cystic/fluctuant Relationship with overlying & underlying structures. Lymph nodes Bimanual palpation for large lesions to determine extent of tumour

Percussion: related teeth. Auscultation: if suspecting vascular lesion. Aspiration: if cystic or contains fluid.

INVESTIGATIONS: IMAGING Plain: LO, PA, OMV, OPG Advanced imaging tech: Computerized tomographic Scans -CT Scans Three dimensional reconstruction CT Complete bone scan / Scintigraphy – to detect distant metastasis if malignancy is suspected Magnetic resonance imaging (MRI) – soft tissue & nodal involvments. Angiographic studies(CT angiogram)

Fine Needle Aspiration Cytology (FNAC) Tissue Biopsy for histological diagnosis – is confirmatory. Techniques– Exfoliative , Aspiration, FNAC, Excisional, Incisional ASSIGNMENT: Discuss the various biopsy methods available for diagnosis of a benign jaw tumours

Principles of Treatment Goals. 1. Complete eradication of tumour. 2. Preservation of normal tissue. 3. Removal with least morbidity. 4. Reconstruction to replace tissue loss and form. 5. Rehabilitation and Restoration of function. 6. Long term follow up to detect recurrence early.

Principles of Treatment The treatment of odontogenic tumours requires correct histological diagnosis. The appropriate choice of surgical treatment method is after proper and adequate evaluation before surgery and depends on: (1) Histological type benign Vs Malignant - encapsulated/ non-infiltrative - non-encapsulated/infiltrative  (2) Anatomical location/ Site of tumour - Oral Cavity -- -- Anterior Vs Posterior -- Maxilla Vs Mandible

Principles of Treatment  (3) Size of Tumour/ confinement to bone- small lesionLocal excision. - large or malignant lesion- Radical/Extensive excision. (4) Age of Pt - ability to withstand stress of radical surgery (5) If malignant--Presence/ absence of distant metastasis. (6) Proximity to adjacent vital structures. (7) Rehabilitation or reconstruction methods.

Treatment methods The best and tested modality of treatment is surgery. Radiotherapy, chemotherapy are usually used as adjuncts or palliative measures in malignant types and therefore have no role in benign odontogenic tumours .

Surgical Treatment Most odontogenic tumours are benign and surgery is the first choice. Adequate resection with margin of normal tissue is the recommended surgical treatment.   Well-circumscribed (encapsulated) non-infiltrative lesions (A.O.T, Ameloblastic Fibroma, Fibro-odontomas , odontomas, cementoblastoma) may however be treated by Conservative surgery . - - Enucleation or Local Excision (Curettage) with or without saucerization or treatment of adjacent bone will suffice.—Chemical Cautery   --- Thermal * Locally invasive (infiltrative) Lesions (Ameloblastoma , ameloblastic odontoma, fibromyxoma, CEOT, KCOT, SOT) a slightly more aggressive approach is needed – Resection with margin of normal bone.

Resection Removal of tumour by cutting through uninvolved tissue around the tumour and delivering the tumour without direct contact with the tumour – en bloc resection. Marginal Resection (Resection with preservation of lower cortical plates if still intact and uninvolved). Also called \Resection without continuity defect (Peripheral Ostectomy or ‘En bloc resection) Partial Resection. (Removing a complete segment of the jaw) Resection with continuity defect). It can vary from a small portion to Hemimandibulectomy / partial maxillectomy.

Resection Total Resection: Removal of the whole involved bone – Maxillectomy or Mandibulectomy Resections can be -- Marginal, partial, total, -- with or without disarticulation. -- Composite resection –for malignant tumours

Reconstruction Surgical resection leads to disfigurement, deviation of jaw during movement, disturbance of function. Therefore, the need for reconstruction to: Restore movement and equilibrium of mandible To maintain normal occlusal plane , floor of mouth and tongue’s anatomical position. To restore function—eg feeding. To restore aesthetics appearance and a more favourable social acceptance

Reconstruction ­+ Reconstruction * Primary (Immediate) or Secondary (delayed) IMMEDIATE : Advantages: Single stage surgery, Early return to function, Minimal compromise of aesthetics, No muscular deformation or scar/ fibrosis limitations. Disadvantages: Recurrence may occur in graft and risk of infection leading to loss of graft. - Intraoral approach .- both intraoral (excision) and Extraoral (grafting) approach. - extra oral approach only

Secondary / delay -- Steinnmans Pin -- Kirschner’s wires -- Acrylic implants -- Metallic implant Reconstruction Plates. --Bowerman-Conroy’s mandibular implant. (All these are temporary materials to maintain tissue space and /or bone continuity if you are planning secondary reconstruction Bone grafts - autogenic (iliac/ribs) alloplastic bone grafts or synthetic materials Microvascular Flap Reconstruction

Rehabilitations Acrylic dentures Obturators with teeth(Maxilla). Dental Implants following bone (Microvascular) grafts. May need RCT for related adjacent teeth if the apices are at risk. Follow up. For many years

Factors for Consideration before surgery Anatomical location of tumour Aggressiveness of Tumour Size of tumour Location of tumour(Confinement to bone). Proximity to adjacent vital structures. Involvement of mandible/maxilla. Rehabilitation or reconstruction methods Age of patient

AMELOBLASTOMA A benign but locally invasive polymorphic neoplasm consisting of proliferating odontogenic epithelium which usually has a follicular or plexiform pattern, lying in a fibrous stroma. Most often a central tumour of jaw bones although peripheral variants are occasionally seen.

Aetiology : Unknown ? Irritation, repetitive trauma or inflammation/infection from difficult eruption since it occurs often in posterior mandible where impaction is common(New 1915, Robinson1934). ? Metabolic disorders e.g. Rickets (Geschickter1935).  ?Viral (Stanley et al 1964 Lucas , 1969,Csiba 1970)- in experimental animals – polyoma virus from dental lamina or its derivatives

Histogenesis: From dental lamina or its derivatives: -enamel organ (Kegel 1932) -epithelial cell rests --cell rests of dental lamina (glands of Serres)or the roots(cell rests of Malassez). lining of odontogenic cysts basal layer of oral mucosa

Clinical features: . Slow – growing usually central jaw lesion . Painless- unless infected . Expands bone - locally infiltrative and erodes cancellous bone. Age: Can occur at any age More common between 2nd – 6th decades (10-59) Peak between 30-40 years.   Sex: Male = Female (Akinosi) Male slightly > female slightly (Adekeye, Arotiba, Ladeinde )

Site:- Mandible > Maxilla Although any part of the jaw may be affected, more commonly seen in the anterior mandible in Nigerians than in Caucasians in which the posterior aspect of the mandible is the predominant site. Clinical Appearance: Hx of Slow growth. Enlargement of bone (expansion of buccal and lingual plates)

Tooth mobility / derangement. Thinning of cortical plates  Depressible bone egg -shell cracking sound. Local bone invasion makes conservative surgery inadequate.

The basic clinical types are: The Solid Multicystic (intraosseous) ameloblastoma. Peripheral (extraosseous) Ameloblastoma. The Unicystic ameloblastoma. Malignant variants Extragnathic – eg craniopharyngioma.

Radiology Multilocular radioluscency - honey comb or soap bubble appearance. - Unicystic radioluscency. . Thinning and expansion of cortical plate . Thinning of lamina dura . Truncation /Amputation of roots.

Histology Non-encapsulated epithelial lesion, infiltrating trabeculae of surrounding bone. It consists of odontogenic epithelium arranged in islands or processes around a connective tissue stroma. The peripheral cells:-tall columnar / cuboidal cells with well polarized nuclei (resembling ameloblast) The central (core) cells :- polyhedral (angular) cells resembling stellate reticulum.  

There are two common basic histologic patterns (i) Follicular (ii) Plexiform Follicular; discrete islands of tumour composed of peripheral layer of tall columnar / cuboidal cells with polarized nuclei . Plexiform:- Irregular Masses (sheets, cords or strands) which are interlacing in appearance. Continuous anastomosing strands

Other less common histological variants are;  (i) Acanthomatous - Squamous metaplasia of the central core of sellate reticulum like cells. Degeneration of these cells leads to formation of keratin. (ii) Granular:- There are granular changes in the cytoplasm of the stellate reticulum like cells. (iii) haemangiomatous:- there is increased vascularization of the stroma (iv) Basal cell type:- Epithelial cells are primitive in appearance resembling the basal cells carcinoma of skin. Desmoplastic:- A lot of collagen deposition in the fibrous stroma. Clear cell variant. Clear cytoplasm with little or no cytoplasmic granules: ? Clear cell odontogenic tumour/carcinoma

Unicystic Ameloblastoma:-  Is a clinical Variant Essentially a cyst lined by normal cell which may show one of the following:- (i) an area if transformation of part of the epithelial lining into cuboidal or columnar, ameloblast-like cells with reversed polarity--( the tumour is confined to the luminal surface of the cyst—luminal unicystic ameloblastoma (ii) A localized nodular projection of ameloblastic cells in the lumen of the cyst- (sometimes called plexiform unicystic Ameloblastoma ) –intraluminal unicystic ameloblastoma. (iii) infiltration of some part of the wall(capsule) of the cyst by plexiform or follicular ameloblastoma - mural ameloblastoma.

SQUAMOUS ODONTOGENIC TUMOUR Locally infiltrative benign tumour - first reported by Pullon and associates (1975). - Sometimes, mistakenly diagnosed as acanthomatous ameloblastoma or epidermoid Ca.   Aetiology – Unknown Histogenesis:- Probably arise from rest cells of Mallassez or derivatives of dental lamina. 

Clinical features: Age:- 2nd – 7th decades (peak- 3rd decade) Sex:- No predilection. Site: Maxilla most common in the incisor/canine area When in Mandible canine premolar areas (Multicentric cases affecting both jaws have been reported) MCQ Usually symptomless at the early stage Advanced stage - Mobility of related teeth - Pain - Tenderness

Xrays:- Unilocular radioluscency (Semi circular or triangular in shape with or without a sclerotic border.) Usually related to the cervical third of the root(s).   Histology:- A locally infiltrative tumour consists of well-differentiated islands of squamous cells, scattered in a fibrous stroma. The peripheral layers of these islands are made up of highly flattened cells, with no pallisading or polarization.

CALCIFYING EPITHELIAL ODONTOGENIC TUMOUR (PINDBORG’S TUMOUR) Is uncommon - Locally invasive epithelial tumour - First classified separately by Pindborg (1958)   Histogenesis: ? enamel organ / dental lamina Clinical features: Age: 20 – 60 years Peak = middle age (40yrs) Sex: No sex predilection Site: - mandible > maxilla -molar-premolar area most affected part

Clinical Appearance:  - Usually asymptomatic slow but progressive bony jaw swelling with associated unerupted tooth / impacted tooth.   Extra-Osseous types have been reported with an average age of 35 years. X-rays:- poorly demarcated irregular radioluscency or circumscribed area of mixed radiolucencies and opacities. There may be irregular bone trabeculations multilocular radiolucency or honeycomb appearance with flecks of radio opacities. 

Histology:- locally infiltrative; shows a lot of variations - Sheets or strands of polyhedral epithelial cells with well-defined borders and prominent intercellular bridges in a bland fibrous tissue stroma that may show degenerative changes.   - Mitosis are rare but there’s nuclear pleomorphism, giant cells, multinucleated cells and cells with prominent nucleoli. - Characteristics presence of round homogenous eosinophilic intra-epithelial substances (similar in staining characteristics to amyloid- ( i.e fluoresce with thioflavin T stain and green birefringence with congo red stain). Controversy does exist as to whether it is a degenerative product or it is actively secreted.

- These substances are extruded into the extracellular spaces later due to cell secretion anddegeneration. - Deposition of calcific material in the concentric eosinophilic masses  Liesesang rings . A variant may show clear cells (vacuolated cytoplasm). - In peripheral or extra osseus types there are fewer foci of calcification and the neoplastic epithelium is less active.

CLEAR-CELL ODONTOGENIC TUMOUR/CARCINOMA This also a locally invasive tumour of odontogenic epithelium recently classified as an entity. First regarded as benign but now believed to be malignant Aetiology: ? Unknown Histogenesis: Probably - derivatives of dental lamina - rest cells of Malassez  Clinical Features: A central jaw tumour can affect either jaw Some patients associated with pain Age more seen above 50 years -More locally aggressive than Ameloblastoma - Data too scanty to give a comprehensive picture.

Radiology:- Radioluscent lesion (may be uni- or multi- locular) with poorly defined margins Histology:- Sheets or islands of uniform vacuolated and clear cells or finely stippled cells in a scanty mature c.t. -No evidence of amyloid or calcific deposits.  -May be similar to clear cell adenocarcinoma or intra-osseus mucoepidermoid carcinoma in histologic appearance.

AMELOBLASTIC FIBROMA Mixed tumour (both epithelial and messenchymal neoplastic elements) - Less common - occur in younger age group than ameloblastoma - Characterized by simultaneous proliferation of both epithelial & mesenchymal tissues without formation of dental hard tissue.   Histogenesis: Epithelial part - Enamel organ or its derivative mesodermal part - dental papilla or follicle

Clinical Features:- Slow growth / Painless Clinical Features:- Slow growth / Painless. Slower than amelo jaw expanding but not infiltrative. Age:-Younger age : 40% below 10 years (most are seen < 25 years ) Average age 15 years.  Sex:- Male = Female   Site:-Mandible > Maxilla (Canine-prem-molar area of the mandible) X-ray: Multilocular or unilocular radioluscency (similar to amelo). Cortical bone expansion, displacement of roots may encompass/include unerupted tooth. The edges are usually smooth or sometimes sclerotic (b/c it does not infiltrate trabeculae)

Histology : Two components epithelial and mesencymal. - Epithelial cells arranged in strands, sheets or scattered islands in a highly cellular c.t. stroma. - The epithelial cells which are cuboidal or columnar may contain small number of stellate reticulum – like cells. - The c.t. is made up of numerous large round or angular cells with little or no collagen and very few blood vessels. - Occasionally some stroma cells may have fine granular cystoplasm (granular cell ameloblastic fibroma)   - Hyalinization around the epithelial cells may also be seen.

AMELOBLASTIC FIBRO-DENTINOMA / FIBRO-ODONTOMA - Rare tumours  - Similar to ameloblastic fibroma (i.e. mixed tumours).  They are characterized by stimultaneous proliferation of epith and messenchy tissues but with inductive changes that lead to dentine or enamel and dentine. - Should not be confused with self limiting developmental anomalies like odontoma.   Age - Occur in children and teenagers as asymptomatic lesions. Characterised by Swelling which may be associated with failure of tooth eruption.

  Sex - Males  Females Site - Maxilla  Mandible X-ray: Both appear as well-circumscribed expansive radioluscencies with large radiopaque masses. Histology:- Proliferating odontogenic epithelium and cell-rich mesencyme with poorly calcified dentine / enamel and dentine around the epithelial cells. Both tumours must not be confused with odontomes (developmental) since they are capable of continuous growth and can reach a relatively large size destroying the jaw bones.

ODONTO AMELOBLASTOMA (Ameloblastic odontoma) Rare Characterized by presence of a relatively undifferentiated epithelial neoplastic component (ameloblastoma) with a highly differentiated mesenchymal tissue (Odontoma). AGE - Affects any age but more common in children   SITE - Mandible > maxilla X-ray: Similar to composite odontomes – multilocular or unilocular radioluscency with numerous small radiopacities. Histology: Similar to ameloblastoma but also with fibrous tissue stroma containing variable amount of cellular odontogenic ectomesenchyme with well formed dentine / enamel.

ADENOMATOID ODONTOGENIC TUMOUR (Adenoameloblastoma) An Intraosseus odontogenic tumour (few extra-osseus cases reported)   - Not common  - It is a benign tumour of odontogenic epithelium with duct-like structures and varying degree of inductive changes in its c.t. Histogenesis: -Enamel organ or its remnant (REE) ? ? from a dentigerous cyst. Disturbance must have occurred after completing of tooth formation (associated with non-defective tooth). 

Clinical Features: Painless progressive swelling expanding bone. Age: All ages: More in 1st – 3rd decades peak 2nd   Sex: Females > males Site: Maxilla > mandible : Canine / premolar. X-RAYS: Radioluscent unilocular lesion with or without sclerotic borders and most of the times enclosing the crown of an unerupted tooth.  * There may be dense radiopaque foci within the lesion.

Histology: Usually encapsulated. - Whorls of Odontogenic epithelium interspersed with duct-like (tubular) structures in a scanty c.t. stroma. - The duct-like structures are lined by columnar / cuboidal (amelobast-like) cells. - Eosinophilic Coagulum are sometimes seen in the “ductal lumen”  - Deposits of amyloid - like substances in between the epithelium cells. - Acidophilic hyaline material deposited in the c.t. suggestive of dysplastic dentine. - Calcific deposits may be scattered throughout the tumour.

CALCIFYING ODONTOGENIC CYST (Gorlins cyst) First described by Gorlin and associates   - Now agreed as a neoplastic lesion although with features of a cyst. - Praetorious et al (1981) described 3 cystic entities and 1 tumour variant each with peculiar histological and clinical features.

Common seen in 2nd/3rd decades of life   - Equal sex distribution - Mandible = maxilla - Central tumour which occur in jaw bones or in soft tissue of tooth bearing areas. X-ray: well-defined radioluscency with varying amount of radiopaque materials. Flecks or nodules of radiopaque material.

Histology: A cystic lesion with epithelial lining which shows well-defined basal layer of columnar cells with an overlying layer (many cells thick) of stellate reticulum like cells.   There are pyknotic epithelial cells (ghost cells) in the epithelial cyst lining or in the fibrous capsule. The ‘ghost’ cells  dysplastic calcification. Dysplastic dentine may be laid down adjacent to the basal layer of the epithelium.

ODONTOMAS These are harmatomatous rather than neoplastic lesions.   (A) Compound:- tooth like structures with various layers (dentine, enamel, cementum & pulp) laid down in regular pattern like normal tooth. (B) Complex:- tooth-like structures with various layers arranged in irregular (harphazard) manner with no semblance to normal tooth.  * Both are – enclosed in a fibrous capsule and a cystic cavity lined by squamous epith.

Clinical features :   - More commonly seen in 1st & 2nd decades  - Females > males - Mandible > maxilla - Compound more common in anterior region incisor / canine while Complex more common in molar/premolar region. - They are usually associated with secondary dentition - Self-limiting Asymptomatic Xray:- Area of well-circumscribed radioluscency at early stage with progressive deposition of radiopaque masses.

ODONTOGENIC FIBROMA Rare - Central or peripheral - A fibroblastic neoplasm  Histogenesis: dental follicle papilla (the c.t. surrounding the enamel region) Clinical Features:- More in children/young adults but can occur at all ages - mandible > maxilla Usually asymptomatic, local enlargement of jaw

Peripheral:- slowly growing, solid, firm, attached to gingival between or close to a tooth. Central:- Very rare. Slowly growing jaw lesion. Xray:- Usually unilocular radiolucency. may Resemble dentigerous cyst radiologically if related to tooth crown. Lesion is however solid and not cystic if multilocular may resemble ameloblastoma.   Histology:- Mass of loosely arranged c.t. in which strands and islands of epithelium are dispersed. There may be calcification in form of dysplastic dentine, osteoid, or cementum like material (calcifying odontogenic fibroma).

ODONTOGENIC MYXOMA (FIBROMYXOMA, MYXOFIBROMA) Benign Locally invasive expansile central tumour - Occur exclusively in jaw bones - Slowly growing but expands bone and destroy the cortex - Little or no encapsulation. Histogenesis: from mesenchymal portion of tooth germ dental papilla / follicle or p.d.l. Clinical features:- slow growth Expands bone causes bone destruction May be associated with an unerupted tooth  Age:- 2nd - 3rd decade rarely below 10years or Sex:- Male = female Site:- Mandible > maxilla (slightly)

FURTHER READINGS Surgical management of Oral Pathologic lesions by Edward Ellis III in Cotemporary Textbook of Oral & Maxillofacial Surgery. ( Chapter 22) Oral & Maxillofacial Pathology by BW Neville, DD Damm, CM Allen & JE Bouquot . Pennsylvania, Philadelphia ; Saunders (2002). Malik NA . Textbook of Oral and Maxillofacial Surgery Jaypee Medical Publishers ( Chapter 36).