Odontogenic tumours/oral surgery courses by indian dental academy


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Odontogenic tumours/oral surgery courses by indian dental academy

  1. 1. GITAM DENTAL COLLEGE & HOSPITAL DEPARTMENT OF ORAL & MAXILLOFACIAL SURGERY SEMINAR ON Odontogenic tumours- current concepts and its treatment modalities. Presented By: Dr. Sambhav K Vora III MDS
  3. 3. INTRODUCTION: - The embryologic events that initiate control and guide the formation of human odontogenic structures take place through a complex and finely regulated series of inductive interactions between epithelium and mesenchyme, which begin during 5th and 6th weeks of intrauterine life and are completed about 16th year after birth. During this extended period, there is ample opportunity for developmental and growth mechanisms to fail in whole or in part, resulting in the formation of malformations, hamartomas and neoplasms. Odontogenic tumors are an imprecise term that encompasses a wide spectrum of lesions and variants that are derived from the specialized dental tissues. These tumors do not always meet the criteria for neoplasia and some appear to represent abortive attempts at odontogenesis. The distinctions among the above mentioned 3 forms of abnormalities might in part depend upon the embryologic stage of initiation and histologic and gross appearance of the lesion at the age of clinical discovery. Odontogenic tumors are primarily intraosseous lesions, although extraosseous variants have been described occasionally. These tumors have a varied clinical and radiographic appearance and can consist of entirely soft tissue, a mixture of soft and calcified tissues or entirely
  4. 4. calcified tissues. A unique feature of these tumors is the wide range of biologic behavior that they express. Because of this wide range of behavior, various methods of treatment have been described for each tumor ranging from conservative to aggressive therapy. Often the proper therapy is selected only after careful consideration has been given to correlate the specific lesion with its clinical behavior pattern. Here let us discuss the various treatment modalities used to treat the odontogenic tumors and the present day concepts regarding the management of the same. CLASSIFICATION: - I. GORLIN, CHAUDHRY AND PINDBORG’S CLASSIFICATION- A. Epithelial odontogenic tumors: 1. Minimal inductive change in the connective tissue- (i) Ameloblastoma. (ii) AOT (iii) CEOT. 2. Marked inductive change in the connective tissue- (i) Ameloblastic fibroma. (ii) Ameloblastic fibrosarcoma. (iii) Odontoma: - • Ameloblastic odontoma. • Ameloblastic dentinosarcoma. • Complex odontoma.
  5. 5. • Compound odontoma. B. Mesodermal odontogenic tumors: 1. Myxoma. 2. Odontogenic fibroma. 3. Cementoma- (i) Periapical cemental dysplasia (ii) Benign Cementoblastoma. (iii) Cementifying fibroma. (iv) Gigantiform cementomas. II. REICHART AND RIES CLASSIFICATION- Ameloblastic Ectomesenchy mal Mesenchym al Neuroectoderm al Ameloblastic Ameloblasto ma. AOT. CEOT. SOT. Ectomesenchy mal AF. AFO. Complex odontoma. Compound odontoma. Cementoblasto ma. Odontogenic Myxoma. Odontogenic fibroma. Dentinoma. Mesenchymal “Adamantino Periapical Fibroma.
  6. 6. ” hemangioma. cemental dysplasia. Gigantiform cementoma. Cementifying fibroma. Lipoma. Hemangiom a. Neuroectoder mal Ameloblasto ma with neurinoma. Central pacinian neurofibroma. Neurofibro ma. Melanotic and Neuroectoderm al tumor of infancy. I. WHO CLASSIFICATION (1992)- I. Neoplasms and other tumors related to the odontogenic apparatus- A. Benign odontogenic tumors: 1) Odontogenic epithelium without odontogenic ectomesenchyme: - (i) Ameloblastoma. (ii) SOT. (iii) CEOT. (iv) Clear cell odontogenic tumor. 2) Odontogenic epithelium with odontogenic ectomesenchyme, with or without dental hard tissue formation: - (i) Ameloblastic fibroma. (ii) AFO and AFD.
  7. 7. (iii) Odontoameloblastoma. (iv) AOT. (v) Gorlin lesion. (vi) Complex odontoma. (vii) Compound odontoma. 3) Odontogenic Ectomesenchymal with or without included odontogenic epithelium: - (i) Odontogenic fibroma. (ii) Myxoma. (iii) Benign Cementoblastoma. B. Malignant odontogenic tumors: 1) Odontogenic carcinomas: - (i) Malignant Ameloblastoma. (ii) Primary intraosseous carcinoma. (iii) Malignant variants of other odontogenic epithelial tumors. (iv) Malignant changes in odontogenic cysts. 2) Odontogenic sarcomas: - (i) Ameloblastic fibrosarcoma. (ii) Ameloblastic fibro-dentinosarcoma and Ameloblastic fibro- odontosarcoma. (iii) Odontogenic carcinosarcoma. II. Neoplasms and other lesions related to bone- A. Osteogenic neoplasms: - 1) Cementifying fibroma (OF, Cementifying fibroma). B. Non-neoplastic bone lesions: -
  8. 8. 1) Fibrous dysplasia of the jaws. 2) Cemento-osseous dysplasias- (i) Florid cemento-osseous dysplasia. (Gigantiform cementoma, familial multiple cementomas). (ii) Other cemento-osseous dysplasias. 3) Cherubism. 4) Central giant cell granuloma (CGCG). 5) Aneurysmal bone cyst. 6) Solitary bone cyst. C. Other tumors: - 1) Melanotic neuroectodermal tumors of infancy. III. REVISED VERSION OF WHO CLASSIFICATION (2002)- I. Neoplasms and tumor-like lesions arising from the odontogenic apparatus- A] Benign: - 1) Odontogenic epithelium with mature, fibrous stroma; odontogenic ectomesenchyme not present: (i) Ameloblastomas.  Intraosseous (central, infiltrative).  Extraosseous (peripheral).  Desmoplastic.
  9. 9.  Unicystic. (ii) SOT. (iii) CEOT. (iv) AOT. 2) Odontogenic epithelium with odontogenic ectomesenchyme, with or without dental hard tissue formation: (i) AF and AFD (neoplastic). (ii) AFD (non-neoplastic).  AFO.  Complex odontoma. (iii) Compound odontoma. (iv) Odontoameloblastoma. (v) Calcifying ghost cell odontogenic tumor. 3) Mesenchyme and /or odontogenic ectomesenchyme with or without included odontogenic epithelium: (i) Odontogenic fibroma (simple). (ii) Odontogenic fibroma (WHO-type). (iii) Odontogenic Myxoma. (iv) Benign Cementoblastoma. B] Malignant (odontogenic carcinomas): - 1) Malignant (metastasizing) Ameloblastoma. 2) Ameloblastic carcinoma- (i) Primary. (ii) Carcinoma in intraosseous
  10. 10. Ameloblastoma (dedifferentiated). (iii) Carcinoma in peripheral Ameloblastoma (peripheral). 3) Primary intraosseous squamous cell carcinoma (i) Solid. (ii) Cystogenic  Non-keratinizing cyst.  OKC. 4) Clear cell odontogenic carcinoma. 5) Calcifying ghost cell odontogenic carcinoma. (Malignant epithelial odontogenic ghost cell tumor). C] Malignant (odontogenic sarcomas): - 1) Ameloblastic fibrosarcoma 2) Ameloblastic fibro-dentino and fibro- odontosarcoma. 3) Odontogenic carcinosarcoma. II. Neoplasms and other lesions occurring in the jaw bones- A) Osteogenic neoplasms: - 1) Cemento-ossifying fibroma. B) Non-neoplastic lesions: - 1) Fibrous dysplasia of the jaws. 2) Cemento-osseous dysplasia (i) Focal cemento-osseous dysplasia. (ii) Florid cemento-osseous dysplasia. 3) Other cemento-osseous dysplasia (i) Cherubism. (ii) Central giant cell granuloma (CGCG).
  11. 11. 4) Pseudocysts of the jaws (i) Aneurysmal bone cavity. (ii) Simple bone cavity. (iii) Lingual and buccal mandibular bone depressions. (iv) Focal marrow containing jaw cavity. C] Other tumors: - 1) Melanotic neuroectodermal tumor of infancy. GENERAL PRINCIPLES OF MANAGEMENT: - IMAGING- I. Plain radiography. II. CT scan and 3-D CT scan. III. MRI. IV. Angiography. BIOPSY- I. Exfoliative cytology. II. Aspiration biopsy. III. FNAC. IV. Excisional biopsy. V. Incisional biopsy.
  12. 12. PRINCIPLES OF SURGICAL MANAGEMENT OF JAW TUMOURS- Goals of treatment- a. Complete eradication of a lesion b. Preservation of normal tissue as permissible c. Excision with least morbidity d. Restoration of tissue loss, form and function e. Long-term follow-up for recurrence. Factors to be evaluated before surgery- (i) Nature of the lesion- Before choosing the most appropriate surgical method, it is a must to identify the lesion histologically with biopsy, whether benign/malignant. (ii) Anatomical location of the lesion- a. The location of the lesion within the jaws may severely complicate the surgical excision and therefore jeopardize the prognosis. A benign tumour in an inaccessible area presents an obvious problem surgically and from the standpoint of the
  13. 13. function rehabilitation of the patient. A more aggressive tumour in an easily reachable and resectable area, as in the anterior mandible, offers a better prognosis b. Maxillary tumours exhibit much more aggressive behaviour than their mandibular counterpart. Proximity to maxillary sinus, nasal cavity, orbital cavity, cranial fossa, and nasopharynx allows these tumours to grow asymptomatically and more extensively to attain a large size with late symptoms. c. Proximity of the benign tumours to adjacent vital structures like neurovascular bundles and teeth is an important consideration because preservation of these structures should be attempted. If the tumour is aggressive, then both these important structures have to be sacrificed. d. The amount of involvement with in a particular site, mandible, has bearing on the type of surgical procedure necessary to obtain a cure with the more aggressive lesions. If the inferior border is not involved in the lesion, marginal resection can be carried out without continuity defect. When the tumour extends through the entire thickness of the involved jaw, a partial resection then becomes mandatory. e. If the tumour is confined to the inferior of the jaw, without perforating cortices, offers a better prognosis than those that have invaded surrounding soft tissues. In the latter case, one
  14. 14. has to carry out wider resection sacrificing the more amount of normal soft tissue along with the resection of the bone. (iii) Aggressiveness of the lesion- Surgical therapy of the odontogenic tumours ranges from enucleation / curettage to composite resection. Histological diagnosis positively identifies and therefore directs the treatment of the lesion. Locally invasive tumours are treated with wider resection in order to prevent recurrence. (iv) Duration of the lesion- Many odontogenic tumours exhibit slow growth and may become static in size. The slower growing lesions seen to follow a more benign course and treatment should be individually tailored to each case. (v) Functional rehabilitation of the patient- After achieving the primary goal of eradicating odontogenic tumours, next most important consideration is the residual defects resulting from the extirpative surgery. Reconstruction is much easier in mandible than in maxilla. When reconstructing defects in the mandible, treatment goals should be established.  Restoration of mandibular continuity-using reconstruction plates.
  15. 15.  Restoration of alveolar bone heights, restore the adequate bulk of the mandible-primary/secondary reconstruction method-to prevent pathological fracture. Gold, Upton and Marx in 1991 have presented a standardized surgical terminology for the excision of lesions in the bone (i) Enucleation (ii) Curettage (iii) Marsupialization (iv) Recontouring (v) Resection without continuity defect (vi) Resection with continuity defect (vii) Disarticulation. 1. Enucleation with/without curettage- Enucleation- removal of an entire structure, without rupture, as one shells kernel of a nut. Curettage- a scraping, usually of the interior of a cavity/tract, for the removal of new growths or other abnormal tissues, or to obtain material for tissue diagnosis using hand instruments. Eventhough, this is mainly used for the cystic lesions; non- aggressive small benign tumours can also make use of enucleation with/without curettage.
  16. 16. Indications- 1) Surgical excision of the tumours, which tend to grow by expansion, rather than by infiltration of the surrounding tissues. 2) Lesions occurring in the bone with a distinct separation between the lesion and the surrounding bone. 3) Often there is a cortical margin of bone that delineates the tumour or cyst from the bone. 4) Indicated in following tumours: (i) Odontogenic tumours- a. Odontoma b. AF. c. AFO. d. AOT. e. Cementoblastoma (ii) Fibro-osseous lesions and nonodontogenic tumours • Ossifying fibroma • Cherubism • CGCG. • Osteoblastoma (iii) Other lesions i. Hemangioma ii. Eosinophilic granuloma
  17. 17. iii. Neurofibroma iv. Neurilemanoma v. Pigmented neurectodermal tumour. Marginal resection or resection without continuity Defect / peripheral osteotomy / en block resection: Enblock resection- this is a procedure that allows complete excision of the tumour, at the same time, a continuity of jawbone is retained. And thus deformity, disfigurement, and the need for secondary cosmetic surgery and prosthetic rehabilitation are avoided. Peripheral osteotomy- a procedure in which scraping usually of the interior of a cavity/tract, for the removal of new growths or other abnormal tissues are done using rotary instruments. Indications- 1. Benign lesions with a known propensity for recurrence. 2. In those lesions that are incompletely encapsulated or tend to grow beyond their surgically apparent capsule. 3. Recurrent lesions 4. Indicated in the following tumours- a. Ameloblastoma b. CEOT c. Myxoma
  18. 18. d. Ameloblastic odontoma e. Squamous odontogenic tumour, f. Benign chondroblastoma g. Haemangioma Intraoral marginal resection (surgical procedure) – The circumgingival incision is taken and the releasing incisions can be extended into the buccal mucosa on either side of the lesion leaving at least one or two adjacent teeth on either side. Using periosteal elevator reflects the full thickness mucoperiosteal flap. Care is taken not to perforate the lesion. If the lesion is perforated, then overlying mucosa should be sacrificed along with the excision of the tumour. The tooth next to the tumour mass should be extracted on either side. The vertical osteotomies are performed through the sockets of the extracted teeth on either side using bur or saw blade. Both the vertical osteotomy cuts are extended from the buccal to lingual cortex. These cuts are joined with a horizontal cut, placed well beyond the tumour mass including margin of the normal bone. Horizontal cut is also completed through and through the buccal and lingual cortex. Using osteotome carries out the complete excision of the tumour along with some amount of normal bone. Teeth involved in the tumour mass are removed with the block in toto. The remaining bony margins should be checked for sharp areas and contoured by using round bur or bone file. The excess mucoperiosteal flap is trimmed off and approximated to suture
  19. 19. the wound. This type of excision can be done under local anaesthesia with sedation for smaller lesions or it can be planned under general anaesthesia. Extraoral peripheral osteotomy- Since complete resection of large segments involving both the horizontal and the ascending rami or disarticulation of the segment causes considerable amount of disability, this method is useful, which will allow complete removal of the pathology, but is less debilitating than complete resection. The procedure is based on the observation that the cortical inferior border of the horizontal body, the posterior border of the ascending ramus and the condyle are not generally involved in the benign tumour process. Bone regeneration will start from such areas even though a thin rim of bone is preserved, especially in young patients result in considerable restoration of the jaw anatomy. Indications- Large lesions involving posterior mandible. Operative procedure- In dentulous patients, intraoral crevicular gingival incision is taken around dentulous area, both buccally as well as lingually. Buccinator and mylohyoid muscles are separated after reflecting the mucoperiosteal flap. In edentulous patients there is no need to take intraoral incision. Extraoral submandibular incision is taken and the inferior border of the mandible is exposed, if required posterior border of the ramus is also
  20. 20. exposed. The site of peripheral osteotomy is already decided by studying CT scans or radiographs. The drill holes are made with the electrical dental drill in the healthy bone around the periphery of the lesion. These holes are connected until the tumour mass is separated from the thin span of bone to be retained. The part to be excised is now separated from the attached soft tissue on the external surface. The masseter and buccinator muscles are detached with care, so that not to injure the branches of the facial nerve. Then the mucoperiosteum of the alveolar process is elevated and the specimen in turned outward to get access to the inner surface to detach the mylohyoid and the internal pterygoid muscles. The temporalis muscle is severed above the coronoid, after which the inferior alveolar nerve and vessels are identified and grasped with a hemostat, ligated and cut off. The remaining bone is now carefully inspected. Intraoral wound is closed with watertight suturing. An immediate bone graft can be inserted through the extraoral wound and fixed with intraosseous wires or bone plates. The wound is closed in layers with a small rubber drain inserted to prevent formation of a hematoma. An external pressure bandage is applied. Careful long-term following up is mandatory. Segmental resection of the jaw- It is carried out for more extensive lesions, which include the inferior border of the mandible. Partial resection- A procedure wherein resection of a tumour by removing the full thickness portion of the jaw is carried out. In mandible, this can
  21. 21. vary, depending on the site of the tumour from a small continuity defect to hemi-mandibulectomy. Disarticulation- Whenever condylar head is included in the resection of the part of the mandible, then a procedure is called as hemi-mandibulectomy with disarticulation. Whenever the condylar head is retained for rehabilitation procedure then the procedure is called hemi-mandibulectomy without disarticulation. Total resection- Excision of a tumour by removal of the involved bone is carried out. Maxillectomy or mandibulectomy procedures can be carried out. Composite resection- Requires much more radical intervention with wider margins of excision of uninvolved tissues. Surgery may include along with resection of the jaw, neck dissection. Radiotherapy or chemotherapy alone or in combination with surgery may be used. This is usually used for malignancies. Indications- 1. For treatment of lesions that are infiltrative or have a tendency to recur. 2. Those lesions, which extend close to the inferior or posterior border of the mandible, the maxillary sinus or the nasal cavity. 3. It is also used for malignant lesions with huge recurrence potential.
  22. 22. 4. Recurrent odontogenic tumours with difficulty in examining and gaining an access surgically. 5. Maxillary ameloblastomas with high recurrence rate. 6. Lesions close to the borders of the jaw, with the possibility of postoperative pathologic fracture. Resection of mandible- Intraoral approach- Advantages- a. Excision of overlying mucosal tissue involved in the lesion is facilitated. b. Easy access for application of arch bars, extraction of involved teeth, ligation of the inferior alveolar neurovascular bundle, closure of the maxillary sinus and maintaining the forward stability of the tongue, whenever required. c. An external scar is avoided. d. An extraoral tissues are preserved for a later reconstruction procedure Disadvantages- a. Contamination of the surgical wound by the oral flora. b. Lack of dependent drainage of the dead space. c. Difficult access to the most posterior portions of the mandible.
  23. 23. d. The risk of damage to the branches of the internal maxillary artery, deep in the wound. e. Immediate bone graft reconstruction by oral route has a higher rate of infection and loss of the bone graft (30%). Surgical procedure- For mandibular lesion extending posterior to the mental foramen, ligation of the inferior alveolar neurovascular bundle prior to resection may prevent significant intraoperative hemorrhage. The incision is designed to expose the lesion on both the facial and lingual aspect with or without inclusion of overlying tissues in the specimen. The same incision is extended posteriorly through the buccal mucosa approximately 7 mm lateral and parallel to the anterior border of the ascending ramus and external oblique ridge. Blunt dissection is carried out along the surface of the buccinator muscle to expose the periosteum and periosteum is elevated lingually to expose the retromolar area of the mandible, internal oblique ridge and medial surface of the ramus, till the lingula. The inferior alveolar neurovascular bundle is located and a curved aneurysmal needle can be passed around it with a ligature threaded through its eye. The neurovascular bundle is ligated at the higher level above the lingula. After this, the entire lesion is exposed by reflecting the mucoperiosteal flap on buccal and lingual side till the inferior margin of the mandible. The anterior and posterior bony cuts are then outlined as planned and the cuts are finished by using bur or saw blade from buccal to
  24. 24. lingual cortex. In the tooth bearing area, one or two teeth may be removed prior to sectioning the jaw, bony cut can be carried out through an empty socket. Separation of the bony cuts can be completed with an osteotome. The specimen is separated from its bony and soft tissue attachments and inferior alveolar neurovascular bundle is sectioned below the ligature level. Whenever the anterior portion of the mandible is removed, it is mandatory to hold the genioglossus muscles with the hemostat prior to separation from the specimen and then these muscles should be secured with a suture in the forward position to the soft tissues of the chin or to the reconstruction plate to prevent airway obstruction due to tongue fall postoperatively. Primary closure of the wound is done. Intermaxillary fixation or reconstruction plate is necessary to preserve the alignment of the fragments. Extraoral approach- 1) Segmental resection with disarticulation: The surgical approach is through a combined postramal (Hinds) and submandibular (Risdon) incision placed at least 2cm below and parallel to the inferior and posterior borders of the mandible. After the incision through the skin, subcutaneous tissue and platysma is taken, the dissection plane is made deep to the platysma, along the investing fascia to the inferior border of the mandible. The pterygomasseteric sling and periosteal layer is divided at the inferior border of the mandible. Subperiosteal reflection of the masseter
  25. 25. muscle is done along the lateral surface of the mandible to expose the coronoid process, sigmoid notch and condylar neck. The anterior portion of the resection is determined and dissected. Care should be taken to prevent an intraoral communication, using the bur or saw blade, the osteotomy is completed. By swinging the specimen laterally, it is freed from its medial attachments subperiosteally. The temporalis muscle is detached from the coronoid process. The condylar head is separated from lateral pterygoid muscle attachments. Care should be taken to prevent damage to the maxillary artery and its branches. The specimen is completely removed and the surgical wound is irrigated. The proximal portion of the segment is smoothened to prevent intraoral perforation. Reconstruction plate with condylar prosthesis is placed and fixed on to the proximal stump with screws. The wound is closed in layers after proper hemostasis. 2) Segmental resection involving the mandibular midline: An incision of at least 2cm is made below the inferior border of the mandible. Incision is taken through the skin, subcutaneous tissue. At the level of platysma muscle the tissues are undermined. Platysma is cut sharply and dissection is followed to the investing layer of the deep cervical fascia. Incision through this layer is taken till the periosteum at the inferior border of the mandible. The dissection is carried out subperiosteally to detach the left and right digastric as
  26. 26. well as the mylohyoid muscle from the medial aspect of the mandible. The genioglossus and geniohyoid muscle attachments are located and a suture is passed around them. Then the muscles are detached from the genial tubercles. The subperiosteal dissection is carried on the buccal surface of the mandible to expose the planned resection portion. The mental nerves are identified and protected. The lateral extent of the resection is defined in the dentulous jaw by extracting the teeth and placing the bony cuts through the sockets. A mucoperiosteal flap is developed intraorally to free the specimen from the soft tissue attachments. Prior to the removal of the specimen, the remaining segments should be stabilized by carrying out temporary intermaxillary fixation. The reconstruction plate is contoured prior to excision of the bone and immediately secured it following the resection by means of screws. This prevents the collapse of the segments and allows jaw function during healing and prior to reconstruction and also prevents scar contraction. The oral mucosa is closed intraorally, using a horizontal mattress suture to obtain as watertight seal as possible. The genioglossus and geniohyoid muscles are pulled forward with suture, which is secured to the reconstruction plate. Extraoral wound is closed in layers. Maxillectomy- Access to the maxilla is generally obtained by designing the classic Weber- Fergusson incision. The eyelids are closed temporarily by taking
  27. 27. tarsorrhaphy sutures. For esthetic good results, it is recommended to tattoo the vermilion border and other points on both sides of the incision with methylene blue. These points are then matched during closure. The typical incision splits the midline of the upper lip. But better cosmetic results can be obtained by incising the philtral ridges and then offsetting the incision at vermilion border. The incision is turned laterally at the base of the columella, then around the alar base and along the side of the nose to within 2mm of the medial canthus. Intraorally the incision is continued down through the gingival margin. It is connected with a horizontal incision at the depth of the labiobuccal vestibule, extending back to the maxillary tuberosity. From here the incision turns medially across the posterior edge of the hard palate. It then turns 900 anteriorly, several mm to the proximal side of the midline, if possible to cross the gingival margin once again. The incision is carried to the bone, except beneath the lower eyelid, where the orbicularis oculi muscle is preserved. The cheek flap is then reflected back to the tuberosity. The central incisor on the involved side is extracted and the gingival and palatal mucosa is elevated back to the midline. The incision extending around the nose is then deepened into the nasal cavity. The palatal bone is then divided near the midline with a saw blade or bur. The basal bone is then separated from the frontal process of the maxilla with an osteotome. The orbicularis oculi muscle is retracted superiorly and the bone cut is extended across the maxilla, just below the infraorbital rim into the zygoma. If the posterior wall of the maxillary sinus
  28. 28. has not been invaded by the tumour, it is separated from the pterygoid plates with a pterygoid chisel. The entire specimen is removed by severing the remaining attachments with a large curved scissors placed behind the maxilla. After removal of the specimen, some amount of brisk bleeding is expected, which is controlled with packing and electrocautery. Branches of the maxillary artery in the pterygomaxillary fissure area may require ligation. While packing in place, the specimen should be inspected to make sure that complete tumour has been excised. All sharp bony projections should be trimmed. The palatal flap is turned up to cover the medial bony margin. A split- thickness skin graft is then sutured to the wound margins to cover the entire defect. Graft is maintained in place by placing softened impression compound ball in the defect. The surgical obturator, which is prefabricated, is placed to seal the defect and support the packing. The obturator is fixed to the remaining teeth by means of interdental wiring. The main cheek flap is then turned back and closed in layers. Modifications- (i) When the tumour extends upto the roof of the maxillary sinus, but does not invade, then the orbital floor should be included in the resection. (ii) When the tumour invades the roof of the maxillary sinus, orbit or the ethmoid sinuses, orbital exenteration is mandatory.
  29. 29. (iii) The tumours, which are confined to the posterior aspect of the maxillary sinus, may be managed with amore conservative resection that spares the premaxilla. Postoperative management- 1) Patients are kept in ICU for first one or two days for cardiovascular monitoring and necessary maintenance of fluid and electrolyte balance. 2) Patients are kept on liquid diet. 3) Instruct to maintain the oral hygiene. 4) Prophylactic antibiotics are advocated for 5-7 days. 5) The surgical obturator is removed after 15 days and the wound is irrigated with warm saline. 6) Excess skin graft and other debris are removed. 7) Long-term follow-up is necessary. RECONSTRUCTION- After surgical resection with continuity defect, there is disfigurement, deviation of the mandible along with resultant altered mandibular movements with facial asymmetry. Need for reconstruction: • For restoration of the movements and equilibrium of the mandible. • For maintenance of normal occlusion, floor of the mouth and tongue’s anatomical position. • For restoration of near normal feeding.
  30. 30. • For acceptable esthetics and function. • For more favourable social acceptance. Immediate reconstruction: Advantages- 1. Single stage surgery. 2. Early return of the function. 3. Minimal compromise of esthetics. Disadvantages: 1) Recurrence in the grafted bone. 2) Loss of graft from infection. Three ways of immediate reconstruction: A] Performing the surgical excision and grafting, both via intraoral approach. B] Surgical excision utilizing both intraoral and extraoral approach, first obtaining the watertight oral closure and grafting is done through extraoral approach. C] Earlier extraction of the involved teeth and waiting for 6-8 weeks for oral healing and then surgery at second stage, with complete procedure via extraoral approach to avoid communication of the graft. Delayed reconstruction (second stage): Here the consideration should be given to maintain the residual mandibular fragments with their normal anatomic relationship with intermaxillary fixation or using reconstruction plate. This is to avoid
  31. 31. cicatricial and muscular deformation and displacement of the segments, which aids in the secondary reconstructive efforts at a later date. Usually six months waiting period is observed for recurrence. I. AMELOBLASTOMA. Synonym: Adamantinoma Introduction: It is a true neoplasm of odontogenic epithelial origin. It is the second most common odontogenic neoplasm. Its incidence combined with its clinical behaviour makes Ameloblastoma the most significant odontogenic neoplasm of concern to oral and maxillofacial surgeons. Opinions differ regarding its terminology, etiology, histological pattern, classification, clinical and biological behaviour, diagnosis, treatment aspect and malignant potential. History: 1827 – first recognized by Cuzack. 1879 – described by Falksson. 1885 – Malassez coined the term Adamantinoma. 1934 – Ivy and Churchill coined the term Ameloblastoma. Definition: Robinson defined Ameloblastoma as usually unicentric, nonfunctional, intermittent in growth, anatomical benign and clinically persistent.
  32. 32. WHO – “ it is a true neoplasm of enamel organ type tissue which does not undergo differentiation to a point of enamel formation.” Types: I. Clinically- a. Central or intraosseous. b. Peripheral or extraosseous. c. Desmoplastic. d. Unicystic II. Histologically- a. Follicular b. Plexiform c. Acanthomatous d. Granular cell e. Basal cell Pathogenesis: The origin of Ameloblastoma is not known with certainty. According to Thoma, Williams in 1993, the tumour may be derived from various origins.  Late developmental sources – cell rests of enamel organ, either remnants of dental lamina or epithelial cell rests of Malassez or remnants of Hertwig’s sheath, follicular sacs.  Early embryonic sources – disturbances of developing enamel organ, dental lamina, tooth buds.  Basal cells of the surface epithelium of the oral mucosa.
  33. 33.  Secondary developmental sources – epithelium of odontogenic cysts, particularly primordial, lateral periodontal cyst, dentigerous cyst and odontomas.  Heterotopic epithelium in other parts of body, especially from the pituitary gland.  With concepts of neoplasia in general, it is likely the result of alterations or mutations in the genetic material of cells involved in odontogenic cysts.  Environmental factors  Patient variables – general health status, nutritional status. Clinical features: Frequency – it accounts for approximately 1% of all oral tumours. 18% of all odontogenic tumours. Age – the average age at diagnosis is around 33 – 39years. And most cases cluster between 1st decades to 7th decade. Sex – men = female. Race – more common in blacks and some studies identifies Asians as most commonly affected population. Site - mandible is most commonly affected area. (5:1). There is a predilection for posterior maxilla and posterior molar-ramus of the mandible. Clinical presentation- (i) Asymptomatic
  34. 34. (ii) C/o swelling and facial asymmetry. (iii) Swelling is usually slow-growing, hard, non-tender, and ovoid which is often large in size. (iv) Pain – occasional sign, if secondarily infected. (v) Ulceration of the overlying mucosa. (vi) Tooth mobility. (vii) Occlusal alterations (viii) Failure of eruption of teeth. (ix) Exfoliation of teeth (x) Ill fitting dentures (xi) Nasal obstruction (xii) Later stage with nerve involvement – sensory changes of the lower lip. (xiii) Large persistent lesions may exhibit fluctuation and egg-shell crackling. If not treated, It invades into the neighboring tissues by replacing them. Invasion into the medullary space is the first feature. When the tumour attains larger size with bone erosion, there is escape into the periosteum mucosa and muscles of adjoining region. Root resorption will occur. Locally aggressive invasion in maxillofacial region – may compress vital structures, obstruct airway, impairs swallowing, erode major arteries, or invade middle cranial fossa.
  35. 35. The extensive tumours can cause gross facial deformity. Size – ranges from 1 cm upto 16 cm. In maxilla, it may enlarge to involve maxillary sinus, and nasal cavity leading to nasal obstruction and even proptosis of eye. Radiographic findings: (i) It presents as a unilocular / multilocular radiolucent lesions. (ii) 50 % of ameloblastomas appear as multilocular radiolucent lesions with sharp borders. 2 % of the Ameloblastomas are peripheral. 6 % appear as Unicystic lesions. (iii) The apparent lesional edge may be distinct or indistinct. (iv) Multilocular cyst like radiolucency with compartmentalized appearance due to bony septa ( honey comb or soap bubble appearance ) resembles fibromyxoma, giant cell lesions. (v) Small or large unilocular or multilocular lesion may contain unerupted deciduous or permanent teeth and may resemble a dentigerous cyst. (vi) Lesions in dentulous area cause root resorption (30 %) and tooth displacement. (vii) Buccolilngual cortical expansion (80%), this tendency is stronger than a cyst. (viii) The displacement of neurovascular bundle at the inferior border is often seen.
  36. 36. (ix) Maxillary lesions often involve the maxillary sinus and change the normal radiolucency of the sinus to a more opacified appearance. (x) The radiographic image of Ameloblastoma is at the most suggestive and not pathognomonic. CT scan with 3-D reconstruction will show the exact extent of the lesion. (xi) One of the variants of the Ameloblastoma – the desmoplastic Ameloblastoma most often found in the anterior maxilla or mandible appears as a relatively radiopaque lesion because of its dense connective tissue content (solid type lesion). Histopathology: The Ameloblastoma is composed of nests, strands and cords of Ameloblastic epithelium, all separated by relatively small amounts of fibrous connective tissue stroma. The characteristic histological features of the Ameloblastoma are the orientation of the outer epithelial cell nuclei, which are positioned (polarized) away from the basement membrane. Two main patterns are seen: 1. Follicular type (resembles tooth follicle) – consists of small to large odontogenic epithelial nests (the follicles) and variously shaped and sized ameloblastomatous islands (more common pattern). Cyst formation is commonly seen. 2. Plexiform type – consists of interlacing strands of narrow or wide odontogenic epithelial trabeculae
  37. 37. resembling the dental lamina. Both these patterns may be observed in the same tumour. Both these types have a columnar or cuboidal outer epithelial cell layer bordering the connective tissue stroma and enclosing the inner epithelial cells. Subtypes – (i) Acanthomatous type – compression of stellate reticulum into a squamoid mass with squamous metaplasia is seen. Sometimes keratin formation in the central portion of the tumour islands is noticed. Occasionally epithelial or keratin pearls may be seen. Usually seen in follicular type of Ameloblastoma or peripheral Ameloblastoma. (ii) Basal cell type – bears resemblance to the basal cell carcinoma of the skin. The inner follicular and outer follicular cells may assume a basal cell appearance throughout the lesion. (iii) Desmoplastic type – variant of solid Ameloblastoma. Abundant fibrous tissue stroma can be seen in this variety. Some areas of calcification also can be seen. Marked stromal desmoplasia is noticed. High recurrence rate. (iv) Granular cell type – stellate reticulum like cells, get transformed into cells with coarse granular, eosinophilic cytoplasm. This type is found to be more aggressive type with high chances of recurrence and metastasis (malignant transformation)
  38. 38. (v) Mural Ameloblastoma –another name for Unicystic lesion, which is found in children and young adults. The Ameloblastic epithelium lines the luminal surface and may proliferate into the cyst (mural growth). Often ‘budding’ aggregates of basal cells, follicular cells, or plexiform strands extend from the luminal lining into the cystic wall. Further growth of the lesion takes place by creation of microcystic and macrocystic formations in the budding Ameloblastic elements that extend and enlarge the primary cystic lumen or the cyst wall by resorption of host bone. Differential diagnosis- II.Radiologically-  Dentigerous cyst,  Odontogenic keratocyst,  Cherubism,  Giant cell granuloma,  Odontogenic myxoma,  ABC. II. CALCIFYING EPITHELIAL ODONTOGENIC TUMOUR. Synonym: Pindborg’s tumour. Acronym: CEOT. Introduction:
  39. 39. CEOT is an uncommon odontogenic tumour that appears to occupy a position between hamartoma and aggressive neoplasm. CEOT has been categorized by 1992 WHO classification as a benign, locally invasive odontogenic neoplasm that is exclusively epithelial in its tissue origin. History: Described by J J Pindborg in 1955. Thoma and Goldman (1946) and Ivy (1948) have erroneously reported the case of CEOT as Ameloblastoma. 1976-Franklin and Pindborg have reported that 113 cases of CEOT have been described in literature since 1955. 2002-Neville, Damn, Allen and Bouguot have reported that around 200 cases of CEOT have been described in the literature. Types: I. Based on site of occurrence-  Intraosseous-within the bone.  Extraosseous-outside the bone. II. Based on histopathology- • Classical type. • Clear cell variant. • CEOT associated with AOT, dentigerous cysts and odontomas. Pathogenesis: -
  40. 40. A confirmed etiology still remains elusive. The probable mechanisms are- i. Reduced enamel epithelium. ii. Stratum intermedium c ells of enamel organ. iii. Immunologic response to stratum intermedium cells. iv. Remnants of the primitive dental lamina. v. Basal layer of oral epithelium. Clinical features- Frequency- uncommon to rare odontogenic neoplasm. Represents less than 1% of all odontogenic neoplasms. Extraosseous-5 to 6% of all CEOT’S. Age – ranges from 8-92 years. Most commonly reported in patient during 4th , 5th and 6th decades of life. Average patient age between late 30’s to early 40’s. 37-43 years. Extraosseous – 12-48years. Sex – no sex predilection. Race – occurs more frequently in whites. Site - mandible is preferred site than maxilla (3:1) may occur in any area of the jaw, but premolar/molar region appears to be favoured. (65%) Extraosseous – anterior region. Predilection for incisor/premolar region. Clinical presentation- Intraosseous lesion-
  41. 41. 2. Usually asymptomatic, discovered through routine radiographic examinations. 3. Present as a slow-growing, painless, expansile, hard, bony swelling – cortical bone thinning – egg-shell crackling – perforation – soft tissue infiltration. 4. May cause associated tooth tipping, rotation, migration and/or mobility secondary to root resorption. 5. In maxilla, the lesion may invade maxillary sinus, pterygoid space, ethmoid and sphenoid sinuses by extension. Extraosseous lesion- a. Painless mucosal-coloured to red swelling of about 6-month duration that may produce saucerization of the underlying bone. b. Sometimes may produce pain. Radiographic features- Not pathognomonic. Radiographic features ranges with regard to
  42. 42. i. Lesion size and ii. Bone pattern. Routine dental radiographic images show- 65% - mixed radiolucent and radiopaque pattern. 32% - completely radiolucent. 3% - totally radiopaque. “ Wind - driven snow” appearance – scattered flecks of calcification throughout radiolucency. May be unilocular and cystic, often associated with an unerupted teeth but cyst like hydraulic pattern of cortical expansion is absent. May be multilocular – i. Honeycomb pattern – locules appearing small, round and somewhat corticated. ii . Soap bubble pattern – large spaces. Radiographic border between tumour and surrounding bone appears to be diffuse / well defined and circumscribed. 3 features associated with teeth that assist in the diagnosis of CEOT – I. Embedded tooth that is rarely impacted e.g. I/II molar. II. Inferior displacement of mandibular unerupted tooth causing protuberance in this region because of penetrating apex of the tooth into the inferior cortex. III. Apical extension of the occlusal c luster that may obscure the embedded tooth.
  43. 43. Erupted teeth may be displaced and root resorption may be seen in adjacent teeth. CT scan- Expansion and thinning of buccal and lingual cortical plates by a well-defined mass containing scattered radiopaque areas of varying size and signal intensity. MRI – Predominantly a hypointense lesion on T1-weighted images. A mixed hyperintense lesion on T2-weilghted images. Hilstopathological features: - Has characteristic histopathologic features- 1. Trabeculae and/or sheets of large, eosionophilic staining, squamoid shaped epithelial cells frequently with prominent intercellular bridges. 2. Tumour cells vary from polygonal to round to oval in shape. It may be irregular, pleomorphic and ominous in morphology. 3. Scattered cells with clear glycogen rich cytoplasmic contents may be seen. 4. Nuclear morphology and staining is highly variable. Single to multinucleated cells that has normal to very large nuclei, abnormal/pleomorphic in shape and have hyperchromaticity with deep basophilic staining characteristics.
  44. 44. 5. Increased number and/or abnormal mitotic figures are uncommon. 6. Connective tissue stroma is usually inconspicuous between the islands and sheets of epithelium. 7. Presence of a homogeneous, eosionophilic substance which has been identified as amyloid-characteristic 8. Ultrastructural studies show 2 forms of amyloid- i. Immunamyloid-arise from the light chain fragments of immunoglobulins. ii. Apudamyloid-arise from the cells of certain endocrine tumours, which may be derived from the endocrine polypeptide cells of neural crest origin of amine precursor uptake and decarboxylation. 9. Immunohistochemical and electron microscopy reveals that the amyloid is derived from- a. Degenerative process involving the cytokeratin intermediate filaments in tumour cells. Or b. Degeneration of type IV collagen associated with basement membrane. 10.Special staining for amyloid- i. Crystal violet – stains metachromatically.
  45. 45. ii. Congo red – display bright orange to red hue when exposed to polarized light – apple green iii. Thioflavin T – fluoresces to a blue colour decreases an UV light. 11.Prominent or scattered calcifications, in concentric crenate like shapes – liesegang rings are seen maturing within the amyloid stroma. 12.Chen et al, reported that CEOT expresses bone sialoprotein. Liesegang’s rings and epithelial cells near them demonstrated positive histochemical staining to bone sialoprotein antibodies evidence of a n in situ hybridization bone sialoprotein mRNA signal respectively. Differential diagnosis- II. Clinically- 1. Ameloblastoma 2. Odontogenic Myxoma 3. Fibro Myxoma 4. Fibroma 5. Ameloblastic fibroma 6. Ameloblastic fibro odontoma 7. Large dentigerous cysts 8. OKC. 9. OF.
  46. 46. 10.CGCG. 11.Central giant cell lesion. 12.Osteoma. 13.Osteoblastoma. 14.Cementoblastoma. 15.Primary odontogenic carcinoma. 16.Metastatic carcinoma of jaws. 17.Osteosarcoma. 18.Chondrasarcoma. III. Radiologically- A. Radiolucent- 1. Dentigerous cyst 2. OKC. 3. Gorlin cyst. 4. AOT 5. Central giant cell lesion 6. Early stage of ossifying fibroma 7. Early stage osteoblastoma B. Mixed- 1. AOT 2. Gorlin cyst 3. Ameloblastic fibroodontoma 4. Maturing / advanced stage of ossifying fibroma
  47. 47. 5. Osteoma 6. Osteoblastoma C. Completely radiopaque- 1. Odontoma 2. Gorlin cyst associated with odontoma 3. AOT associated with odontoma IV. Histologically- 1. Squamous cell carcinoma. 2. Metastatic carcinoma of jaws. 3. Unknown primary metastatic adenocarcinoma. 4. Primary intraosseous mucoepidermoid carcinoma. 5. Osteosarcoma. Management- The surgical treatment of CEOT should be case specific and is dependent on: (i) Size and location of the neoplasm (ii) Patient’s overall medical condition or tolerance to withstand the surgical procedure. (iii) Clinical activity (perforation of the cortical bone, periosteal/nerve involvement etc.) (iv) Recognized behavioural characteristics (v) Skill / experience level of the operator
  48. 48. Small, intrabony mandibular lesions with well-defined borders – simple complete but conservative tumour enucleation / curettage followed by indicious removal of a thin layer of bone adjacent to the tumour. Small maxillary lesions – surgically excised by either through intrabony curettage or conservative enblock resection. Maxillary tumours can be treated more aggressively than a similar sized lesion in the mandible. Resection without continuity defect or resection with continuity defect can also be used. Resection with continuity defect – segmental resections-significant bone discontinuity requiring either distraction osteogenesis/graft and reconstruction procedures. Treatment of atypical/frankly malignant CEOT- Early intervention essential. Radical resection of the affected jaw portion and associated soft tissue with no less than 1cm in every dissection. Adjunctive external beam radiotherapy-local spread to cervical lymph nodes Adjunctive chemotherapy-controls distant organ metastasis. Radiotherapy in lieu of surgical resection is contraindicated for CEOT. Treatment of peripheral CEOT – According to Houston and Fowler, simple local excision. Prognosis-
  49. 49. Local recurrence rate 10%-20% Incidence of malignant transformation to odontogenic calcifying epithelial pindborg tumour is extremely low. No reported recurrences in patient treated for peripheral CEOT. II. ADENOMATOID ODONTOGENIC TUMOUR Synonyms- a. Adamantoma b. Epithelial odontome c. Tooth germ cyst of the jaw d. Adenoameloblastoma e. Glandular Ameloblastoma f. Adenomatoid Ameloblastoma g. Ameloblastic adenomatoid tumour Acronym- AOT Introduction- AOT is a benign, nonaggressive odontogenic tumour characterized by the formation of “duct like structures” by the epithelial component of the lesion. AOT is considered as an odontogenic tumour because- a. Occurs only in the tooth – bearing area of the jaws.
  50. 50. b. Its histomorphologic resemblance to components of tooth germ. AOT is the fourth most frequent odontogenic tumour. Some investigators consider AOT as an hamartomas because- i. Limited size of most cases ii. Lack of recurrence Others consider AOT to be a non-aggressive, non-invasive benign neoplasm because – i. The limited size of the most cases stems from the fact that most are detected early and removed before slow-growing tumour reaches a clinically noticeable size. ii. The microscopic features of the lesional tissues show greater departure from the arrangement of the normal odontogenic apparatus, than should be expected in a developmental anomaly. Gardner describes AOT as “benign embryonal neoplasm” History- 1909-James and Forbes reported case as “epithelial odontome” almost certainly an AOT (England).
  51. 51. 1915- earliest irreputable case reported by HARBITZ, Norway, as “Adamantoma”. 1916-Ist acceptable American case reported, “Tooth germ (chorioblastomatous) cyst of the jaw” by Wohl. 1948-Stafne reported first series of AOT as “epithelial tumours associated with developmental cysts of the maxilla. 1950-BERNIER AND TIECKE, coined the term “adenoameloblastoma” 1951-V annual American Academy of Oral Pathology meeting simple Ameloblastoma and adenoameloblastoma as separate entities “was presented for further consideration but was not adopted. 1961-GORLIN et al introduced the term “Ameloblastic adenomatoid tumour. (AAT) 1963- SHAFER et al adopted the term “AAT’ in his 2nd edition of Textbook of Oral Pathology. 1968-ABRAMS et al suggested the term “odontogenic adenomatoid tumour” 1969-PHLIPSEN AND BIRN, proposed the name “AOT’. 1971-the term AOT was adopted in the initial edition of WHO “Histological typing of Odontogenic tumours, jaw cysts and allied lesions.” 1992- retained in the 2nd edition of WHO “Histological Typing of Odontogenic Tumours, jaw cysts and allied lesions” Types-  Based on the location-
  52. 52. 1. Intraosseous/central/intragnathic 2. Extraosseous/peripheral/extragnathic  Radiographically- 1. Pericoronal 2. Extracoronal Pathogenesis- A variety of ultrastructural studies attempting to clarify the origin of AOT have been carried but in vain. The specific stimulus that triggers the proliferation of the progenitor cells of AOT is unknown. Nearly all investigations have agreed upon the cytologic resemblance of the structures of AOT to the dental lamina and components of enamel organ. Thoma suggested a dual origin for AOT- (i) Salivary (ii) Odontogenic This was ruled out by Smith et al in 1979 who showed the presence of hemidesmosomes and basal lamina at the luminal pole of the cells that form the duct like structures. This was supported by negative reactivity of these cells to lactoferrin and L1 antichymotrypsin antibodies. (Takahashi et al). The duct forming cells and non-duct forming cells exhibit secretory granules and coated vesicles near the luminal pole resembling inner enamel epithelium cells as they develop through preameloblast stage.
  53. 53. (Smith et al, Schlosnagle and Sameren, Yamamoto et al and Poulson and Greer). Spindle cells that are between cell-rich nodules resemble ultrastructurally the stellate reticulum and those that are immediately adjacent to the nodules resembles stratum intermedium of enamel organ. The cell present in the tumour resembles the outer enamel epithelium cells (Hatakeyama and Sujuki). The cells present in the tumour have been described to resemble odontoblasts. (Khan et al). Philipsen et al, 1992 argued that AOT arises from remnants of the successional lamina/accessional dental lamina. Clinical features- Frequency-3%-7% of all odontogenic tumours. Intraosseous-97% Extraosseous-3% Age – ranges from 3-82 years of age. Its predilection for young patients is well established. 88% diagnosed in the 2nd and 3rd decades of life. (Intraosseous) Extraosseous 12-14years Sex – females are commonly affected (2:1) intraosseous extraosseous F; M= 14:1 Race – more common in b lacks. (Just harvesting phenomenon).
  54. 54. Site – maxilla more commonly affected than mandible (2:1). Marked predilection for anterior jaw. 85 % of lesions appear anterior to the II premolar (central and peripheral) Clinical presentation – Intraosseous (i) Usually asymptomatic, but patient may be aware of an area of jaw enlargement. (ii) Discovered on routine dental radiographic examination. (iii) Delayed eruption of permanent tooth or slow-growing bony expansion – discovery of the central AOT’s (iv) Mobility of teeth, swelling of the cheek, and asymmetrical facial swelling has been reported less frequently. (v) Infection of the tumour or fracture of the mandible – rarely led to discovery of the lesion. (vi) Nasal obstruction – rarely encountered. Extraosseous- (i) Gingival coloured mass that ranges from 1 – 1.5 mm in diameter. (ii) Epulis like fibrous swelling that mimics periodontal disease if bone erosion occurs. (iii) 10 times more prevalent in maxillary gingival. (iv) Painless
  55. 55. (v) Peripheral lesions represent central lesions that erupted with tooth, to complete their development in the gingival. Radiographic features- A. Pericoronal—70 % of AOT’s are associated with the crown of an unerupted tooth. 6% associated with two or more unerupted teeth. 60% of AOT’s associated with cuspids. 40% with maxillary cuspids. 3% associated with permanent molars. B. Extracoronal – 30% of AOT’s The relationship to the roots of adjacent / nearby teeth that ranges from that lateral / interproximal to Periapical to no relationship at all. 89% of extracoronal AOT’s occurred adjacent to permanent cuspids. Radiographic presentation- 1. Not pathognomonic. 2. As well-circumscribed, pear-shaped radiolucency lying between the diverging roots of the canine and I premolar teeth or 3. As unilocular, radiolucent lesion that is well-circumscribed exhibiting smooth corticated border. 4. Most lesions are pericoronal or juxta coronal, but the radiolucency may extend apically beyond the CEJ.
  56. 56. 5.Rare multilocular lesions have been reported and a scalloped border is observed occasionally. 6. Lesion may range from 1.5 – 7 cm and more. 7. May be associated with one or more impacted teeth. 8. Maxilla – slight buccal expansion of cortex. 9. Mandible – significant expansion present. 10. Maxillary lesions may grow into nasal fossa and antrum and may obliterate the antrum and expand the orbital floor. 11. Evidence of calcification within the lesion (65%) – faint/quite dense radiopaque foci. Patterns of calcifications –  Snowflakes  Animal prints  Hand / foot prints  Doughnuts  Semicircles  Groups of dots. Predominant pattern-even distribution throughout the lesion. 12. Occasionally, intralesional radiopacity may be identified usually eccentrically positioned within the lesion. 13. Unique feature – presence of capsular space 0.3 –0.8 cm wide – well defined, radiolucent band, that partly / most often completely surrounds the periphery of the lesion.
  57. 57. 14. Divergence of the roots and displacement of teeth occurs frequently. 15. Root resorption is rare. 16. Gingival lesions rarely are detectable radiographically but those may be slight erosion of the underlying alveolar bone cortex. Histologic features- A. Macroscopic features –  Soft, roughly spherical mass with a discernible fibrous capsule.  White to tan solid to crumbly tissue or one/more cystic spaces of varying size.  Minimal yellow – brown fluid to semisolid material.  Fine, hard gritty granular material.  One to several larger calcified masses. B. Microscopic features- Tumour is made up of a cellular multinodular proliferation of spindle, cuboidal, and columnar cells in a variety of patterns; usually scattered duct like structures, eosinophilic material, and calcifications in several forms; and a fibrous capsule of variable thickness. 6. Cell-rich epithelial nodules (hyaline droplets / tumour droplets) 7. Microcysts 8. Internodular epithelial cells
  58. 58. 9. Basaloid epithelial cells 10.Calcifying epithelial odontogenic tumour-like foci 11.Cystic space 12.Reduplicated basement membrane 13.Dysplastic dentin/dentinoid 14.Calcified bodies 15.Stroma 16.Fibrous capsule 17.Cytologic atypia Differential diagnosis- I. Clinically –  Central odontogenic tumours and cysts  Benign fibroosseous lesions  Benign mesenchymal neoplasms Gingival lesions –  Gingival fibroma  Peripheral cemento ossifying fibroma  Peripheral giant cell lesions  Other peripheral odontogenic tumours II. Radiographically – 1. Pericoronal – 1. Dentigerous cyst 2. OKC
  59. 59. 2. COC 3. Unicystic Ameloblastoma 4. Ameloblastic fibroma 5. Early Ameloblastic fibro-odontoma 6. Odontogenic fibroma 7. CEOT. 2. Extracoronal – a. Aforementioned odontogenic tumours and cysts b. Central giant cell lesion c. Benign fibroosseous lesions (early C-OF). d. Lateral periodontal cyst e. Lateral radicular cyst f. Apical radicular cyst g. Central benign mesenchymal neoplasms (neurilemoma). III. Histologically – 1. Vascular Ameloblastoma 2. Plexiform type of Ameloblastoma Treatment – Because of uniformly benign biologic behaviour of AOT and consistent presence of a well-developed fibrous capsule – conservative
  60. 60. complete surgical excision by means of enucleation and curettage – treatment of choice. Impacted teeth incorporated within the lesion should be removed. Teeth whose radicular bone cover has been resorbed by the lesion – endodontically treated or removed. Several reported cases have resolved or failed to progress following incomplete removal of varying extent – not a preferred treatment – incisional biopsy above or subtotal excision following confirmatory incisional biopsy or marsupialization followed by cystectomy. Prognosis- 1. Growth rate – slow / very slow growing tumour, but no report of measurements of growth rate over a course of time could be located 2. Recurrence rate – till date only 5 cases of recurrence have been reported. Unequivocal case of recurrence has not been reported. Association of AOT with other odontogenic cysts and tumours-  Dentigerous cyst  Combined epithelial odontogenic tumour  Odontoma  Ameloblastoma  COC Unusual cases –
  61. 61. (i) Melanotic AOT (ii) Multilfocal AOT. Future research- Modern research methods have facilitated the advancement of our understanding of the histogenesis of this lesion but unanswered questions remain. We await the results of in situ hybridization, DNA microassay analysis, gene rearrangement studies and other developing molecular biology techniques to solve the remaining mysteries. IV. SQUAMOUS ODONTOGENIC TUMOUR Synonyms –  Benign epithelial odontogenic tumour  Acanthomatous Ameloblastoma  Acanthomatous Ameloblastic fibroma  Hyperplasia and squamous metaplasia of residual odontogenic epithelium  Benign odontogenic tumour, unclassified. Acronym – SOT. Introduction – SOT is a relatively rare, benign, but locally infiltrative and occasionally aggressive odontogenic epithelial lesion that appears to have hamartomatous and neoplastic characteristics. History-
  62. 62. 1975 – first described by PULLON et al. Since then a number of papers have amplified details of the clinical presentations and range of biologic activity of SOT. Types – I. Based on the site of occurrence –  Intraosseous  Extraosseous II. Based on histopathology -  Solid type  Cystic type Pathogenesis- May be multifactorial. (i) Cell rests of Malassez} intraosseous (ii) Dental lamina (iii) Surface stratified squamous epithelium} extraosseous (iv) Cell rests of Serrae Clinical features – Frequency – rare odontogenic epithelium. 1 case of extraosseous lesion described. Age – SOT occurs over a wide range of age ranging from 2nd – 7th decade and reported incidence peaks in the third decade of life.
  63. 63. Sex – no sex predilection. But some studies show slight male preponderance and some others show slight female preponderance. Race – no racial predilection. But SOT was diagnosed in whites, blacks and Asians. Site – maxilla = mandible. Some studies show that mandible is commonly affected. Maxilla – lesions centered around the incisor cuspid region Mandible – lesions had a predilection for the bicuspid molar area. Lesions may be found singly or multicentrically in all areas of both jaws. Clinical presentation- (i) Often asymptomatic. Casually discovered by routine radiographs. (ii) Lesions involving dentate areas – alveolar resorption around the teeth – tooth mobility and pain. (iii) Tender on percussion – positive (iv) Occasionally abnormal sensations present. (v) If cortical bone is penetrated by the lesion, tumour infiltrates gingival, occasionally unattached alveolar mucosal, palatal soft tissue and rarely the buccal mucosal. (vi) Aggressive maxillary tumours may infiltrate the maxillary sinus and nasal floor and nasal spine. (vii) Familial SOT’s have been reported. Radiologic features-
  64. 64. Not pathognomonic of SOT. Presents as a triangular / semicircular radiolucency within the alveolar bone between the roots of several teeth. Displacement of one / both the adjacent roots. Destruction of crestal bone. Presence of smooth sclerotic border at the margin of the lesion. Some lesions are cystic / are associated with cysts. Thus they may appear radiographically as dentigerous, periodontal / Periapical in form. Extraosseous – saucerization of underlying bone. Histologic features- I. Solid type- (i) Consists of numerous islands of squamous epithelium dispersed in a connective tissue stroma. (ii) Islands are distributed in a uniform fashion and are well demarcated from the surrounding connective tissue stroma. (iii) The basal cell layer consists of flat to cuboidal cells and the internal cells exhibit squamous differentiation. (iv) The central areas of islands show foci of parakeratin or keratin calcification or cellular degeneration. (v) The epithelial cells are uniform and without pleomorphism or nuclear hyperchromatism or mitotic activity. II. Cyst type-  Contains many islands of squamous epithelium in the connective tissue wall, either completely separated from the odontogenic
  65. 65. epithelium lining the lumen or appearing to arise directly from the luminal epithelial lining.  These islands often exhibit vacuolization and microcyst formation.  Chronic inflammation may be seen. Differential diagnosis- I. Clinically – 1. Periodontal disease II. Radiographically – 1. Dentigerous cyst 2. Apical periodontal cyst III. Histologically –  Acanthomatous and Desmoplastic Ameloblastoma  SCC Treatment – Complete excision is required depending on the clinical and radiographic extent of the lesion. Intraosseous – 1. Enucleation 2. Curettage 3. Local excision
  66. 66. Clinically aggressive lesions – enbloc excision Intrabony lesion involving the soft tissue due to the penetration of cortical bone – soft tissue should be included in the excision. Teeth within the lesional area – extracted. Cystic lesion – treated conservatively. Complete excision by enucleation and / or curettage. Prognosis- SOT exhibits a biologic behaviour pattern of aggression that appears unaccountable in strictly histologic terms. Recurrences of incompletely excised lesions have been reported. V. ODONTOGENIC FIBROMA Introduction- A benign, relatively rare connective tissue tumour that contains a variable amount of inactive odontogenic epithelium. It has a benign behavioural course. Types- (i) Based on site of occurrence- a. Intraosseous / central. b. Extraosseous /peripheral. CENTRAL ODONTOGENIC FIBROMA Introduction-
  67. 67. The odontogenic fibroma is a central tumour of the jaws which is seen so infrequently that little is known about this neoplasm. There is lack of unanimity of definition of the lesion. Hence lots of uncertainty regarding this tumour. WHO classified COdF under “Odontogenic ectomesenchyme with / without included odontogenic epithelium” Slater et al (2001) considers this to be a mixed epithelial Ectomesenchymal neoplasm. Philipsen and Reichart (2002) , believes that the fibrous connective tissue component is of a mature mesenchymal type and not that of an Ectomesenchymal type. Definition- WHO defines COdF as a “fibroblastic neoplasm containing variable amounts of apparently inactive odontogenic epithelium and in some cases, calcified material resembling dysplastic dentin or cementum – like material.” Types- 1. Simple type – composed of delicate fibrous and myxoid tissue with scant numbers of inactive appearing islands and strands of odontogenic epithelium 2. WHO type / complex type – composed of cellular, mature, fibrous tissue containing numerous strands and islands of odontogenic
  68. 68. epithelium without palisading, reverse polarization or Stellate reticulum. Handlers et al (1991) concluded that COdF need not be separated into simple and WHO types because their histologic patterns did not correlate with clinical behaviour. The tumour formerly classified as the simple type was subclassified as a myxofibroma under Myxoma section in WHO histological typing of odontogenic tumours. Basic concepts concerning COdF- 1. It is a lesion around the crown of an unerupted tooth resembling a small dentigerous cyst. 2. It is a lesion of fibrous connective tissue, with scattered islands of odontogenic epithelium, bearing some resemblance to the dental follicle – because of size it may attain appearing to constitute a neoplasm. 3. It is a lesion as described by WHO, as previously mentioned. Pathogenesis- 1. Cells in dental follicle – gives origin to COdF associated with unerupted teeth. 2. Periodontal ligament – gives rise to COdF not associated with unerupted teeth. Clinical features-
  69. 69. Frequency – 4% -5% of all odontogenic tumours. Ranges from 0 – 14%. Age – 5 – 80 years. Mean 37 years. Sex – female predilection (2.8: 1) Race – occurs more frequently in whites. (95.5%) Site – occurs more frequently in mandible (52%). Fonseca found a predilection for maxilla. 77% of cases were located anterior to the I molar. Clinical presentation- 1. Asymptomatic 2. Mild tenderness / sensitivity – discomfort. 3. Paresthesia 4. Size 0.3 – 6.0 cm (Avg. 2.2 cm) 5. Duration few weeks to months to years. 6. Slow growing progressive enlargement 7. Unusual finding – presence of a cleft / depression or sinus tract like defect involving palatal gingival and palatal mucosal. 39% of maxillary COdF anterior to I molar had an associated palatal cleft. Mechanism of formation of such palatal clefts is poorly understood - attributed to the presence of myofibroblasts. COdF extends through a perforation in the palatal bone adhering to the periosteum and infiltrating the palatal mucosal. The palatal mucosa clinically seems to collapse into the bony defect. Radiographic features- 1. Expansile, multilocular radiolucency – majority.
  70. 70. 2. May have mixed density or completely radiopaque mass. 3. May also be manifested as unilocular lesion 4. May have loculated / scalloped periphery. 5. Most lesions are well defined, with a sclerotic border. But in some lesions the borders were ill-defined or irregular. 6. May also show – cortical expansion External resorption of the tooth roots Displacement of teeth Tooth mobility Erosion / perforation of cortical bone Displacement of the inferior alveolar canal. 7. May be associated with residual odontogenic cyst / roots of erupted tooth / unerupted tooth. Histological features- The microscopic components of COdF are – 1. Fibrous tissue of variable cellularity and density. 2. Variable amounts of inactive – appearing odontogenic epithelium. 3. Variable presence of calcifications resembling dysplastic dentin, cementum – like tissue or bone 1. Fibrous tissue-  Mesenchymal component varied from loosely collagenized to well collagenized, with/without myxoid areas.
  71. 71.  Myxoid areas, when present, were focal to prominent in distribution.  Cellularity varied from sparse to moderate to cellular.  Mitotic activity also was observed.  Eosinophilic, amorphous globules, which stain weakly for amyloid but may represent enamel matrix protein – infrequent.  Pleomorphic plump, stellate shaped and binucleated fibroblasts – Gunhan et al. 2. Odontogenic epithelium- a. Inactive. b. Present as islands / cords ranging from few to numerous. c. Epithelial cells exhibited cytoplasmic vacuolization. d. A zone of hyalinization may surround islands of epithelium. e. Presence of microcystic spaces in epithelial strands – Dunlap. 3. Calcifications- a. Ranged from focal to florid in distribution. b. These were interpreted as- Nonspecific calcifications. Cementum /cementum – like Cementum /dentin Cementum and osteoid Woven bone None of the COdF’s were encapsulated.
  72. 72. Differential diagnosis- 1. Giant cell granuloma 2. Odontogenic fibromyxoma 3. Desmoplastic fibroma 4. Neurofibroma 5. Ameloblastic fibroma 6. Follicular sac surrounding the crown of an unerupted tooth. 7. Metastatic carcinoma 8. CEOT 9. Ameloblastoma 10.CEOC 11.CGCG 12.Cementifying fibroma Treatment- This tumour is treated by surgical excision. But the excision is dependent on – clinical extent and anatomic involvement of the individual lesion. Most lesions can be managed by – enucleation and curettage. The lesions tended to shell out easily and completely from the surrounding bone. The lesions associated with palatal defect – dissection of the defect at their junction with palatal mucosa and periosteum. If the tumour incorporates the mandibular neurovascular bundle, an attempt should be made to preserve it. Teeth in the lesional area – extracted. The recurrent lesions can be treated conservatively. Rare is a resection required.
  73. 73. Prognosis- Recurrence rate 26%. Length of follow up ranges from 1 – 10 years. The time interval between first surgical procedure and the first recurrence ranged from 14 – 48 months. The spectrum of histologic patterns bears no correlation with the biologic behaviour. PERIPHERAL ODONTOGENIC FIBROMA Synonyms-  Odontogenic gingival epithelial hamartomas  Peripheral Ameloblastic fibrodentinoma  Peripheral hamartomas of dental lamina rest  Calcifying fibrous epulis. Acronym- POdF Introduction- POdF is considered to be the gingival counterpart of the COdF and is rare in occurrence. POdF can be confused with peripheral ossifying fibroma, a reactive lesion. Clinical features- Frequency – 1.2% of all odontogenic cysts and tumours. Age – ranges from I to VIII decades. Sex – M=F Site – mandible > maxilla. Found anterior to the II premolar.
  74. 74. Clinical presentation- (i) Measures around 1 – 3 cm in diameter. (ii) The lesions may be on the attached gingival or alveolar ridge. (iii) May be pedunculated / sessile. (iv) May have a normal gingival colour. (v) Large lesions may displace teeth but do not involve the underlying bone usually. Radiographic features – Radiographs reveals calcification in POdF more often than in the COdF. Histologic features- POdF mirrors central lesion in histologic appearance. Unencapsulated proliferation of cellular fibrous or fibromyxomatous connective tissue that exhibits variable amounts of odontogenic epithelium and sometimes foci of calcification in the form of dentinoid, cementicles or bone. Differential diagnosis – 1. Peripheral giant cell granuloma 2. Pyogenic granuloma 3. Giant cell fibroma 4. Simple fibroma 5. Peripheral ossifying fibroma 6. Neurofibroma
  75. 75. 7. Fibroepithelial polyp Treatment – The lesion should be excised to the interface with bone and a modest perimeter of the uninvolved tissue. Teeth incorporated in the tumour should be extracted. Prognosis- Unknown potential for recurrence. 39% recurrence rate in a 3 – 4 year interval. (Daley et al, 1994 and Gardner, 1982). VI. GRANULAR CELL ODONTOGENIC TUMOR. Synonyms-  Granular cell odontogenic fibroma  Granular cell Ameloblastic fibroma  Granular cell tumour of the jaws. Acronym – GCOT Introduction- Rare, benign odontogenic neoplasm that contains variable amounts of large eosinophilic granular cells and apparently inactive odontogenic epithelium. Types- 1. Central GCOT 2. Peripheral GCOT Pathogenesis –
  76. 76. Uncertain. Microscopic studies and immunohistochemical studies support a mesenchymal origin for the granular cells. Clinical features- Frequency – rare. Only 30 cases have been reported. Age – ranges from 16 – 77 years. Average – 45.5 years. Sex – F > M (73.3%) Site – mandible > maxilla (3:1). Premolar / molar region most common site. Clinical presentation –  Asymptomatic.  Cortical bone expansion – initial examination  Duration – ranges from months to years  Displacement of the teeth  Facial swelling  Intraoral ulceration  Cortical perforation  Maxillary sinus involvement  Displacement of mandibular canal Radiographic features- (i) May be radiolucent / mixed density / radiopaque. (ii) Patterns ranged from unilocular to multilocular often with a sclerotic border. Histologic features-  Specific.
  77. 77.  Consists of sheets / lobules of round to polygonal cells with abundant, eosinophilic granular cytoplasm with round to ovoid nuclei,  Scattered among the granular cells are cords and nests of odontogenic epithelium. Epithelial cells often possess clear cytoplasm.  Thin septae of fibrous connective tissue separate the lobules of granular cells.  The islands of epithelium do not form stellate reticulum.  Scattered small cementum – like or dystrophic calcifications seen (50%). Florid distribution of cementum like calcifications has been reported.  Ultrastructural studies supported the presence of lysosomes within the cytoplasm of granular cells.  Immunohistochemical studies have shown that the granular cells express – Vimentin α1 antiltrypsin Antichymotrypsin Lysozyme CD68 HLA –DR But stains negative for cytokeratins and S-100 protein.
  78. 78. Differential diagnosis- 1. Ameloblastic fibroma 2. COdF Treatment- Treated using conservative approach – enucleation / curettage. Prognosis- Does not show an aggressive biologic behaviour but can recur. VI MYXOMA Synonyms- (i) Odontogenic Myxoma (ii) Myxofibroma (iii) Odontogenic fibromyxoma Introduction- Benign, neoplasm of uncertain histogenesis with a characteristic histologic appearance, often behaves in a locally aggressive, infiltrating fashion. This is grouped under the subheading “Odontogenic ectomesenchyme with / without included odontogenic epithelium according to WHO classification.” Traditionally, myxomas are considered to be neoplasm of odontogenic origin. The odontogenic derivation of Myxoma is believed to origi9nate from the primitive mesenchymal portion of the developing tooth germ as an
  79. 79. inductive effect of nests of odontogenic epithelium on mesenchymal tissue or as a direct myxomatous change of fibrous tissue in an odontogenic fibroma. Definition- WHO defines myxoma as a locally invasive neoplasm consisting of rounded and angular cells that lie in an abundant mucoid stroma. Types- 2 forms of myxomas are recognized in head and neck region. 1. Those derived from the soft tissue. 2. Those derived from facial skeleton – nearly nonexistent. a. Odontogenic myxomas b. True Osteogenic myxomas. Clinical features- Frequency – 3% - 6% of all odontogenic tumours. Occurs 2 – 4 times less frequently than Ameloblastoma. Age – occurs from 11 months to 7th decade. 75% occurred between 2nd and 4th decades. 7% occurred in the I decade. Sex – slight female preponderance. F: M = 1.5: 1 Site – 66% occurs in mandible. 34 % occurs in maxilla. Mandible: maxilla = 2:1. Has a definite predilection for molar and premolar regions in both jaws. May also occur in – sinonasal tract, facial bones, extracranial skeleton. Clinical presentation-
  80. 80. 1. Usually asymptomatic. 2. Painless 3. Slow growing lesion and unilateral, some may cross the midline. 4. Mandible – buccal and lingual swelling. 5. Maxilla – swelling if sinus not involved. 6. Exophthalmos and nasal obstruction. Radiographic features- 1. Periapical radiographs and panoramic radiographs – I indicators of Myxoma of jaws. 2. Not pathognomonic. 3. Ranges from small unilocular lesions to large multilocular lesions. 4. Often displaces the teeth. 5. Rarely resorb the roots of the teeth. 6. The multilocular pattern – honeycomb, soap bubble, tennis racket, wispy and spider web in appearance. 7. Multilocular myxomas > 4.0 cm. Unilocular – smaller. 8. 5 % of myxomas associated with unerupted teeth. 9. May appear as – radiolucent – common. Mixed density – 12.5% Radiopaque – 7.5% 10.1/3rd exhibited diffuse / poorly defined borders. 11.CT & MRI should be used to clearly define tumour margins and to define the true extent of the Myxoma before surgery is performed.
  81. 81. 12.Imaging help to determine the true extent and involvement of the neoplasm. 13.Significant cortical expansion and perforation of the cortex with invasion into the soft tissues.’ 14.In maxilla, extension into the antrum – sunburst / hairbrush appearance. 15.Extension into nasal fossa and zygoma and thinning the orbital floor and hard palate. Histological features- I. Macroscopic features- 1. Well-delineated, unencapsulated, gray-white to tan-yellow mass that can be rubbery, soft or gelatinous in texture. 2. Margins are ill defined in gelatinous specimens 3. On cut surface, it is glistening, translucent and homogenous. II. Microscopic features- Bland in appearance. 1. Composed of loosely arranged, evenly dispersed spindle shaped, rounded and Stellate cells with long protoplasmic processes with a lightly eosinophilic cytoplasm in a mucoid – rich, intercellular matrix. 2. Mild nuclear pleomorphism / hyperchromatism exist. Mitosis / binucleate cells occasionally be present.
  82. 82. 3. Myxoid matrix is rich in hyaluronic acid and chondroitin sulphate. 4. Myxomas have a fine network of reticulin fibres and some have low collagen content. 5. Inconspicuous vascularity – supports the diagnosis. 6. Occasional island / rest of inactive – appearing odontogenic epithelium may be found. 7. Non encapsulated and may pervade surrounding bone by expansion. Differential diagnosis- 1. Enlarged dental follicle with myxoid change 2. Odontogenic fibroma 3. Dental papilla of a developing tooth 4. Malignant tumours of the jaws 5. Myxoid neurofibroma 6. Myxoid liposarcoma 7. Myxoid chondrosarcoma 8. Desmoplastic fibroma 9. Ameloblastoma 10.Hemangioma 11.CGCG 12.ABC. 13.Hyperparathyroidism
  83. 83. 14.Central neurilemmoma Treatment- The standard treatment for Myxoma is surgical excision. Radiation therapy and chemotherapy are ineffective treatments. A number of surgical methods have been advocated – 1. Excision 2. Enucleation and curettage 3. Curettage with / without electrical or chemical cautery. 4. Enbloc resection 5. Wide resection with and without immediate grafting. GOLD’S MANAGEMENT PROTOCOL- 1. Biopsy performed in a central area of the lesion and at the radiographic lesion – host bone interface histologically identifies the lesion. 2. Excision of the lesion by enucleation and curettage is restricted to unilocular lesions of no more than 1-2cm in diameter. Chemical cauterization (e.g. Carnoy’s solution) of the tumour bed may be of value. Teeth and alveolar process at the edge or within the radiographic and clinical limits of the lesion should be removed. 3. Extensive lesions should be excised by resection without continuity defect or resection with continuity defect including a perimeter margin of tumour – free bone of 1 cm depending upon the anatomic extent of the lesion.
  84. 84. 4. The neurovascular bundle of the mandible should not be sacrificed routinely, even in lesions that require resection with continuity defect. 5. The decision for immediate or delayed reconstruction is dependent upon the a. Clinical and / or histologic certainity of the complete excision of the tumour. b. Tissue requirements for reconstruction. Prognosis- Benign but aggressive tumour that has a propensity to infiltrate vital structures. Recurrence rate ranges from 10% - 33%. Recurrences of myxomas are related to incomplete removal than to the intrinsic biologic behaviour of the tumour. VII. AMELOBLASTIC FIBROMA Synonyms-  Soft mixed odontogenic tumour  Soft mixed odontoma  Fibroademantoblastoma Acronym- AF Introduction- Relatively rare, true benign mixed tumour in which epithelial and the Ectomesenchymal elements are neoplastic. It is characterized by the simultaneous neoplastic proliferation of the mesenchymal and epithelial
  85. 85. components without formation of dental hard tissues, namely dentin and enamel. Definition- WHO defines AF and related lesions as “neoplasms composed of proliferating odontogenic epithelium embedded in a cellular Ectomesenchymal tissue that resembles the dental papilla, and with varying degrees of inductive change and dental hard tissue formation.” History- First reported by Kruse in 1891. Types- 1. Intraosseous 2. Extraosseous Pathogenesis- Arises denovo during odontogenesis – result of overproduction of the basal lamina without odontogenic differentiation. Clinical features- Frequency – 1% - 2% of all odontogenic tumours. Age – predominantly in children and young adults with an age range of 6 months to 42 years (average 14. 6 – 15.5 years). Sex – no sex predilection (Tradahl). Some authors have reported male preponderance (Slootweg). Some authors have reported female dominance.
  86. 86. Site – mandible most commonly affected. Most frequently in the I permanent molar and II primary molar region. (80%). Rarely in the posterior maxilla and anterior regions of the jaws. Clinical presentation –  Asymptomatic. 20 % of the lesions discovered on routine radiography.  Painless, slow-growing and expansile neoplasm.  Exhibits slower clinical growth than Ameloblastoma and does not tend to infiltrate bone.  Enlarges by gradual expansion – periphery of the lesion often remains smooth.  Initial presentation – pain, tenderness or mild swelling of the jaw, discharge, and failure of teeth to erupt.  Associated with an impacted tooth 75%). Radiographic features – no pathognomonic radiographic features. a. Appears as a large, expansile pericoronal radiolucency and is well defined, unilocular / multilocular with a smooth, well- defined outline and often with a sclerotic opaque border. b. Small lesions are typically unilocular, whereas large mandibular lesions are multilocular. They may range in size from 1-8cm in diameter. c. Associated with unerupted teeth / impacted tooth. d. May be completely with in the bone or perforate the cortex.
  87. 87. e. Root resorption and inferior displacement of the mandibular canal may be seen. Histologic features- I. Macroscopic features- Appears as a solid, soft tissue mass with a smooth surface and often exhibits lobulated configuration. A well-defined capsule may not be present. II. Microscopic features – A. Ectodermal portion-  Proliferating islands, cords and strands of odontogenic epithelium with a peripheral layer of cuboidal / columnar cells and central area resembles the Stellate reticulum of embryonic enamel organ. (Tumour islands are found “opening”).  Mitotic activity uncomm9on.  Epithelial cells may be rounded / cuboidal. arranged in slender strands.  Amount and density of epithelial component may vary from area to area.  Cystic degeneration usually not seen. B. Ectomesenchymal portion-
  88. 88. 1. Embryonic, cell-rich mesenchyme that mimics the dental papilla. 2. The cells are rounded / angular and are fibroblast like, with little collagen. 3. Degree of cellularity varies. 4. A cell free zone / zone of hyalinization may be formed around the epithelial – connective tissue interface ultrastructural examination. 5. Degrees of thickening of lamina densa by granulofilamentous material. III. Immunohistochemistry-  Odontogenic epithelial cells positive for cytokeratins  Immature dental-papilla-like mesenchymal tissue positive for tenascin.  Some areas of dental papilla-like cells and in the basement membrane positive for vimentin of epithelium.  Collagen IV predominantly found, collagen I and protocollagen III were found less.  Unduliln not detected.  Proliferating cell nuclear antigen (PCNA). + Rarely encountered – slow growing nature.  MIB – 1 expression – recurrent AF and Ameloblastic fibrosarcoma.
  89. 89. Growth pattern of AF occurs usually by smooth expansion within the jaws – cortical bone thinning and occasional resorption. Surgical description – “finger like projections of the tumour extend into the bone” Treatment- AF has been managed by a conservative surgical approach unless the size of the lesion has dictated the anatomic need for resection procedures. (i) Most, if not all, recurrences probably result from incomplete excision. A conservative first approach to management is acceptable if the lesion is encapsulated. (ii) Presence / absence of the encapsulation should be established during the first stages of the surgical procedure. Despite encapsulation, some lesions may have loculi of the tumour that escape detection and excision. (iii) Enucleation and curettage result in successful excision of unilocular, encapsulated lesions. Careful histologic study of multiple sections of different areas – detect dysplastic changes. (iv) Extensive / multilocular lesions are more definitely managed by resection with continuity defect or resection with continuity defect from the outset. (v) Huge lesions require resection without continuity defect or resection with continuity defect and bone graft. To maintain anatomic integrity of the jaws.
  90. 90. (vi) Long term clinical and radiological follow up evaluation is required. Prognosis- Recurrence rate 43.5 % (Trodahl’s 1972). 18 % (Zallen et al). Recurrences are probably regrowth of residual tumour. 45% of Ameloblastic fibrosarcomas evolve from untreated / incompletely treated AF. VIII. AMELOBLASTIC FIBRO – ODONTOMA Acronym- AFO. Introduction- Benign, mixed odontogenic tumour that appears to be a combination of AF and forming complex odontoma. The lesion has expansile growth potential of AF and inductive ability of complex odontoma. AF represented the least histologically differentiated lesion that evolves from a moderately differentiated form of AFO to odontoma. (Cahn and Blum). Some investigators believe that AF and AFO are variations of the same process. This represented a hamartomatous lesion. Definition- WHO defines AFO as “a lesion similar to AF, but showing inductive changes that lead to formation of dentin and enamel.” History- First delineated by Hooker in 1972 and was clearly separated from Ameloblastic odontoma.
  91. 91. Pathogenesis- Similar to AF. Clinical features- Frequency – 1% -3% of odontogenic tumours. Age – found in I and II decades of life. 98% of tumours occur before the age of 20 years. Sex – M: F = 3:1 Site – mandible = maxilla. Some studies show mandibular preponderance. Premolar – molar region. Most commonly in the mandibular posterior region followed by maxillary posterior region. Clinical presentation- Usually asymptomatic.  Exclusively central / intraosseous lesion.  Painless, slow growing, expansile lesion.  Presents with swelling and failure of tooth eruption.  Most AFO’s associated with unerupted tooth. Radiographic features- (i) The tumour is unilocular / multilocular, with well-defined sclerotic borders and well-defined pericoronal radiolucency. (ii) May be seen as mixed radiopaque – radiolucent larger extensive lesions.
  92. 92. (iii) Associated with unerupted teeth / anodontia / absent teeth. (iv) Maxillary lesions may involve entire maxillary sinus and displace the involved tooth proportionately forts size. Cause more tooth displacement. (v) These lesions are generally not more than 1 – 2 cm in size. Histological features- (i) Composed of strands, cords, islands, fingers, and rosettes of primitive odontogenic columnar or cuboidal epithelial cells, resembling dental lamina. (ii) These epithelial components are distributed in a cell-rich, dental papilla like Ectomesenchymal stroma with delicate fibrils interspersed by large primitive fibroblasts. (iii) Varying amounts of osteodentin / dentin like material and occasional enamel matrix present. (iv) Odontogenic epithelium adjacent to the enamel matrix seems to be preameloblast like. (v) More calcified lesions exhibits mature dental hard tissues that resemble rudimentary teeth or a conglomerate of enamel and dentin. (vi) May / may not be well encapsulated. Differential diagnosis- Treatment-
  93. 93. (i) Noninvasive. Expansile characteristics encapsulation / well circumscribed. – Conservative excision by enucleation. (ii) Concurrent removal of associated unerupted tooth. (iii) Bosselated projections / lobular areas of the tumour – carefully removed. (iv) Huge lesions – resection (resection without continuity defect / resection with continuity defect). a. Site b. Extent c. Anatomic involvement. Prognosis- Recurrence is probable if residual lesion remains. Ameloblastic sarcomatous transformation has been reported. IX. AMELOBLASTIC FIBRO-DENTINOMA. Synonym – Dentinoma Acronym – AFD Introduction- Extremely rare, benign odontogenic mixed tumour and a variant of AF, in which odontogenic mesenchyme is induced to form dentin or a dentine-like product by the odontogenic epithelium. AFD is also considered as an hamartomas rather than a neoplasm. Some authors consider that AFD is a variant of AFO. Clinical features-
  94. 94. Frequency – about 35 cases have been reported 1936 – 1994. Age – ranges from 4 – 60 years of age. Usual age below 30 years. Sex – slight male predilection noted. (2:1). Site – mandible: maxilla (3:1). Lesions in children are associated with unerupted / missing deciduous teeth and are usually found in the anterior jaw. Lesions in adults, involving permanent teeth, show a preference for the posterior region of the jaw. Clinical presentation – (i) Asymptomatic (ii) Painless facial swelling / enlargement of the jaws (iii) Failure to deciduous / permanent teeth to erupt. – brings the patient to dentist. Radiographic features- (i) Small / extensive. (ii) Unilocular / multilocular. (iii) Often with well-defined borders with a thin rim of sclerotic bone. (iv) Present as a pericoronal radiolucency with radiopaque flecks consisting of calcified dentinoid. (v) Associated with unerupted deciduous / permanent teeth. (vi) Root resorption of the adjacent teeth. Histological features- I. Macroscopic features- (i) Can be encapsulated.
  95. 95. (ii) Described as mushroom – like and has white, rubbery consistency. II. Microscopic features- 1. Epithelial component-  Strands and islands of odontogenic epithelium proliferation in a mesenchymal, cellular, dental papilla – like connective tissue.  Peripheral epithelial cells induce a dentinoid matrix at interface. 2. Mesenchymal component-  Mesenchymal tissue may appear hypocellular, eosinophilic, and hyalinized.  Various stages of inductio9n of dentine may be demonstrated – dentinoid, osteodentin and rarely, tubular dentine.  The dentine may be infrequently and poorly mineralized. Treatment- 1. Complete excision of AFD. 2. The form of excision is case dependent – enucleation if possible. Resection without continuity defect / resection with continuity defect – if surgical circumstance requires. Prognosis- Recurrence is not expected. But residual lesion has the capacity to grow. A long-term follow up is a must. X. ODONTOAMELOBLASTOMA Synonyms-
  96. 96. (i) Ameloblastic odontoma (ii) Adamanto odontoma (iii) Soft and calcified odontoma Acronym- OA. Introduction- Rare, controversial epithelial odontogenic neoplasm that is composed of distinct areas of Ameloblastoma and odontoma. (Composite). Characterized by peculiar proliferation of tissue of the odontogenic apparatus in an unrestrained pattern, including complete morphodifferentiation, as well as apposition and even calcification. Unusuality of this lesion – a relatively undifferentiated neoplastic tissue is associated with a highly differentiated tissue – both may show recurrence. Definitions- 1. WHO – a very rare neoplasm, which includes odontogenic ectomesenchyme, in addition to odontogenic epithelium that resembles an Ameloblastoma both in structure and in behaviour. Because of the presence of the odontogenic ectomesenchyme, inductive changes take place leading to formation of dentine and enamel in parts of tumour. 2. Gorlin and Torsell and Shafer – tumour in which there is simultaneous occurrence of Ameloblastoma and a complex or compound odontoma with in the same tumour.
  97. 97. 3. Regezi and Scuiba – rare variant that is essentially an Ameloblastoma in which there is focal differentiation into an odontoma. History – 1944 – Thoma et al reported 1st case of Odontoameloblastoma. 1953 – Frissell and Shafer reported a case, which showed Ameloblastoma like areas and dental hard tissue but ghost cells were also present. 1980 – Labnola et al reported a case with definitive Ameloblastoma with a hard tissue component. 1986 – Gupta and Gupta reported a case with Ameloblastoma like tissue but hard tissue component. 1991 – Kaugars and Zussman 2002 – Masqueda – Taylor et al reported most recent series of OA. Pathogenesis – OA and AFO are one entity (Wachter et al). Clinical features – Frequency – very few cases are reported. Age – common in children I and II decades. Sex – male predilection. Site – posterior regions of both the jaws. Mandible > maxilla. Clinical presentation – 1. Slowly expanding lesion of the bone – facial asymmetry / deformity.
  98. 98. 2. Central lesion – considerable destruction of bone. 3. Mild pain 4. Delayed eruption of teeth. Radiological features- 1. Small, large / extensive lesion. 2. Well-circumscribed lesion with central radiopaque mass surrounded by a radiolucent zone or may contain irregular small / large radiopaque masses interspersed with radiolucent areas and usually surrounded by a sclerotic border. 3. No radiographic impression of infiltration. 4. Central destruction of bone with expansion of cortical plates is prominent. Histologic features- 1. Unusual and characteristic 2. Consists of a great variety of cells and tissues in a complex distribution – columnar, squamous and undifferentiated epithelial cells as well as ameloblasts, enamel and enamel matrix, dentine, osteodentin, dentinoid and osteoid material, Stellate reticulum – like cells, dental papilla, bone and cementum as well as stromal connective tissue. 3. Many structures resembling normal / atypical tooth germs may be found, with / without the presence of calcified dental tissues.
  99. 99. 4. An outstanding characteristic – presence of sheets of typical Ameloblastoma, usually basal cell, follicular / plexiform type. 5. Few mitotic figures are present. Differential diagnosis- 1. AFO 2. Ameloblastoma 3. Developing odontoma 4. Dentinogenic ghost cell tumour. Treatment- OA initially treated conservatively, including recurrences extensive maxillary lesion – hemimaxillectomy (LaBriola et al) Twice recurrent lesion – resection without continuity defect (Frissell and Shafer) 1. Lesions those are primarily radiopaque and circumscribed by sclerotic bone – treated enucleation and careful curettage. 2. Lesions that contain significant areas of radiolucency in addition to calcified odontomatous masses should be biopsied in several areas.  Histologic assessment determines the presence / absence of a capsule and the quantity and distribution of Ameloblastic elements.  If capsule present – lesion excised by enucleation and curettage.  If capsule not present – lesion excised by enucleation and careful curettage / at most resection without continuity defect.
  100. 100.  Histologic analysis of the specimen determines whether a further surgical procedure is indicated. Rarely resection with continuity defect is justified. Management depends on clinical features, radiological features and anatomic involvement. Prognosis- Recurrence rare. Due to growth of residual lesion. X. ODONTOMA Introduction- Most common abnormalities of the jaws. Believed to be a hamartomas. Odontoma is the end product of the anomalous completion / incompletion of tooth formation by odontogenic epithelium and odontogenic ectomesenchyme. WHO classifies odontoma under the category of tumours containing odontogenic epithelium with odontogenic ectomesenchyme, with / without dental hard tissue formation. History – 1866 – Broca first coined the term odontome. Thoma and Goldman narrowed the term odontoma to include tumours that were composed of well-differentiated tooth structure. Definition – Broca’s – tumour formed by an overgrowth of complete dental tissue.
  101. 101. Shafer and Gorlin – tumour that has developed and differentiated enough to produce enamel and dentin. Types –  Complex odontoma – a malformation in which all of the dental tissues are represented, and individual tissues mainly are well formed but occur in a disorderly pattern.  Compound odontoma – a malformation in which all of the dental tissues are represented in a more orderly pattern than in the complex odontoma so that the lesion consists of many tooth – like structures. Pathogenesis- Complex odontoma is formed from other mixed odontogenic tumours. AF / AFD. I step. AFO. II step. Complex odontoma. final step. Compound odontoma is a malformation, which is more differentiated, and its pathogenesis more closely is related to the creation of supernumerary teeth, especially mesiodens. This hypothesis is supported strongly by the preponderance of compound odontomas in the anterior maxilla. Origin- Unknown. Several theories have been proposed.